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The effect of the manipulation of blood lactate on the integrated EMG of the vastus lateralis muscle… Seburn, Kevin L. 1988

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THE EFFECT OF THE MANIPULATION OF BLOOD LACTATE ON THE INTEGRATED EMG OF THE. VASTUS LATERALIS MUSCLE.. DURING INCREMENTAL EXERCISE By KEVIN L. SEBURN B.P.E., The University of B r i t i s h Columbia, 1982 A THESIS SUBMITTED IN PARTIAL FULFILLMENT OF REQUIREMENTS FOR THE DEGREE OF MASTER OF PHYSICAL EDUCATION i n THE FACULTY OF GRADUATE STUDIES (School of Physical Education) We accept t h i s thesis as conforming to the required standard THE UNIVERSITY OF BRITISH COLUMBIA OCTOBER, 1988 ©Ke v i n L. Sebum, 1988 In presenting this thesis in partial fulfilment of the requirements for an advanced degree at the University of British Columbia, 1 agree that the Library shall make it freely available for reference and study. I further agree that permission for extensive copying of this thesis for scholarly purposes may be granted by the head of my department or by his or her representatives. It is understood that copying or publication of this thesis for financial gain shall not be allowed without my written permission. Department The University of British Columbia Vancouver, Canada DE-6 (2/88) ABSTRACT This study was designed to t e s t the hypothesis that the electromyographic signal recorded from a working muscle r e f l e c t s changes i n blood lactate concentrations. A group of trained c y c l i s t s performed two incremental exercise tests on a cycle ergometer. The Control T r i a l was a incremental t e s t with power increments of 23.5 watts per minute. Cadence was monitored and maintained at 90+/-1 revolutions per minute. The Experimental T r i a l consisted of a high i n t e n s i t y arm exercise protocol designed to elevate blood l a c t a t e above 8 mmol/1. The arm protocol was followed by f i v e minutes of rest and the incremental exercise protocol used i n the Control T r i a l . Expired gases were sampled every f i f t e e n seconds and calculat e d values for oxygen uptake, v e n t i l a t i o n , excess C0 2, and R.Q. were averaged to give a mean value for each minute i n both t r i a l s . Heart rate was monitored and recorded every minute f o r both t r i a l s . Electromyographic data were sampled from the vastus l a t e r a l i s of the r i g h t leg for the f i n a l eight seconds of each workload i n both t r i a l s . The data were integrated for each pedal cycle and averaged to give a mean integrated value for each cycle (CIEMG) for each workload. During both t r i a l s blood samples were drawn from the cephalic vein of the l e f t arm during the l a s t ten seconds of each workload. The anaerobic threshold (Tlac) was determined i i using the log-log transformation as outlined by Beaver et a l . , (1985). Control T r i a l lactate concentration showed a marked i n f l e c t i o n point a f t e r an i n i t i a l slow increase. The mean maximal l a c t a t e concentration was 18.21 +/- 5.54 i n the Control T r i a l s . This i n f l e c t i o n point occurred at a mean lact a t e concentration of 5.58 +/- 1.05 mmol/1. The mean oxygen uptake at the i n f l e c t i o n point was 2.28 +/- 0.37 1/min which represented a mean of 72.6 +/- 7.20 % of maximum. Experimental T r i a l mean plasma l a c t a t e at the beginning of incremental exercise was 26.61 +/- 8.86 mmol/1. The plasma la c t a t e concentration decreased s t e a d i l y for the i n i t i a l loads to a mean low concentration of 10.78 +/- 5.78 mmol/1 at Tlac and then increased to a mean of 19.08 +/- 6.66 mmol/1 at t e s t completion. Plasma lactate concentration was greater i n the Experimental T r i a l at a l l workloads though the values tended to converge once Tlac was surpassed. No v i s u a l l y i d e n t i f i a b l e i n f l e c t i o n point i n the p l o t of CIEMG vs Power could be determined i n any of the pl o t s . An analysis of the slope of the CIEMG vs. Power rel a t i o n s h i p was therefore performed. An analysis of variance demonstrated no s i g n i f i c a n t difference i n the slope of the rel a t i o n s h i p within or between t r i a l s i n three d i f f e r e n t comparisons. The slope of the l i n e was not s t a t i s t i c a l l y d i f f e r e n t when compared over: (a) the entire sample (b) pre Tlac and (c) post Tlac. Correlations performed between plasma lactate i i i concentrations and CIEMG were s i g n i f i c a n t i n f i v e of six subjects during the Control T r i a l (r = 0.57 to 0.97). During the Experimental T r i a l only three of the s i x subjects showed s i g n i f i c a n t c o r r e l a t i o n s and they were i n the opposite d i r e c t i o n (r = -0.62 to -0.96). Correlations between power output and CIEMG were for a l l subjects i n both t r i a l s (r = 0.92 to 0.99 Control, r = 0.91 to 0.99 Experimental). The increase seen i n CIEMG with increased power output r e f l e c t s poorly the changes in blood l a c t a t e concentrations under the conditions of t h i s investigation. Plasma lactate showed a dramatic increase in the Control T r i a l and a steady decrease from an i n i t i a l high concentration followed by a marked increase i n the f i n a l workloads of the Experimental T r i a l . In contrast the CIEMG increased i n a near l i n e a r fashion f o r a l l subjects i n both t r i a l s . The changes i n CIEMG showed highly s i g n i f i c a n t correlations with changes i n VOz or power output i n both t r i a l s for a l l subjects. These r e s u l t s indicate that changes i n the surface electromyogram are highly related to changes i n power output. However the surface electromyogram changes are not driven by changes i n l a c t a t e concentration under the conditions of t h i s i n v e s t i g a t i o n and may not be a s e n s i t i v e enough indicator of these changes to be employed i n the determination of Tlac. iv The Dynamics of Lactate and pH During Incremental Exercise 2 0 Mechanisms of Lactate Accumulation 21 Blood Lactate as an Estimator of Muscle Lactate 2 3 Dynamics of Lactate During Recovery from Exercise 24 pH Changes with Lactate Accumulation 2 6 Ef f e c t s of Decreased pH on the Contractile Apparatus 27 Neuromuscular Response to Incremental Exercise. . 3 0 The Integrated EMG as an Indicator of Muscle Tension 3 0 Relationship Between Isometric Tension and EMG 31 Relationship Between Dynamic Contractions and EMG ' 34 The Integrated EMG as a Non-Invasive Indicator of the Lactate Threshold •••• 3 6 Proposed Rationale for the use of IEMG as an Indicator of the Anaerobic Threshold 38 Possible E f f e c t s of Cadence on the Electromyographic Signal 41 Timing and Duration of E l e c t r i c a l A c t i v i t y as a Possible Confounding Factor 4 3 3. PROCEDURES 44 Research design 4 4 Subjects 44 Control Condition Protocol 45 Experimental Condition Protocol 45 P r e t r i a l Muscle Warming 46 v i Data C o l l e c t i o n 46 Procedures for Lactate Sampling 4 6 Procedures for Lactate Determinations 47 Procedures for EMG Recording 47 Data Analysis 48 Integration of EMG Data 48 Timing and Duration of E l e c t r i c a l A c t i v i t y 48 Determination of Lactate Threshold 48 Determination of Rate of Change (Slope) of CIEMG vs. Power Output 49 4. RESULTS 51 Description of Subjects 51 Analysis of Cardio-Respiratory Data 51 Control T r i a l Cardiorespiratory Data 51 Experimental T r i a l Cardiorespiratory Data... 53 Analysis of Lactate Data 53 Control T r i a l Lactate Data 54 Experimental T r i a l Lactate Data 56 Anaerobic Threshold Determination Using Plasma Lactate 57 Analysis of Integrated EMG Data 58 Control T r i a l Integrated EMG Data 58 Experimental T r i a l Integrated EMG Data 60 Examination of the Relationship Between Lactate and CIEMG 61 5. DISCUSSION 65 Cardiorespiratory and Metabolic Data 65 v i i Response of EMG to Plasma Lactate 66 Plasma Lactate Changes i n the Control T r i a l 66 The E f f e c t of Lactate on the CIEMG i n the Control T r i a l 67 Plasma Lactate Changes i n the Experimental T r i a l 71 The E f f e c t of Lactate on the CIEMG During the Experimental T r i a l 73 Explanation of C o n f l i c t i n g Results 75 6. Summary, Findings, Conclusions and Recommendations 84 Summary 84 Findings 85 Conclusions 86 Recommendations 87 APPENDIX A - COMPLETE CARDIORESPIRATORY DATA 89 APPENDIX B - PLASMA LACTATE DATA 94 APPENDIX C - ELECTROMYOGRAPHIC DATA 95 APPENDIX D - INDIVIDUAL SUBJECT PLOTS OF CIEMG AND PLASMA LACTATE FOR BOTH TRIALS 96 APPENDIX E - SELECTED DATA SUMMARY TABLES 102 REFERENCES 104 v i i i LIST OF TABLES 1. Analysis of Variance of Selected Cardiorespiratory Measures 54 2. Slope of IEMG vs V02 Plot for the Total Exercise Period and Before and After the Lactate Threshold.. 60 3. Analysis of Variance of Slopes of I EMG vs V0 2 Plots 61 4. Correlations C o e f f i c i e n t s for CIEMG and Power Output and CIEMG and Plasma Lactate 64 ix LIST OF FIGURES 1. Plots of Mean Cardiorespiratory Data - Control and Experimental Conditions 52 2. Mean Plasma Lactate vs Oxygen Uptake - Control and Experimental Condition 55 3. Plot of CIEMG vs. Power Output - Control and Experimental T r i a l 59 4. Group Data - Mean CIEMG and Plasma Lactate vs. Power Output - Control and Experimental T r i a l s 63 x ACKNOWLEDGEMENTS I would l i k e to express my sincerest appreciation to several people who were instrumental i n my completing t h i s t h e s i s . To Dr. Don Mckenzie for his i n i t i a l support and enthusiasm i n my project without which I might never have attempted to bring i t to completion. Also, for Don's e s s e n t i a l p r a c t i c a l assistance i n s e t t i n g up my project and i n c o l l e c t i o n of my data. To Dr. Angelo Belcastro for his he l p f u l discussions, guidance and p r a c t i c a l assistance with my data analysis. To my colleague and friend Peggy McBride f o r her repeated assistance and constant support which made the d i f f i c u l t times less so. F i n a l l y , to Dr. David Sanderson for the countless hours of assistance and guidance. The dedication and high standards which Dave demands serve not only to motivate but heighten a sense of accomplishment upon completion. I am proud to have been part of the UBC Biomechanics Laboratory and hope my contribution has come near to what I have derived from the experience. x i Chapter 1 INTRODUCTION During incremental exercise on a cycle ergometer changes occur i n the human metabolic environment which eventually contribute to a decreased a b i l i t y to perform muscular work. At a power output representing approximately 60% of maximal oxygen uptake the human organism cannot supply energy through aerobic g l y c o l y s i s at an adequate rate to sustain performance (Davis, 1985). At t h i s point the body begins to r e l y more heavily on anaerobic g l y c o l y s i s . This change i n the predominant energy supply system i s indicated by changes i n the metabolic environment. The point at which the t r a n s i t i o n takes place i s commonly termed the anaerobic threshold. The metabolic c h a r a c t e r i s t i c s of the blood and muscle during incremental exercise r e f l e c t increasing muscular power output. As the power output of a muscle increases the rate at which energy must be supplied increases. The rate of energy production determines the predominant energy system and therefore the end product of g l y c o l y s i s . At submaximal power outputs the aerobic energy system favors the production of pyruvate which i s completely metabolized to carbon dioxide and water v i a the TCA cycle and the electron transport system. However as power output increases toward maximal l e v e l s the production of lactate i s favored over pyruvate oxidation (Wasserman, 1986). The amount of lactate produced i n the muscle i s related to the intensity, mode and duration of work, 1 the t r a i n i n g status of the i n d i v i d u a l , as well as the glycogen content and type of muscle f i b r e involved (Farrel et a l . , 1979, Graham, 1978). The unbalancing of muscular l a c t a t e production and u t i l i z a t i o n r e s u l t s i n a i n f l e c t i o n point i n a p l o t of blood l a c t a t e vs. oxygen uptake. This i n f l e c t i o n point i n blood l a c t a t e i s used as an invasive estimation of the anaerobic threshold or l a c t a t e threshold (Tlac). During the performance of muscular work the human body adjusts the functional coupling of cardiovascular and respiratory a c t i v i t y to supply the c e l l s with an adequate supply of oxygen. The changes i n the demand for oxygen as the body adjusts to the increased metabolic need r e f l e c t accurately the i n t e n s i t y of the work being performed. This i s evidenced by the l i n e a r r e l a t i o n s h i p between oxygen uptake and power output. As the power output increases the a b i l i t y of the c i r c u l a t i o n to supply a l l c e l l s with oxygen may be inadequate. This brings about a change i n the redox state of the working muscle such that the production of l a c t a t e i s favored over pyruvate entry into the mitochondrion (Wasserman, 1986, and Wasserman et a l . , 1986) increasing the concentration of muscle l a c t a t e . P r i o r to the production of l a c t a t e due to an a l t e r e d redox state the increased energy need i s met by a rapid acceleration of g l y c o l y s i s whose end product, pyruvate, i s produced at a rate greater than the rate at which i t can be oxidized completely (Wasserman et a l . , 1985). This r e s u l t s i n an increased production of l a c t a t e . These changes indicate the 2 body's increased reliance on muscle glycogen and anaerobic g l y c o l y s i s . This increased reliance r e s u l t s i n an unbalancing of muscular l a c t a t e u t i l i z a t i o n and production. At physiological pH lactate i s 99% dissociated and must be buffered. Some portion of t h i s buffering i s performed by the bicarbonate system (Wasserman et a l . 1967). This r e s u l t s i n increased hydrogen ion concentration i n the muscle which decreases muscle pH. The increase i n i n t r a c e l l u l a r l a c t a t e concentrations i s l i n e a r l y related to the decrease i n i n t r a c e l l u l a r muscle pH (Sahlin, 1978) and has been highly correlated with changes i n v e n t i l a t o r y parameters due to the increased C02 production. The following set of equations summarizes the process. HLA < Lactate Dehydrogenase > H+ + LA 1 H+ + HC03"< Carbonic Anhydrase > H 2 C 0 3 2 H 2C0 3 < > H20 + C02 3 Because of the relat i o n s h i p between v e n t i l a t i o n , changes i n l a c t a t e concentration, and the subsequent change i n pH numerous studies have demonstrated the usefulness of these v e n t i l a t o r y changes i n estimating the anaerobic threshold. The anaerobic threshold (Tvent) i s estimated to occur at the percentage of oxygen uptake where a non-linear increase i n VE and excess C0 2 occurs accompanied by an increased V E/V0 2 r a t i o without a concomitant increase i n V E/VC0 2 r a t i o (Davis, 1985). While some studies have have demonstrated a high c o r r e l a t i o n between Tlac and Tvent during incremental exercise t e s t s 3 others have introduced conditions where a d i s s o c i a t i o n of the two i n f l e c t i o n points has been evident (Farrel and Ivy, 1987). Despite the uncertainty of t h i s r e l a t i o n s h i p these two methods, one invasive and one non-invasive, have proven useful as estimators of the t r a n s i t i o n point i n energy production from predominantly oxidative phosphorylation to anaerobic g l y c o l y s i s r e s u l t i n g i n l a c t a t e production. Several studies (Moritani, 1980, Nagata et a l . , 1981, Miyashita et a l . , 1981, Moritani et a l . , 1984, V i i t a s a l o et a l . , 1985) have demonstrated a r e l a t i o n s h i p between muscle a c t i v a t i o n as determined by surface electromyogram and the anaerobic threshold. These studies have shown that with incremental increases i n power output there i s a point where a sudden increase i n Integrated EMG (IEMG) occurs. The sudden increase seems to exceed that expected due to increased power output. This i n f l e c t i o n point occurs at a percentage of oxygen uptake which correlates highly with the percentage of maximal oxygen uptake at which the i n f l e c t i o n point i n v e n t i l a t o r y parameters or blood l a c t a t e concentration occurs (Moritani, 1980, Nagata, 1981). These studies have concluded that since IEMG seems to respond to changes i n l a c t a t e the Integrated EMG could serve as a non-invasive i n d i c a t o r of Tlac. The electromyogram r e f l e c t s the f i r i n g rate, amplitude, recruitment pattern and f i b r e type of motor units of the muscle being recorded (Basmajian, J.V., 1978, Komi et a l . , 4 1970, Moritani, 1986). The t h e o r e t i c a l basis of increased e l e c t r i c a l a c t i v i t y with increased force development stems from studies by Milner-Brown et a l . (1972) and Milner-Brown et a l . , (1976). These studies demonstrated that increased force was achieved by i n i t i a l l y increasing the number of f i b r e s recruited and l a t e r increasing the f i r i n g rate of the f i b r e s involved. The orderly recruitment of f i b r e s from small to large and the greater amplitude and maximum f i r i n g frequency of the larger f i b r e s produce increasing recorded e l e c t r i c a l a c t i v i t y . Any changes i n the metabolic environment which a f f e c t the recruitment pattern or f i r i n g frequency within a c e r t a i n muscle or a l t e r the a c t i v a t i o n pattern of a muscle group w i l l be r e f l e c t e d i n changes i n the recorded surface electromyogram and the integrated EMG. There have been numerous studies which characterized the r e l a t i o n s h i p between the electromyogram and muscle tension or force i n both dynamic and isometric contractions of unfatigued muscle. Some studies have indicated a l i n e a r r e l a t i o n s h i p between isometric contraction force and IEMG (Lippold, 1952, Inman et a l . , 1952, Close et a l . , 1960, Dejong et a l . , 1967, Moritani et a l . , 1986) while others have demonstrated non-l i n e a r relationships (Zuniga et a l . , 1969, Komi et a l . , 1970, Kuroda et a l . , 1970, Heckathorne et a l . , 1981). During dynamic c y c l i n g exercise a l i n e a r r e l a t i o n s h i p was demonstrated between EMG a c t i v i t y (Root Mean Square) of the l a t e r a l quadriceps and load (Bigland-Ritchie and Woods, 1974). 5 This r e l a t i o n s h i p was l a t e r extended by Petrofsky et a l . , (1979) who "showed that i n the absence of fatigue" the l i n e a r r e l a t i o n s h i p existed for loads up to an independently determined maximum. The exact nature of the re l a t i o n s h i p i s d i f f i c u l t to characterize. Measures of force or muscle tension represent summations of a c t i v i t y within a muscle or group of muscles that may not be r e f l e c t e d by the surface electromyogram which provides a s t a t i s t i c a l sampling of the e l e c t r i c a l a c t i v i t y . The majority of evidence suggests that a l i n e a r r e l a t i o n s h i p e x i s t s between the recorded electromyogram signal and measured force. However evidence i n d i c a t i n g some other type of re l a t i o n s h i p suggests that caution must be used i n a t t r i b u t i n g changes i n the electromyographic signal to variables other than increased force or muscle tension. The presence of fatigue i n a muscle a l t e r s the re l a t i o n s h i p between the IEMG and force. The r e l a t i o n s h i p has been shown to change with sustained submaximal isometric contractions, i n a muscle that was previously fatigued and during sustained maximal contractions (Komi, 1984). These changes have been related i n some instances to changes i n the metabolic environment. The accumulation of lactate i n the muscle decreases the pH i n the muscle and subsequently i n the blood (Hermansen et a l . , 1977, Sahlin, 1978). The decrease i n muscular pH has been suggested to be the cause of fatigue for high i n t e n s i t y 6 exercise. Evidence has shown that the decrease i n muscle pH a f f e c t s the e x c i t a t i o n contraction coupling of muscle contraction. Several steps i n the c o n t r a c t i l e process are affected by a decrement i n muscular pH. They include: (a) increased Ca + + requirement (Donaldson, 1978); (b) decrease i n myosin ATPase a c t i v i t y (Schadler c i t e d i n Sahlin 1978) ; (c) an increase i n the binding constant of the sarcoplasmic reticulum for Ca + + (Nakamura and Schwartz, 1972). The decreased a b i l i t y of the muscle to produce force correlates highly with increasing l e v e l s of lactate and has been hypothesized to be the r e s u l t of a combination of these mechanisms. In dynamic incremental c y c l i n g exercise to determine maximal oxygen uptake, an i n f l e c t i o n point i n IEMG, apparently unrelated to changes i n workload, has been shown to occur. (Moritani, 1980, Nagata et a l . , 1981, Miyashita et a l . , 1981, Moritani et a l . , 1984, V i i t a s a l o et a l . , 1985). This i n f l e c t i o n point, caused by changes i n the e l e c t r i c a l c h a r a c t e r i s t i c s of the muscle, i s hypothesized to be the r e s u l t of the decreased pH caused by increased l a c t a t e conc-entration (Tesch et a l . (1983) i n Komi 1984). This explanation i s l o g i c a l because both increased l a c t a t e concentrations and increased e l e c t r i c a l output can be shown to be related to increased percentages and recruitment of fa s t g l y c o l y t i c f i b r e s (Tesch et a l . , 1978, Tesch et a l . , 1983). The increase i n IEMG with fatigue r e s u l t s from the f a i l u r e of some working f i b r e s r e s u l t i n g i n increased 7 recruitment of fa s t twitch g l y c o l y t i c f i b r e s as well as increased f i r i n g rate of some already r e c r u i t e d f i b r e s (Hakkinen et a l . 1986). This change i n muscle f i b r e r e c r u i t -ment and f i r i n g frequency would r e s u l t i n altered e l e c t r i c a l c h a r a c t e r i s t i c s i n the muscle as a r e s u l t of the greater amplitude and f i r i n g frequency of the fa s t twitch f i b r e s . This, i n combination with the increasing work load could r e s u l t i n an accelerated, non-linear increase, or i n f l e c t i o n point i n the IEMG of the working muscle. However several studies (Edwards et a l . , 1972, Karlsson et a l . , 1975, Broman, 1977, Petrofsky, 1980, Komi 1984, Boubrit, 1983) have pointed out that the time course of recovery from exercise for l a c t a t e and pH requires one to several hours depending upon conditions of recovery while the recovery of maximum twitch tension and amplitude as well as mean power frequency of the EMG signal have shown an almost immediate recovery to pre-exercise or r e s t i n g l e v e l s . M i l l s and Edwards (1984) examined changes i n the electromyogram of myophosphorylase d e f i c i e n t patients who are incapable of producing l a c t a t e . They demonstrated changes s i m i l a r i n d i r e c t i o n to normal controls but greater i n magnitude. This indicated that under the conditions c i t e d above the e l e c t r i c a l c h a r a c t e r i s t i c s of a muscle are independent of the metabolic environment and using EMG as an indicator of underlying p h y s i o l o g i c a l changes may not be v a l i d . The i n i t i a l study using incremental cycle ergometer 8 exercise u t i l i z e d constant power output ergometers and allowed cadence to range from 50 to 80 revolutions per minute (Moritani, 1984). Because power output i s the product of the applied force and cadence, a constant power output i s possible with any combination of the two variables. I t i s quite l i k e l y that these d i f f e r e n t combinations cause the muscle to respond d i f f e r e n t l y depending on whether the increase i n power output i s achieved through increasing force or by increasing cadence. There i s evidence to suggest that changes i n cadence at constant power output a l t e r s metabolic response (Coast and Welch 1985) . A change i n the metabolic response of the working muscle could indicate an al t e r e d a c t i v a t i o n pattern. Such a l t e r a t i o n s could have an e f f e c t on the electromyographic signal recorded from the working muscle. Further i t i s possible that some predictable changes i n cadence occur during incremental work which could r e s u l t i n the observed changes i n the IEMG. I t i s important that cadence be monitored and addressed as a possible contributor to observed changes i n the IEMG with incremental exercise. Statement of the Problem Previous studies have demonstrated a r e l a t i o n s h i p between both Tlac and an Integrated EMG i n f l e c t i o n point. The conclusion that IEMG could be used as an indicator of the observed dramatic increase i n blood lactate concentrations during incremental exercise suggests a high degree of s e n s i t i v i t y . I f t h i s method of lactate threshold 9 determination i s to be of p r a c t i c a l use the implied s e n s i t i v i t y i s a necessity. Such a high degree of s e n s i t i v i t y has not been demonstrated. I f the proposed r e l a t i o n s h i p does ex i s t between blood lactat e and IEMG i t should respond predictably to changes i n blood lactat e accumulation under varied conditions. Hypotheses 1. I t was hypothesized that a strong p o s i t i v e c o r r e l a t i o n would be seen between the percentage of maximal oxygen uptake at which an i n f l e c t i o n point i n blood l a c t a t e occurred and the percentage of maximal oxygen uptake at which an i n f l e c t i o n point i n CIEMG occured i n the Control Condition. 2. In the Experimental Condition i t was hypothesized that the i n f l e c t i o n point would be s h i f t e d to the l e f t i n the la c t a t e vs. power output p l o t . Further the CIEMG vs. power output p l o t would show a s i m i l a r s h i f t i n the i n f l e c t i o n point. Significance of the Study The s i g n i f i c a n c e of t h i s study i s that i t w i l l provide data which c l a r i f y the rel a t i o n s h i p between changing amounts of l a c t a t e and the e l e c t r i c a l c h a r a c t e r i s t i c s of muscle. The integration of data concerning the metabolic state of the muscle and i t s e f f e c t on the e l e c t r i c a l functioning or v i c e versa i s important because of the m u l t i f a c t o r i a l nature of 10 muscle fatigue. I t should provide a s t a r t i n g point for further studies which could focus on monitoring, manipulation and description of some of the other factors which are known to e f f e c t both muscle function and IEMG. In addition, i f a v a l i d r e l a t i o n s h i p i s supported between la c t a t e and IEMG during incremental exercise some i n i t i a l p r a c t i c a l applications may be made. These applications would require further study into the application of IEMG i n the monitoring of t r a i n i n g i n t e n s i t y and i t s effectiveness as compared to other more conventional methods. D e f i n i t i o n of Terms Incremental Exercise Test. A t e s t performed on a cycle ergometer with four minutes of unloaded c y c l i n g and increasing i n steps of 23.5 watts per minute u n t i l the subject could no longer maintain the prescribed cadence of 90 revolutions per minute. Anaerobic Threshold. The point i n incremental exercise to maximum where energy i s increasingly supplied by anaerobic g l y c o l y s i s . This term w i l l be used interchangeably with Tlac. Tlac. The int e r s e c t i o n point i n a log-log p l o t of Lactate concentration vs. Oxygen uptake of two regression l i n e s . One from t e s t commencement to a v i s u a l l y determined d i v i d i n g point and one from the d i v i d i n g point to maximum (Beaver et a l . , 1985). Tlac w i l l be determined for each subject from t h e i r Control T r i a l data. 11 Tvent. The percentage of oxygen uptake where a non-l i n e a r increase i n VE and excess C0 2 occurs accompanied by an increased V E/V0 2 r a t i o without a concomitant increase i n V E/C0 2 r a t i o (Davis, 1985). Integrated Electromyogram (IEMG). The i n t e g r a l of the f u l l wave r e c t i f i e d EMG s i g n a l . Cycle Integrated Electromyogram (CIEMG). The integrated value f o r each burst of a c t i v i t y (from TDC to TDC) at each work load i s calculated. Each cycle i s averaged to give a mean integrated per cycle value (CIEMG) for each workload. Top Dead Centre (TDC). The p o s i t i o n of the pedal at the top of the cycle, when the crank i s perpendicular to the f l o o r . A TTL pulse of +/- 5 v o l t s indicates the p o s i t i o n of r the crank. Delimitations Measurements of pC0 2, p0 2, pH, and HCO"3 w i l l not be performed on a r t e r i a l blood samples which then could be combined with a r t e r i a l lactates for a more se n s i t i v e and accurate determination of lactat e threshold (Nagata et a l . 1981). The determination of the lactat e threshold from venous lac t a t e measurements i n the arm i s a v a l i d r e f l e c t i o n of the changes i n o v e r a l l blood lactat e (Simon et a l . , 1986). Venous blood l a c t a t e concentrations w i l l be taken to r e f l e c t the d i r e c t i o n of change i n muscle lactate concentrations only. 12 Chapter 2 REVIEW OF THE LITERATURE This review i s divided into four major subsections: (a) p h y s i o l o g i c a l responses to incremental exercise; (b) the existence and s i g n i f i c a n c e of the anaerobic threshold; (c) the dynamics and interactions of l a c t a t e and pH during incremental exercise; (d) the neuromuscular response to exercise. Physiological Responses to Incremental Exercise At the onset of exercise the human body begins a series of adaptations which are aimed at maintaining c e l l u l a r homeostasis. During incremental exercise from low i n t e n s i t y to maximal e f f o r t a t y p i c a l pattern of responses i s evident i n a number of d i f f e r e n t measures. Skinner and McClellan (1979) divided these responses into three d i s t i n c t phases moving from almost purely aerobic metabolism through a t r a n s i t i o n phase to almost purely anaerobic metabolism. During the f i r s t phase the demand for oxygen by the working tissues increases r e s u l t i n g i n greater extraction of oxygen from the blood causing a s l i g h t decrease i n the f r a c t i o n of expired oxygen ( F E 0 2 % ) . Concomitantly the amount of carbon dioxide produced increases causing a s l i g h t increase i n the f r a c t i o n of expired C02 (F EC0 2%) . Linear increases occur i n V e n t i l a t i o n (V£) , Heart Rate, and Oxygen uptake (V02) . That t h i s stage i s aerobic i s indicated by only small 13 increases i n the respiratory quotient (R or VC0 2/V0 2) which remains between 0.7 and 0.8. As well blood l a c t a t e [La] which i s an indicator of the degree of anaerobiosis, r i s e s only s l i g h t l y above re s t values. The second stage or the t r a n s i t i o n phase i s characterized by continuing l i n e a r increases i n Heart Rate and V0 2 and an i n i t i a l r i s e i n blood lactate, usually to l e v e l s approximately twice that of res t i n g values. This increase i n l a c t a t e causes an increased production of H* ions thereby decreasing pH (Hermansen and Osnes, 1972, Sahlin, 1978, Metzger and F i t t s , 1987). These ions are buffered v i a several mechanisms. These mechanisms include metabolic buffering processes such as the u t i l i z a t i o n of creatine phosphate, the production of ionosine monophosphate r e s u l t i n g from the combination of hydrogen ions with ATP and the oxidation of amino acids. These metabolic processes account for approximately 40% of the ava i l a b l e buffering capacity. The remaining buffering capacity i s v i a physico-chemical processes which account for approximately 60% of the t o t a l buffering capacity (Parkhouse and McKenzie, 1984) . These include the absorption of hydrogen ions by plasma proteins and inorganic phosphate. Sahlin (1978) reported that approximately 15 - 18 % of the hydrogen ions produced are buffered v i a the bicarbonate system according to the following s i m p l i f i e d equations. HLa + NaHC03 < > NaLa + H 2C0 3 4 H 2C0 3 < > H20 + C02 5 14 The increased production of C02 as a r e s u l t of the d i s s o c i a t i o n of the carbonic acid i n equation f i v e r e s u l t s i n a steady increase i n the F £C0 2. The respiratory centers respond to the decreased pH and the increased production of C02 by increasing V£ r e s u l t i n g i n a marked increase i n VC0 2. A d i s t i n c t increase i n the V E/V0 2 r a t i o i s seen due to an increase i n VE and VC02 greater than the increase i n V0 2. Because of the disproportionate increase i n VE i n comparison with V0 2 there i s a decreased extraction of oxygen from the inspired a i r r e s u l t i n g i n an increased F E0 2%. This combination of responses, non-linear increases V£ and VC02 with a r i s e i n F E0 2 without concomitant increases i n VC02 , along with increased lactat e concentration was proposed to represent the anaerobic threshold (Wasserman et a l . , 1973). These changes occur at power outputs which correspond to oxygen uptakes of approximately 40-60% of maximum. The f i n a l phase outlined by Skinner and McClellan (1978) occurs as the power output approaches approximately 65-90%. The l i n e a r increases i n Heart Rate and V0 2 continue u n t i l near maximal l e v e l s where a l e v e l i n g o f f i s t y p i c a l l y seen. The increase i n VE continues but i s not adequate to compensate for the increased l e v e l s of C02 thus a decrease i n VC02 occurs and the F E0 2 continues to r i s e . A rapid increase i n La i s evident and continues u n t i l maximal power output i s reached. These changes, decreased F £C0 2, a sharp increase i n La and hyperventilation have been i d e n t i f i e d by MacDougall, (1978) 15 and Green et a l . (1979) as representing the anaerobic threshold. These adaptations to incremental exercise r e s u l t from the increased power output and r e f l e c t changes i n the r e l a t i v e contribution of aerobic and anaerobic energy systems to the energy supply of the working muscle. The Existence and Significance of the Anaerobic Threshold Precise physiological mechanisms responsible f o r a threshold have not yet been determined. Further while the anaerobic threshold concept i s of p r a c t i c a l importance using i t to in t e r p r e t underlying physiological interactions i s d i f f i c u l t . Despite controversy concerning the i n t e r p r e t a t i o n of the relevant data and the subsequent terminology associated with t h i s evidence (Davis, 1985, Brooks, 1985), there i s a general agreement on a functional d e f i n i t i o n . The anaerobic threshold can be defined as the point during incremental exercise above which the energy u t i l i z e d i s increasingly derived from anaerobic g l y c o l y s i s (Jones and Ehrsam, 1982, Helal et a l . , 1987). Anaerobic g l y c o l y s i s depends pr i m a r i l y on glycogen reserves as f u e l and generates metabolites which appear to i n d i r e c t l y contribute to the i n h i b i t i o n of energy production and thus i s s e l f - l i m i t e d i n i t s a b i l i t y to supply energy over long periods of time (Coyle and Coggan, 1984). The existence of the anaerobic threshold i s empirically supported by research which correlates anaerobic threshold determinations with predictions of a maximal maintainable rate of work. 16 Prediction of Performance Using Anaerobic Threshold  Determinations. Rhodes and Mckenzie, (1984) determined the anaerobic threshold using v e n t i l a t o r y excess C0 2. Performance times i n a marathon were then predicted using the running v e l o c i t y at the determined threshold. They demonstrated a high c o r r e l a t i o n (r = 0.94) between predicted and actual performance times suggesting that running v e l o c i t y at the anaerobic threshold represents optimal running pace or a pace which t h e o r e t i c a l l y would be d i f f i c u l t to exceed and maintain because doing so would cause greater reliance on anaerobic g l y c o l y s i s . Tanaka and Matsura (1984) performed a s i m i l a r study to examine the differences i n marathon performance pr e d i c t i v e a b i l i t y between the quantit a t i v e l y defined (ie 4mmol) onset of blood lactat e accumulation (OBLA) and the anaerobic threshold defined as the point of systematic increase of la c t a t e above a rest i n g base-line value. The running v e l o c i t y at the anaerobic threshold as determined by the l a t t e r method, showed a higher c o r r e l a t i o n with the predicted marathon race v e l o c i t y than did OBLA. F a r r e l et a l . (1979) investigated the relat i o n s h i p between the accumulation of plasma la c t a t e and distance running performance over various distances. They demonstrated that regardless of competitive l e v e l s the treadmill v e l o c i t y and VOz which corresponded with the systematic increase of plasma la c t a t e above a base-line correlated very highly (r = 0.91) with distance running performance. These investigations support 17 the existence of the anaerobic threshold as defined by Jones and Ehrsam (1982) and Helal et a l . (1987). They e s t a b l i s h the p r a c t i c a l s i g n i f i c a n c e of the threshold or a t r a n s i t i o n phase but do not provide evidence which c l e a r l y demonstrates the responsible mechanisms. Fibre Type and Substrate Depletion During Incremental  Exercise. The existence of the anaerobic threshold i s also empirically supported by research examining f i b r e type d i s t r i b u t i o n and substrate depletion. There are two primary types of muscle f i b r e s which comprise human s k e l e t a l muscle. Gollnick et a l . (1972) distinguished the f i b r e s on the basis of t h e i r myosin ATPase a c t i v i t y while others have i d e n t i f i e d the d i f f e r e n t types on the basis of oxidative enzyme concentrations or g l y c o l y t i c capacity (Essen et a l . , 1975). The types have been variously named but for the purposes of t h i s investigation the f i b r e s w i l l be referred to using the nomenclature Slow Oxidative (SO) and Fast G l y c o l y t i c (FG). This nomenclature i s useful i n that i t denotes both the c o n t r a c t i l e c h a r a c t e r i s t i c s (Fast, Slow) and the predominant type of energy supply system ( G l y c o l y t i c , Oxidative). An intermediate f i b r e , Fast Oxidative G l y c o l y t i c (FOG) has also been i d e n t i f i e d . The SO f i b r e s are enzymatically and s t r u c t u r a l l y designed to function primarily during low i n t e n s i t y aerobic work. These f i b r e s are r i c h i n mitochondrion and the enzymes necessary for oxidative metabolism. Muscle glycogen l e v e l s which are the primary 18 energy source for anaerobic g l y c o l y s i s are r e l a t i v e l y small i n these f i b r e s . FG f i b r e s function optimally at high l e v e l s of muscular work. They have fewer mitochondrion and enzyme p r o f i l e s which are best suited for energy production v i a anaerobic g l y c o l y s i s (Gollnick and Hermansen, 1973). The FOG f i b r e s have c h a r a c t e r i s t i c s of both the SO and FG f i b r e s and may a l t e r c h a r a c t e r i s t i c s somewhat depending upon the type of t r a i n i n g they have undergone. During incremental exercise recruitment of the d i f f e r e n t f i b r e s depends on the i n t e n s i t y of the work being performed with the SO f i b r e s being recruited f i r s t at low i n t e n s i t i e s and FG f i b r e s being re c r u i t e d l a t e r (Milner-Brown et a l . , 1973). Essen, (1978) demonstrated that during submaximal exercise the SO f i b r e s had a more pronounced depletion of glycogen than the FG f i b r e s while during sustained high i n t e n s i t y exercise glycogen depletion was more marked i n FG f i b r e s supporting the increasing r o l e of g l y c o l y t i c f i b r e s as power output increases. Tesch et a l . (1978) found a p o s i t i v e c o r r e l a t i o n between the percentage of FG f i b r e s and muscle lactate concentration. Ivy et a l . (1980) demonstrated high correlations between the percentage of SO f i b r e s and both maximal oxygen uptake and muscle respiratory capacity. Consequently Ivy et a l . (1980) noted a high c o r r e l a t i o n between both the r e l a t i v e and absolute l a c t a t e thresholds and the percentage of SO f i b r e s i n the vastus l a t e r a l i s muscle of humans. The higher the percentage of SO f i b r e s the higher the percentage of V0 2 at which the l a c t a t e 19 threshold occurred. I t i s suggested that t h i s i s due to the high g l y c o l y t i c capacity and greater lactat e production of FG f i b r e s which are recruited i n greater numbers as power output increases. The empirical evidence for the existence of a t r a n s i t i o n phase or anaerobic threshold i s substantial. These investigations also demonstrate a l i n k between the changing p r o f i l e of muscle f i b r e types being recruited for force production and the changing metabolic p r o f i l e during incremental exercise. The Dynamics and Interactions of Lactate and pH During  Incremental Exercise The production of lactat e i n the muscle has been shown to be highly related to metabolic rate (Donovan and Brooks, 1983, Brooks et a l . , 1984). As power output increases the recruitment of the FG f i b r e s increases (Milner-Brown et a l . , 1973). These f i b r e s have a high g l y c o l y t i c capacity and t h e i r recruitment r e s u l t s i n the production of pyruvate at a rate which exceeds the a b i l i t y of the pyruvate dehydrogenase complex to convert pyruvate to acetyl CoA and enter the mitochondrion. The excess pyruvate produced i n the muscle i s then converted into Lactate [La] r e s u l t i n g i n increased La concentration. I t has been suggested that the increased g l y c o l y t i c metabolism was due to a d e f i c i t i n oxygen supply which i n h i b i t e d energy production v i a oxidative metabolism ( H i l l et a l . , 1924). I t has become clea r through t r a c e r 20 k i n e t i c experiments that the production and u t i l i z a t i o n of la c t a t e i s a constant ongoing process which occurs both at rest and during exercise (Eldridge et a l . , 1974, Eldridge, 1975, Issekutz B. J r . et a l . , 1976, Issekutz B. J r . , 1984). The r e s u l t s of these investigations invalidate the theory that accelerated anaerobic metabolism and the subsequent increase i n muscle la c t a t e concentration i s due s o l e l y to an inadequate oxygen supply. Mechanisms for Lactate Accumulation. Wasserman (1986) and Wasserman et a l . (1986), proposed that there are two mechanisms responsible for the accumulation of l a c t a t e i n working muscle. (a) Glycolysis increases so r a p i d l y that pyruvate i s produced at a rate which i s too fas t f o r i t to be moved into the mitochondrion for complete oxidation. This r e s u l t s i n the accumulation of pyruvate i n the cytosol which causes the accelerated formation of la c t a t e . The formation of l a c t a t e allows maintenance of g l y c o l y t i c metabolism. (b) The mitochondrial shuttle which c a r r i e s the reduced NAD into the TCA cycle to transfer electrons and protons to coenzymes f o r eventual combination with oxygen i s no longer capable of maintaining the redox state. Wasserman et a l . (1986) point out that t h i s might occur i f the oxygen available to the cytochrome oxidase reached a value low enough to change the c e l l redox state to favor the conversion of pyruvate to l a c t a t e and accelerated g l y c o l y s i s . This model of mechanisms for l a c t a t e accumulation i s supported by research (Wasserman 21 et a l . , 1985) showing that a t r a n s i t i o n i n the mechanism for the increase i n l a c t a t e concentration seems to occur during incremental exercise. These authors examined the lactate/pyruvate r a t i o s and showed that at work i n t e n s i t i e s up to the Tlac the increase i n l a c t a t e was p a r a l l e l e d by increases i n i t s precursor pyruvate. This i s a necessity for the mass action conversion of pyruvate to l a c t a t e , the basis of the mechanism proposed i n one above. However beyond some c r i t i c a l oxygen uptake represented by Tlac the increase i n l a c t a t e f a r exceeded the increase i n pyruvate concentration. This supports the second mechanism described above since the increase i n l a c t a t e would have to come from a change i n redox state where the production of l a c t a t e from pyruvate would be favored. The accumulation of lac t a t e i s due to a greater increase i n production of lactate v i a the mechanisms described above, than the increase i n the a b i l i t y to remove l a c t a t e . The removal of lac t a t e during exercise i s however considerable. The r e s u l t s of tracer studies by Issekutz (1984) and Eldridge et a l . (1974) indicate that l a c t a t e i s an important substrate during exercise and that the major avenue fo r l a c t a t e removal i s oxidation. Brooks (1986) demonstrated that approximately 50% of the lactate produced at r e s t was oxidized and that during exercise at 50% of maximum, oxidation accounted f o r nearly 90% of the l a c t a t e removal. The same inve s t i g a t i o n indicated that both the r e l a t i v e and absolute 22 oxidation rates of lactate increased with increasing power output. Despite the use of lactat e as a substrate during exercise the production of lactat e during exercise eventually exceeds the a b i l i t y of the various metabolic pathways to remove i t . This r e s u l t s i n the accumulation of l a c t a t e both i n the muscle and the blood that i s seen during incremental exercise. Blood Lactate as an Estimator of Muscle Lactate. The appearance of lactat e i n the blood i s subsequent to i t s production i n the muscle. The concentration of l a c t a t e i n the blood i s dependent upon the balance of production, u t i l i z a t i o n and removal i n muscle. Diamant et a l . (1968) provided evidence which suggested a concentration gradient for lactate from muscle to blood. Karlsson (1971) and J o r f e l d t et a l . (1978) found s i g n i f i c a n t l y higher l a c t a t e concentrations i n human muscle than i n venous blood during work and reported that several minutes were required f o r blood lactate to e q u i l i b r a t e with muscle l a c t a t e . Similar r e s u l t s were reported by Hirche et a l . (1971) fo r i s o l a t e d dog gastrocnemius with a concentration gradient e x i s t i n g at a l l times between muscle la c t a t e and blood l a c t a t e during exercise. The gradient favored movement of l a c t a t e into venous blood. These authors also pointed out that the gradient was increased markedly at power outputs above 70% of maximum. They concluded that the production of l a c t a t e i n working muscle was greater than i t s release into the blood. 23 Graham (1978) reported that blood lactat e concentrations depend upon blood flow, sampling time and muscle f i b r e type and d i d not always represent accurately absolute muscle lac t a t e values. The evidence above suggests that estimation of absolute l a c t a t e concentrations of muscle from blood l a c t a t e concentrations i s not v a l i d . Karlsson (1971) measured blood la c t a t e values immediately following maximal exercise which were approximately h a l f the simultaneously measured muscle la c t a t e values. However the evidence also indicates that during incremental exercise beginning from rest the d i r e c t i o n of change i s s i m i l a r . That i s , during incremental exercise increases i n blood lactat e r e f l e c t increases i n muscle la c t a t e of the working muscle. Dynamics of Lactate During Recovery from Exercise. The increased l a c t a t e concentration which accompanies incremental exercise disturbs the homeostasis of the muscle c e l l eventually reaching a point where i t can no longer function. The return of lactat e concentrations to pre-exercise l e v e l s has been shown to depend on both the duration, i n t e n s i t y and mode of exercise used to produce the increased concentration, and on the i n t e n s i t y of a c t i v i t y following the exercise (Brooks and Fahey, 1984). Brooks (1986) estimated that up to 70% of the lactat e produced i n exhaustive exercise i n rats was removed v i a oxidation during recovery. Approximately 20% of the lactat e was converted into muscle and l i v e r glycogen, 24 5-10% were converted into protein constituents, less than two percent was traced to glucose and l a c t a t e and the remaining ten percent was not s p e c i f i c a l l y located. These estimates are supported by tracer studies (Issekutz, 1984, and Eldridge et a l . , 1974) which also indicate that the major avenue fo r l a c t a t e removal was oxidation. The r e s u l t s from these studies indicate the importance of lac t a t e as a substrate during exercise. The l i n e a r r e l a t i o n s h i p demonstrated between la c t a t e extraction and a r t e r i a l l a c t a t e concentration i n muscle during both rest and exercise (Brooks, 1986) c l e a r l y indicates that an elevated l a c t a t e concentration r e s u l t s i n increased uptake by working muscle. Belcastro and Bonen (1975) demonstrated that elevated blood l a c t a t e l e v e l s produced by exercise above Tlac can be reduced by exercise at an i n t e n s i t y below Tlac. Such evidence highlights the balance between l a c t a t e production, e f f l u x , and u t i l i z a t i o n which ultimately determines measured concentrations i n the blood or muscle. Submaximal l e v e l s of exercise w i l l lower l a c t a t e to pre-exercise concentrations more rapid l y than passive recovery (Jo r f e l d t , 1970, Essen et a l . , 1975, Hermansen et a l . , 1973, and Issekutz et a l . , 1976). Lactate appears to be used p r e f e r e n t i a l l y as a substrate p a r t i c u l a r l y i n the case of p r i o r elevated l a c t a t e concentrations. The accumulation of lactate i s i n i t s e l f not detrimental to the muscle function (Sahlin, 1986) and i n fact forms a useful metabolic substrate of considerable importance 25 necessary i n the maintenance of g l y c o l y t i c energy production. The fate of the lactate accumulated above that which can be metabolized by active muscle, inactive muscle, the l i v e r , and the heart does however have important implications f o r the understanding of the ef f e c t s that increased anaerobic metabolism may have on the c o n t r a c t i l e mechanism. pH Changes with Lactate Accumulation. The low pK of l a c t i c acid (3.9) re s u l t s i n i t being almost e n t i r e l y dissociated at c e l l u l a r pH and necessitates that the r e s u l t i n g protons be buffered immediately. Sahlin (1978) demonstrated that the production of lactate r e s u l t s i n an equivalent release of hydrogen ions causing a decrease i n intramuscular pH. This investigation demonstrated a l i n e a r r e l a t i o n s h i p between Total Muscle pH and lactate + pyruvate concentration a f t e r both isometric and dynamic exercise. The accumulation of protons and t h e i r measured e f f e c t on pH i s a r e s u l t of interactions between proton production and proton removal. Protons are produced due to the d i s s o c i a t i o n of the acids which are the end products of two pathways f o r energy production. Oxidation produces the weak acid C02 while g l y c o l y s i s produces the stronger l a c t i c acid. Due to the low pK of l a c t i c acid i t produces greater amounts of protons explaining the greater drop i n pH during work which requires use of the g l y c o l y t i c pathways. The removal of protons which are produced i n the muscle c e l l depend e s s e n t i a l l y on two processes (a) movement of acid or bases across the c e l l 26 membrane, (b) the removal of the acid or supply of the base from the e x t r a c e l l u l a r space v i a c i r c u l a t i n g blood. At some point the appearance of protons i s exceeded by t h e i r removal r e s u l t i n g i n a decrease i n muscle pH. Hermansen and Osnes (1972) demonstrated a decrease i n muscle pH from a r e s t i n g value of 6.93 to a low of 6.40 a f t e r both intermittent and continuous exercise. Sahlin et a l . (1972), and Sahlin et a l . (1976) found s i m i l a r values with a decrease from 7.08 at rest to 6.60 and 6.56 following dynamic and isometric exercise respectively. Metzger and F i t t s (1987) investigated the changes i n muscle pH with both high and low frequency stimulation to fatigue of i n v i t r o preparations of rat diaphragm muscle. Their r e s u l t s showed comparable decrements i n pH from r e s t i n g values of 7.06 to a low value of 6.33 following fatiguing contractions. A l l of the above studies measured decrements i n the pH of working muscle. A rela t i o n s h i p has been shown to e x i s t between t h i s decrease i n the pH of the muscle and i t s a b i l i t y to perform. E f f e c t s of Decreased pH on the Cont r a c t i l e Mechanism. The decrease i n muscular pH or increase i n H+ ions has been suggested to be the cause of fatigue for high i n t e n s i t y exercise. Sahlin (1986) i d e n t i f i e d four steps i n the c o n t r a c t i l e process which previous investigators have shown to be affected by the decrement i n muscular pH. (a) An increased Ca + + 27 requirement, (b) decreased maximal tension with decreased muscle pH (Donaldson, 1978), (c) a decrease i n myosin ATPase a c t i v i t y as the pH decreased from 6.5 to 7.5 (Schadler, 1967), and (4) an increase i n the binding constant of the sarcoplasmic reticulum for Ca + + with decreased pH (Nakamura and Schwartz, 1972). This increased a f f i n i t y of the sarcoplasmic reticulum for Ca + + could i n t e r f e r e i n the ex c i t a t i o n contraction coupling. Any of these changes could e f f e c t the a b i l i t y of the affected muscle c e l l s to contract. The detrimental e f f e c t of decreased pH i s supported by investigations which have demonstrated increased a b i l i t y of muscles to perform work by increasing the buffering a b i l i t y of both the muscle and the e x t r a c e l l u l a r f l u i d ( C o s t i l l et a l . , 1984) . These authors also demonstrated a decrease i n pH to be accompanied by a corresponding decrease i n HCO"3. This would be predicted by equation 7 which i n the presence of hydrogen ions and HCO~3 would cause a s h i f t to the r i g h t . HLA < > H+ + LA" 6 H+ + HC03" < > H 2C0 3 7 H 2C0 3 < > H20 + C02 8 Mainwood and Renaud (1985) reported that while changes i n pH are c l e a r l y related to the a b i l i t y of the muscle to develop tension they cannot be considered to be causal. The authors reported that the recovery of force development could be delayed over an hour by maintaining an e x t r a c e l l u l a r pH of 6.4. In the same experiment an increase i n the e x t r a c e l l u l a r 28 pH from 6.4 to 8.0 during recovery resulted i n a rapid increase i n force development. This increase was more rapid than would be predicted due to the increased proton e f f l u x . The authors postulated that there may be other more d i r e c t mechanisms at work i n the recovery process. They supported t h i s idea with r e s u l t s from further experiments employing proton e f f l u x i n h i b i t o r s . These i n h i b i t o r s had no e f f e c t on the recovery of twitch tension at a pH of 7.4. Of p a r t i c u l a r relevance to the present investigation i t was reported that a s i m i l a r decrease i n developed tension was seen during stimulation of frog sartorius muscle with external pH's of 6.4 and 8.0. This r e s u l t i s d i f f i c u l t to explain because proton load increases with i n t e n s i t y and decreased external pH has been shown to decrease the e f f l u x of protons. Once again i t would appear that some other factor may p a r t i c i p a t e i n the i n b i l i t y to decrease tension although i s l i k e l y that the r e s u l t may be due to methodology. In a more recent study Mainwood et a l . , (1987) decreased lactat e e f f l u x from i s o l a t e d s k e l e t a l muscle by increasing e x t r a c e l l u l a r pH. Under these conditions they showed that muscle tension did not return to normal during recovery but that there was a further decrease i n tension. These authors also showed that muscles loaded with a l a c t a t e load s i m i l a r to that seen i n fatigue reversed l a c t a t e f l u x and produced a reduction i n i n t r a c e l l u l a r pH. The a r t i f i c i a l l a c t a t e load increased twitch duration and time to peak tension. The a l t e r a t i o n s were s i m i l a r to those seen 29 i n normally fatigued muscle but were smaller i n magnitude. I t i s c l e a r that there i s a r e l a t i o n s h i p between muscle function, l a c t a t e and pH changes. The r e l a t i o n s h i p i s complex and i t seems l i k e l y that other factors are involved. The model presented by Mainwood must be applied cautiously since the l a c t a t e loads u t i l i z e d (20 - 30 umol) are l e s s than the l a c t a t e loads observed i n humans during exercise. The cascade of events r e s u l t i n g i n an increased l a c t a t e concentration and subsequent decreased blood and muscle pH have been related to observed changes i n the e l e c t r i c a l p r o f i l e of muscle. These changes could r e s u l t i n previously recruited f i b r e s becoming i n e f f e c t i v e i n force production r e s u l t i n g i n changes i n the e l e c t r i c a l c h a r a c t e r i s t i c s of the e n t i r e muscle as i t adapted i n order to continue to produce the required l e v e l of tension. Neuromuscular Response to Exercise The Integrated EMG as an Indicator of Muscle Tension. The e l e c t r i c a l c h a r a c t e r i s t i c s of the two primary f i b r e types are also d i f f e r e n t and are related to the metabolic c a p a b i l i t i e s of the f i b r e . The FG f i b r e s have a higher recruitment threshold and are therefore recruited p r i m a r i l y at higher l e v e l s of force output than the SO f i b r e s (Tanji and Kato, 1972). The SO f i b r e s are enervated by alpha motorneurons which are smaller i n diameter than those innervating the FG f i b r e s r e s u l t i n g i n lower nerve conduction v e l o c i t i e s and longer time to peak force development fo r the 30 SO f i b r e s . The FG f i b r e s have a greater peak amplitude and f i r i n g frequency and produce greater peak forces than the SO f i b r e s (Milner-Brown et a l . , 1973). Thus, due to the recruitment pattern and the greater amplitude and f i r i n g frequency of f i b r e s recruited at higher tensions i t i s c l e a r that with increasing load t h e i r should be an increase i n the e l e c t r i c a l output of the muscle. The surface electromyogram r e f l e c t s the f i r i n g rate, amplitude, recruitment pattern, and f i b r e type of motor units of the muscle being recorded (Basmajian, J.V., 1978, Komi et a l . , 1970, Moritani 1986). There have been numerous studies which characterized the r e l a t i o n s h i p between the electromyogram and muscle tension or force i n both dynamic and isometric contractions. Relationship Between Isometric Tension and EMG. Zuniga et a l . (1969), examined the r e l a t i o n s h i p between tension and continuously averaged EMG for tensions covering the f u l l range of voluntary isometric contractions of the biceps b r a c h i i muscle and reported that a parabolic curve provided a much better f i t than a l i n e a r one. The authors contend that the difference i n the r e l a t i o n s h i p shown by t h e i r data and some previous data resulted from the use of a f u l l range of tensions (up to maximum). The l i n e a r i t y of t h e i r data occurred at loads that had not been previously used i n i n v e s t i g a t i n g the r e l a t i o n s h i p . However the c o e f f i c i e n t of v a r i a t i o n for t h e i r average EMG data was 53% and ranged from 45 to 68% i n 31 i n d i v i d u a l subjects. Further observation of t h e i r data shows that the l i n e calculated for the l i n e a r regression f a l l s well within the error bars on the plots of EMG vs. tension. Komi and Buskirk (1970) supported the existence of a non-linear r e l a t i o n s h i p while researching the r e p r o d u c i b i l i t y of d i f f e r e n t electrode types i n electromyographic recording. A quadratic r e l a t i o n s h i p was exhibited between mean IEMG and and isometric tension of the biceps b r a c h i i muscle. Kuroda et a l . (1970) reported a l i n e a r r e l a t i o n s h i p between average EMG and force while force was maintained at submaximal l e v e l s . Once the l e v e l of force exceeded submaximal l e v e l s the l i n e a r i t y of the r e l a t i o n s h i p decayed. These authors used a linear-plus exponent function to describe the EMG-force re l a t i o n s h i p over the entire range of forces. Heckathorne and Childress (1981) also used a c i n e p l a s t i c preparation of the human biceps b r a c h i i muscle of an amputee i n which tension was recorded d i r e c t l y from the d i s t a l biceps tendon v i a a s u r g i c a l l y produced tunnel. These authors demonstrated a non-l i n e a r r e l a t i o n s h i p between IEMG and tension at several muscle lengths for both isometric and isotonic contractions. Heckathorne and Childress suggest that the l i n e a r i t y demonstrated by other researchers may be due to the s y n e r g i s t i c action of other muscles i n a normal i n t a c t limb. Contrary to these re s u l t s some investigators have indicated l i n e a r relationships. In an early study, Lippold (1952), demonstrated a l i n e a r r e l a t i o n s h i p between the 32 amplitude of the integrated EMG and the tension produced i n a voluntary isometric contraction of the gastrocnemius muscle. Inman et a l . (1952) using both inserted wire electrodes and surface electrodes, reported a s i m i l a r r e l a t i o n s h i p i n c i n e p l a s t i c muscle preparations of amputees and concluded that the IEMG could be used as an index of muscle tension during isometric contractions of the biceps b r a c h i i muscle. Edwards and Lippold (1956), showed that the previously demonstrated l i n e a r r e l a t i o n s h i p between IEMG and tension of an unfatigued muscle was maintained with a previously fatigued muscle with only v a r i a t i o n s i n the slope of the rel a t i o n s h i p being evident. Close et a l . (1960), used indwelling wire electrodes placed i n the soleus muscle to determine the rel a t i o n s h i p between action potential counts and both isometric and isoton i c contractions. They demonstrated a l i n e a r r e l a t i o n s h i p between isometric tension and action p o t e n t i a l counts for ten second isometric contractions at s ix d i f f e r e n t muscle lengths. These authors r e s u l t s also suggested that a l i n e a r r e l a t i o n s h i p existed between tension developed i n is o t o n i c contractions and IEMG. Dejong and Freund (1967), studied the relat i o n s h i p between the twitch tension and the amplitude of the action p o t e n t i a l i n the adductor p o l l i c i s brevis muscle. They concluded that a strong l i n e a r association existed between the action p o t e n t i a l amplitude and the twitch tension with e l e c t r i c a l l y evoked contractions v i a the motor nerve. Devries (1968), reported a 33 l i n e a r r e l a t i o n s h i p between maximal isometric tension of the elbow f l e x o r group and the root mean square of the EMG. More recently Moritani and Devries (1978) demonstrated a s i m i l a r l i n e a r r e l a t i o n s h i p between the integrated EMG and force of voluntary isometric contractions of the elbow f l e x o r muscle group. They demonstrated that a l i n e a r function f i t the data better than eit h e r exponential, quadratic, or power functions fo r both standardized group data and i n d i v i d u a l data. Relationship Between Dynamic Contractions and EMG. There has been less research done on the re l a t i o n s h i p between dynamic r e p e t i t i v e contractions and EMG. Bigland-Ritchie & Joseph (1974), used dynamic c y c l i n g exercise to demonstrate a l i n e a r r e l a t i o n s h i p between EMG a c t i v i t y (Root Mean Square) of the l a t e r a l quadriceps and load for unfatigued muscle at submaximal loads. This r e l a t i o n s h i p was l a t e r extended by Petrofsky (1980) who showed that i n the absence of fatigue the l i n e a r r e l a t i o n s h i p existed for loads up to an independently determined maximum. In contrast during dynamic exercise at power outputs equal to or greater than 60% of maximum t h e i r was a steady increase i n the amplitude of the RMS EMG that was unrelated to changes i n workload. I t was concluded that fatigue complicated the relat i o n s h i p between e l e c t r i c a l output and tension and made EMG i n v a l i d as an indicator of muscle tension. The v a r i e t y of experimental protocols, EMG recording and processing techniques make i t d i f f i c u l t to compare the re s u l t s 34 from the preceding investigations. The preponderance of evidence suggests however that the r e l a t i o n s h i p between the IEMG and tension or force as recorded by surface electrodes i s i n f a c t l i n e a r for an unfatigued muscle performing both isometric and isoto n i c contractions. As well IEMG recorded during dynamic r e p e t i t i v e exercise such as c y c l i n g has been demonstrated to have a l i n e a r r e l a t i o n s h i p i n the absence of fatigue (Petrofsky et a l . , 1980). This research was confirmed by p i l o t data c o l l e c t e d i n our laboratory which demonstrated a c l e a r l y l i n e a r r e l a t i o n s h i p between power output and IEMG during b r i e f bouts of dynamic c y c l i n g exercise f o r increasing power outputs, decreasing power outputs and with randomly selected power outputs. I t i s also c l e a r from the reviewed research that fatigued muscle responds d i f f e r e n t l y to increased loads with e l e c t r i c a l output showing increases that appear unrelated to changes i n power output. During incremental exercise to maximum a number of changes occur i n the metabolic p r o f i l e of the working muscle which do not occur i n the muscle during b r i e f periods of work. The electromyogram i s s e n s i t i v e to 'changes i n f i b r e type, recruitment, f i r i n g rate, and amplitude of muscle. Therefore any changes i n the metabolic environment which a f f e c t any of these parameters should be r e f l e c t e d i n changes i n the surface electromyogram and the Integrated EMG. In p a r t i c u l a r the accumulation of l a c t a t e and the r e s u l t i n g decrease i n pH have been hypothesized to be responsible for some of the changes 35 seen i n the e l e c t r i c a l p r o f i l e of the muscle during incremental exercise. The Integrated EMG as a Non-Invasive Indicator of the Lactate  Threshold There have been several studies which demonstrated a re l a t i o n s h i p between the anaerobic threshold and muscle a c t i v a t i o n as determined by electromyography (Moritani 1980, Nagata et a l . , 1981, Miyashita et a l . , 1981, Moritani et a l . , 1984, V i i t a s a l o et a l . , 1985). An i n i t i a l i n v e s t i g a t i o n by Moritani (1980) provided data which was used to v a l i d a t e an IEMG-Power Method for the non-invasive determination of the anaerobic threshold. The r e s u l t s indicated that an i n f l e c t i o n point i n the IEMG of the vastus l a t e r a l i s appeared during incremental exercise at a oxygen uptake value which correlated very highly (r = 0.99 to 0.863, p<0.0001) with the oxygen uptake value at the anaerobic threshold. The anaerobic threshold was determined using cardiorespiratory measures or Tvent as e a r l i e r defined. Nagata et a l . (1981) validated further t h i s method of non-invasive determination of the anaerobic threshold by showing high c o r r e l a t i o n (r = 0.921 p<0.001) between the anaerobic threshold determined using a r t e r i a l blood la c t a t e , P0 2, PCOz , HC0"3 and pH with the anaerobic threshold determined using the IEMG-Power method. In addition Nagata et a l . (1981) demonstrated an abrupt increase i n the frequency band width at 70% of peak frequency which occurred immediately a f t e r the 36 anaerobic threshold. The increase i n the width of t h i s frequency band, which was postulated to be the most active was taken as an i n d i c a t i o n of previously reported decreases i n mean power frequency noted i n muscular fatigue. Moritani (1984) supported h i s own hypothesis by demonstrating high co r r e l a t i o n s between blood lactat e and both IEMG and Mean Power Frequency (MPF) (0.977 to 0.857, p<0.001 and -0.962 to -0.862, p<0.001 respectively) during incremental forearm exercise to exhaustion. V i i t a s a l o et a l . (1985) monitored f i v e d i f f e r e n t muscles separately during both the ascending and descending phases of the pedal cycle. The r e s u l t s of te s t s at f i v e d i f f e r e n t power outputs indicated an apparent non-linearity i n the IEMG of a l l muscles at a power output i d e n t i f i e d by the authors as the aerobic threshold (Skinner and McClellan, 1979) but no further change i n the non-l i n e a r i t y at the anaerobic threshold. The MPF was also monitored but no difference was noted above and below the anaerobic threshold. These studies contend that with increases i n power output there i s a point where a sudden increase i n Integrated EMG (IEMG) a c t i v i t y occurs which i s apparently unrelated to changes i n workload. This i n f l e c t i o n point occurs at a percentage of oxygen uptake which correlates well with the percentage of maximal oxygen uptake at which Tlac occurs. A l l of these studies have concluded that t h i s r e l a t i o n s h i p would allow for the use of Integrated EMG as a non-invasive indicator of Tlac or the anaerobic threshold. 37 Proposed Rationale for the Use of the IEMG as an  Indicator of the Anaerobic Threshold. The i n f l e c t i o n point i n the IEMG vs. Power p l o t i s caused by changes i n the f i r i n g frequency and/or the amplitude of the muscle above that r e s u l t i n g from increased load. As previously discussed, accumulation of lac t a t e i n the muscle decreases the muscle pH (Hermansen et a l . , 1977, Sahlin 1978). I t i s hypothesized that these changes are the r e s u l t of the decreased muscle pH. Research reviewed e a r l i e r indicated that changes i n pH i n t e r f e r e with the function of the c o n t r a c t i l e apparatus. I t i s proposed that t h i s interference d e b i l i t a t e s c e r t a i n f i b r e s and necessitates changes to maintain tension or power output. Hakkinen et a l . (1986) showed decreased pH to be related to increased recruitment of fast twitch g l y c o l y t i c f i b r e s as well as increased f i r i n g rate of already recruited f i b r e s . This change i n muscle f i b r e recruitment and f i r i n g frequency would r e s u l t i n altered e l e c t r i c a l c h a r a c t e r i s t i c s i n the t o t a l muscle as a r e s u l t of the greater amplitude and f i r i n g frequency of the fa s t twitch f i b r e s . These altered c h a r a c t e r i s t i c s i n combination with the increasing work load could r e s u l t i n an accelerated, non-linear increase, or i n f l e c t i o n point i n the Integrated EMG of the working muscle. The presence of fatigue i n a muscle, defined as the i n a b i l i t y to maintain or produce a given force, a l t e r s the r e l a t i o n s h i p between the IEMG and force. Komi (1984) points to three well documented e f f e c t s of fatigue on the IEMG. 38 1) An increase i n IEMG a c t i v i t y i s observed during a sustained submaximal isometric contraction. The slope of the r e l a t i o n s h i p i s dependent on the l e v e l of tension with the increase being greater at higher tensions. The time to exhaustion i s also shortened with increasing tension. 2) The r e l a t i o n s h i p between IEMG and force i s s h i f t e d to the l e f t across the e n t i r e range of forces i n fatigued muscle. 3) During maximal contractions maximum force decreases and the maximum IEMG also declines. I t i s c l e a r that a l t e r a t i o n s i n the e l e c t r i c a l c h a r a c t e r i s t i c s of muscle occur as the muscle reaches maximal l e v e l s and fatigues. These changes have been related i n some instances to changes i n the metabolic environment i n p a r t i c u l a r increases i n l a c t a t e concentration and decreases i n pH. One measure that has been used i n the analysis of changes i n muscle function i s the mean power frequency or power spectrum. During fatiguing contractions the power spectrum has been shown to s h i f t to lower frequencies (Moritani et a l . , 1986). Komi (1984) c i t e s studies (Komi and Tesch, 1979, V i i t a s a l o and Komi, 1978 and Tesch et a l . , 1983) which showed a negative r e l a t i o n s h i p between percentage of f a s t twitch f i b r e s which produce high l e v e l s of l a c t a t e and the decrease i n mean power frequency of the EMG s i g n a l . Tesch et a l . (1983) indicated a negative r e l a t i o n s h i p between mean power frequency and both increasing l e v e l s of l a c t a t e and percentage of fa s t 39 twitch f i b r e s . Moritani et a l . (1984) showed the marked increase i n venous blood l a c t a t e was accompanied by a s t a t i s t i c a l l y s i g n i f i c a n t increase i n RMS amplitude and decrease i n mean power frequency during incremental forearm exercise. However several studies (Edwards et a l . , 1972, Karlsson et a l . , 1975, Broman, 1977, Petrofsky, 1980, Komi 1984, Boubrit, 1983) have pointed out that the time course of recovery from exercise for l a c t a t e and pH requires one to several hours depending upon conditions of recovery while the recovery of maximum twitch tension and amplitude as well as mean power frequency have shown an almost immediate recovery to pre-exercise or r e s t i n g l e v e l s . M i l l s and Edwards (1984) studied subjects with myophosphorylase deficiency who are incapable of producing lactate and demonstrated a frequency s h i f t i n t h e i r EMG signal greater than that observed i n normal controls. These studies i n combination with the conclusion by Mainwood and Renaud (1986) that i n c e r t a i n types of fatigue " . . . i n t r a c e l l u l a r l a c t a c i d o s i s i s not the main cause of the suppressed tension..." (p. 648) point to the necessity for further investigation into the proposed r e l a t i o n s h i p between IEMG and l a c t a t e . The r e l a t i o n s h i p has come under recent scrutiny. Boubrit (1983) showed a d i s s o c i a t i o n of the previously demonstrated r e l a t i o n s h i p between decreased MPF and l a c t a t e i n recovery re-examined the r e l a t i o n s h i p . Helal et a l . (1987) examined the response of the power and frequency of the EMG signal during incremental exercise i n nine subjects. 40 A breakpoint was found i n the PEMG which occurred at a power output of 275 watts s i m i l a r to the breakpoint i n l a c t a t e which occurred at 250 watts. The mean EMG data was found not to represent c o r r e c t l y represent the i n d i v i d u a l data to the c h a r a c t e r i s t i c high inter-subject v a r i a b i l i t y . Therefore the i n d i v i d u a l subject data was examined. They observed the breakpoint i n the PEMG of the vastus l a t e r a l i s i n only f i v e of the nine subjects. S i m i l a r l y only s i x of the nine show a decrease i n the MPF and the decrease occurred at the f i n a l workload. Possible e f f e c t s of cadence on the electromyographic  s i g n a l . The i n i t i a l study which examined the r e l a t i o n s h i p between IEMG and lactat e during incremental c y c l i n g exercise u t i l i z e d a constant power output ergometer. Cadence was allowed to vary between 50 and 80 revolutions per minute. (Moritani, 1980). Coast and Welch (1985) and Boning et a l . (1984) have both demonstrated a parabolic r e l a t i o n s h i p between oxygen uptake and cadence at a constant power output. Force and cadence may be combined i n many combinations to provide the same power output. I t i s l i k e l y that d i f f e r e n t combinations of cadence and force, producing equivalent power outputs, would r e s u l t i n an e n t i r e l y d i f f e r e n t recruitment strategy by the muscle. Such recruitment strategies would be r e f l e c t e d i n the recorded electromyographic s i g n a l . The work by Coast and Welch (1985) suggests the existence of an optimal cadence which would support the premise of altered recruitment 41 strategy f o r d i f f e r e n t cadences. Also, changes i n cadence could a f f e c t the IEMG simply because with a constant sampling period increases or decreases i n cadence would r e s u l t i n s i m i l a r increases or decreases i n the t o t a l amount of a c t i v i t y per sampling period such v a r i a t i o n should be considered i n analysis of electromyographic data. In subsequent studies however (Nagata et a l . , 1981, Miyashita et a l . , 1981, V i i t a s a a l o et a l . , 1985), s i m i l a r r e s u l t s were obtained and cadence was "...maintained constant". These studies did not report monitoring of cadence over the course of the t e s t nor was cadence used as the c r i t e r i o n for determining the end of the t e s t . The use of IEMG makes a constant cadence important since v a r i a t i o n s w i l l a l t e r the amount of a c t i v i t y which i s recorded i n a given period of time. In a recent study Helal et a l . (1987) maintained cadence "rigourously" at 80 rpms. They also reported i n f l e c t i o n points i n recorded EMG but i n only f i v e of nine subjects. I t i s important that cadence be monitored and c o n t r o l l e d when examining changes i n IEMG of a muscle. The r e s u l t s from the investigations above suggest cadence i s unrelated to the observed i n f l e c t i o n points. However the area needs further i n v e s t i g a t i o n to ascertain i f the observed r e l a t i o n s h i p between la c t a t e and IEMG i s not simply an a r t i f a c t of v a r i a t i o n s i n cadence which a l t e r the recruitment pattern of the muscle. 42 Timing and duration of e l e c t r i c a l a c t i v i t y as a possible  confounding factor. A further possible confounding factor that has not been examined i s possible changes i n the timing and duration of the e l e c t r i c a l a c t i v i t y i n r e l a t i o n to the sampling i n t e r v a l . I f such changes occurred i n a systematic manner with incremental exercise they could r e s u l t i n systematic changes i n the IEMG of the working muscle. Timing and duration should be monitored because of the possible contribution of these factors to changes i n the recorded electromyographic s i g n a l . Elimination of these factors would allow stronger conclusions regarding the e f f e c t s of the metabolic state of the muscle on the electromyographic s i g n a l . The surface electromyogram represents a s t a t i s t i c a l summation of the e l e c t r i c a l a c t i v i t y i n a muscle and may not be sen s i t i v e enough to detect metabolic changes at the l e v e l of the Tlac. I f IEMG i s to be used i n the non-invasive determination of the anaerobic threshold or Tlac t h i s s e n s i t i t v i t y i s required. Evidence demonstrating a breakdown i n the proposed r e l a t i o n s h i p between lac t a t e and the IEMG suggest that the re l a t i o n s h i p may be coincidental. 43 Chapter 3 PROCEDURES The purpose of t h i s study was to examine the e f f e c t of changes i n blood lactat e concentration during an incremental exercise t e s t on the Integrated EMG of the vastus l a t e r a l i s . These changes were observed i n order to t e s t the v a l i d i t y of the IEMG-Power Method for the determination of the l a c t a t e threshold. This chapter contains a description of the methodology and instrumentation used to obtain and analyze the experimental data as follows: (a) Research Design; (b) Subjects; (c) Control Condition Protocol; (d) Experimental Condition Protocol; (e) Data C o l l e c t i o n ; (f) Data Analysis. Research design An attempt was made to t e s t the v a l i d i t y of the IEMG -Power Method for determining the lactat e threshold by c o r r e l a t i o n of the percent oxygen uptake at the point of i n f l e c t i o n i n a Mean Plasma Lactate vs Power p l o t with the percent of oxygen uptake at the point of i n f l e c t i o n i n the IEMG vs Power p l o t . Because no i n f l e c t i o n point could be determined i n either condition from the IEMG vs Power plo t s an analysis of the rate of change of the IEMG vs Power p l o t (Slope) was performed to determine i f any difference could be detected between the Control and Experimental Conditions. Subi ects The subjects were s i x trained male c y c l i s t s accustomed to 44 maximal e f f o r t s . A l l subjects had at le a s t two years of racing experience. Control Condition Protocol In the Control Condition an incremental cycle ergometer t e s t was used to determine maximal oxygen uptake. The protocol consisted of four minutes of unloaded c y c l i n g at 90 revolutions per minute (rpm) with subjects receiving v i s u a l feedback to a s s i s t i n maintenance of cadence within +/-1. Increases i n power output of 23.5 watts/minute continued u n t i l the subject reached a work load which caused the cadence to drop below 90 rpms for more than f i v e seconds. Expired gases were monitored and the following v e n t i l a t o r y parameters VE, V02, Excess C0 2, F E0 2, F EC0 2, Respiratory Quotient (R.Q.) were calculated and recorded. Heart Rate (M.H.R.) was monitored and recorded for each workload. Lactate measures were taken at r e s t and then once during the f i n a l eight seconds of each workload. Raw EMG was also amplified, f i l t e r e d and sampled at 500 hz for the f i n a l eight seconds of each workload and stored on floppy disk for l a t e r analysis. Experimental Condition Protocol The Experimental Condition u t i l i z e d a high i n t e n s i t y arm exercise protocol on a Monark Arm Ergometer to produce elevated blood lactates. Each subject performed two three minute bouts of arm work at a power output equal to between 0.90 and 1.00 watt per kilogram of body weight. The two 45 exercise bouts were separated by one minute of rest. A rest period of f i v e minutes followed the completion of the second bout of arm exercise. At the end of f i v e minutes a blood sample was drawn and used to determine the Post Arm Exercise l a c t a t e concentration. The Control Condition protocol was repeated immediately following the sampling of the blood. P r e - t r i a l Muscle Warming. A l l t r i a l s were preceded by the warming of the vastus l a t e r a l i s muscle by a p p l i c a t i o n of an external hot pack to achieve a surface temperature of approximately 40 degrees centigrade to minimize the e f f e c t s of muscle temperature on the amplitude and conduction v e l o c i t y of the action p o t e n t i a l . Data C o l l e c t i o n Procedures for Lactate Sampling. In the Control Condition samples of approximately 2 ml were taken from the cephalic vein of the arm at rest and then once every minute a f t e r the onset of exercise u n t i l t e s t completion. During the Experimental Condition a sample was taken f i v e minutes a f t e r the arm exercise protocol and then once every minute as i n the Control Condition. Sampling occurred during the f i n a l eight seconds of each workload i n order that the electromyographic data corresponded with the metabolic data. Samples were centrifuged and the plasma was frozen and stored for l a t e r analysis. Procedures for Lactate Determinations. Lactate determinations were performed enzymatically (Sigma) using a 46 method involving conversion of lactate to pyruvate following the introduction of lactate dehydrogenase and NAD*. Values were obtained by comparison of samples with a serie s of measurements of a stock solution i n the 0 - 6 . 6 mmol/1 range. A l l samples were analyzed i n duplicate a f t e r adding 0.1 ml of the sample to 2.9 ml of reagent solution. Samples were then measured for o p t i c a l density at 340 nm. Lactate values were calculated from a lea s t squares regression equation based on the standards from the stock solution. Procedures for Electromyographic (EMG) Recording. The myoelectric signals were recorded with s i l v e r / s i l v e r chloride b i p o l a r recording electrodes placed over the d i s t a l portion of the r i g h t vastus l a t e r a l i s muscle at an interelectrode distance of 4 cm. A reference electrode was placed over the volar aspect of the anterior crest of the ilium. Skin resistance was reduced by abrading. The EMG signal was f i r s t introduced into a Voltage Coupler (Beckman 9878) with a frequency range of 5-2000 hertz (hz) and a maximum s e n s i t i v i t y of 5 microvolts (uv). The signal was then passed through a Variable Preamplifier (Beckman R411) and into a custom made bioamplifier with a frequency range of 20-1000 hz, a gain of 1000, an input impedance of ten megaohms and a common mode re j e c t i o n r a t i o (CMMR) of greater than 100 db. The preamplifier s e t t i n g was adjusted by having the subject perform a single b r i e f isometric contraction with the pedal 47 crank at 90 degrees past TDC. The preamplifier s e t t i n g was selected to give an output which would be near ten v o l t s at the highest power output. EMG data sampling was i n i t i a t e d by a f i v e v o l t Transitor Transistor Logic (TTL) pulse which was generated by breaking a photoelectric beam at Top Dead Centre (TDC) of the pedal cycle. The TDC pulse was recorded simultaneously with the EMG s i g n a l . The EMG signals were sampled at a rate of 500 hertz for the f i n a l 8 sees of each work load. The signal was amplified, low passed f i l t e r e d at 1 kHz, and stored for l a t e r analysis on floppy disk using a Data General MicroNova mini computer system. Data Analysis Integration of EMG Data. Integration was performed over each pedal cycle (CIEMG, TDC to TDC). Integration was performed by a computer program using an algorithm based on the Trapezoid r u l e . Timing and Duration of EMG A c t i v i t y . The duration and timing of the EMG a c t i v i t y f or each pedal cycle was calculated i n r e l a t i o n to the TDC pulse. The duration and timing values were expressed as a percentage of t o t a l cycle time for each burst. A mean duration, beginning point and end point of a c t i v i t y f o r each cycle was then calculated for each workload. Determination of Lactate Threshold Two d i f f e r e n t methods were tested to determine the most appropriate method of estimating Tlac from the data c o l l e c t e d . 48 The f i r s t method i s that proposed by Beaver et a l . (1985) which u t i l i z e d a p l o t of Log-Log transformations f o r l a c t a t e and V02 . The second method was that employed by Hughson, Weisiger and Swanson (1987) which used a continuous exponential plus constant model for defining a p l o t of lactat e and V0 2. A computer program developed by Hughson compared the f i t of the two models to the data by c a l c u l a t i n g the residual sum of squares and mean square error for the two models. The Log-Log model f i t the present data best and was therefore employed to estimate Tlac. Tlac was taken to be the point of i n t e r s e c t i o n of two regressions l i n e s calculated for points l y i n g on eith e r side of a v i s u a l l y i d e n t i f i e d i n f l e c t i o n point. A more complete description of the method i s a v a i l a b l e i n Beaver et a l . (1985). Tlac was estimated using each subjects Control T r i a l data and due to the proximity i n time of the t e s t i n g sessions was assumed to be the same for the Experimental T r i a l . Tlac was expressed i n terms of oxygen uptake i n l i t r e s per minute. Determination of Rate of Change (Slope) of IEMG vs Power  Output A post-hoc analysis was performed of the slope of the l i n e described by the p l o t of CIEMG vs Power Output p l o t for each subject over the entire t e s t duration. As well the slope of the l i n e was determined for the l i n e p r i o r to Tlac and for the l i n e a f t e r Tlac. The mean slope for each l i n e was then calculated for both the Experimental and Control Conditions and an analysis of variance was performed to determine i f there was any s i g n i f i c a n t difference i n the rate of change i n IEMG. In addition Pearson's Product-Moment Correlation was performed between lactate and CIEMG and power output and CIEMG to determine which of the two better predicted the changes i n CIEMG. 50 Chapter 4 RESULTS The following chapter contains a presentation and analysis of the data obtained from t h i s i n v e s t i g a t i o n . The data are categorized as follows: (a) Description of subjects; (b) Analysis of cardio-respiratory data; (c) Analysis of lac t a t e data; (d) Analysis of Integrated EMG data. Description of Subjects Six trained male c y c l i s t s volunteered as subjects for t h i s study. The basic descriptive data on a l l subjects i s included i n Appendix E. The subjects' mean age, height and weight were 22 +/-4.1 years, 175.6 +/- 1.2 cm., and 66.0 +/- 5.9 kg. respectively. Analysis of Cardio-Respiratorv Data The mean cardiorespiratory data was calculated using values up to minute 15. A l l subjects completed t h i s workload i n the Control t r i a l and a l l except one completed i t i n the Experimental T r i a l . There was no s i g n i f i c a n t difference i n the mean duration of the incremental exercise t e s t s performed i n the Control and Experimental T r i a l s (t = 1.074 p = 0.308) with only one subject (Subject 6) showing a marked difference i n duration. Control T r i a l Cardiorespiratory Data. Figure l a shows the mean Control T r i a l response i n VD2 . The t y p i c a l l e v e l i n g o f f of V02 at the f i n a l workloads i s not evident. S i m i l a r l y , 51 (b) LU a. LU X O 4.5 4-3.5-3-2.5-2-1.5 1 0.5-1 0 Legend A CONTROL X EXPERIMENTAL 1 1 1 i I I I I I I 0 2 4 6 8 10 12 14 16 18 20 TIME (MIN) 160 -j 130-Z 1 1 0" ^ 9 0 -£ 70 6 o ^ 30 10 0 2 X EXPERIMENTAL 6 I 1 I I I I 1 8 10 12 14 16 18 20 TIME (MIN) (c) 50-] 4 5 -•z. 4 0 -3 5 -- J CM 3 0 -o > 25-LU > 2 0 -15-10-Legend & CONTROL X EXPERIMENTAL 0 2 4 6 8 10 12 14 16 18 20 TIME (MIN) •z. 2 CN O o to CO LU CJ X LU 26-i 21-16-6 J Legend A CONTROL X EXPERIMENTAL 0 2 4 6 8 10 12 14 16 18 20 TIME (MIN) Fiaure 1 (a) Oxygen Uptake - Control and Experimental T r i a l s . (b) V e n t i l a t i o n - Control and Experimental T r i a l s . (c) V E/V0 2 Ratio - Control and Experimental T r i a l s . (d) Excess C 0 2 - Control and Experimental T r i a l s . 52 heart rate data does not show the normal l e v e l i n g o f f . High R.Q. r a t i o s i n (Appendix E - Table 2a, p. 113) do indicate r e l i a n c e on anaerobic g l y c o l y s i s at higher power outputs. However these values represent the maximums within the constraints of the incremental protocol and are l i k e l y less than subjects 7 absolute maximum. The mean maximal oxygen uptake value f o r the Control T r i a l was 3.15 +/- 0.52 1/min and the mean maximal V e n t i l a t i o n was 133.51 +/- 9.22 1/min. Figures l b , l c , and Id indicate t y p i c a l responses to incremental exercise i n V E, Excess C0 2, and V E/V0 2. Experimental T r i a l Cardiorespiratory Data. The maximal oxygen uptake and v e n t i l a t i o n were 3.29 +/- 0.61 1/min and 127.58 +/- 18.67 1/min respectively. The p l o t s i n Figures l a , l b , l c , and Id shows the mean response of the cardiorespiratory measures for the Experimental T r i a l were very s i m i l a r to those of the Control T r i a l . The r e s u l t s of the analysis of variance displayed i n Table 1 show no s i g n i f i c a n t difference i n the maximal values f o r V £, V0 2 and Excess C02 between T r i a l s . Analysis of Lactate Data Values for lactat e determination represent the mean of two spectrophotometric determinations. Mean Plasma Lactate values at r e s t and for each workload for both the Experimental and Control T r i a l s are displayed i n Appendix B - Table 1. A l l values are l i k e l y somewhat higher than the true values. This i s due to the haemolysis of some samples. The haemolysis also 53 Table 1 Analysis of Variance of Selected Cardiorespiratory Measures Comparison of C a r d i o r e s p i r a t o r y Parameters Between Control and Experimental ANALYSIS OF VARIANCE SUMMARY TABLE SOURCE SUMS OF SQUARES MEAN SQUARES DF F RATIO P BETWEEN SUBJECTS ERROR 708.4485 141.6897 5 WITHIN SUBJECTS-TRIALS (CONT. vs. EXPER.) ERROR 61.3872 380.2730 61.38720 76.05460 1 5 .807 .410 V02, VE, EXCESS C02 ERROR 110503.4 991.454 55251.68 99.14536 2 10 557.280 .00001 TRIAL x V02, VE, C02 ERROR 57.35253 609.4042 28.67627 60.94042 2 10 .471 .638 explains some of the observed v a r i a b i l i t y i n t h i s measure since the degree of haemolysis was not consistent. As well no correction was performed for the expected plasma water s h i f t that occurs during exercise and the samples were not deproteinized. The spectrophotometric analysis i s s e n s i t i v e to the degree of haemolysis and would r e s u l t i n a r t i f i c i a l l y high values. The lack of correction for the plasma water s h i f t and deproteinization would have a s i m i l a r e f f e c t on the lact a t e concentration determinations though to a les s e r extent. There was no s i g n i f i c a n t difference between the res t i n g l a c t a t e values (t=0.234 p>.25) of the control and experimental t r i a l s . Control T r i a l Lactate Data. Figure 2a shows the Mean Plasma Lactate r i s i n g s l i g h t l y above res t i n g values and remaining r e l a t i v e l y constant u n t i l the tenth minute (235.5 watts) when a steady increase to a Mean Maximum Plasma Lactate of 18.21 +/- 5.46 mmol/1 i s reached during the f i f t e e n t h 54 (a) O LU CJ < CO < 36-j 33-30-27-24-21-18-15-12-9-6-3-0 — A CONTROL i ( i i i i i i i 0 47 94 141 188 235 282 329 376 423 POWER OUTPUT (WATTS) (b) IS CJ < CO < 36-n 33-30-27-24-21-18-15-12-9-6-3-l I I I I I I i i 47 94 141 188 235 282 329 376 423 POWER OUTPUT (WATTS) Figure 2 (a) Mean Plasma Lactate vs. Power Output Control T r i a l (b) Mean Plasma Lactate vs. Power Output Experimental T r i a l 55 minute. The lactate value at the f i f t e e n t h minute i s used as the maximum Mean Plasma Lactate for the Control T r i a l because a l l subjects completed that workload. The averaged data i n Figure 2a i s representative i n d i r e c t i o n of the i n d i v i d u a l data (See Appendix D). The complete data (Appendix E - Table 2a, p.10) shows that Subjects two and s i x had t e s t durations of 18 and 16 minutes respectively and that i n d i v i d u a l subject's maximum lactates ranged from 15.21 to 27.68 mmol/1 at the end of the Control T r i a l . Experimental T r i a l Lactate Data. The p l o t i n Figure 2b for Mean Plasma Lactate i n the Experimental T r i a l shows a markedly d i f f e r e n t trend than the Control T r i a l . The arm ergometer protocol performed by subjects i n the Experimental T r i a l s i g n i f i c a n t l y elevated Mean Plasma Lactate to 26.61 +/-8.86 mmol/1 p r i o r to the commencement of the incremental exercise protocol. A l l subjects with one exception (Subject 2) began the incremental exercise protocol i n the Experimental T r i a l with plasma lactate values that were greater than the maximal values reached at the end of the incremental exercise protocol i n the Control T r i a l . The Mean Plasma Lactate values i n the Experimental T r i a l are c l e a r l y higher than those of the Control T r i a l at a l l workloads except for the f i n a l few workloads. The high degree of v a r i a b i l i t y evident i n the mean lactates of the Experimental T r i a l (Figure 2b) can be attri b u t e d to the v a r i a b i l i t y i n the response of the 56 i n d i v i d u a l subjects to the arm work. Because of the r e l a t i v e l y untrained state of the arms and upper body musclature of these c y l i s t s a more variable response to exercise using these muscles i s expected. The v a r i a b i l i t y decreases s l i g h t l y during the course of the incremental protocol but remains quite large. This demonstrates the i n d i v i d u a l v a r i a b i l i t y i n the response to a l a c t a t e load and i t s removal. The varied a b i l i t y to handle elevated l a c t a t e loads i s apparent i n the control t r i a l as well with the v a r i b i l i t y increasing markedly a f t e r Tlac. Anaerobic Threshold Determination Using Plasma Lactates The anaerobic threshold (Tlac) was determined using the log-log model of Beaver, Wasserman and Whipp (1985) which f i t the data more accurately than the continuous model proposed by Hughson, Weisiger and Swanson (1987). The threshold i s expressed i n terms of oxygen uptake both i n absolute values and percentage of maximum achieved. Complete Tlac data for subjects i s presented i n Appendix E - Table 3. The mean anaerobic threshold was 2.28 +/- 0.37 1/min and i s indicated by the arrow i n Figure 2a. The anaerobic threshold of the Control T r i a l was used as the anaerobic threshold i n both t r i a l s for a l l subjects. This was due to the al t e r e d dynamics of l a c t a t e removal and appearance when lactates are elevated p r i o r to incremental exercise. As well an i n f l e c t i o n point was undetectable i n three of the s i x subjects during the Experimental T r i a l . The anaerobic threshold as estimated from 57 the mean p l o t of l a c t a t e and V02 represents a mean power output of 203.9 watts and a value which represents 72.6% of maximum achieved. The estimates of the anaerobic threshold are used i n the following analysis of the EMG data. Analysis of Integrated EMG Data The i n t e g r a l of the e l e c t r i c a l a c t i v i t y during each pedal cycle within each sample was calculated. The i n t e g r a l s of each pedal cycle were then averaged to give a mean per cycle value at each workload (CIEMG). Mean CIEMG was plotted against power output and i n i t i a l l y examined fo r the existence of an i n f l e c t i o n point which could be used to estimate the l a c t a t e threshold using the IEMG -Power method as outlined by Moritani (1980). This method requires that an i n f l e c t i o n point be v i s u a l l y determined p r i o r to deriving i t s exact location. Control T r i a l Integrated EMG Data. An i n f l e c t i o n point i n the v i c i n i t y of Tlac could not be v i s u a l l y i d e n t i f i e d for any of the subjects i n the Control T r i a l so the IEMG-Power method could not be employed. The trend of the Mean CIEMG data was therefore examined by c a l c u l a t i n g the slope of the IEMG vs. Power Output for three d i f f e r e n t sections of each p l o t . This method also eliminated the problem of high v a r i a b i l i t y between subjects seen (Figures 3a and 3b) i n the absolute CIEMG values. The slopes were calculated for both t r i a l s using sections of each p l o t as i d e n t i f i e d by: (a) Total Exercise Period; b) Pre-Tlac; and c) Post T-Lac. The slope values are 58 (a) 1-i 0.75-00 O 0.50-LU CO > CD UJ (b) 0.25 0 -0.25-1 -0.50 0.75 CO CJ 0.50 H LU CO ^ 0.25 yj 0 (J -0.25--0.50 • CONTROL i 1 r — i 1 1 1 1 1 47 94 141 188 235 282 329 376 423 POWER OUTPUT (WATTS) EXPERIMENTAL I I \ I I I 188 235 282 329 376 423 47 94 14  POWER OUTPUT (WATTS) Figure 3a - CIEMG vs. Power Output - Control Figure 3b - CIEMG vs. Power Output - Experimental 59 displayed i n Table 2. An analysis of variance was performed to determine i f any s i g n i f i c a n t difference existed between the slope of the l i n e s for these comparisons. Table 3 indicates there was no s i g n i f i c a n t difference in the slopes of the IEMG vs. Power Output f o r any of the comparisons made. Table 2 Slope of IEMG vs. Power Output Plot for the Total Exercise Period and Before and A f t e r the Lactate Threshold CONTROL TRIAL | I EXPERIMENTAL TRIAL Subj. Slope Slope of Slope of 1 Slope Slope of Slope of # Total CIEMG CIEMG I Total CIEMG CIEMG Durat. Pre-Tlac Post-Tlac 1 Durat. Pre-Tlac Post-Tlac 1 .111 .125 .098 I I .117 .126 .018 2 .191 .173 .091 1 .078 .097 .061 3 .121 .073 .429 1 .131 a a 4 .121 .115 .055 I .088 .102 .051 5 .082 .054 .182 | .114 .118 .182 6 .221 .148 1.82 1 .108 .080 .229 Mean .141 .115 .445 1 I .106 .105 .109 S.D. .050 .040 .631 1 I .020 .020 .082 Note. indicates that there was an i n s u f f i c i e n t number of points beyond the anaerobic threshold to determine a slope. This subject was not included i n the analysis of var i a n c e . Experimental T r i a l Integrated EMG Data. No i d e n t i f i a b l e i n f l e c t i o n point existed i n the v i c i n i t y of Tlac i n any of the t r i a l s i n the Experimental T r i a l . Table 3 indicates that there was no s i g n i f i c a n t d i f f e r e n c e between Pre-Tlac and Post-Tlac slopes of the IEMG vs. Power pl o t for the Experimental T r i a l and that no s i g n i f i c a n t difference existed between Control and Experimental T r i a l s i n Total Exercise Period slopes, Pre-Tlac or Post-Tlac slopes. 60 Table 3 Analysis of Variance of Slopes of IEMG vs. Power Output Plots Comparison of Slope of IEMG vs. Power Output Between Control and Experimental ANALYSIS OF VARIANCE SUMMARY TABLE SOURCE SUMS OF SQUARES MEAN SQUARES DF F RATIO P BETWEEN SUBJECTS ERROR .5207872 .1301968 4 WITHIN SUBJECTS TRIALS (CONT. vs. EXPER.) ERROR .1357441 .3984209 .1357441 .0996052 1 4 1.363 .308 PRE & POST TLAC & TOTAL ERROR .1716329 .9004025 .085816 .1125503 2 8 0 .762 .498 TRIAL x PRE,POST,TOTAL ERROR .1606889 609.4042 .0803444 60.94042 2 10 1.079 .385 The rate of increase i n e l e c t r i c a l output of the vastus l a t e r a l i s was not s i g n i f i c a n t l y d i f f e r e n t i n ei t h e r t r i a l . Further there was no s i g n i f i c a n t difference i n the pre- and post-Tlac comparisons for any of the subjects i n ei t h e r t r i a l . The p l o t s i n Figure 3a and 3b graphically confirm these conclusions. The high degree of intra-subject v a r i b i l i t y i n the mean CIEMG and mean Plasma Lactate i s evident i n both measures f o r both t r i a l s . However examination of i n d i v i d u a l p l o t s (Appendix E, p. 91-96) show that i n d i v i d u a l subjects data are very s i m i l a r i n d i r e c t i o n for both l a c t a t e and CIEMG. Examination of the Relationship Between Lactate and CIEMG In order to determine the degree to which changes i n plasma la c t a t e are r e f l e c t e d i n changes i n the CIEMG Pearson's Product Moment Correlation was performed for la c t a t e and CIEMG. In the Control T r i a l only f i v e of the s i x subjects showed s i g n i f i c a n t correlations with c o e f f i c i e n t s ranging from 0.57 to 0.97. The mean r value for the subjects showing 61 s i g n i f i c a n t correlations i n the Control T r i a l was 0.81+/-0.15. In the Experimental T r i a l only three of the s i x subjects showed s i g n i f i c a n t correlations between lactate and CIEMG. The s i g n i f i c a n t r values i n the Experimental T r i a l were a l l negative and ranged from -0.62 to -0.96. The mean r value for the Experimental T r i a l was -0.84+/-0.15. The negative value i s expected i n the Experimental T r i a l data since l a c t a t e was decreasing f o r the majority of the t e s t while CIEMG increased s t e a d i l y throughout. Correlation c o e f f i c i e n t s f o r each subject i n both t r i a l s are contained i n Table 4 below. A further c o r r e l a t i o n performed between Power Output and CIEMG demonstrated highly s i g n i f i c a n t c o r r e l a t i o n s f o r a l l subjects i n both t r i a l s . The c o e f f i c i e n t s are displayed i n Table 10 above. The r values ranged from 0.92 to 0.99 and from 0.91 to 0.99 i n the Control and Experimental T r i a l s respectively. A l l r values except one were s i g n i f i c a n t at the .00001 l e v e l . The mean r value for the Control T r i a l was 0.96+/-0.02 and the mean r value for the Experimental T r i a l was 0.95+/-0.03. The mean r 2 value for the Control and Experimental T r i a l s was 0.90 and ranged from 0.84 to 0.98 which indicates that on average 90% of the v a r i a b i l i t y i n the CIEMG i s explained.by the v a r i a t i o n i n the power output. In contrast the mean r 2 value for the Control T r i a l f or la c t a t e versus CIEMG i s only 0.66. Thus only 66% of the v a r i a b i l i t y i n the CIEMG i s explained by the v a r i b i l i t y i n the plasma l a c t a t e . I t should also be noted once again that 62 (a) O LU < CO < 0.75 -0.50 -0.25 O CO O UJ CO >UJ o --0.25 i i i i i i i r 47 94 141 188 235 282 329 376 423 POWER OUTPUT (WATTS) -0.50 (b) LU is cj < CO < i i i r 141 188 235 282 329 376 423 0.50 47 94 POWER OUTPUT (WATTS) Figure 4a - Mean CIEMG and Plasma Lactate vs. Power Output Control T r i a l Figure 4b - Mean CIEMG and Plasam Lactate vs Experimental T r i a l Power Output 63 c o r r e l a t i o n was s i g n i f i c a n t i n f i v e of s ix subjects. A s i m i l a r analysis of the r values i n the Experimental T r i a l would indicate that 71% of the v a r i a b i l i t y i n CIEMG i s explained by the v a r i a b i l i t y i n plasma lactate. However the negative correlations would suggest that increasing l a c t a t e causes a decrease i n CIEMG. This i s c l e a r l y not the case and indicates the complete reversal of the rel a t i o n s h i p between l a c t a t e and CIEMG during the Experimental T r i a l . Table 4 Correlations C o e f f i c i e n t s f o r CIEMG and Power Output and CIEMG  and Plasma Lactate for both T r i a l s POWER OUTPUT VS. CIEMG S LACTATE VS. CIEMG Control Experimental H Control Experimental # R P R P R P R P 1 0.99 10-6 * 0.93 10-6 * 0.82 .0003* -0.93 .0008* 2 0.92 10-6 * 0.97 10-6 * 0.57 .02 * -0.62 .02 * 3 0.94 10-6 * 0.99 10-6 * 0.97 10-5 * -0.96 .0004* 4 0.97 10-6 * 0.96 10-6 * 0.62 .05 -0.34 .41 5 0.94 10-6 * 0.95 10-6 * 1 0.86 .004 * 0.31 .36 6 0.96 10-6 * 0.91 .000006*H 0.71 .03 -0.47 .11 H ' x- 0.96 10-6 * 0.95 .000009*1 0.76 .02 -0.50 .15 sd 0.02 n/a 0.03 .000001*1 0.13 .02 0.43 .17 Note. - * ind i c a t e s R value i s s i g n f i c a n t l y greater than 0. 64 Chapter 5 DISCUSSION The r e s u l t s of the investigation presented i n the previous chapter w i l l be discussed i n d e t a i l here under the following subsections: (a) Cardiorespiratory and metabolic data; (b) Response of EMG to Plasma Lactate; (c) Explanation of c o n f l i c t i n g r e s u l t s . Cardiorespiratory and Metabolic Data The cardiorespiratory and metabolic data c o l l e c t e d on the subjects i n t h i s investigation are i n general agreement with previous r e s u l t s . The mean maximal oxygen uptake value reported for trained c y c l i s t s by Simon et a l . (1986) was 63.8 +/- 1.3 ml/kg/min. In t h i s investigation a somewhat lower mean value of 47.1 +/-5.62 ml/kg/min was found. The high R.Q. r a t i o s do indicate a heavy reliance on anaerobic g l y c o l y s i s and more importantly the anaerobic or lactat e threshold was c l e a r l y surpassed i n a l l subjects for both t r i a l s . The somewhat lower than expected oxygen uptake values are inconsequential for the purposes of t h i s study because Tlac was the point being examined for comparison. However the fact that absolute maximums were not reached may be important i n l i g h t of the present r e s u l t s and w i l l be considered i n the f i n a l section. A l l other cardiorespiratory measures showed t y p i c a l progressions for incremental exercise. Values were lower than could be expected from trained c y c l i s t s but commensurate with 65 the oxygen uptake values. A l l values obtained for the cardiorespiratory measures are representative of maximum under the constraints of the protocol used. The absolute values for plasma lactate concentrations are higher than those reported by other investigators. In the Control T r i a l a mean maximum value (at 15 minutes) of 18.21 +/- 5.5 mmol/1 was found as compared to the mean maximal value of 10.5 +/- 1.1 mmol/1 reported by Simon et a l . (1986). The plasma l a c t a t e determinations of the present study were not corrected for plasma water s h i f t s known to occur during exercise and many of the samples were haemolysed. These factors both would have the e f f e c t of elevating plasma l a c t a t e concentrations which were spectrophotometrically determined. Response of EMG to Plasma Lactate Plasma Lactate Changes i n Control T r i a l . The IEMG has been reported to be useful as a non-invasive estimate of the lact a t e threshold (Nagata et a l . , 1981, Moritani et a l . , 1984, V i i t a s a l o et a l . , 1985) during incremental work. The r e s u l t s of the present investigation do not support the conclusions of previous work. The trend of the changes i n mean plasma l a c t a t e concentration with incremental work for the Control T r i a l are t y p i c a l with a very c l e a r and d e f i n i t e i n f l e c t i o n point. The anaerobic threshold (Tlac) as defined for t h i s i n v e s t i g a t i o n was i d e n t i f i e d and determined by computer analysis (Hughson et 66 l a c t a t e accumulation. Muscle lactate accumulation i s related to the observed decrement i n muscle pH (Keul et a l . , 1972 and Sahlin, 1978) and has been shown to be related to detrimental e f f e c t s on the c o n t r a c t i l e apparatus (Fuchs et a l . , 1970, Donaldson, 1978, Schadler, 1967, Nakamura and Schwartz, 1972). These detrimental e f f e c t s have been related to a l t e r e d e l e c t r i c a l c h a r a c t e r i s t i c s which may be r e f l e c t e d i n the EMG s i g n a l (Hakkinnen et a l . , 1986, Komi, 1984, Moritani, Muro and Nagata, 1986, Komi and Tesch, 1979, V i i t a s a l o and Komi, 1978, and Tesch et a l . , 1983) I t has been postulated that these relationships should allow for the use of the EMG i n the detection of the Tlac. The E f f e c t of Lactate Accumulation on the CIEMG During  the Control T r i a l . The analysis of the CIEMG data showed no i d e n t i f i a b l e i n f l e c t i o n points when plotted against power output. This made the use of the IEMG-Power method for anaerobic threshold determination as outlined by Moritani (1980) and validated by Nagata et a l . (1981) impossible since i t i s predicated on p r i o r v i s u a l i d e n t i f i c a t i o n of an i n f l e c t i o n point. This study produced r e s u l t s which are contrary to Moritani et a l . (1984). Using incremental forearm exercise with a modified handgrip dynamometer Moritani et a l . (1984) were able to show very high correlations for a l l f i v e subjects between venous lactate, IEMG and MPF (0.977 to 0.857 and -0.960 to -0.862 resp e c t i v e l y ) . In the present invest i g a t i o n c o r r e l a t i o n c o e f f i c i e n t s for venous la c t a t e and 67 CIEMG were s i g n i f i c a n t i n only four of s i x subjects (0.57 to 0.97) . I t i s notable that Moritani did not employ h i s own IEMG-Power method for determination of the l a c t a t e threshold i n t h i s i nvestigation. In fact the study by Moritani et a l . (1984) used no objective c r i t e r i o n to determine any of the i n f l e c t i o n points. A f t e r i d e n t i f y i n g the l a c t a t e threshold as "...an abrupt increase i n lactate concentration. 1 1 Moritani et a l . (1984) showed s i g n i f i c a n t differences i n IEMG, MPF, and venous l a c t a t e between points on either side of the l a c t a t e threshold. However close examination of Moritani's data do not support the rationale used to explain h i s findings. The r e s u l t s show the lac t a t e threshold occuring at a mean venous lactate concentration of approximately 2 mmol/1. This l a c t a t e load i s l e s s than that shown by previous investigators to be sustainable and demonstrates the possible existence of other mechanisms for the observed i n f l e c t i o n points. Moritani (1984) contends that l a c t a t e and the accompanying decrement i n pH has detrimental e f f e c t s on the c o n t r a c t i l e apparatus at venous concentrations of approximately 2 mmol/1 and a r t e r i a l concentrations of 1.5 mmol/1. J o r f e l d t (1970) examined the uptake and u t i l i z a t i o n of lactate using radioactive tracers during steady state forearm exercise at 1.634 watts a f t e r a r t e r i a l l a c t a t e concentrations were a r t i f i c i a l l y elevated. Subjects had t h e i r a r t e r i a l lactate concentrations a r t i f i c i a l l y elevated by continuous infusion and then 68 exercised f o r a period of 60 minutes. The a r t e r i a l l a c t a t e concentrations a f t e r 10 minutes of exercise were 3.35 mmol/1 and a f t e r 40 minutes were only 3.36 mmol/1. Measurements of pH of a r t e r i a l blood taken simultaneously showed values of 7.43 and 7.47 at 10 and 40 minutes respectively. These values are i n agreement with data presented i n Keul et a l . (1972) from a previous study by Keul et a l . (1967) which showed that at a r t e r i a l concentrations of 2 mmol/1 pH has decreased very l i t t l e to a value of approximately 7.3. The values presented by Keul et a l . (1972) give somewhat higher estimates of pH both at r e s t and a f t e r maximal exercise than some more recent studies (Sahlin et a l . , 1972 and Sahlin et a l . , 1976). However despite differences i n the absolute values the r e l a t i v e decrement would be expected to be s i m i l a r given the highly s i g n i f i c a n t negative correlations between l a c t a t e and pH (Sahlin, 1978, Keul et a l . , 1972). The intramuscular pH would be lower than these e x t r a c e l l u l a r values but i t seems un l i k e l y that a decrement i n pH can explain the observed changes i n the IEMG with an a r t e r i a l l a c t a t e load of only 1.5 mmol/1 (Moritani ,1984). In fact to suggest that changes observed were related to metabolic a l t e r a t i o n s i s questionable p a r t i c u l a r l y i n view of the subjective manner of determining the i n f l e c t i o n points. The protocols of the J o r f e l d t (197 0) and Moritani et a l . (1984) were d i f f e r e n t therefore one could expect some differences i n the dynamics of l a c t a t e accumulation but the accumulation would s t i l l be expected to 69 have a s i m i l a r e f f e c t on pH making i t d i f f i c u l t to a t t r i b u t e changes i n the IEMG to small changes i n pH. Moritani (1984) did not report l a c t a t e values per kilogram of body weight making quantitative comparisons inconclusive. In the present investigation the r e s t i n g l a c t a t e l e v e l s of the Control T r i a l were more than twice venous l a c t a t e l e v e l s demonstrated by Moritani et a l . (1984) at the l a c t a t e threshold. At the l a c t a t e threshold present values were more than three times Moritani's values. This i s expected given the much larger muscle mass of the vastus l a t e r a l i s muscle and the elevated absolute lactate values of the present invest i g a t i o n . However i f the r e l a t i o n s h i p between la c t a t e and IEMG i s to be supported i t would be expected that changes previously observed i n the IEMG would be c l e a r l y evidenced at these l a c t a t e loads. The lack of an i n f l e c t i o n point i n the CIEMG refutes the existence of a predictable r e l a t i o n s h i p between la c t a t e and CIEMG under the conditions of the present invest i g a t i o n . However the difference i n r e s u l t s may be a t t r i b u t a b l e i n part to differences i n methodology and the previously demonstrated rela t i o n s h i p may e x i s t under c e r t a i n s p e c i f i c conditions. To determine i f a v i s u a l l y undetectable change was occuring an analysis of the slopes of these plots was performed using a method adapted from V i i t s a a l o et a l . (19851). V i i t s a a l o reported a s i g n i f i c a n t difference i n slope of the IEMG-Power rel a t i o n s h i p at power outputs below and above the 70 a r t e r i a l l a c t a t e threshold. In the present i n v e s t i g a t i o n the CIEMG recorded during the Control T r i a l increased i n a near l i n e a r fashion despite a marked rapid increase i n the plasma lac t a t e concentration once the lactate threshold was reached. The slope of the CIEMG vs Power Output p l o t was not s i g n i f i c a n t l y d i f f e r e n t when compared before and a f t e r the la c t a t e threshold for any of the subjects i n the Control T r i a l . The r e s u l t s of t h i s analysis indicate that the CIEMG shows no s e n s i t i v i t y to changes i n blood l a c t a t e concentration during incremental exercise using the present protocol and that the use of IEMG as an indicator of the la c t a t e threshold or anaerobic threshold i s not r e l i a b l e under a l l conditions. Plasma Lactate Changes i n Experimental T r i a l . The re l a t i o n s h i p between lactate and IEMG was tested further by a l t e r i n g the normal dynamics of lactate u t i l i z a t i o n and production. The trend of the changes i n mean plasma l a c t a t e concentrations of the Experimental T r i a l show a c l e a r and marked a l t e r a t i o n i n the dynamics of lactate production and u t i l i z a t i o n as compared to the Control T r i a l . The steady decrease i n lactate concentration from the i n i t i a l l y high value indicates p r e f e r e n t i a l u t i l i z a t i o n of the la c t a t e produced p r i o r to incremental exercise. As expected t h i s steady decrease continues u n t i l the lactate threshold i s reached when a sudden increase occurs. At a l l workloads for a l l subjects the plasma lactate concentration of the Experimental T r i a l was greater than those of the Control 71 T r i a l . Karlsson et a l . (1975) demonstrated that l a c t a t e l e v e l s were elevated i n non-exercising muscle following exhaustive short term exercise by other muscle groups and concluded that: ...muscles which have been engaged i n heavy exercise e x h i b i t a d e f i n i t e influence on the metabolic s i t u a t i o n i n other "non-exercised" muscles which w i l l l i m i t t h e i r performance, (p. 766) These investigators showed a decrease i n performance time when la c t a t e was elevated p r i o r to an exercise bout. They attr i b u t e d t h i s decrease i n performace to "... one or more l o c a l metabolic f a c t o r s . . . " and i d e n t i f i e d phosphagen depletion or l a c t a t e accumulation as possible candidates. This would support the premise that the increased concentration of l a c t a t e produced through the high i n t e n s i t y arm protocol of the present experiment would have a detrimental e f f e c t on the vastus l a t e r a l i s during c y c l i n g . However a s i g n i f i c a n t difference i n performance time was not found. The present i n v e s t i g a t i o n u t i l i z e d an incremental exercise protocol following the elevation of plasma l a c t a t e . This would make the presence of lac t a t e less detrimental i n i t i a l l y and could explain the lack of a s t a t i s t i c a l difference i n mean te s t duration between the two t r i a l s . Recent research has shown c l e a r l y that l a c t a t e i s an important oxidative substrate during exercise (Eldridge, et a l . , 1974 and Issekutz, 1984). Further the u t i l i z a t i o n of l a c t a t e as a substrate i n oxidation i s increased with increasing exercise i n t e n s i t y . This 72 u t i l i z a t i o n i s c l e a r l y r e f l e c t e d i n the steady decrease i n plasma la c t a t e concentration seen i n the Experimental T r i a l . Despite the use of lactate as a substrate, production or appearance of la c t a t e eventually exceeds u t i l i z a t i o n or disappearance and accumulation occurs (Wasserman, 1986, and Wasserman et a l . , 1986). This i s evidenced by the increase i n the plasma lactate seen around Tlac of the Experimental T r i a l . Despite the considerable u t i l i z a t i o n of la c t a t e the concentration of the lactate was higher i n the Experimental T r i a l than i n the Control T r i a l f or a l l subjects throughout the exercise period i t would be expected that the proposed detrimental e f f e c t s of increased lactate concentration would have been accelerated i n the Experimental T r i a l . The s e n s i t i v i t y of the CIEMG to changes i n plasma la c t a t e should be c l e a r l y evidenced under these circumstances i f previous research i s to be supported. The E f f e c t of Lactate Accumulation on the CIEMG During  the Experimental T r i a l . During the Experimental T r i a l a near l i n e a r increase, very s i m i l a r to the Control T r i a l was again demonstrated i n the CIEMG. This trend continued during periods of both decreasing and increasing plasma la c t a t e concentrations. The CIEMG did not respond as predicted i n the Control T r i a l and was also impervious to the c l e a r l y altered l a c t a t e dynamics of the Experimental T r i a l . In fac t the nature of the relat i o n s h i p between lactate and CIEMG was e n t i r e l y reversed during the Experimental T r i a l with 73 s i g n i f i c a n t negative c o r r e l a t i o n c o e f f i c i e n t s i n only three of the s i x subjects (-0.62 to -0.97). The negative co r r e l a t i o n s i n the Experimental T r i a l are not unexpected. The rationale used to support the existence of a r e l a t i o n s h i p between lac t a t e and IEMG points to decreased pH as a factor i n the observed change i n IEMG. In the early submaximal loads of the Experimental T r i a l a decrease i n pH would not be expected because there i s net lactat e u t i l i z a t i o n and therefore no net proton accumulation. However the lack of a consistent r e l a t i o n s h i p f o r a l l subjects i n the Experimental T r i a l indicates that changes i n lactate do not a f f e c t the CIEMG i n a predictable or consistent manner. This demonstrates an i n s e n s i t i v i t y of the EMG signal to changes i n the plasma lac t a t e concentration during incremental exercise protocol of the present investigation. I t i s important to note that the CIEMG of the Experimental T r i a l responded almost i d e n t i c a l l y to the CIEMG of the Control T r i a l . The metabolic changes that occur with an increased lactat e load would not be al t e r e d i n absolute terms from those of the Control T r i a l however they would be accelerated and the sudden increase i n l a c t a t e accumulation (Tlac) would be expected to occur e a r l i e r than the Tlac of the Control T r i a l . A subjective comparison of the Experimental and Control T r i a l (Appendix E) p l o t s indicates that Tlac did occur e a r l i e r i n the Experimental T r i a l than i n the Control T r i a l i n f i v e of the s i x subjects. In a l l instances Tlac was s h i f t e d one workload to the l e f t i n 74 the Experimental T r i a l . This demonstrates that the la c t a t e accumulation and therefore the decrement i n pH would have begun e a r l i e r i n the Experimental T r i a l . Previous r e s u l t s (Moritani, 1980, Nagata et a l . , 1981, Moritani et a l . , 1984, and V i i t a s a l o et a l . , 1985) would suggest that the IEMG (CIEMG) should have been sensi t i v e to t h i s s h i f t . Explanation of C o n f l i c t i n g Results The rat i o n a l e provided by previous investigators f o r the re l a t i o n s h i p between the IEMG and plasma l a c t a t e has been that the increase i n lactate causes a decrement i n muscle pH which i n turn impairs some of the contracting f i b r e s through several possible mechanisms. The muscle compensates for t h i s d e f i c i t i n c o n t r a c t i l i t y by r e c r u i t i n g more motor units or by increasing the f i r i n g frequency of already r e c r u i t e d f i b r e s . As the power output increases an increasing number of the r e c r u i t e d f i b r e s are fas t g l y c o l y t i c f i b r e s . These f i b r e s produce greater amounts of lactate and have greater peak amplitudes and f i r i n g frequency. I t i s suggested that t h i s would r e s u l t i n an increase i n the IEMG greater than that a t t r i b u t e d to the increasing power output r e s u l t i n g i n the observed i n f l e c t i o n point. The t h e o r e t i c a l l o g i c i s sound and i s supported by previous work which has demonstrated a re l a t i o n s h i p between al t e r a t i o n s i n the IEMG of a working muscle during exercise and changes i n the metabolic environment. The data of the present investigation can also be 75 supported by recent research which would suggest that the r e l a t i o n s h i p between IEMG and lactate during incremental exercise i s conincidental (Bourbrit, 1983, M i l l s and Edwards, 1983, Komi, 1984, and Helal et a l . , 1987). Previous research suggesting that IEMG can be used as an estimate of the l a c t a t e threshold i s based upon research which indicates a r e l a t i o n s h i p between lactate accumulation and changes i n the amplitude and frequency spectrum of a working muscle (Lindstrom et a l . , 1970, Mortimer et a l . , 1970, V i i t a s a l o and Komi, 1978, Komi and Tesch, 1979, Tesch et a l . , 1983, Komi, 1984 and Moritani et a l . , 1986). This i s further supported by research which demonstrates that muscles which are higher i n FG f i b r e s and therefore produce greater amounts of l a c t a t e show a greater decrease i n the center frequency than muscles of predominantly SO f i b r e s (Komi and Tesch, 1979, Tesch et a l . , 1983). This rela t i o n s h i p i s well substantiated. The c o n f l i c t i n g data on the nature of the r e l a t i o n s h i p between IEMG and power output i n the absence of fatigue must be considered. A number of investigations have demonstrated non-linear rela t i o n s h i p s . A l l previous studies examining the postulated IEMG - lactate r e l a t i o n s h i p have reported high cor r e l a t i o n s between these two variables. None of these studies have reported correlations between power output and IEMG. In the present investigation s i g n i f i c a n t c o rrelations between la c t a t e and CIEMG were demonstrated for f i v e subjects (Control). However i n both t r i a l s a l l subjects data showed 76 power output to be more highly correlated with the changes i n CIEMG than was l a c t a t e . I t i s possible that previously observed i n f l e c t i o n points i n the IEMG during incremental work are simply the r e s u l t of a non-linear r e l a t i o n s h i p between CIEMG and power output which has been previously demonstrated i n the absence of lactat e accumulation. The existence of higher co r r e l a t i o n s between IEMG and power output does not eliminate the p o s s i b i l i t y of a r e l a t i o n s h i p between l a c t a t e and IEMG. However i t suggests the r e l a t i o n s h i p may be conincidental and i s c l e a r l y not causal under a l l conditions. Comparison of previous r e s u l t s with present r e s u l t s must also consider methodological differences. There were two major differences between the present inves t i g a t i o n and those that employed incremental c y c l i n g exercise protocols i n previous studies. They were: (1) Cadence (2) Subject's c y c l i n g experience. Power output was used as measure of i n t e n s i t y i n a l l investigations. Power output on a cycle ergometer i s a product of the cadence and the applied force. Equivalent power outputs may be obtained by varying e i t h e r of these two factors. There i s some data which indicates (Coast and Welch, 1985, Boning et a l . , 1987) that equivalent power outputs at d i f f e r e n t cadences do not e l i c i t equivalent metabolic responses. Coast and Welch (1985) reported a parabolic r e l a t i o n s h i p between oxygen uptake and increasing cadence at equivalent power outputs during incremental exercise. These researchers did not monitor EMG but i t i s 77 possible the altered metabolic response would be r e f l e c t e d i n the EMG s i g n a l . I t i s possible to speculate that a muscle's recruitment pattern/strategy would be e n t i r e l y d i f f e r e n t with a l i g h t load and high cadence when compared to a heavy load and low cadence. The present investigation used higher cadence (90 rpm) than any of the previous investigations which demonstrated a re l a t i o n s h i p between IEMG i n f l e c t i o n points and l a c t a t e i n f l e c t i o n s points. As well none of the previous studies monitored cadence or used i t as a c r i t e r i o n for ending the exercise t e s t . Helal et a l . (1987) used a cadence of 80 rpm and reported the i n f l e c t i o n points i n only f i v e of t h e i r nine subjects. I t i s possible then that the l a c t a t e - IEMG rel a t i o n s h i p may only e x i s t under c e r t a i n conditions with a p a r t i c u l a r type of muscle recruitment strategy dictated by a c e r t a i n force and cadence combination. I t i s possible to speculate that the i n f l e c t i o n point may disappear at higher cadences used i n the present i n v e s t i g a t i o n and as seems to be occurring i n the investigation by Helal et a l . (1987). The influence of the varying cadence on recruitment during incremental exercise has not been examined and would provide data to confirm or refute such speculation. Also the use of a drop i n cadence of only one rpm as the c r i t e r i o n f o r stopping the t e s t seems to have not allowed subjects ot a t t a i n t h e i r true maximum. This i s evident i n both the oxygen uptake values and the heart rate data neither of which showed the t y p i c a l l e v e l i n g o f f . I t i s possible that 78 CIEMG i n f l e c t i o n points may have become apparent i f true maximum had been reached. However t h i s does not a l t e r the present conclusion that CIEMG does not respond to increased l a c t a t e concentration following under the conditions of t h i s i n v e s t i g a t i o n . The present investigation also d i f f e r e d i n that i t was the only study to employ experienced trained c y c l i s t s . I t i s possible that such athletes could have developed a d i f f e r e n t recruitment strategy than t h e i r untrained counterparts during incremental c y c l i n g exercise. Such differences may account i n part for the present c o n f l i c t i n g r e s u l t s but no evidence i s av a i l a b l e at t h i s point. The use of IEMG to estimate the la c t a t e threshold implies that the IEMG i s s u f f i c i e n t l y s e n s i t i v e to and driven by changes i n la c t a t e concentration and the subsequent decrement i n pH. The use of the IEMG to predict the l a c t a t e threshold would require that the r e l a t i v e l y small changes i n pH at the point of the threshold cause a l t e r a t i o n s i n the EMG signal immediately. Data are available which indicate a drop i n pH of only 0.5 units from rest to maximal exercise. The la c t a t e l e v e l s at Tlac are s i g n i f i c a n t l y greater than submaximal l e v e l s but les s than the maximal l e v e l s that are attained at the point of exhaustion. A commensurate decrement i n pH would be expected at Tlac. The data of Keul et a l . (1972) indicate that at the mean lactate l e v e l s of Tlac i n the Control T r i a l (7.18 +/-0.74 mmol/1) of the present experiment a decrement 79 of approximately 0.1 units i n pH from the re s t i n g pH of the a r t e r i a l blood could be expected. Further a decrement of only 0.05 pH units would be expected i n the pH from the pH value one minute p r i o r to Tlac. These small decrements i n pH may have an e f f e c t on the e l e c t r i c a l c h a r a c t e r i s t i c s of the working muscle. I t seems u n l i k e l y that t h i s small decrement would be r e f l e c t e d i n the EMG given the global nature of the surface electromyogram as a measurement t o o l . The r e s u l t s of the present experiment c l e a r l y do not support the suggestion of such a high degree of s e n s i t i v i t y . In fact these r e s u l t s suggest that changes i n l a c t a t e concentration are poorly related to changes i n CIEMG (IEMG) of the muscle during incremental exercise and show no measureable changes at the i n t e n s i t y represented by the l a c t a t e threshold. This conclusion i s supported by recent research which shows a an uncoupling of the proposed lactate - IEMG re l a t i o n s h i p (Bourbrit, 1983, M i l l s and Edwards, 1983, Komi, 1984, and Helal et a l . , 1987). The time course for recovery of increased l a c t a t e concentration has been demonstrated to be d r a s t i c a l l y d i f f e r e n t than the time course for the recovery of the amplitude and frequency c h a r a c t e r i s t i c s of the EMG s i g n a l . Investigations examining t h i s subject have noted that l a c t a t e may require anywhere from several minutes to a few hours to return to normal while amplitude and mean power frequency have been shown to recover almost immediately upon the cessation of exercise (Edwards et a l . , 1972, Karlsson et a l . , 1975, Broman, 80 1977, Petrofsky, 1980, Komi, 1984). Bourbrit (1983) showed s i m i l a r r e s u l t s but i n addition showed that the frequeny spectrum had returned to normal even while l a c t a t e concentration was s t i l l increasing. M i l l s and Edwards (1983) supported further the lack of a causal r e l a t i o n s h i p between increased l a c t a t e concentration and change i n the IEMG of a muscle. They showed a greater frequency s h i f t i n subjects with myophophorylase deficiency who produce absolutely no l a c t a t e during exercise than i n normal controls. This would indicate the existence of some other mechanism or mechanisms responsible for the altered EMG signals. In the present investigation the increase i n CIEMG was nearly l i n e a r and showed highly s i g n i f i c a n t c o r r e l a t i o n s with power output for a l l subjects i n both conditions. In a l l subjects the c o r r e l a t i o n between power output and CIEMG was greater than the c o r r e l a t i o n between lactate and CIEMG. The changes i n CIEMG were predicted better by changes i n power output than by changes i n l a c t a t e . The suggested r e l a t i o n s h i p between IEMG and lact a t e i s based upon the e f f e c t s l a c t a t e accumulation has on pH and the subsequent e f f e c t s i t has on the c o n t r a c t i l e apparatus. The use of the surface electromyogram and the IEMG to determine the l a c t a t e threshold suggests that the e f f e c t of increased lactat e accumulation and decreased pH has an immediate measureable e f f e c t on the recruitment and f i r i n g frequency of the working muscle at the l e v e l of the l a c t a t e threshold. However a majority of the 81 evidence i n t h i s area reports e f f e c t s on the IEMG which are relat e d to metabolic changes only at or near maximal l e v e l s . While the l a c t a t e threshold represents a "point of no return" fo r sustained performance the muscle i s s t i l l capable of maintaining or even increasing developed tension f o r a considerable period of time beyond t h i s point. The r e l a t i o n s h i p between muscle la c t a t e and a l t e r a t i o n s i n the IEMG at the lactate threshold of a working muscle appear to be fortuitous. A change i n the IEMG of a muscle as recorded by surface electrodes requires there be: (a) a change i n the number of motor units recruited; (b) a change i n the f i r i n g frequency of already recruited f i b r e s or newly recruited f i b r e s (Bigland and Lippold, 1954, and Milner-Brown et a l . , 1975). Changes i n these parameters have been shown to be related to changes i n lactate concentration and to several other factors. However these parameters may also be alter e d simply by changes i n recruitment patterns within a group of muscles performing a complex movement. Consideration of t h i s p o s s i b i l i t y i s important given the summative nature of the surface electromyogram. Procedural d i f f i c u l t i e s inherent i n the use of surface electromyogram must also be considered. The c h a r a c t e r i s t i c high i n t e r - i n d i v i d u a l v a r i a b i l i t y makes grouping of EMG data for analysis d i f f i c u l t . Individual subject data i s often presented as c h a r a c t e r i s t i c making v a l i d generalizable conclusions impossible. Further the problems i n examining data for i n f l e c t i o n points without employing an 82 objective c r i t e r i o n and then performing correlations on the i d e n t i f i e d points introduces greater p o s s i b i l i t y of error and makes subsequent conclusions questionable. On the other hand given the differences i n methodology discussed above i t i s possible that the re l a t i o n s h i p does e x i s t under c e r t a i n conditions. The issue of the e f f e c t of varying cadence on the recruitment pattern during incremental exercise i s important and must be resolved to make any conclusive statements concerning the e f f e c t of a changing metabolic environment on the electromyographic s i g n a l . The evidence to date i n combination with the present r e s u l t s would suggest that while a relat i o n s h i p between la c t a t e and IEMG seems to e x i s t t h i s r e l a t i o n s h i p may be the r e s u l t of the two variables responding independently to some other factor or factors. 83 Chapter 6 SUMMARY, CONCLUSIONS, FINDINGS, AND RECOMMENDATIONS Summary This investigation was designed to t e s t the hypothesis that changes i n plasma lactate concentration drive changes i n the electroymyographic p r o f i l e of working muscle during incremental exercise. The hypothesis was tested by a l t e r i n g the dynamics of lactate production and u t i l i z a t i o n of the vastus l a t e r a l i s during incremental cycle ergometer work and comparing the changes recorded i n the IEMG of the same muscle. The anaerobic or lact a t e threshold was determined for each subject using a log-log transformation of a lactate vs oxygen uptake p l o t . The lact a t e threshold was not detectable using the IEMG Power method as presented by previous researchers. Subsequently an analysis of the slope of the IEMG vs oxygen uptake pl o t s was performed before and a f t e r the lactate threshold f o r both conditions. Correlations were determined between l a c t a t e concentration and the CIEMG and between power output and CIEMG. The data were c o l l e c t e d on s i x male c y c l i s t s (22.0 +/-4.1 years). Each subject performed two incremental exercise t r i a l s on a cycle ergometer. The protocol consisted of 4 minutes of unloaded c y c l i n g followed by l i n e a r increases of 84 23.5 watts per minute at 90 revolutions per minute. The tests were ended when the c y c l i s t deviated from the prescribed cadence f o r more than f i v e seconds. The same protocol was used for the Experimental T r i a l s but was preceded by two bouts of high i n t e n s i t y arm work followed by f i v e minutes of re s t . Findings The mean Tlac as determined using log-log p l o t s of the lac t a t e vs oxygen uptake data was found to occur at 77.7 +/-9.50% of maximum achieved. An analysis of the slope of the CIEMG vs Power Output plots demonstrated that there was no s i g n i f i c a n t difference i n the slope of the l i n e before and a f t e r the la c t a t e threshold i n either condition. Further i t was demonstrated that there was a steady increase i n CIEMG despite decreasing concentrations of la c t a t e from i n i t i a l l y elevated l e v e l s i n the Experimental T r i a l . The changes i n CIEMG were s i g n i f i c a n t l y correlated with changes i n power output i n a l l subjects i n both t r i a l s . The changes i n CIEMG were s i g n i f i c a n t l y correlated with changes i n la c t a t e i n only four of the s i x subjects i n the Control T r i a l and the correlations were less s i g n i f i c a n t than those demonstrated for power output i n a l l cases. In the Experimental T r i a l only three of the s i x subjects showed s i g n i f i c a n t correlations between lactate and CIEMG. In addition the s i g n i f i c a n t correlations were a l l negative i n d i c a t i n g a completely opposite r e l a t i o n s h i p i n the Experimental T r i a l . 85 Conclusions The following conclusions were made under the conditions of t h i s i nvestigation. 1. I t was hypothesized that a strong p o s i t i v e c o r r e l a t i o n would be seen between the percentage of maximal oxygen uptake at which an i n f l e c t i o n point i n blood l a c t a t e occured and the percentage of maximal oxygen uptake at which an i n f l e c t i o n point i n CIEMG occured i n the Control Condition. This hypothesis was not supported as no detectable i n f l e c t i o n points i n CIEMG were found i n any subjects i n the Control Condition. I t i s concluded that under the conditions of t h i s i n v e s t i g a t i o n the CIEMG i s not a v a l i d estimator of the la c t a t e threshold during incremental exercise. 2. In the Experimental Condition i t was hypothesized that the i n f l e c t i o n point would be s h i f t e d to the l e f t i n the lac t a t e vs. power output p l o t . Further the CIEMG vs. power output p l o t would show a s i m i l a r s h i f t i n the i n f l e c t i o n point. This hypothesis was not supported as no i n f l e c t i o n point was i d e n t i f i e d i n CIEMG for any of the subjects during the Experimental Condition. A subjective evaluation of the la c t a t e data indicated that Tlac may have been s h i f t e d to the l e f t with no observable e f f e c t on the CIEMG. I t can be concluded that the CIEMG does not respond d i f f e r e n t l y to increased l e v e l s of plasma lactate during incremental exercise. 3. The CIEMG i s highly correlated with and predicted by 86 power output. 4. These findings are supported by research which indicates that the relat i o n s h i p between increasing l a c t a t e concentrations and IEMG i s not v a l i d under a l l conditions. Recommendations The present study u t i l i z e d well trained c y c l i s t s as subjects. I t i s possible that trained c y c l i s t s have developed an a b i l i t y to compensate for metabolic changes through altered recruitment patterns and reduce the e f f e c t s such changes might have on the recorded electromyogram s i g n a l . At present there i s no evidence to support t h i s hypothesis. The present investigation sampled the electroymyographic signal at a rate of 500 hz. This rate i s slower than has been previously used. I t would not be expected to eliminate the previously observed rela t i o n s h i p between lactate and EMG but could r e s u l t i n reduced resolution of the expected i n f l e c t i o n points. The previous v a l i d a t i o n of the IEMG-Power method f o r the non-invasive determination of the anaerobic or la c t a t e threshold i s not supported by the present research. The present research would suggest that the previously demonstrated re l a t i o n s h i p between the IEMG and lac t a t e i s for t u i t o u s . The t h e o r e t i c a l rationale for the existence of the r e l a t i o n s h i p suggests a s e n s i t i v i t y i n the EMG which i s un l i k e l y given the nature of the the electromyogram and i s not 87 supported a considerable body of previous work. The present r e s u l t s cast doubt regarding the s e n s i t i v i t y and r e l i a b i l i t y of the IEMG as an indicator of the metabolic state of the muscle at the l e v e l of Tlac. The r e l a t i o n s h i p could be examined further. I t would be of i n t e r e s t to examine the postulated r e l a t i o n s h i p by: 1. Comparing the IEMG and lactat e concentration changes of a group of untrained subjects with those of the trained subj ects. 2. Increasing the i n t r a c e l l u l a r l a c t a t e d i r e c t l y of the muscle being monitored to determine the e f f e c t on the IEMG during incremental exercise. 3. Monitor as many of the muscles as possible involved i n c y c l i n g to determine i f recruitment patterns between trained and untrained c y c l i s t s d i f f e r during incremental exercise. 4. Validate the IEMG - Power method of determining Tlac or anaerobic threshold by monitoring only IEMG and then p r e d i c t i n g maximal performance l i m i t s during long term exercise. 5. Examining the power spectrum of the present data. 6. Performing measures of pH to be support l a c t a t e data. 7. Use NMR spectroscopy to determine intramuscular changes i n pH and t h e i r r e l a t i o n s h i p to observed changes i n the recorded EMG s i g n a l . 88 APPENDIX A - COMPLETE CARDIORESPIRATORY DATA TABLE 1 - Oxygen Uptake (l/min) - Control Trial OXYGEN UPTAKE L/MIN - CONTROL TRIAL # 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 1 1.070 1.093 1.218 1.425 1.518 1.818 1.953 2.233 2.619 2.759 3.084 3.480 3.815 3.983 4.142 3.940 2 0.850 1.015 1.093 1.407 1.676 1.838 1.860 2.181 2.215 2.462 2.402 2.476'2.747 2.720 3.021 2.888 3.350 3.257 3 0.720 0.843 1.076 1.291 1.732 1.874 2.111 2.309 2.245 2.374 2.420 2.504 2.539 2.714 2.729 4 0.738 0.835 1.099 1.259 1.483 1.637 1.840 1.965 1.885 2.037 2.076 2.238 2.469 2.738 2.791 2.840 5 0.647 0.834 0.986 1.172 1.351 1.650 2.030 2.317 2.511 2.409 2.792 2.818 2.933 3.075 3.265 6 0.717 0.778 0.939 1.036 1.175 1.404 1.644 2.098 2.350 2.431 2.394 2.351 2.375 2.432 2.541 2.592 MEAN 0.790 0.900 1.069 1.265 1.489 1.704 1.906 2.184 2.304 2.412 2.528 2.645 2.813 2.944 3.082 3.065 3.350 3.257 S.D. 0.139 0.113 0.089 0.134 0.188 0.162 0.150 0.123 0.235 0.210 0.324 0.414 0.484 0.501 0.526 0.518 TABLE 2 - Oxygen uptake (ml/min) - Experimental Trial OXYGEN UPTAKE ML/MIN - CONTROL TRIAL # 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 1 14.93 15.25 16.98 19.87 21.17 25.36 27.24 31.14 36.52 38.47 43.01 48.54 53.21 55.55 57.77 54.95 2 11.02 13.17 14.18 18.25 21.74 23.84 24.13 28.29 28.73 37.93 31.15 32.11 35.63 35.28 39.19 37.45 43.45 42.25 3 10.77 12.60 16.09 19.29 25.88 28.01 31.56 34.52 33.55 35.49 36.17 37.42 37.95 40.57 40.79 4 12.77 14.45 19.01 21.79 25.65 28.32 31.83 34.00 32.62 35.24 35.92 38.72 42.71 47.38 48.29 49.10 5 10.48 13.49 15.95 18.97 21.86 26.70 32.84 37.49 40.63 38.98 45.18 45.60 47.46 49.76 52.84 6 11.60 12.58 15.18 16.75 19.00 22.70 26.58 33.93 37.99 39.31 38.71 38.02 38.39 39.33 41.08 41.91 MEAN 11.93 13.59 16.23 19.15 22.55 25.82 29.03 33.23 35.01 37.57 38.36 40.07 42.56 44.65 46.66 45.85 43.45 42.25 S.D. 1.53 0.97 1.51 1.53 2.46 2.07 3.21 2.88 3.87 1.62 4.67 5.46 6.11 6.89 6.90 6.71 89 TABLE 3 - Oxygen Uptake (l/min) - Control Trial OXYGEN UPTAKE L/MIN - EXPERIMENTAL TRIAL # 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 1 0.865 1.031 1.197 1.287 1.546 1.733 1.774 2.018 2.104 2.296 2.369 2.637 2.863 3.030 3.158 2 0.668 0.955 1.141 1.375 1.652 1.677 1.739 2.019 2.121 2.385 2.405 2.867 3.059 3.479 3.774 4.026 4.233 4.407 3 0.634 0.664 1.037 1.145 1.264 1.503 1.734 1.878 2.015 2.186 2.171 2.240 2.348 2.464 2.393 4 0.783 0.853 1.101 1.295 1.501 1.609 1.890 1.968 2.019 2.105 2.156 2.309 2.523 2.732 3.014 3.198 5 0.845 1.002 1.203 1.548 1.864 2.077 2.256 2.491 2.619 2.841 3.043 3.160 3.246 3.390 3.590 6 1.158 1.243 1.394 1.650 1.892 2.254 2.420 2.577 2.755 2.765 3.058 2.903 3.089 MEAN 0.826 0.958 1.179 1.383 1.620 1.809 1.969 2.159 2.272 2.430 2.534 2.686 2.855 3.019 3.186 3.612 4.233 4.407 S.D. 0.171 0.176 0.112 0.169 0.216 0.267 0.270 0.271 0.299 0.279 0.377 0.329 0.321 0.385 0.483 0.414 TABLE 4 - Oxygen Uptake (ml/min) - Experimental Trial OXYGEN UPTAKE ML/MIN - EXPERIMENTAL TRIAL # 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 1 12.26 14.62 16.97 18.25 21.92 24.57 25.14 28.61 29.83 32.56 33.58 37.38 40.58 42.95 44.77 2 8.78 12.54 14.99 18.07 21.70 22.03 22.85 26.54 27.87 31.35 31.61 37.68 40.20 45.72 49.59 52.90 55.62 57.91 3 9.48 9.92 15.49 17.10 18.88 22.45 25.89 28.05 33.55 32.65 32.42 33.46 35.06 36.81 35.74 4 13.50 14.75 19.05 22.40 25.97 27.84 32.69 34.05 34.93 36.42 37.30 39.94 43.65 47.20 52.15 55.33 5 13.63 16.17 19.41 24.97 30.06 33.50 36.39 40.18 42.24 45.82 49.08 50.97 52.35 54.68 57.90 6 18.67 20.04 22.46 26.59 30.49 36.33 39.00 41.53 44.40 44.56 49.28 46.78 49.78 MEAN 12.72 14.67 18.06 21.23 24.81 27.79 30.33 33.16 35.47 37.73 38.87 41.04 43.60 45.47 48.03 54.12 55.62 57.91 S.D. 3.242 3.114 2.562 4.000 4.780 5.960 6.630 6.490 6.620 6.410 8.210 6.550 6.460 5.818 7.463 1.215 90 TABLE 5 - Ventilation (l/min) - Control Trial CONTROL TRIAL - 7 £ SUBJECT 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 1 2 3 4 5 6 27.90 28.17 30.82 35.45 36.95 42.12 46.16 51.26 55.55 58.22 63.16 72.10 89.12 104.8 128.1 148.1 32.58 28.95 35.20 40.13 45.86 50.00 59.74 61.26 67.02 69.97 74.66 77.57 82.88 88.00 96.29 116.6 123.64 142.45 23.73 26.48 29.51 32.57 38.27 42.82 47.39 55.58 58.14 64.91 77.53 83.66 94.26 106.2 125.8 23.49 28.84 31.88 36.62 39.42 44.65 50.62 57.16 65.09 72.03 81.03 93.62 107.3 117.0 131.7 18.31 21.75 24.12 28.64 30.62 36.08 44.50 53.60 63.55 73.96 84.39 89.15 108.7 121.6 131.8 19.98 25.04 28.44 27.86 34.57 35.31 40.93 50.20 57.01 61.97 66.04 77.94 90.12 105.8 121.2 MEAN S.D. 24.33 26.83 29.95 33.55 37.62 41.83 48.22 54.84 61.06 66.84 74.47 82.34 95.36 107.2 121.5 132.4 123.64 142.45 4.22 2.44 2.78 4.35 3.91 4.58 5.78 4.25 5.65 7.81 9.33 12.68 13.3 14.5 13.8 16.0 TABLE 6 - Ventilation (l/min) - Experimental Trial EXPERIMENTAL TRIAL - V £ SUBJECT 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 1 2 3 4 5 6 24.94 26.61 28.06 28.42 32.43 36.56 37.48 42.60 48.67 54.96 61.29 69.12 77.07 92.09 112.1 20.92 26.51 27.56 33.58 39.94 44.70 48.51 55.32 59.55 66.38 71.23 80.40 87.11 101.6 116.0 130.9 144.7 158.69 26.15 23.79 30.37 34.37 36.76 39.14 46.25 50.93 57.33 61.20 66.78 74.86 84.16 99.07 110.1 21.92 24.39 27.89 30.89 34.87 38.96 45.09 51.02 56.98 64.98 71.98 80.99 92.01 107.1 118.7 129.6 26.01 27.95 29.65 33.45 39.55 43.57 49.36 53.21 63.53 70.57 78.29 88.81 98.13 118.4 144.5 42.19 43.44 42.30 45.27 45.95 52.30 55.45 56.84 64.63 71.30 82.77 96.74 110.3 MEAN S.D. 27.02 28.78 30.97 34.33 38.25 42.54 47.02 51.65 58.44 64.89 72.06 81.82 91.46 103.7 120.3 130.2 144.7 158.69 7.07 6.71 5.17 5.29 6.36 6.23 5.76 6.55 6.88 8.61 11.26 13.16 7.12 8.82 12.46 0.625 91 TABLE 7 - Excess CO, (l/min) - Control Trial CONTROL TRIAL - EXCESS COL, SUBJECT 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 1 5.80 6.39 6.58 6.60 6.74 7.67 7.92 9.13 10.92 11.19 11.73 16.48 23.79 25.8 29.53 27.26 2 2.80 3.05 1.17 1.42 2.23 3.10 4.85 6.28 6.76 7.40 8.42 9.75 9.62 10.59 12.31 14.74 18.23 19.98 3 3.90 4.03 4.22 4.96 6.86 8.83 9.75 11.82 11.75 13.35 15.48 16.64 18.87 22.02 26.56 4 4.36 1.99 5.72 6.56 7.58 8.47 9.85 10.98 11.85 13.3 13.59 15.43 18.56 22.75 24.79 27.79 5 3.36 3.55 3.99 4.90 5.36 5.81 8.42 9.64 12.79 16.44 17.6 17.98 23.28 25.69 31.90 6 1.67 1.43 2.01 2.52 1.40 3.11 3.41 4.62 7.66 9.51 10.86 11.28 13.99 17.03 20.49 24.46 MEAN 3.65 3.41 3.95 4.49 5.03 6.16 7.37 8.75 10.29 11.87 12.95 14.59 18.02 20.65 24.26 23.56 18.23 19.98 S.D. 1.29 1.60 1.91 1.93 2.38 2.36 2.42 2.53 2.26 2.92 3.02 3.01 4.98 5.36 6.49 5.25 TABLE 8 - Excess CO^ - Experimental Trial EXPERIMENTAL TRIAL - EXCESS C02 SUBJECT 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 EXPERIMENTAL TRIAL 1 2.99 3.03 2.92 2.25 3.17 3.74 3.83 5.38 6.54 8.08 9.28 12.40 15.84 17.97 23.36 2 1.98 2.29 2.01 3.25 3.97 3.98 5.26 6.03 7.40 8.07 9.66 11.64 13.22 15.71 19.38 23.54 27.17 29.39 3 3.55 2.51 2.29 3.50 3.70 4.11 5.65 6.89 8.52 9.53 11.39 13.52 16.55 21.25 23.34 4 5.21 5.36 5.80 6.46 7.68 8.42 9.56 10.78 11.94 13.51 13.81 16.01 18.96 23.05 25.83 28.01 5 3.94 2.99 2.97 1.88 3.61 4.34 5.74 7.24 8.46 10.46 12.20 13.38 15.38 20.45 23.03 6 7.35 6.94 5.29 5.37 5.47 7.70 8.99 9.76 12.69 15.14 18.02 21.35 23.83 MEAN 4.17 3.85 3.55 3.80 4.60 5.38 6.51 7.60 9.25 10.79 12.39 14.72 17.29 19.69 22.99 25.78 27.17 29.39 S.D. 1.72 1.71 1.46 1.65 1.70 2.09 2.25 2.13 2.48 2.92 3.22 3.57 3.69 2.57 2.07 2.24 92 TABLE 9 - ' E / v ° 2 " Control Trial CONTROL TRIAL - VE/VG2 SUBJECT 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 1 26.07 25.77 25.30 24.88 24.34 23.17 23.64 22.96 21.21 21.10 20.48 20.72 23.36 26.30 30.92 37.58 2 34.16 32.10 26.49 25.02 23.94 24.95 26.88 27.39 27.66 27.22 29.13 30.15 28.24 30.47 29.13 33.34 34.81 37.96 3 32.96 31.41 27.43 25.23 22.10 22.85 22.45 24.07 25.90 27.34 32.04 33.41 37.12 39.11 46.08 4 28.55 28.13 26.24 25.32 24.69 24.08 24.27 25.76 30.32 31.95 34.70 36.21 37.92 39.20 41.91 46.38 5 28.30 26.08 24.46 24.44 22.66 21.87 21.92 23.13 25.31 30.70 30.23 31.64 37.06 39.56 40.36 6 26.51 25.68 26.67 27.45 23.71 24.62 21.48 19.51 21.36 23.45 25.89 28.09 32.82 37.06 41.65 46.75 MEAN 29.43 28.20 26.10 25.39 23.57 23.59 23.44 23.80 25.29 26.96 28.74 30.04 32.75 35.28 38.34 41.01 34.81 37.96 S.O. 3.07 2.65 0.96 0.97 0.91 1.07 1.81 2.46 3.25 3.78 4.57 4.88 5.37 5.09 6.16 5.75 TABLE 10 - Vg/vOj, - Experimental Trial EXPERIMENTAL - VE/V02 SUBJECT 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 1 28.83 25.81 23.44 22.08 20.98 21.10 21.13 21.11 23.13 23.94 25.87 26.21 26.92 30.39 35.51 2 31.32 27.76 24.15 24.42 24.18 26.65 27.90 27.40 28.08 27.83 29.62 28.04 28.43 29.20 30.73 32.51 34.18 36.01 3 41.25 35.83 29.29 30.02 28.03 26.04 26.67 27.12 28.45 28.00 30.76 33.42 35.84 40.21 46.01 4 27.99 28.59 25.33 23.85 23.23 24.21 23.86 25.92 28.22 30.87 33.39 35.08 36.47 39.21 39.37 40.53 5 30.78 27.89 24.65 21.61 21.22 20.98 21.88 21.36 24.26 24.84 25.73 28.10 30.23 34.93 40.24 6 36.43 34.95 30.34 23.93 23.20 22.91 22.06 23.46 25.79 27.07 33.32 35.69 MEAN 32.77 30.14 26.20 24.32 23.47 23.65 23.91 24.40 26.32 27.09 29.78 31.09 31.59 34.79 38.33 36.52 34.18 36.009 S.D. 4.65 3.82 2.64 2.75 2.33 2.21 2.54 2.57 2.08 2.26 3.12 3.75 3.88 4.46 5.09 4.01 93 APPENDIX B - PLASMA LACTATE DATA TABLE 1 - Plasma Lactate Concentrations (mrol/l) at Each Workload - Control Trial PLASMA LACTATE CONCENTRATIONS AT EACH WORKLOAD CONTROL TRIAL # REST ARM 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 1 5.18 ***** 5.32 3.60 3.86 4.36 2 3.67 ***** 4.24 4.69 5.14 5.62 ^ ^ ill A A A A Irtrtctt 'trtr&rit ^ 07 ^A^WF ^ J 39 A A A A A ^ A A A A ^ 2^  AiWnfc 5 3.9! *****4.9o 3.93 5.29 3.71 ^ ^ 39 ^^AlHWf ^ A A A A ^ 2^  4rA^4r 3.06 **** 4.09 4.71 6.30 4.68 4.52 4.84 3.99 5.33 4.41 4.73 J /|/| A^Wnlr J A A A A £ AAnfcA A A A A A A A A Q 2^  A A A A ^ ^ 2Q 5.03 4.90 3.58 4.72 4.09 4.82 5.87 **** 5.01 4.13 5.45 6.46 7.82 9.56 14.08 16.45 18.81 *END* 5.70 5.39 6.05 6.73 7.88 8.64 11.47 15.2 7.69 9.35 12.25 14.66 18.96 *END* 7.09 10.88 12.99 17.27 22.10 *END* 7.01 10.50 14.04 17.38 23.31 27.68 *END* 7.77 11.74 *END* MEAN 4.63 4.59 4.07 4.48 4.56 4.78 4.87 5.01 4.72 5.22 5.58 7.18 9.57 11.88 14.50 18.21 18.16 11.47 15.21 S.D. 0.71 0.44 0.46 0.38 0.79 0.97 0.03 1.54 0.42 0.90 1.05 0.74 2.03 2.99 4.00 5.46 9.52 TABLE 2 - Plasma Lactate Concentrations (mrol/l) at Each Workload - Experimental Trial PLASMA LACTATE CONCENTRATIONS AT EACH WORKLOAD EXPERIMENTAL TRIAL # REST ARM 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 1 5.54 23.48 23.72 ***** 19.91 ***** 7.89 ***** 10.67 ***** 5.09 4.71 5.99 5.36 *END* 2 3.01 10.34 9.67 8.95 7.99 7.69 7.15 5.69 5.62 5.54 5.02 5.05 5.64 5.56 6.64 7.89 9.69 13.0 17.1 20.1 3 3.40 35.43 29.91 ***** 28.42 ***** 26.82 ***** 23.91 ***** 19.42 15.88 17.70 16.73 20.35 *END* 4 5.01 29.37 23.72 ***** 19.91 ***** ***** ***** 15.57 ***** ***** ***** 16.05 13.71 17.27 20.51 24.34 *END* 5 3.23 24.18 16.45 ***** 14.75 ***** 13.62 ***** 11.32 ***** 10.36 9.19 9.62 13.03 13.50 19.11 23.21 *END* 6 6.64 36.84 32.68 33.51 33.51 28.62 28.66 25.62 28.28 22.33 24.31 19.08 24.01 27.37 27.99 MEAN 4.47 26.61 22.69 21.23 20.75 18.16 16.83 15.66 15.90 13.94 12.84 10.78 13.17 13.63 17.15 15.84 19.08 13.02 17.16 20.07 S.D. 1.35 8.86 7.77 12.28 8.39 10.47 9.21 9.97 7.87 8.41 7.78 5.78 6.67 7.44 7.09 5.65 6.65 94 APPENDIX C - ELECTROMYOGRAPHIC DATA TABLE 1 - Cycle Integrated EMG (CIEMG) for Each Workload - Control Trial * CONTROL TRIAL CYCLE INTEGRATED EMG (CIEMG) FOR EACH WORKLOAD # 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 1 2 3 4 5 6 0.03|0.08|0.11|0.14|0.17|0.19|0.21|0.23|0.26|0.28|0.33|0.36|0.37|0.41|0.43| | | 0.19|0.27|0.30|0.34|0.39|0.43|0.42|0.46|0.46|0.47|0.53|0.52|0.78|0.57|0.63|0.63|0.64| 0.06|0.09|0.11|0.13|0.14|0.16|0.18|0.19| 0.2|0.19|0.22|0.24|0.27|0.34|0.42| | | 0.07|0.10|0.12|0.15|0.18|0.19| 0.2|0.22|0.25|0.28| 0.3| 0.3|0.29|0.29|0.31| | | 0.06|0.07|0.08|0.09|0.11|0.12|0.14|0.15|0.16|0.18|0.21|0.21|0.21|0.23|0.36| | | 0.08|0.12|0.16|0.19|0.22|0.22|0.29|0.31|0.35|0.35|0.41|0.42|0.45|0.59|0.75| | | MEAN S.D. 0.OS|0.12|0.15|0.17|0.20|0.22|0.24|0.26|0.28|0.29|0.33|0.34|0.40|0.41|0.48|0.63|0.6 0.05|0.07|0.07[0.08|0.09|0.10|0.09|0.10|0.10|0.10|0.11[0.11|0.19|0.14|0.16| 0| 0| TABLE 2 * - Cycle Integrated EMG (CIEMG) - Experimental Trial EXPERIMENTAL TRIAL CYCLE INTEGRATED EMG (CIEMG) FOR EACH WORKLOAD # 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 1 0.08|0.15|0.20|0.21|0.26|0.24|0.25|0.16|0.29|0.32|0.34|0.36|0.39|0.38|0.37|0.42| | 2 0.06|0.09|0.12|0.15|0.16|0.17|0.19|0.19|0.21|0.21|0.23|0.25|0.26|0.29| | | | 3 0.05|0.09|0.11|0.13|0.15|0.18|0.20|0.20|0.24|0.27|0.29| I I I I I I 4 0.06|0.08|0.10|0.12|0.16|0.18|0.17|0.18|0.20|0.21|0.23|0.23|0.24|0.23|0.25| | | 5 0.07|0.11|0.12|0.17|0.23|0.26|0.26|0.24|0.26|0.31|0.29|0.29|0.36|0.39|0.47| | | 6 0.11|0.13|0.14|0.17|0.19|0.20|0.22|0.23|0.25|0.26|0.26|0.30|0.45|0.51| | | | MEAN 0.07|0.11|0.13|0.16|0.19|0.21|0.22| 0.2|0.24|0.26|0.27|0.29|0.34|0.36|0.36|0.42| | S.D. 0.O2|0.G2|O.(B|0.GB|0.()4|0.a3|0.Q3|0.GB|0.O3|0.04|0.04|0.04|^  | | 95 APPENDIX! D - INDIVIDUAL SUBJECT PLOTS" OF -PLASMA LACTATE FOR BOTH TRIALS figure 1 - Control. TriaLlSubjecr 1 CIEMG- AND U J is < CO < -0.75 -0.50 CO o LU CO -0.25 C~ > (J UJ CJ --0.25 t i i i i i r 47 94 141 188 235 282 329 376 423 POWER OUTPUT (WATTS) 0.50 Figure 2 - Experimental Trial Subject 1 LU is CJ < CO < -0.75 -0.50 -0.25 O CO CJ LU CO >UJ u "i 1 1 1 1 r 0 47 94 141 188 235 282 329 376 423 POWER OUTPUT (WATTS) 0.25 0.50 96 Figure 3 - Control Trial Subject 2 Figure 4 - Experimental Trial Subject 2 97 Figure 5 - Control Trial Subject 3 36-j _! 33 -_ 1 o 3 0 -27-24-TE 21-TA 18-c j 15-< _i 12-< 9-C O 6 -< 3-C L 0 -C O o CO > U J --0.25 i 1 r 47 94 141 188 235 282 329 376 423 POWEff OUTPUT (WATTS) -0.50 Figure 6 - Experimental Trial Subject 3 U J 36 33 -30 -27-24-21-< H 18-< 15 29H A LACTATE • CIEMG r1 0.75 C O 0.50 O L U C O 0.25 ^ U J 1 1 I I I I l 1 47 94 141 188 235 282 329 376 423 POWER OUTPUT (WATTS) h-0.25 0.50 9 8 Figure 7 - Control-Triai.Subject.4 3.6-1 __l 33-1 o 30-27-:§ 24-LU 21-I— TA 18-CJ 15-< 12-< 9-CO 6 -< _ l 3-0. 0.75 -0.50 -0.25 cS --0.25 n i i i i i r 94 141 188 235 282 329 376 423 POWER OUTPUT (WATTS) 0.50 Figure 8 - Experimental Trial Subject 4 36-i _! 33-_J o 30-27-24-UJ 21-< 18-CJ 15-< _ l 12-< 9 -CO 6-< _ 1 3-0_ 0-A LACTATE © CIEMG [-1 -0.75 -0.50 -0.25 0 h-0.25 1 r 47 94 141 188 235 282 329 376 423 POWER OUTPUT (WATTS) -0.50 99 Figure 9 - Control Trial Subject:5 36n 33-_J o 30-27-24-TE 21-TA 18-u 15-< 12-< 9-CO 6-< 3-0_ 0--0.75 -0.50 CO CJ U J CO -0.25 O > UJ CJ --0.25 "i r 1 1 r 94 141 188 235 282 329 376 423 POWER OUTPUT (WATTS) 0.50 Figure 10 - Experimental Trial Subject 5 36-j 3 3 -_J o 3 0 -27-24-UJ i — 21-TA" 18-CJ 15-< _ j 12-< 9-CO 6-< — I 3 -Q_ 0 --0.75 -0.50 -0.25 C~ CO CJ UJ CO >CD UJ CJ 0.25 i i i i i i r 94 141 188 235 282 329 376 423 POWER OUTPUT (WATTS) 0.50 100 Figure 11 - Control Trial Subject. 6 APPENDIX E - SELECTED DATA SUMMARY TABLES TABLE 1 Age,Height, and Weight of Subiects SUBJECT AGE(YRS) HEIGHT(CM) WEIGHT(KG)| 1 19 174.0 70.54 2 25 174.0 76.10 3 29 176.3 66.95 4 23 176.7 58.40 5 18 175.4 62.00 6 18 177.0 62.05 MEAN 22 175.6 66.01 RANGE 18-29 174.0 -176.7 62.00-76.10 S.D. 4.1 1.212 5.957 Table 2a Selected Individual Maximum Ca r d i o r e s p i r a t o r y Values of Control T r i a l CARDIORESPIRATORY DATA SUMMARY MAXIMUM VALUES - CONTROL TRIAL SUBJECT TEST MAXIMAL OXYGEN UPTAKE EXCESS Ivc/V0, I R.Q. I DURATION . C CO-(MINS) (L/MIN) (ML/KG) (L/MIN) (L/MTN) (L/MIN) 1 16 4.14 54.95 148.10 27.26 37.58 1 19 2 19 3.34 43.28 142.45 25.05 37.97 1 20 3 15 2.73 40.79 125.80 26.56 46.08 1 35 4 16 2.84 49.10 131.70 27.79 46.38 1 26 5 15 3.27 52.84 131.80 31.90 40.36 1 30 6 15 2.59 41.91 121.20 24.46 46.75 1 28 MEAN 16 3.15 47.01 133.51 27.17 42.52 1 26 S.D. 1 0.52 5.62 9.22 2.41 3.98 0 06 Table 2b Selected Individual Maximum Cardiorespi ratory Values of Experimental T r i a l CARDIORESPIRATORY DATA SUMMARY MAXIMUM VALUES - EXPERIMENTAL TRIAL "X" SUBJECT TEST DURATION (MINS) MAXIMAL OXYGEN UPTAKE (L/MIN) (ML/KG) E (L/MIN) EXCESS C0 ? (L/MTN) V E / v 0 2 | R.Q. (L/MIN) 15 18 14 15 15 13 16 41 46 01 59 09 44.77 57.91 36.81 52.15 57.90 49.78 112.10 158.69 110.10 129.60 144.50 110.30 23.36 29.39 23.34 28.01 23.03 23.83 35.51 36.01 46.01 40.53 40.24 35.69 1.22 1.21 1.28 1.27 1.10 1.18 MEAN S.D. 15 1.5 3.29 0.61 49.89 7.43 127.58 18.67 25.16 2.55 38.99 3.77 21 06 102 Table 3 Anaerobic Threshold from Log-Log Plot of IEMG vs. V0 2 Subj. # 1 2 3 4 5 6 X S.D. A.T. l/min 2.75 2.48 2.32 1.97 2.51 1.64 2.28 0.37 A.T. watts 235.5 235.5 188.0 188.0 211.5 164.5 203.9 26.2 | % Maximum 66.4 74.3 85.1 69.4 76.8 63.4 72.6 7.. 1 Table 4a Heart Rate Data - Control T r i a l # 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 1 105 101 120 126 120 127 127 138 137 154 160 169 174 178 182 185 2 80 86 93 104 112 118 120 119 137 138 141 155 162 162 162 177 176 3 86 94 103 105 120 131 131 142 149 158 168 174 178 182 189 4 63 77 89 88 98 107 121 128 143 149 163 170 178 185 185 187 5 92 100 102 105 115 123 133 149 154 165 171 179 184 188 192 6 100 112 100 121 121 140 142 158 166 172 180 185 189 194 196 X 87.7| 112| 101| 108| 114| 124| 129| 139| 148| 156| 164| 172| 189| 182| 196| 183| 176| S.D.13.8|11.2J9.79|12.4|7.97|10.3|7.51|12.9|10.2j10.9j12.0|9.35|8.44j10.0j11.0|4.32j 0| Table 4b Heart Rate Data - Experimental T r i a l # 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 1 112 115 117 121 124 130 137 143 150 158 161 166 172 176 180 2 69 81 88 97 102 108 112 120 122 130 138 146 155 161 168 172 177 3 110 116 114 131 132 142 147 156 161 166 170 178 178 187 187 4 120 125 129 140 140 152 156 163 165 174 178 182 185 187 187 5 115 118 118 125 132 135 142 144 158 163 170 174 180 187 189 192 6 129 131 134 138 150 153 163 170 178 185 194 196 199 X 109| 131| 117| 125| 130| 137| 143| 149| 156| 163| 169| 174| 199| 180| | 182| 177| S.D 19.0|15.9|14.6|14.3|14.9|15.3|16.2|16.3|17.3|17.0|17.0|15.3|13.3|10.2|7.73| 10 j 0| 103 Basmajian, J.V., ( 1 9 7 8 ) . 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