UBC Theses and Dissertations

UBC Theses Logo

UBC Theses and Dissertations

The relationship between anaerobic threshold, excess CO² and blood lactate in elite marathon runners Hearst, William Edward 1982-12-31

You don't seem to have a PDF reader installed, try download the pdf

Item Metadata

Download

Media
831-UBC_1982_A7_5 H43.pdf [ 3.53MB ]
Metadata
JSON: 831-1.0077391.json
JSON-LD: 831-1.0077391-ld.json
RDF/XML (Pretty): 831-1.0077391-rdf.xml
RDF/JSON: 831-1.0077391-rdf.json
Turtle: 831-1.0077391-turtle.txt
N-Triples: 831-1.0077391-rdf-ntriples.txt
Original Record: 831-1.0077391-source.json
Full Text
831-1.0077391-fulltext.txt
Citation
831-1.0077391.ris

Full Text

THE RELATIONSHIP BETWEEN ANAEROBIC THRESHOLD, EXCESS C02 AND BLOOD LACTATE IN ELITE MARATHON RUNNERS by WILLIAM EDWARD HEARST B.P.H.E., Lakehead University, Thunderbay, 19 77 A THESIS SUBMITTED IN PARTIAL FULFILLMENT OF THE REQUIREMENTS FOR THE DEGREE OF MASTERS OF PHYSICAL EDUCATION in THE FACULTY OF GRADUATE STUDIES School of Physical Education and Recreation We accept this thesis as conforming to the required standards. THE UNIVERSITY OF BRITISH COLUMBIA October, 19 82 (c) William Edward Hearst, 19 82 . In presenting this thesis in partial fulfilment of the requirements for an advanced degree at the University of British Columbia, I 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 of The University of British Columbia 1956 Main Mall Vancouver, Canada V6T 1Y3 Date DE-6 (3/81) ABSTRACT The purpose of this study was to investigate the use of excess CC>2 (ExC02) as a determinant of the anaerobic threshold (AT) and the subsequent relationship to blood lactate (La). Four highly trained marathon runners (x values, age=30.6 years; % body fat= 8.2; V02max = 6 8 ml-kg "*"'min "*") volunteered to participate in this study. Metabolic and respiratory exchange variables were assessed by an open circuit method utilizing a Beckman metabolic measurement cart interfaced on-line with a Hewlitt Packard..3052A data acquisition system. V02max and the treadmill velocity at the threshold of anaerobic metabolism (V ) were obtained from a progressive, treadmill run (.81 kph. ^ min.) until volitional fatigue. vtam (Kilometers per hour, Kph) was calculated from the point of .a non-linear increase in ExC02. Subjects performed set treadmill runs of 10 minutes on alternate days. Variations (latin square) included runs at V /V n, t cim t cirri i x ^tam+2' an<^ Vtam-1" Analysis of variance with preplanned orthogonal comparisons and Scheffe post hoc contrasts were used to determine the effects of the treadmill variations on La and ExC0„. There was no significance found between V. and 2 y tam Vj_ . for La or ExC0o. Significance (p^ .05) was evident with tam-1 2 ^ ^ -V. -CV. .ir for La and V. i V. for ExCO„. tam tam+1 tam tam+2 tam tam+2 2 An overall correlation of .; 89 (p^.005) demonstrated a high positive,.relationship between ExCC>2 and La. Findings indicate to be a critical point in determining the anaerobic tam ^ 3 iii threshold in marathoners, and performance above this demarcation results in a state of anaerobiosis. iv ACKNOWLEDGMENT The author would like to thank those, individuals who assisted him in completing this thesis: Committee chairman Dr. E. Rhodes, committee members Dr.D.McKenzie, Dr. J. Taunton and Dr. K. Coutts.for their valuable guidance and patience; and to all my subjects my great admiration. The author would also like to express additional thanks to Mr. D. Dunwoody, Mr. W. Parkhouse, Dr. D. Montgomery, Dr. R. Schutz, my parents Lillian and Roy Hearst, and my wife Tonia E. Hearst, for their support throughout this project. V ' TABLE OF CONTENTS Page ABSTRACT • • ii ACKNOWLEDGMENT— v LIST OF FIGURES ; • vii LIST OF TABLES • viii Chapter 1. INTRODUCTION '• 1 STATEMENT OF THE. PROBLEM —— 7 HYPOTHESIS 7 RATIONALE 8 DELIMITATIONS 9 LIMITATIONS • 9 DEFINITION OF TERMS — • . 10 2. REVIEW OF SELECTED LITERATURE 12 INTRODUCTION : 1LACTIC ACID • 12 FORMS OF LACTIC ACID • 14 LACTIC ACID ASSAY- 15 LACTATE CONCENTRATION 6 C02——— — 21 ANAEROBIC THRESHOLD 23 THE MARATHONER •- 29 EFFECTS OF TRAINING ON AT : v- 30 REPRODUCIBILITY OF AT 31 vi 3. METHODS AND PROCEDURES : 32 SUBJECTS 3TESTING PROCEDURES 32 TESTING PROTOCOLS 3 EXPERIMENTAL DESIGN AND DATA ANALYSIS 34 4. RESULTS AND DISCUSSION 35 RESULTS 3DISCUSSION : 45 5. SUMMARY AND CONCLUSIONS 56 SUMMARY 5CONCLUSIONS 8 RECOMMENDATIONS 59 BIBLIOGRAPHY 6 0 APPENDIX : : 69 yii LIST OF FIGURES FIGURE PAGE I Common Variables Used for AT Determination 4 II Hypothetical Model Of Three Phase, Double Breakaway Model 6 III Means + S.D. For Four Subjects Over Four Conditions - La • 41 IV Means ± S.D. For Four Subjects Over Four Conditions - ExCO_, 42 V Correlation Between ExCO„ and La 43 yiii LIST OF TABLES TABLE PAGE I Physical Characteristics of Subjects 36 II Relevant Data • 37 III Analysis of Variance With Preplanned Orthoganal Comparisons and Scheffe'Post Hoc Contrasts 38 IV Correlation Coefficients: La and EXCO2 39 V Summary of Hypothesis Testing 40 CHAPTER I INTRODUCTION TO THE PROBLEM The "anaerobic threshold" as defined by Wasserman et al (196 4) is synonymous with the onset of metabolic acidosis. Anaerobic threshold has been measured via gas exchange variables and direct blood lactate sampling with considerable success (Wasserman et al, 1973; Wasserman and Whipp, 1975; Davis et • alf-'19 76;'. Katch, 19 79; Farrell et al, 19 79). Respiratory exchange variables.: measured during a constant increase in.work reveal the following: 1. V„ (minute ventilation) and VCO„ (Volume of C0_ hj A Z. produced) initially increases with VO2/* 2. At the anaerobic threshold the V02 remains linear * • with work rate, but VC02 increases faster than V02 primarily due to the buffering of lactate by the bicarbonate system; * • 3. V„ increases in proportion to VCO„; 4. End tidal PC02 does not change, but end-tidal P02 increases; 5. Because VC02 increases above V02, R increases; As work rates become higher (approximately 80% of • * maximum), the increased V„ increases VCO„ with a consequent reduction of end-tidal PC0o (Wasserman and Whipp, 19 75). 2 The measurement of the aerobic-anaerobic transition via the appearance of lactate in the blood in.excess of resting levels reveal the following pattern: 1. At very low work rates: no increase in blood lactate; 2. At moderate work rates: lactate peaks early in work and then returns to resting values as V02 reaches a steady state (lactate is oxidized to CC>2 and H^O in the tissue); 3. At heavy intensities: Lactate increases and then may decrease slightly, but is maintained at higher than resting values by a balance between sustained production and removal; 4. At severe intensities: lactate continues to increase throughout the work (Diamant et al, .19 68) . Lactate accumulation leads to a decrease in bicarbonate (buffering of lactic acid), to the appearance of excessive (relative to the resting metabolic level) amounts of CO^ (ExC02) and to the production of hydrogen ions (which stimulate the chemoreceptors to increase the ventilation rate). Volkov et al (19 74) states that it is possible to determine the level of anaerobic metabolism from the excess of released CO ' through the following calculation: 3 ExC02 = AIR • VC>2 = VG02 - (R)rest«V02, -1 -i • where ExC02 is excess C02 (ml-kg/; :-.min ), VC>2 is the level of oxygen consumption during work (ml-kg "'"•min "*") * -1 -1 VC02 is the level of CO^ released (ml-kg •min ).. Therefore, at work rates at or above the anaerobic threshold, additional CC>2 is added to the expirate primarily through the/following reaction, which involves the buffering of lactic acid produced through the glycolytic pathways: Na HC03~ + H+ lactate —> Na+ lactate + H2C03 —> C02t + H20 Consequently, the anerobic threshold is postulated to occur when there is a sudden curvilinear increase in excess CC>2 elimination, ventilation rate and respiratory exchange ratio, with a concomitant increase in blood lactate levels (above resting values). (Figure I) . Costill and Fox (1969) have shown that marathon runners are able to utilize approximately 75% of their VC>2 max with little lactic acid production. In addition, Farrell et al (1979) found that the "marathoner1 can maintain an average velocity during a race which is only slightly above.his anaerobic threshold. Kinderman et al (19 79) found that endurance trained athletes achieve higher work intensities before lactate production FIGURE I Common Variables Used for A.T. Determination 5 10 15 20 25 Time (Min.) 5 exceeds its removal. Costill et al (19 73) found that at all running speeds above 70% max, the faster distance runners accumulated less blood lactate than the slower runners at similar speeds and relative percentages of their aerobic capacities. It has been suggested that the metabolic adaptations of the running musculature have been oxidative rather than glycolytic. In addition, intensities above the anaerobic threshold, according to Wasserman et al (1973), can be maintained with slightly elevated lactic acid for prolonged periods of time. The terminology used today to define the interplay between aerobic and anaerobic sources is varied. These include the anaerobic threshold of Wasserman et al (1964), the onset of plasma lactate accumulation (OPLA) of Farrell et al (19 79), an intensity threshold as defined by Sady et al (1980), the lactate threshold of Ivy et al (1980), the onset of blood lactate accumulation (OBLA) of Sjodin et al (19 81), and the three phase double breakaway model of Skinner and McLellan (1980) and Kindermann et al (1979). (Figure II) In addition, investigations in Europe by Stegmann et al (1981) display the need for individual anaerobic threshold (IAT) determination, via lactate kinetics, due to interindividual variability. The curvilinear increase in ExCOn elimination as defined FIGURE II Hypothetical Model of Three Phase, Double Breakaway Model (adapted from Skinner and McLellan, 19 80) PHASE I PHASE II PHASE III REST AEROBIC THRESHOLD ANAEROBIC THRESHOLD V02 MAX -Predominant type of metabolism -Predominant Substrate -Predominant Muscle Fiber Type -Relative Intensity (% V02Max) -Heart Rate (Beats per min.) -Blood Lactate (mM/L) Aerobic Fat > Carbohydrate 40 - 60 130 - 150 /v 2 I, IIA Anaerobic Carbohydrate > Fat I, IIA, IIB 65 - 90 100 - 180 ^4 7 by Volkov et al (1974) and used by Rhodes et al (1981) to predict marathon racing times is also suggestive of a critical intensity above which metabolic acidosis becomes a limiting factor on performance. The role of the anaerobic threshold has been used for testing hospital patients (Wasserman and Whipp, \ 19 7.5), athletes (Costill, 19 70) and models of the hyperpnea of dynamic muscular exercise (Whipp, 19 77) . However, the study, of the role of the anaerobic threshold and its relationship to performance of elite endurance runners is in stages of preliminary investigation. Statement of Problem The purpose of this study was to elucidate the relationship between ExCC^ as a determination of anaerobic threshold and the appearance to blood lactate. Hypotheses For each of the following dependent variables, it was hypothesized that: 1. Blood lactate at specific Vta__, ie. (LaVtam) (a) LaV ' ,, will have a value equal to or tam-1 lower than LaV, (1 km/hr below V, ); tarn tarn (b) LaV. will have a lower value than LaV , tarn tam+1 (1 km/hr above V, ); tarn (c) LaV" ,, will have a lower value than LaV. tam+1 tam+2 (2 km/hr above V ); tarn 8 (LaV, ,~ > LaV^. >'LaV. ^ LaV. m .) tam+2 tam+1 tam tam-1 2. Excess C02 production at specific ^tam (ExC02Vtam^ (a) ExCO„V, . will have a value equal to 2 tam-1 or lower than ExCO„V, 2 tam (b) ExCC>2Vtam will have a lower value than ExCC> V^ _, , ; 2 tam+1 (c) ExC0oV. will have a lower value than ' 2 tam+1 ExCO-V^ ' _; 2 tam+2 (ExCO„ V,. ExCO_V. , _ > ExC0oV, 35 ExCO_V, ^ ) 2 tam+2 2 tam+1 2 tam 2 tam-1 3. There will be a significant correlation between excess C0„ and blood lactate (LaV^ and ExCC" V. ) for 2 tam 2 tam V,_ , , V. , , .and V. ,n . tam-1 tam tam+, tam+2 Rationale The anaerobic threshold has been defined as that work rate just below the point at which there is the first significant elevation of blood lactate in excess of resting levels, with a concomitant increase in excess C02 elimination. Studies have shown that elite marathon runners appear to utilize the highest percentage of their maximal oxygen consumption (70% - 85% VC^max), with a minimum amount of lactic acid production. The aerobic pathways then, are already operating.at an extreme level and any increase in intensity will necessitate an increasing contribution through 9 glycolytic/anaerobic metabolism. Although there is no definitive line between aerobic and anaerobic metabolism, there does appear to be a critical work intensity above which metabolic acidosis is observable. Although metabolic acidosis has; been measured via noninvasive (ExCG^) or direct venous blood lactate techniques, no attempt has been made to elucidate upon the use of ExCC>2 through lactate analysis at critical running speeds in elite marathon runners during treadmill exercise. Delimitations This study is delimited by: (1) the sample type; (2) the sample size (N=5); (3) the sample's fitness level (endurance trained); (4) the.speed of the treadmill at which the subject will run; Limitations This study's results are limited by: (1) data collection capabilities of the Beckman Metabolic Meaurement Cart and the Hewlett Packard Data Acquisition system interfaced with it; (2) the methods.of anaerobic threshold determination; (3) the individual's metabolic response to the protocols; 10 (4) blood lactate measurement technique. Definitions For the purpose of clarification, the following definitions and abbreviations were considered applicable throughout this study: (1) Anaerobic threshold (AT) - the work rate just below the point at which lactate production exceeds its removal by oxidative means (ie. first significant elevation of blood lactate above resting level) with which there is a concomitant increase in excess CC^. (2) Excess CC>2 (ExCC^) - the relationship between the amount of nonmetabolic CC^ being produced in proportion to the amount of non-metabolic ©2 being consumed as energy for a given workload. ExC02 - VC02 ~ (resting R.Q. x VC^) where CO^ is the total expired CO^ O2 is the total expired R.Q. is the resting respiratory quotient VCC>2 produced 0„ consumed - -(3) velocity of treadmill (V. ) at time of onset . tarn of anaerobic metabolism - treadmill speed (km/hr) 11 corresponding to the anaerobic threshold, (as determined by a curvilinear increase in excess CC^). (a) V\ , = 1 km/hr below AT; tam-1 (b) V,. = treadmill velocity (km/hr) at AT; tam J (c) vtam+l = ^m/nr aD°ve AT; (d) ^0 = 2 km/hr above AT. tam+2 12 CHAPTER II REVIEW OF LITERATURE Introduction The capability of the human body to perform physical work of varying intensities and duration involves the recruitment of muscle, consequently, any factors which limit this will limit performance (Wenger and Reed, 19 76). One of the metabolic factors associated with muscluar fatigue during aerobic .and anaerobic work is an increase in lactate production. This increase can result in a decrease in muscle and blood pH which inhibits the reaction velocity of phosphofructokinase thus slowing down the rate of ATP production (Edgerton et al, 1973), decreases Ca++ sensitivity inhibiting the contractile process and inhibits the conversion of phosphorylase b to a thus decreasing glycogen degradation, (Hultman and Sahlin, 19 81). Furthermore, the effects of the increased lactate will, inhibit fat mobilization from adipose tissue thus straining the limited glycogen stores (Boyd et al, 19 74). It will be the purpose of this review to present current research pertaining to lactic acid and its subsequent relationship to CO^ production, the anaerobic threshold concept and the endurance athlete. Lactic Acid In the nineteenth century, Berzelius (180 7) demonstrated 13 the presence of lactic acid in human and muscle tissue. Virtually all tissues of the body are capable of producing lactic acid, although the best known physiological example is muscular exercise during which lactate accumulates in the tissues and blood stream. The accumulation is because of relative oxygen lack and the inability of lactate removal mechanisms to keep up with production, thus causing metabolic acidosis (Cohen et al, 19 76) . The removal of accumulated lactate is necessary since lactic acid may inhibit the performance of subsequent exercise (Karlson et al, 1975). This may result from the inhibitory action that lactic acid has on the glycolytic enzymes phosphofructokinase (Keul et al, 19 72; Newsholme, 19 74 ) and phosphorylase (Hultman and Sahlin, 1901), and/or on free fatty acid mobilization (Issekutz and Millar, 1962). During exercise, the muscles go into debt for oxygen despite an increase in metabolism. The energy requirements of the muscle supersede the ability of the cardio-vascular system to supply oxygen, consequently energy is supplied by anaerobic production through the breakdown of glucose or glycogen to lactate (Alpert, 1965) . Jobsis and Stainsby (196 8) however, stated that the lactate formation is not caused by hypoxic stimulation of anaerobic glycolysis, but rather an inbalance between pyruvate production by aerobic 14 glycolysis and pyruvate utilization in the Kreb Cycle. Consequently, pyruvate accumulates and is converted to lactate. Farrell (19 79) suggests that .the plasma lactate concentrations are the result of the production of lactate in muscle, and diffusion of lactate from muscle to blood and the uptake of lactate by numerous tissues. The lactate may be acted upon within the muscle itself (Hermanson & Vaage, 1977), or be released into the blood where it may be removed by the heart (Carlsten,1961), kidney (Mole et al, 1973), skeletal muscle (Jorfeldt, 1970; Issekutz et al, 1976), brain (Belcastro and Bonen, 19 75) and liver (Cori and Cori, 1929) . Forms of Lactic Acid Lactic acid occurs in two stereoisometric forms and in a so-called racemic mixture of these two isomers. The stereoisomers have been named D(-) Lactic Acid and L(+) Lactic Acid. The L(+) isomer represents the form of lactic, acid produced in muscle metabolism as a result of muscle cell anaerobiosis and/or the ordinary glycolytic oxidation of glucose in all cells. (Cori, 1962; Lockwood et al, 1965). COOH COOH H^OH CH3 D(-) Lactic Acid ic Acid Although Moriya in 1904 stated that almost all of the 15 lactate formed by various animal tissues was of the L(+) form, Dakin and Dudley (1913) found that some animal tissues formed D(-) lactate. Cori1s (1931) classical experiment showed that D(-) lactate is poorly metabolized and that 30 - 40% of the lactate ingested is excreted in the urine, compared with none of the L(+) form. However, recent investigations have shown that D(-) lactate can be metabolized by the rat and probably the human (Schumer, 19 79) . Thus the definitive- values placed on lactate determination via L(+) specific assays is questionable in relationship to all lactate in the human serum. Lactic Acid Assay The preferred stereospecific analytical method for L(+) lactic acid is based on the reduction of nicotinomide adenine dinucleotide (NAD+) by L(+) lactic dehydrogenase (LDH) in the presence of L(+) lactic acid, where the change in optical density at 340 ny/ is read (Olson, 1962). C02H rnu C09H | - . LDH | 2 + 0=0 + NADH + H => HOCH + NAD CII3 " CH3 (Pyruvic acid) L(+) Lactic Acid The liberated hydrogens are transferred to NAD (nicotinomide adenine dinucleotide) to form NADH. It is this reduced form which is capable of absorbing light. The 16 increase in absorbance is directly proportional to lactate concentration (Kragenings, 1978). There are at least five distinct forms of lactic dehydrogenase (LDH) which arise from the combination of two types of protein "H" type and "M" type. The LDH form composed of four identical "M" subunits (M^) is found in skeletal muscle and the H^ form is characteristic of heart-type tissues (Cahn et al, 1962). The intermediate electrophoretic forms of LDH, which are molecular hybrids of muscle and heart-type LDH, include M^H and MH^. The M4 and M^H isoenzymes are predominantly found in fast-twitch, glycolytic skeletal fibers (Thorstensson et al, 19 77; Schumer, 19 79), which facilitate the reduction- of pyruvate to lactate; and the MH^ and isoenzymes predominate in slow-twitch oxidative tissue (Sjodin, 1976; Schumer, 1979), which facilitate the oxidation of lactate to pyruvate and its subsequent use in the Krebs Cycle. The results of a study by Taunton et al, 0-981) suggests that the glycolytic enzyme activity is a function of fiber composition rather than training. Consequently recent studies have not resulted in LDH enzyme alterations in either endurance or power athletes (Green et al, 1979). Lactate Concentration Cohen and Woods (19 78) state that the main metabolic 17 pathways involved in lactate concentration are glycolysis, gluconeogenesis and lactate oxidation. The functions of glycolysis include the provision of energy in the form of adenosine triphosphate and the provision of intermediates for subsequent biosynthesis of other metabolites. Margaria (196 7) showed that under conditions of maximal exercise, when the oxygenation of tissue is lowered, energy is provided via glycolysis. Under anaerobic conditions the sole product of glycolysis is lactic acid; whereas under aerobic conditions the lactic acid formed can either be used for the resynthesis of glucose or oxidation via the tricarboxylic acid cycle. It should be noted though, that energy sources are seldom strictly aerobic or anaerobic, inferring a serial relationship (Astrand and.Rodahl, 1977). Gluconeogenesis refers to the formation of glucose from lactate and amino acids (Cohen and Woods, 1978). The pathway includes some of the glycolytic reactions through which the net flux is in the reverse direction. muscle glycogen —-> blood lactate t 4 blood glucose < liver glycogen (Cori Cycle) Recently the quantitative significance "of the "Himwich-Cori Cycle" for removal of lactate has been questioned. Hermansen and Vaage (19 80) state that although some of the lactate produced in muscle during exercise diffuses out 18 into the blood and other fluid compartments, part of the lactate produced is "stored" within the muscle. Furthermore, they showed that only about 10% of the lactate disappearance from human muscle during its recovery from maximal exercise, can be accounted for by an efflux from muscle into the circulation. This suggests that 90% is metabolized within the muscle itself ie. 15% through oxidation to CO^ and ^O; 75% through (re)conversion to glycogen. Both Gisolfi et al (1966) and Davies et al (196 8) alluded to the fact that moderate aerobic workloads during recovery increased the rate of disappearance from blood, suggesting that a greater fraction of lactate may have been utilized as substrate. More recently, Bonen and Belcastro (19 76) demonstrated greater lactate removal during recovery speeds between sets of one mile runs : in highly trained endurance runners than in untrained subjects. The investigations into the fate of lactate has led to some controversy. Rowell et al (1966) indicated that approximately 50% of lactate produced during moderate prolonged exercise is resynthesized into glycogen by the liver, whereas the studies by Hermansen and Vaage (19 80) conclude that 75% of lactate found in muscles at the end of anaerobic exercise is converted into glycogen in the same muscle. These data suggest that lactate concentration and subsequent 19 removal may be intensity specific. The oxidation of lactate via the tricarboxylic acid cycle to C02 and H^O depends on the activity of pyruvate dehydrogenase and not that of lactate dehydrogenase. The enzyme is maintained in an inactive state when the concentration of ATP and acetyl CO-A are kept high by the oxidation of fuels such as fatty acids (Cohen and Woods, 19 78) . Resting man probably produces a lactate concentration of 0.7 -1 mM/L, a 70 kg. man having a total lactate production approximating 1300 mM/day. Of this, 53% is apparently metabolized by liver (Cohen, 1975). Practical and physiological factors also influence the concentration of lactate. Practical factors include the technique of venipuncture, musclular contraction in.'the limb from which the blood is obtained, and the method of blood collection, all which yields spuriously high lactate concentrations (Cohen et al, 1976; Huckabee, 1958(b)). Physiological factors include the site of sampling, arterial values being lower than peripheral venous values (Jervell, 19 28; Huckabee 1961(a)), and the state of an individual, since lactate concentration can rise following a meal or during exercise. Turrell and Robinson (19 42) :showed that blood lactate concentrations can reach 22 mM/L during maximal exercise, the accumulation causing a metabolic acidosis which Barr 20 et al (1923) termed "lactic acid acidosis". A question crucial to the interpretation of blood lactate concentration, and its subsequent use to indicate the quantity of anaerobic work performed is whether it bears any relationship to tissue lactate concentrations. Skinner and McLellan (1981) state that, depending on the time of blood sampling, blood lactate may or may not be indicative of muscle lactate. It would appear that the higher the exercise intensity, the later blood lactate reaches peak values. However, Green et al (1982) showed that the elevation in muscle anaerobic glycolysis precedes both the VC^AT and the blood LaAT in a progressive exercise test. Furthermore, Taunton et al (19 81) stated that rapid removal rates during recovery in long distance runners will lead to lower blood lactate values if taken 5 minutes post exercise. Further research is required in this area as related to specificity of training. Neither muscle lactate concentration nor the muscle-to-blood gradient for lactate was related to lactate released into the blood (Graham et al, 1976) . In addition, blood lactate concentration is influenced by muscle fiber composition and recruitment as mentioned previously. Graham (19 78) showed a muscle lactate concentration to be three times as high in Type II fibers as that found in 21 Type I fibers. He hypothesized that the Type II fibers would be more likely to become hypoxic due to lower values for capillary-fiber ratio, mitochondrial concentration and the rate of oxidative metabolism. Due to what appears to be a preferential recruitment patter from Type I to Type IIA to Type IIB fibers during various phases of progressive exercise (Essen, 1977), as related to glycogen depletion studies, recruitment may influence lactate concentration. "Thus, it would appear that blood lactate levels reflect the production, release, and oxidation of lactic acid by muscle and that, in turn, is influenced by muscle fiber composition and the type of fiber being recruited at any given time" (Skinner, P.238, 1981), in addition to the type of exercise performed and the intensity at the onset of exercise. C02 -The control of pulmonary ventilation during exercise, and the subsequent CO^ and hydrogen ion mediators in the blood, are of special importance to the discussion of aerobic-anaerobic metabolism and the subsequent determination of the anaerobic threshold. In 1905, Haldane and Priestley stated that CO^ production could fully account for the increase in ventilation o 22 seen during exercise. In the years from 1911 - 1914, European researchers indicated that the hydrogen ion was the blood borne mediator of ventilatory control in exercise. Today, we realize that CC^ can be produced by the aerobic metabolism of fat and carbohydrate. During anaerobic metabolism, lactic acid is also formed thus constituting an .additional source of CO,,. The entry of lactate into the red blood cells is associated with the entry of hydrogen ions which react with HCO^ leading to E^CO^ and thus the CC>2 which is excreted by the lungs . The question at times is the availability of carbonic anhydrase. There is no carbonic anhydrase in plasma, but an abundant supply in red blood cells. HLa + NaHC03~ > NaLa + H2C03 ; H„CO_ -—> CO- + H_0 2 3 * 2 2 (Wasserman andiMcIlroy., 1964; Wasserman et al, 1973) Turrell and Robinson (19 42) earlier had shown that an increase in lactate is accompanied by a decrease in base bound as bicarbonate, which, causes a decrease in the CO^ combining capacity of the blood. Some hydrogen ions will stimulate the chemoreceptors located in the medulla oblongata, the carotid and aortic bodies thus causing the respiration rate to increase (Guyton, 1976) . 23 The diffusion coefficient is twenty times higher for CC>2 than for 02 therefore C02 diffuses easily out of the cells into the interstitial fluid then into the blood. Once in the blood, C02 is carried via three major forms: (a) 10% of dissolved C©2 forms some bicarbonate ions, but this is a very slow process in the plasma; C0o + H_0 H„C0^ => H+ + HCO ~ Z Z ^ Z 3 ^ -J The H+ is buffered by plasma protiens: (b) 20% of C02 carried forms a loose combination with carbamine Hb; (c) 70% of C02 diffuses into the red blood cells which carries high concentrations of the enzyme carbonic anhydrase. Carbonic anhydrase converts C09 to H„CO,. through the following reaction: CA C02 + H20 H2C03 > H + HC03-Once these reactions occur the (H*) ions are picked up by the Hb and buffered in order to control the pH and the HCO^ diffuse out into the plasma in exchange for CL (CL shift or Hamburger shift). The C02 is carried via venous return to be excreted by the lungs. (Ganong, 19 79) . Anaerobic Threshold From the early studies of Margaria et al (19 64) and 24 Bang (19 36) the concept of "anaerobic threshold" grew. These researchers considered that lactate production would be restricted to the first few minutes of exercise when the oxygen supply would be limited. However, research by Hubbard (197 3) showed that lactate production could occur even at low intensities and that uptake probably increases with increasing intensity. Knuttgen (1962) showed that there was a "critical" level of work where lactate first appears in the blood and in 1964, Wasserman and Mcllroy postulated that the "anaerobic threshold" was the level of work just below which a subject could exercise for prolonged periods in a steady state, without developing metabolic acidosis. They measured the AT via .an .increase in blood lactate concentration, a decrease in arterial blood HCO and pH, and an increase in R. 3 In 19 61, Issekutz and Rodahl stated that there was a high correlation between blood lactate levels and excess C02 and ventilation (r=0.92) suggesting that the diffusion of bicarbonate C02 (non-metabolic C02) was more rapid than lactate. This showed that excess C02 follows anaerobic metabolism more closely than blood lactate levels. However, Bouhuys et al (1966) found that R and ExC02 were associated with lactate accumulation, but the reverse was not always true. As the workload increased, the increase in lactate 25 was greater than the decrease in standard bicarbonate causing them to allude to the fact that the measurement:of R and ExCG^ would only be an indirect sign of the degree of exercise acidemia. Furthermore, they were unable to reproduce the excellent correlation found by Issekutz and Rodahl in 1961. Issekutz, Birkhead and Rodahl (196 2) first recognized that there would be a concomitant increase in C02 output by the lungs with increased lactic acid production. They suggested that an increase in the respiratory quotient would indicate lactic acid production, where, R = volume of CO^ produced/volume of CC^ consumed Wasserman-and Mcllroy (1964) expanded this concept in cardiac patients and in 196 7, Clode, Clark and Campbell quantified the approach, recognizing that the volume of excess CC^ rather than R would be stoichiometrically equivalent to lactic acid production, ie. the numerical relations of chemical elements/compounds and the mathematical laws of chemical changes.. Volkov in 19 75 supported Issekutz and Rodahl (19 61) when he found that lactate accumulation led to a decrease in HCO^ and to the appearance of excessive amounts of CC^ • He states that it is possible to determine the level of anaerobic metabolism from the excess of release C0„ through the following 26 equation: ExC02 = OR • V02 = VC02 — [R(rest) x VcJ -1 -1 • where ExC02 is excess C02 (ml* kg • min ), V02 is the level of oxygen consumption during work (ml-kg - min "*") . Diamont et al (1968) found muscle tissue lactate to differ from blood lactate (19.1 to 11.4 mM/L respectively): after maximal exertion therefore suggesting a possible delay in diffusion capacity for lactate from muscle tissue to the blood. This was supported by Graham (19 78) . Jorfeldt et al (19 78) suggested that the< delay may be due to the inadequate relationship between recruited fibers and available draining capillaries. Wasserman et al (19 73) used a breath by breath technique for determining the anaerobic threshold and found that the end-tidal CC>2 and C>2 tensions were more sensitive indicators, because they allowed for the detection of hyperventilation. This hyperventilation may obscure the gas exhange parameters, ie. VC02, V , and R. This was supported by Wasserman and Whipp (19 75) who also suggested that for non-invasive AT determination, a one minute work increment would be optimal for showing the change in metabolism at the start of anaerobiosis. Kao (1977) however, suggests that the hyperventilation is partially due to alterations of the neural component and to the altered recruitment of fiber. 27 Today the anaerobic threshold terminology has been disputed by various investigators (Kinderman et al, 19 79; Skinner and McLellan, 1980) who suggest that there is a three phase two breakaway model during the progressive transition from exercise of low to maximal intensity. The phases are conveniently termed aerobic phase, aerobic-anaerobic transition phase, and anaerobic phase. The following pattern would be observed: 1) Aerobic Phase: at low intensitity exercise, there is a linear increase in oxygen intake (VO^), ventilation (JJ^) , volume of CO^ expired (VC02) and heart rate, with an R of .7 to .8 and little or no lactate formed; in addition, there would be a decrease in Fe02 and an increase in FeC02; 2) Aerobic-Anaerobic Transitional Phase: at an exercise intensity of 40 - 60% of V02 max, the » V02 and heart rate continue to rise linearly and there is a rise in lactate to appoximately 2 mM/L; due to buffering of the H+ produced by the lactate by the bicarbonate, there will be an increased VCC>2 and a continuing rise in FeCC>2 consequently V and VCC>2 will be greater than the rise in VC>2; since there is an increased V to compensate for the metabolic acidosis there will be a decrease in FeO„; this 2 8 breakaway point corresponds to the AT of Wasserman et al (19 73) and the aerobic threshold of Skinner and McLellan (1981). 3) Anaerobic Phase: at an exercise intensity of 6 5 - 90% V02max the VC>2 and heart rate continue to rise linearly to maximal plateaus; the lactic acid is approximately 4 mM/L and takes a curvilinear increase accompanied by another V breakaway and a continuing rise in VC02; there is a drop-off in FeC02 due to hyperventilation while Fe02 continues to rise; this breakaway point corresponds to the AT of MacDougall (1978) . . • Rupp et al (1982) looked specifically at non-invasive measures of the aerobic threshold and AT and found the best prediction of aerobic threshold to be the initial increase in V"e out of proportion to V02. They further stated that no effective non-invasive prediction could be found when using the second breakaway V"e and/or a decrease in FeC02. Sucec et al (19 82) demonstrated that blood lactate measurement of AT is reproducible and that gas exchange may be validly employed to determine AT for exercise. Ponton et al (19 82) supported these findings and also suggested that different workload durations of one to three minutes do not 29 seem to affect the threshold point. The Marathoner The marathon is a 42.195 km. (26 mile, 385 yard) running race. The pace, set through the eyes of the moder elite marathoner, is between 17.74 km/hr and 19.35 km/hr;. The physiological consequence of the biochemical adaptations to this form of exercise from an untrained state to a trained state is well documented (Holloszy et al, 1977; Holloszy, 1973). These include increases in mitochondrial content and respiratory capacity of skeletal muscle, increased VG^niax and subsequent absolute work rates, increased rate of myocardial protein synthesis resulting in a physiological cardiac hypertrophy, a lower utilization of glycogen in the working muscles, an enhanced capacity to oxidize fatty acids (which helps to protect against glycogen depletion), increases in number of capillaries per number of muscle fibers and increases in type II muscle fiber mitochondrial volume (Holloszy et al, 1977; Howald et al, 1982) . Costill and Fox (1969) have shown that marathon runners were able to utilize 75% of their VC^max with little lactic acid production. Later in 197 3, Costill et al found that at all running speeds above 70% VC^max, the faster distance runners accumulated less blood lactate than the slower runners at similar speeds and relative•percentages of their aerobic capacities. 30 The ability of the endurance runner to maintain a high velocity during a race which is only slightly above his anaerobic threshold was reported by Farrell et al (1979). Rhodes et al (19 81) demonstrated that there was indeed a high correlation between the velocity at the anaerobic threshold and the marathon running pace. This appears to be appropriate for specific specialties as Svendenhag and Sjodin (19 82) found that the running velocity corresponding to a blood lactate concentration of 4 mM/L was the best single parameter in differentiating between runners with different distance specialties. Effects of Training on AT The effects of training on the anaerobic threshold has received some attention as of late. Daniels et al (1980) suggests that training delays the onset of blood lactate accumulation "as a function of exercise intensity", indicating that the accumulation of venous lactate is reversible during steady state exercise. MacDougall (19 77) and Robinson and Sucec (1980) , state that both moderate (85% VO^max) and intensive (125% VOc,max) training increase the anaerobic threshold. They included both high intensity endurance-interval and long duration sub-maximal training. Lafontaine et al (19 82) found that for moderate fit individuals, medium intensity/high quantity and high intensity/low quantity 31 increased the anaerobic threshold over other combinations of low/medium/high intensity with low or high quantity over a 10 week, 5 sessions per week, training schedule. Reproducibility of AT The reproducibility of the AT via gas exchange and venous blood lactate measurements has been investigated. Sucec et al (1982), using V , VCC>2, v"e/V02 and FeC>2 for the gas exhange variables and venous blood lactates drawn 15 seconds prior to changing the work rate, to determine the AT, found the blood lactate measurements of AT to be reproducible and that non-invasive determination may be validly employed in assessing AT for exercise on the bicycle ergometer. . Ponton et al (1982) studied the validity and reproducibility of the lactate threshold for a continuous protocol on the treadmill for trained runners and found the lactate threshold to be a valid and reliable measure. The role of the anaerobic threshold has been used for testing hospital patients (Wasserman and Whipp, 19 75), athletes (Costill, 1970) and models of hyperpnea in non-athletes (Whipp, 19 77) . However, the study of the role of the anaerobic threshold and its relationship to performance of elite endurance runners is. in stages of .preliminary investigation. 32 CHAPTER III METHODS AND PROCEDURES Subjects Five male subjects (mean age = 30.6 - 5.64 years) were selected from track training clubs in the Vancouver lower mainland. Each subject had a VO^max of approximately 65 ml-kg •min or greater, and had run a sub 2:30 marathon. Information regarding training program, best time at various distances and medical history was also compiled. Testing Procedures The subjects were tested on five separate days with at least one day between each session. They were asked to refrain from any heavy training 24 hours prior to and on the test day. Testing was administered at approximately the same time of day and under similar environmental conditions. During the first session after an appropriate consent form had been signed (see Appendix), height, weight, body composition ; assessment (Hydrostatic weighing), anaerobic threshold and maximal oxygen consumption (V02max) were determined. The remaining four sessions consisted of a short warm-up, followed by a 10 minute constant speed run, after which 2 ml. of blood was drawn from an anti-cubital vein (every minute for four minutes) in the arm of each subject. 33 Testing Protocols All testing was performed in the J. M. Buchanan Fitness and Research Centre at U.B.C Heart rate was monitored by direct ECG utilizing an Avionics 4000 Electrocardiograph with oscilloscope and ST depression computer and display. Expired gases were continually sampled and analyzed by a Beckman Metabolic Measurement Cart (BMMC) interfaced into a Hewlett Packard 30 52A Data Acquisition system for fifteen second determination of respiratory gas exchange variables. Physical characteristics included height, weight and percent body fat. Assessment of percent body fat was carried out via hydrostatic weighing (Katch et al, 196 7) . VC^max and anaerobic threshold were determined using a continuous treadmill protocol. Each subject walked on the treadmill at 8.06 km/hr (for.' five minutes) as a warm-up. The speed was then increased to .81 km/hr at the end of each minute with subject running until volitional, fatigue. Maximal oxygen consumption and ExCC^ at max were determined by averaging the highest four consecutive fifteen second values. Values reported for the 10 minute constant speed runs were mean i S.D. The anaerobic threshold and the Vtam were determined by visual inspection of the ExCC^ elimination curve (Volkov, 19 75) . Three investigators carried out the determination and came to an agreed point of break away. 34 The determination of the anaerobic threshold was consistent with the definition by Wasserman et al (19 64) . The blood samples were drawn from an anti-cubital vein via a 21 gauge butterfly catheter, at the end of the 10 minute constant speed run, and each subsequent minute for four minutes. Samples were immediately centrifuged and plasma pipetted and frozen for future analysis. Blood lactate was calculated in mM/L via a standard enzymatic method, and peak lactates were recorded (Gutmann and Wahlefeld, 1974) . Experimental Design and Data Analysis There were two dependent variables: Blood lactate and ExCC^. The independent variable was the speed of the treadmill with four levels of variation: 1. 1 km/hr below V. tarn 2. at V_ tarn 3. 1 km/hr above V" ' tam 4. 2 km/hr above V, ' tam A latin square was used to assign the subjects to these variations. Analysis of variance with preplanned orthogonal comparisons and Scheffe post hoc contrasts were used to determine the effects of the treadmill variations on La and ExCC^• The Pearson product-moment correlation coefficient using raw scores was employed, in correlating La and ExCC^. 35 CHAPTER IV RESULTS AND DISCUSSION Results The physical characteristics of the five subjects are summarized in Table I. The pertinent variables for four of the subjects are represented in Table II. The results of the statistical analysis for blood lactate (La) and excess CQ2 (ExCO,,) are displayed in Table III. The correlation coefficients between La and ExC02 are represented in Table IV. Table V contains a summary of the hypotheses testing. Figures III and IV represent the means and standard deviation of La versus treatments and ExC02 versus treatments respectively. Figure V shows the relationship between La and ExC02. Individual summary sheets for the metabolic parameters and the subsequent anaerobic threshold curves, for determination of Vtam appear in Appendix A. It was revealed during the blood lactate determination that subject NW had been assessed at a V, which was well J tam above the accepted values for anaerobic threshold determination, as outlined by Wasserman et al (1964) . The following values for La (mM/L) were found: V,. . • V ' V" , , V^_ , „ tam-1 < tam tam+1 tam+2 NW 5.096 8.261 11.927 14.053 LH 1.479 2.493 4.570 9.26JT 2.05 3.397 4.191 6.978 JH .1.747 3.837 8 .077 8 .945 SP 2.774 2.908 4.277 9.3836 TABLE 1 • / PHYSICAL CHARACTERISTICS OF SUBJECTS (SUBJECT AGE HEIGHT WEIGHT % VD^ A.T.- MARATHON TIME (YRS.) (CM.) (KG.) BODY . . ., % VO„ (hr: min: sec) FAT (ml-kg 'rain ' 2max NW 34 171.7 67.1 5.2 69.80 88 2:29:27 LH 36 182.1 72.0 - 67.01 86 2:29:00 JT 34 182.2 68.5 11.2 64.11 87 2:26:14 JH 25 177.1 70.5 8.7 67.47 91 2:18:33 SP 24 182.0 68.5 7.9 72.42 82 2:15:56 X 30.6 179.02 69.32 8.25 68.16 86.8 2:23:50 +S.D. -5.64 ±4.63 ±1.93 ±2.47 ±3.12 ±3.27 ±6:13 37 TABLE II RELEVANT DATA VARIABLES V, tam-1 V tam V tam+1 V, tam+2 MAX Velocity of treadmill (KPH) VCL -1 -1 (ml «kg -min ) |vo2 (percent MAX) iExC02 (ml-kg-1-min-1) |ExC02 (percent MAX) [Blood lactate (irM/L) (Heart Rate Xb.p.m.) \J (STPD) e 16.61±.77 J7.58-.77 18.55±.77 19.52±.77 22.74±.77 52.67±1.48 58.64±2.42 62.05±1.96 63.32^4.54 67.75±3.45 77±3 87±3 91-5 93±4 100 11.09±1.54 14.35±1.34 17.06±3.15 21.61±2.53 28.8si4.55 39±10 50-7 59-2 15-8 100 2.01±.56 3.16±.58 5.28±1.87 8.64±1.13 162±8 167±9 174±9 182±8 +_ .+ . pfeight (kg.) 76.49-2.8 89.90-2.66 99.08-8.59 113.89-7.74 130.55-4.35 69.3 ±1.5 69.2 ±1.4 69.2 ±1.6 69.-1 ±2 67.7 ±2 * - + (All values are X - S.D.; N=4 unless *, where N=3) 38 . TABLE III ANALYSIS OF VARIANCE WITH PREPLANNED ORTHOGONAL COMPARISONS AND SCHEFFE'S POST HOC CONTRASTS F Probability (p*) Blood Lactate'. F Probability (p^) ExC02 Between Groups V,. ,, V, , tam-1' tam 24.95 0.01 15.46 0.01 Vtam+1' Vtam+2 Comparison 1 tam-1 tam/ 56.24 0.01 34.15 o;oi tam+1 tam+2 Comparison 2 tam-1 tam 1.93 non-sig. 4.15 non-sig. Comparison 3 V - V tam+1 tam+2 16.65 0.01 7.89 ; .0.05 Scheffe's V, , and V, .. tam-1 -:.. tam+1 11.62 0.05 2.33 non-sig. V^, . , and V, .„ tam-1 tam+2 47.78 0.01 43.23 0.01 V^. and V. tam tam+1 4.88 non-sig. 2.87 non-sig. v and V^_ . . tam tam+2 32.64 0.01 20.59 0.05 TABLE TV CORRELATION COEFFICIENTS: HLa and ExCO. SUBJECT r LH .949* JT .998** JH .995** SP .948* OVERALL .886** ** p<*.005 40 TABLE V SUMMARY OF HYPOTHESES TESTING DEPENDENT VARIABLES PROPOSED RELATIONSHIPS RESULTS ExC02 (ml*kg "'"•min 1) tam-1-" tam V • y V tam tam+1 V V tam+1^ tam+2 Supported Non-Supported Supported HLa (iriM/L) Vtam-1—Vtam V ^ V tam ^- tam+1 V ^ V Tam+1 *~ tam+2 Supported Non-Supported Supported ExC02/HLa High Correlation Supported FIGURE III Means - s.D. For Four Subjects Over Four Conditions 43 i rH I •H 30 25'-•2,0 h FIGURE V Correlation Between ExCC^ and La (r = .89) 15 CN O U w -1.0 2 5: 1) '9 i'O-Blood Lactate (mM\L ) O LH + JT" O JH' * SP 44 In addition, subject NW was able to complete only 7:30 ;(min) of the 10 (min) vtam+2 work task. Subsequently, he was injured and unable to further complete a second testing. Consequently, his data only appears in Appendix A and was not included in any statistical analysis. Blood lactates and ExC02 demonstrate a significant F for the between group; .variation (p^O.01). This indicates that the velocity of the treadmill (V^^, "V^, Vtam+1, Vtam+2) affected both the La and ExC02 values. The between groups variance was then divided into preplanned orthogonal comparisons and . statistical significance was found for both La and ExCO„ for the comparison V. , and V. versus 2 tam-1 tam V_ ,. and V_ , „ • (p* 0 .01 for La; p*0.05 for ExCC- ). tam+1 tam+2 c c 2 No significance was found for V. . and V. for either La 3 tam-1 tam or ExC02. Scheffe's multiple comparison of means was computed on both La and ExCC>2. to further locate significance. Vtam_i and V\ , , were found to be significantly different (p^-0.05 tam+1 3 for blood lactate, whereas V, , and V. (p-J 0.01) and tam-1 tam+_ also V_ and V. (p^eO.Ol for La; p-<0.05 for ExCOJ tam tam+2 - > c . 2 demonstrated significant differences for both La and ExC02. No significance was found for vtam_j and Vtam+1 for ExC02' nor for v\ and V\ ,, for both La and ExC0o. tam tam+1 , 2• The individual correlations between La and ExC02 are 45 highly significant. The overall correlation,of .886 (p<0.05) demonstrates a high positive correlation between La and ExC02. Discussion The main objective of this study was to elucidate the procedure of utilizing the non-linear increase in ExCC>2, as outlined by Volkov (1975), for the subsequent determination of the anaerobic threshold, as defined by Wasserman et al (1964). Although the sample size (N=4) limited statistical treatment, analysis of variance with preplanned orthogonal comparisons and Scheffe' post hoc contrasts reveal similar patterns between La and ExCC^ over the four conditions, ie. tam-1 tam tam+1 tam+2 The subjects are representative of the usual elite class marathoner. They have a low percentage of body fat (X = 8.25-^ 2.47%); are capable of consuming large volumes of oxygen (VG^max) during an exhaustive effort (X =67.76 - 3.45 ml-kg • min "'") ; and have the ability to maintain a large fraction of their V02max (AT - % VC>2max) for prolonged periods.. (Costill, 1967, 1979; Saltin arid Astrand, 1967; Costill et al, 1970). According to Volkov (1975), the more aerobically trained a runner is, the higher V,_ (or AT - % VO.max) . This study reported tam 2 an AT - % V02max of 86 .8 - 3.27 %. (17.58 km/hr) which is higher than most distance runners who employ 75 - 80%. 46 However, some elite runners have been recorded at 86 - 90% V02max (Costill and Fox, 1969; Costill, 1970'; MacDougalL 1977). Further research should consider the AT - %V02max as an additional indicator of performance potential. The critical percent of VG^max which one can maintain for prolonged periods of time has been defined as the anaerobic threshold (Wasserman et al, 1964) . The velocity of the treadmill just below the point of a non-linear increase in. ExCC>2 elimination was used as the anaerobic threshold determinant and labelled V\ (Volkov et al, 19 74) . tam ' Prior research has already indicated an increase in lactate at a critical level of work (Knuttgen, 1962; Margaria et al, 19 63; Issekutz and Rodahl, 19 61; Naimark et al, 1964; Bouhuys et al, 1966), above which the limited energy from anaerobic metabolism and tissue acidosis probably determines optimal running pace. In earlier studies, this critical level would be revealed via a dramatic increase in R (respiratory quotient), increased La and a decrease in HCO^ . The increase in R is attributed to the ExC02 produced by metabolic acidosis which displaces C02 from bicarbonate (Naimark et al, 19 64). Wasserman and Mcllroy (1964) alluded to the fact that ExCC»2 was released when acids formed during anaerobic metabolism were buffered, principally by HCO . Therefore, 47 an increase in the volume of C02 produced and eliminated.would yield a higher value for ExCC^ since: ExC02 = [vC02 -(R(rest) x VO^j (Volkov, 19 75) It should be pointed out that in metabolic acidosis only 15 - 20% of the acid load is buffered by the H2C03-HC03~ system in the interstitial fluid. The majority of the buffering occurs as an intracellular process, largely by protien and organic phosphates which bind H+ and liberate Na+ and K+. (Ganong, 19 81; Hultman and Sahlin, 19 81) . In actuality the rise in plasma H+ stimulates the ventilation rate enabling the level of H2C03 to be reduced otherwise an uncompensated acidosis would be evident with a decrease in pH. Crandall and Bidani (19 81) have shown that a reduction in PJJCQ3~ leads to a reduction in pulmonary C02 elimination of up to 30%, whether or not carbonic anhydrase activity is available to plasma. They suggested that the red cell HGp3 /CL exchange partially limits C02 elimination or capillary gas transfer when its speed is abnormally slow. This may be the case at extreme workloads. The measurement of Vtam can be affected by hyperventilation (in addition to errors in visual inspection) which liberates stored C02 and transiently increases R, therefore due to the 48 decreased R. ^_ more C0o will be excreted and the volume ACO2 z of ExC02 will increase. Consequently vtam maY be over estimated in these cases where a breath by breath analysis is not employed. (Wasserman et al, 19 73). Wiley (unpublished M.P.E. Thesis, 1980), studying the relationship between oxygen debt and V , showed that V tam tam is useful in determining primarily aerobic work intensity above which metabolic acidosis occurs. Dunwoody (1981 M.P.E. Thesis) showed that V m was probably easier to determine in the highly trained individuals as opposed, to the, lesser trained. Although using different variables for the determination of a threshold, other investigators have demonstrated significant correlations between the onset of anaerobic metabolism and race time (Weiser et al, 19 78; Farrell et al, 19 79, Sucec, 19 79; Sjodin et al, 1981; Sady.et al, 1981). A recent article by Rhodes et al (19 81, CJASS abstract in press), examined the relationship between predicted marathon, times, calculated from V , and actual performance times, in a marathon, and found a highly significant zero order correlation (R - .94, p^O.01) between the predicted and actual marathon times. This relationship established V, tam as a critical point in determining marathon running speed and possibly to the onset of metabolic acidosis. The present study not only shows high individual correlation 49 between La and ExCO,,, but a high overall correlation (r = .886 , p«-0.005), indicating that there exists a high positive relation between La and ExCC^ (Table IV, Figure V). Recently the use of the term "anaerobic threshold" has been questioned (Kinderman et al, 19 79; Skinner and McLellan, 1981) . The authors suggested that the ability of the aerobic cycle to supply fuel to the working muscle and to remove any metabolic by-products will eventually" be exceeded at a critical point labelled the aerobic threshold (^2 mM/L. La) (the anaerobic threshold of Wasserman et al, 1964). The transitional stage whereby the percent contribution of aerobic mechanisms is gradually diminished and the percent contribution of anaerobic metabolism increases was labelled the aerobic-anaerobic transition (<**'2 - 4 mM/L La). As the percent of the anaerobic contribution increases, a third phase becomes evident, labelled the anaerobic threshold (*M mM/L La)(Mader et al, 1976). For the purpose of discussion, the three phase double breakaway model reported by Skinner and McLellan (19 81) will be used. In the present study, V^ demonstrated a La concentration * 2 tam of 3.16 mM/L which is higher than the accepted value of approximately 2 mM/L defined by Wasserman, and more closely located in the aerobic-anaerobic transition stage reported by Kinderman et al (1979) and Skinner and McLellan (1981). The 50 La value of 5.28 mM/L reported for vtam+]_ i-s markedly above the 4 mM/L mark for contemporary terminology which indicates that V\ ,, is above the anaerobic threshold as tam+1 reported by MacDougall (19 78) and Mader et al (19 76) . In order to shew a*transitional zone though, serial sampling may be necessary and differences.may be due to the range of treadmill speeds. The fact that •significance was demonstrated between V\ , and V\_ versus V\ „,, and tam-1 tam tam+1 V. , „ -(p<0.01) for both ExCO- and La indicates that the tam+2 ^ 2 values are closer to the anaerobic threshold or the upper limits of the aerobic-anaerobic transitional stage, above which metabolic acidosis is evident by the increasing concentration of La. Inter-^individual variability among the runners may account for differing. ;La concentrations. Derek Clayton in one series of experiments; was required to run at a treadmill speed which equalled his best marathon performance .'(328 m/min. or 4:54 sec./mile). His heart rate response was constant during the run at 16 7 beats/min. which equals the X- heart at V\ for this study and that reported by Parkhouse tam et al (1982) . Venous blood lactate values at 10 and 30 minutes were 2.1 and 2.3 mM/L. respectively, which is similar, to the X - La value reported for vtam_T_- H:LS ability to run at 86-9 0% of V02max with La concentrations only slightly above 51 resting values (1.3 mM/L) is probably a function of muscular adaptations to endurance training. In the present study the 3.16 mM/L reported at vtam is above the aerobic threshold. V. as used by Rhodes • tam -* et al (19 81 CJASS .Abstract) has been shown to have a high correlation to marathon running pace (r - .9 2). The fact that the values reported differ from accepted threshold concentrations of 2 mM/L and 4 mM/L derhonstate the need^for the determination of individual anaerobic threshold (IAT) via lactate kinetics as pointed out by Stegmann et al (1981) . Furthermore, the incorrect assessment of subject NW's V, J tam supports the need for the development of a method of evaluating vtam which would be more sophisticated than visual inspection alone. At this stage, it should be apparent that the discussion of a specific point or threshold is misleading. Since the plasma lactate concentrations are the result of the production of lactate in muscle, diffusion of lactate from muscle to blood, and the uptake of lactate by numerous tissues, caution must be used in interpreting the AT as the onset of anaerobiosis (MacDougall, 19 78; Farrell et al, 19 79) . It appears to be a point in a transition stage which varies from individual to individual. Many researchers believe that there is a critical pH which can affect rate limiting enzymes 52 ie. PFK or the Ca dependent contractile mechanism. As you get closer to the critical pH a very small decrease in pH may be quite important. (Roos and Baron, 19 81; Hultman and Sahlin, 1981) . The significance demonstrated between v\ 3 tam+1 and vtam+2 offers some indirect support for this. The high correlation of .886 shown between La and ExCC>2 does not necessarily indicate a cause/effect situation since a third variable (or more) may be involved. It does indicate that both appear to increase in a linear fashion as intensity increases.. Although out of the scope of this study the intracellular buffering and the determination of intramuscular pH seem to be obvious candidates to consider. The increased ventilation rate as a result of H+ accumulation helps to compensate for an impending acidosis should intensity continue to increase. Above a critical intensity though extra CC^ is added to the expirate primarily through the B^CO^/HCO^ buffering system. Consequently, above V, one should see further increases in ExCO„ elimination tam 2 as the body's ability to maintain a tolerable pH leads to fatigue. In a practical situation, this would necessitate a slowing of pace ora cessation of the run. Fatigue in this case is interpreted according to the four basic processes outlined by Simonsen (19 81): depletion of substances necessary for activity, accumulation of substances, changes 53 of physico-chemical state of substrate and disturbance of regulation and coordination. In an exercise situation, • the majority of the (H+) which reflects pH is from lactic acid (97%) and pyruvate malate, etc. (3%). The use of ExCC^ is of particular importance for determining running pace for an endurance athlete since it measures the CC^ produced as a by-product from metabolic acids and is non invasive therefore much easier to ascertain than La. (Issekutz et al, 1962; Naimark et al, 1964; Rhodes et al, 1981). It was hypothesized that V, , _c V, -C V, ,, V. Jjr tam-1 tam tam+1 tam+2 for both La and ExCC^. Results, represented in Table III, support this. Although no significance was found between v^am and vtam+j xt maY possibly be due to the small N and variability and/or as discussed, part of a transition stage above which a more significant increase in La and ExCC^ is seen. This was supported by the significant difference seen between V +^ and vtam+2 (P^O.Ol for La; P<0.05. ExC02) . The greater the workload, the greater the accumulation of La and the subsequent ExCC>2 elimination. The implications of this study to the coach and athlete has yet to be established. The use of ExCC^ in determining the present pace status of a marathon runner, above which fatigue processes become limiting upon performance, appears to be adequate. Some research has been carried out on 54 the effects of intensity and training quantity on the A.T. and medium intensity/high quantity and high intensity/low quantity both increased A.T. (LaFontaine et al, 19 82).. In addition to a high v02max and high percent V02max' tra:Lnin9" volume is associated with success in marathon running. (Hagan and Gettman, 19 82; Sjodin and Jacobs, 19 82) . Specific guidelines for an individual would necessitate tabulating data in a large population of marathon runners to establish some general norms and then identifying that individual's strong and weak areas. Certainly, the moire elite a runner becomes, the smaller the room for improvement and the more sophisticated the tools of analysis. In summary, although other factors such as the difference between subjects in storage capacity in muscle for lactate, lactate tolerance and in diffusion of this lactate from the muscle to blood, coupled to differences in fiber type and recruitment, ventilatory responses, storage and buffer capacity for metabolic acids, the analysis of La and ExCO^ in this study revealed similar patterns of significance and a high positive correlation. These findings support the relationship between the increase in ExCG^ and the onset of plasma lactate accumulation as a limiting factor in performance of elite marathon runners. (Issekutz et al, 19 62; Naimark et al, 1964; Volkov, 1975; Farrell et al, 19 79; Rhodes et al, 1981; Sjodin and Jacobs, 19 81). 55 Further investigation is required into the range of transition from aerobic to anaerobic metabolism via breath by breath analysis of respiratory measurements in conjunction with La values or perhaps La Kinetics (serial sample for a better look at time changes). The effect of training below, at and above this critical level as related to endurance athletes may yield optimal training specificity for peak performances. CHAPTER V .. SUMMARY AND CONCLUSIONS Summary The term "anaerobic threshold" grew from the early studies of Bang (1936) and Margaria et al (1964) . In 1962, Knuttzen showed that there was a critical level of work where lactate first appears in the blood. The increase in lactate is associated with muscular fatigue which limits performance at a given intensity. Wasserman and Mcllroy (19 64) later postulated that the anaerobic threshold was the level of work just below which a subject could exercise for prolonged periods in a steady state, without developing metabolic acidosis. Recently the use of excess CO2 as a non-invasive measure for determination of anaerobic threshold has been shown to correlate highly with marathon running pace (Rhodes.et :al, 1981). The present study attempted to elucidate the relationship between ExC02,.as used in determining the anaerobic threshold, and the appearance to blood lactate in elite marathon runners. Since lactate has been used to determine the degree of acidemia, during exercise of varying intensities, similar patterns in EXCO2 may reveal a non-invasive tool indicative of metabolic acidosis. Five male subjects (mean age 30.6) who had a VX^max °^ approximately 65 ml«kg "'"•min \ and had. runa sub 2:30 marathon were tested on five separate days. During the .first session, after ah appropriate consent form had. been .signed, height, weight,, body composition 57 assessment, anaerobic threshold and maximal oxygen uptake were determined. The remaining four sessions consisted of a short warm-up, followed by a 10 minute constant speed run (V\ , , V\ j V. , , , V\ after which 2 ml. of blood was tam-1 tam tam+1' tam+2 drawn from an anti-cubital vein. Due to the small number of subjects under investigation, statistical analysis was limited. Nevertheless, analysis of variance with preplanned orthogonal comparisons and Scheffe's post hoc contrasts revealed similar patterns,of significance between ExC02 and blood, lactate over the four treatments. The overall correlation coefficient of .886 (p<.005) between ExC02 and blood lactate revealed a high positive relationship between the two variables. ExC©2 (ml-kg "''•min ^) was used as the determinant of the onset of metabolic acidosis in the prediction of the anaerobic threshold. The similar patterns of significance and high correlation, although indicative of a relationship, should not be interpreted as a cause-effect relationship as other variables may be involved (ie. intramuscular buffering). In addition the use of ExCC>2 in determining the AT. as defined by Wasserman et al (1964) needs re-evaluation as the mean lactate was higher than accepted values (3.16 mM/L as opposed to an accepted value of approximately 2.0 mM/L). Consequently, when using 58 contemporary terminology the estimation of AT, via ExCC^ is located slightly above the aerobic threshold and in the aerobic anaerobic transition phase. The fact that a mean of 3.16 mM/L was reported indicates that elite endurance runners are able to run at a pace which is slightly above their aerobic threshold and that the use of ExCC^ in identifying this is an excellent prediction of pace. Consequently, the application of this point to athlete and coach needs to be assessed in terms of. training regimes. The fact that research has shown increase in AT. with training at or above the AT, identifies the .ExCC>2 determination as a viable prediction of a threshold intensity that the athlete should train about. Conclusions 1. Similar patterns of significance were revealed for ExCO„ and blood lactate over the four treatments (V. n, 2 tam-1' Vtam' Vtam+1' Vtam+2) 2. A high positive correlation was demonstrated between ExC02 and blood lactate (r=.886 p<.005),-3. ExCC>2 signifies a rough measure of metabolic acidosis because other variables may account for the high correlation reported. 59 Recommendations 1. Serial measurements of blood lactate in conjunction with ExCC>2 values during and following a progressive treadmill run for the determination of an individual anaerobic threshold needs to be compared in relationship to other variables which may contribute to metabolic acidosis; ie. pH, buffering capacity, fiber composition, and so on; 2. The use of an assumed RQ for the calculation of ExCG^ may vary the actual ExCG^ values since: ExC02 = VC02 - (resting R.Q. x VC>2) ; 3. Further research is required into the effects of varying intensities and. duration of training upon the AT (as assesed by ExCC>2) and subsequent race pace in marathon runners; 4. The use of other non-invasive predictions in addition to ExC02 for visual determination of AT should be included (ie. ventilation versus ExC02) to eliminate any error, as a. result of inter-investigator variability. 60 BIBLIOGRAPHY Alpert, N.R., Lactate production and removal and the regulation of metabolism. Annals of the New York Academy of Science. 119(3): 995-1011, 1965. Astrand, P.O. and H. Rodahl. Textbook of Work Physiology. McGraw-Hill, New York, 19 77. Bang, 0. The lactate content of the blood during and after muscular exercise in man. Skand. Arch. Physiol. 74: 51-82 (Suppl. 10),1936 . Barr, D.P., H.E. Himwich and R.P. Green. Studies in the physiology of muscular exercise. I. Change in acid-base equilibrium following short periods of vigorous muscular exercise. J. Biol. Chem. 55: 495, 1923. Belcastro, A.N. and A. Bonen. Lactic acid removal rates during controlled and uncontrolled recovery exercise. Amer. J.  Physiol. 39: 932-936, 1975. Bonen, A. and A.N. Belcastro. Comparison of self-selected recovery methods on lactic acid removal rates. Med. Sci.  Sports. 8(3): 176-178, 1976. Bouhuys, A., J. Pool, R.A. Binkhurst, and P. Van Leeuwen. Metabolic acidosis of exercise in healthy males. J. Appl.  Physiol.1 21(3): 1040-1046, 1966. Boyd, A.E., S.R. Giamber, M. Mayer and H.E. Lebovitz. Lactate inhibition of lipolysis in exercising man. Metabolism. 23(6): 531-542, 1974. Cahn, R.D., N.O. Kaplan and E. Zwilling. Science. 136: 39 2, 1962 . Carlsten, A. Myocardial.metabolism of glucose, lactic acid and fatty acids in healthy human individuals at rest and at different workloads. Scan. J. Clin. Lab. Invest. 13: 8-828, 1961. Clode, M., T.J.H. Clark and E.J.M. Campbell. The immediate CO^ storage capacity of the body during exercise. Clin.  Sci. 32: 161-165, 1967. Cohen, P.J., Editorial views. More on lactate. Anesthesiology. 43: 614-616, 1975. Cohen, R.O. The production and removal of lactate. Lactate in Acute Conditions. Int. Symp., Basil. 10-19, 19 78. 61 Cohen, R.D. and H.F. Woods. Clinical and Biochemical Aspects  of Lactic Acidosis. Blackwell Sci. Pub. Oxford, 19 76. Cori, C.F. Mammalian carbohydrate metabolism. Physiol. Rev. 11: 143-275, 1931. Cori. C.F. and G.T. Cori. Glycogen formation in liver from d and L-lactic acid. J. Biol. Chem. 81: 389-403, 1929. Costill, D.L. The relationship between selected physiological variables and distance running performance. J. Sports  Med, and Phy. Fit. 7: 61-66, 1967. Costill, D.L. Metabolic responses during distance running. J. Appl. Physiol. 28(3) ; 251-255, 1970. Costill, D.L. A Scientific Approach to Distance Running. Track and Field News. 19 79. Costill, D.L. and E.L. Fox Energetics of marathon running. Med. Sci. Sports. 1: 81-86, 1969. Costill, D.F., H. Thomason and E. Roberts. Fractional utilization of the aerobic capacity during distance running. Med. Sci. Sports. 5(4): 2 4 8-252, 19 73. Costill, D.F. and E. Winrow. Maximal oxygen intake among marathon runners. Arch. Med. Rehab. 51: 317-320, 1970. Crandall, E.D. and A. Bidani. Effects of red blood cell HC03_ /CL~exchange kinetics on lung C02 transfer: theory. J. Appl Physiol.: Respirat. Environ. Exercise Physiol. 50(2): 265-271, 1981. Dakin, H.D. and H.W. Dudley. J. Biol. Chem. 14: 423, 1913. Danforth, W.H. Control of energy metabolism activation of glycolytic pathway in muscle. In; Control of Energy  Metabolism. B. Chance (ed.) New York. Academic Press. 287-297, 1965. Daniels, W.L., D.S. Sharp, D. Bascik and D.M. Kowal. Lactic accumulation in runners and non-runners during steady state exercise. Med, and Sci. in Sport and Exercise. 12 (2) : 87, 1980 . Davies, C.T.M., A.V. Knibls and J. Musgrove. The effect of recovery exercise on the removal of lactic acid from the blood. J. Physiol. 196: 61, 1968. Davis, J.A.,,P. Vodak, J.H. Wilmore, J. Vodak and P. Kurtz. Anaerobic threshold and maximal aerobic power for three modes of exercise. J. Appl. Physiol. 41 (4): 554-550, 19 76 . 62 Diamont, B., J. Karlsson, and B. Saltin. Muscle tissue lactate after maximal exercise in man. Acta. Physiol.  Scand. 72: 383-384, 1968. Dill, D.B., H.T. Edwards, E.V. Newman and R. Margaris. Analysis of recovery from anaerobic work. Arb. Physiol. 9: 299, 1936. Dunwoody, D.W. A comparison of respiratory exchange variables between untrained, aerobically and anaerobically trained individuals. Unpublished M.P.E. Thesis. University of British Columbia, 19 81. Edgerton, R.V., B. Saltin, B. Essen and D.R. Simpson. Glycogen depletion in specific types of human skeletal muscle fibers after various work routines. Second International Symposium in Biochemistry of Exercise. Magglinden; 19 73. Essen, B. Intramuscular substrate utilization during prolonged exercise. Annals of the New York Academy of Science. 301: 30-44, 1977. Farrell, P.A., J.H. Wilmore, E.F. Coyle, J. Billing, and D.L. Costill. Plasma lactate accumulation and distance running performance. Med. Sci. Sports. 11(4): 338-344, 1979. Ganong, W.F. Review of Medical Physiology. ,(9 ed.) Los Altas, California. 19 79. Gisolfi, F., S. Robinson and E.S. Turrell. Effects of anaerobic work performed during recovery from exhausing work. J. Appl Physiol. 21: 1767-1772, 1966. Graham, T. Oxygen delivery and blood and muscle lactate changes during muscular activity. Can. J. of Appl. Sport  Sci. 3: 153-159, 1978. Graham, T., D. Sinclair and C. Chapler. Metabolic intermediates and lactate diffusion in active dog skeletal muscle. Amer. J. of Physiol. 3: 153-159, 1976. Green, H.J., R.L. Hughson, G.W. Cerr and D.A. Ranney. Interrelationship between anaerobic threshold, blood lactate and muscle metabolites during progressive exercise. Med, and Sci. in Spt. and Ex. 14(2): 160, 1982. (abstract). Gutmann, I.';?ari<3 LA.W. Wahlefeld. L-( + )-lactate determination with lactate dehydrogenase and NAD. In: Methods of Enzymatic Analysis, edited by H. U. Bergmeyer. New York: Academic, 1974, vol. Ill, p. 1464-1468. Guy-ton, A.C. Textbook of Medical Physiology. Saunders Co., Toronto, Ontario. 1976. Haldane, J.S. and J.S. Priestley. The regulation of the lung ventilation. J. Physiol. 32: 225-266, 1905. Hermansen, L. and I. Stensvold. Production and removal of lactate during exercise in man. Acta. Physiol. Scand. 86: 191-201, 1972. Hermansen, L. and O. Vaage. The quantitative significance of the "Himwich-Cori Cycle" for removal of lactate during recovery after maximal exercise in man. Lactate: Physiologic, Methodologic and Pathologic Approach. Springer-Verlag, Berlin, Heidelberg, 1980. Holloszy, J.O. Biochemical Adaptations to Exercise: Aerobic Metabolism. P. 45-71, 1973. Holloszy, J.O., M.J. Rennie, R.C. Hickson, R.K. Conlee and J.M. Hagberg. Physiological consequences of the biochemical adaptations to endurance exercise. Annals of New York Academy of Science. 440-450, 1977. Howald, H., H. Claasen, O. Mathieu, R. Straub and H. Hoppeler. Increase of mitochondrial volume in different muscle fiber types due to training at the A.T. Med. Sci in  Spt. and Ex. 14(2): 141, 1982. Hubbard, J. The effect of exercise on lactate metabolism. J. Physiol. 231: 1-18, 1973. Huckabee, W.E. Relationship of pyruvate and lactate during anaerobic metabolism. II..Exercise and formation of 0„ debt. J. Clin. Invest. 37, 255, 1958b. Huckabee, W.E. Abnormal resting blood lactate. I. The significance of hyperlactatemia in hospitalized patients. Amer. J. Med. 30, 833, 1961a. Hultman, E. and K. Sahlin. Acid-base balance during exercise. Exercise and Sport Sciences Reviews. 8: 41-128, 1980. Issekutz, B. Jr., N. Birkhead and K. Rodahl. Use of respiratory quotient in assessment of aerobic work capacity. J. Appl Physiol. 17(1): 47-50, 1962. Issekutz, B. Jr. and H. Millar. Plasma free fatty acids during exercise and the effect of lactic acid. Proc. Soc. Expth. Biol. Med. 110: 237-239, 1962. 64 Issekutz, B. Jr. and R. Rodahl. Respiratory quotient during exercise. J. Appl. Physiol. 16(4): 606-610, 1961. Issekutz, B. Jr., W.A.S. Shaw and A.C. Issekutz. Lactate metabolism in resting and exercising dog. J. Appl. Physiol. 40: 312-319, 1976. Ivy, J.L., D.L. Costill, P.J. Van Handel, D.A. Essig and R.W. Lower. Alteration in the lactate threshold with changes in substrate availability. Int. J. Sports Medicine. 2(3): 139-142, 1981. Ivy, J.L., R.T. Withers, P.J. Van Handel, D.H. Elger and D.L. Costill. Muscle respiratory capacity and fiber type as determinatns of the lactate threshold. J. Appl. Physiol.  Respirat. Environ. Exercise Physiol. 48(3): 5 2 3-52 7, 1980 . Jervell, 0. Investigation of the concentration of lactic acid in blood and urine under physiologic and pathologic conditions. Acta. Med. Scand. (Suppl) 24: 1, 19 28. Jerfeldt, L. Metabolims of L(+) Lactate in human skeletal muscle during exercise. Acta. Physiol Scand. (Suppl.) 388, 19 70. Jorfeldt, L., A. Jahlin-Dannfeldt and J. Karlsson. Lactate release in relation to tissue lactate in human skeletal muscle during exercise. J. Appl. Physiol. 44(3): 350-352, 1978. Kao, F. The peripheral neurogenic drive: An experimental study In: J. Dempssey and C. Reed (Eds..), Muscular exercise and the lung. Madison: University of Wisconsin Press, 1977. Karlsson, J. Lactate in working muscles after prolonged exercise. Acta. Physiol. Scand. 82: 123-130, 1970. Karlsson, J., B. Hulten and B. Sjodin. Effects of previous exercise with arms or legs on metabolism and performance in exhaustive exercise. J. Appl. Physiol. 38: 763-767, 1975. Katch, V., E.D. Michael, S.M. Howath. Estimation of body volume by underwater weighing: Description of simple method. J. Appl. Physiol. 23: 811-813, 196 7. Katch, V., A. Weltman, S. Sudy and P. Freedson. Validity, of the relative precent concept for equating training intensity. Eur. J. Appl. Physiol. 39: 219-227, 1978. 65 Keul, J. Energy metabolism of the human muscle. Medicine and Sport. V.7. Baltimore: Univ. Park Press, 19 72. Kinderman, W., G. Simon and J. Keul. The significance of the aerobic-anaerobic transition for the determination of work load intensities during endurance training. Eur. J. Appl. Physiol. 42(1): 25-34, 1979. Knuttgen, H. Oxygen debt, lactate, pyruvate and excess lactate after muscular work. J. Appl. Physiol. 17(4): 639-644, 1962. Kragenings, I. Methodology of lactate assay in Lactate in Acute . Conditions. Int. Sym. on Lactate in Acute Conditions. Basel p.20-28, 1978. Komi, P.V., A. Ito, B. Sjodin, R. Wallenstein and J. Karlsson. Muscle metabolism, lactate breaking point and biomechanical patterns of endurance running. Int. J. Sports Medicine. 2 (3) : 148-153, 1981. Lafontaine, T., B.R. Donderee, L. Foy and T. Barrett. The effect of intensity and quantity of exercise on the aerobic and anaerobic thresholds. Med. Sci. in Spt. and Ex. 14 (2) : 127, 1982. Lockwood, L.B., D.E. Yoder. and M. Mienty. Lactic Acid. Annal of the New York Academy of Sciences. 119(3): 854-865, 1965. MacDougall, J. The Anaerobic threshold: Its significance for the endurance athlete. Can. J. of Appl. Spt. Sciences.-2: 137-140, 1978. Mader, V.A., H. Liesen, H. Heck, H. Philippi, R. Rost, P. Schurch and W. Hollmann. Zur Beurteilung der sportart-spezif ischen:. Ausdauerleistungsfahigkeit. Sportarzt and  Sport Medizin. 27: 80, 1976. Margaria, R. Aerobic and anaerobic energy sources in muscular exercise. In: Exercise in Altitude Exerpta Medica, Foundation, New York, 196 7. Margaria, R., P. Cerretelli and F. Mangibi. Balance and Kinetics of anaerobic energy release during strenuous exercise in man. J. Appl Physiol. 19: 623-628, 1964. Margaria, R., H.T. Edwards and D.B. Dill. The possible mechanisms of contracting and repaying the oxygen debt and the role of lactic acid in muscular contraction. Amer. J. Physiol. 106: 689, 1933. 66 Mole, P.A. Enzymatic pathways of pyruvate metabolism in Skeletal Muscle: adaptations to exercise. Amer. J. Physiol. 224: 50-54, 1973. Moriya, G.Z. Physiol. Chem. 43: 397, 1904. Naimark, A., K. Wasserman and M. McTlroy. Continuous measure ments of ventilatory exchange ratio during exercise. J. Appl. Physiol. 19: 644-652, 1964. Newsholme, E.A. and C. Start. Regulation in Metabolism Toronto: John Wiley and Sons. 19 74. Olson, G.F. Optimal Conditions for the enzymatic determination of L(+)-Lactic Acid. Clin. Chem. 8: 1-10, 1962. Parkhouse, W. Buffer capacity of human skeletal muscle; relationship to fiber composition and anaerobic performance. M.P.E. Thesis, University of British Columbia, 1982. Ponton, L.J., A.A. Sucec, S.R. Tucker and B. Macy. Validity and reproducibility of the lactate threshold for a continuous protocol on the treadmill. 14(2): 160-161, 1982 . Robinson, T. and A.A. Sucec. The relationship of training intensity and anaerobic threshold to endurance performance. Med. Sci. in Spt. and Ex. 12(2): 124, 1980. Rowell, L.B., K.K. Kraining II, T.O. Evans, J.W. Kennedy, J.R. Blackman and F. Kusumi. Splanchnic removal of lactate and pyruvate during prolonged exercise in man. J. Appl. Physiol. 21: 1773-1783, 1966. Rhodes, E.W., D.C. McKenzie, J.P. Wiley, D.W. Dunwoody and W.S. Parkhouse. Relationship between anaerobic threshold and actual marathon time. Can. J. Appl. Spt. Sci. Dec. 1981 (abstract) Roos, A. and W.F. Boron. Intracellular pH. Physiol. Rev., 61(2): 296-434, 1981. Rupp, J.R.., A.D. Kanochoff, R.L. Bartels, and E.L. Fox. Noninvasive measures of aerobic and anaerobic thresholds: A validation study. Med. Sci. in Spt. and Ex. 14(2): 161, 1982. Sady, S., V.Katch, P. Freedson and A. Weltman. Changes in metabolic acidosis: Evidence for an intensity threshold. J. Sports Med. 20: 41-46, 1980. 67 Saltin, B. and P.O. Astrand. Maximal oxygen uptake in athletes. J. Appl. Physiol. 23: 347-352, 1967. Schumer, W. Cell metabolism and lactate. Lactate in Acute Conditions: International Symposium, Basel, 1-9, 19 79. Simonsen, E., Physiology of Work Capacity and fatigue. Springfield, 111.: Charles C. Thomas, 19 71. Sjoden, B. Lactate dehydrogenase in human skeletal muscle. Acta. Physiol. Scand., (Suppl.) 436: 1-32, 19 76. Sjoden, B and I. Jacobs. Onset of blood lactate accumulation and marathon running performance. Int. J. Sports Med. 2 (1) : 23-26 , 1981. Sjoden, B., J. Jacobs and J. Karlsson. Onset of blood lactate accumulation and enzyme activities in medical vastus lateralis in man. Int. J. Sports Medicine. 2(3): 166-170, 19 81. Skinner, J.S. and T.H. McLellan. The transition from aerobic to anaerobic metabolism.. Research Quarterly. 50(1) : 234-248, 198.0 . Stegmann, H., W. Kindermann and A. Schnabel. Lactate Kinetics and individual anaerobic threshold. Int. J. Sports Med. 2(3): 160-165, 1981. Sucec, A.A., S. Tucker, L. Ponton, and B. Macey. The reproducibility of the A.T. by venous blood lactate and gas exchange measurements. Med, and Sci. in Spt. and Ex. .14(2): 127, 1982. Sutton, J.R. and N.L. Jones. Control of pulmonary ventilation during exercise and mediators in the blood: CO2 and hydrogen ion. Med. Sci. Sports. 11(2): 198-203, 1979. Svendenhag, J. and B. Sjodin. Physiological characteristics of elite middle and long distance runners. Med, and Sci. in Spt. and Ex. 14(2): 104, 1982. Taunton, J.E.,,H. Maron and J.G. Wilkinson. Anaerobic performance in middle and long distance runners. Can. J.  Appl. Spt. Sci. 6(3): 109-113, 1981. Tesch, P.A., D.S. Sharp and W.L. Daniels. Influence of fiber type composition and capillary density on onset of blood lactate accumulation. Int. J. Sports Medicine. 2.(4): 252-255, 1981. 68 Thorstensson, A., B. Sjodin, P. Tesch and J. Karlsson. Actomyosin ATPase, myokinase, CPK and LDH in human fast and slow twitch muscle fibers. Acta Physiol. Scan. 99: 225-229, 1977. Turrell, E.S. and S. Robinson. The acid-base equilibrium of the blood in exercise. Amer. J. Physiol. 137: 742, 1942. Volkov, N., E. Sherkavets and V. Borilkevich. Assessment of aerobic and anaerobic capacity of athletes in treadmill running. Eur. J. Appl. Physiol. 34(2): 121-130, 1975. Wasserman, K.. and M. Mcllroy. Detecting the threshold of anaerobic metabolism in cardiac patients during exercise. Amer. J. Cardiology. 14: 844-852, 1964. Wasserman, K. and B. Whipp. Exercise physiol. in health and disease. Amer. Rev. Resp. Disease. 112: 219-249, 1975. Wasserman, K., B. Whipp, S. Koyal and W. Beaver. A.T. and respiratory gas exchange during exercise. J. Appl. Physiol. 35 (2) : 236-243, 1973. Wenger, H.A. and A.T. Reed. Metabolic factors associated with muscular fatigue during aerobic and anaerobic work. Can. J. of Appl. Spt. Sci. Vol. 1: 43-48, 1976. Weiser, P.C., C. Narton and L. Krogh. Anaerobic threshold and the running speed for 3.2 km. Med. Sci. Sports. 10(1): 43, 1978 (abstract). Whipp, B. The hyperpnea of dynamic muscular exercise. Ex. Spt.  Sci. Rev. 5: 295-311, 1977. Wiley, J.P. The relationship of individual anaerobic thresholds to total, alactic and lactic oxygen debts after a set treadmill run. Unpublished M.P.E. Thesis. University of British Columbia, 1980. 69 A P P E ND I X 70 Subject: NW V7ARIART.KS Vtam-1 Vtam Vtam+1 Vtam+2 MAX Velocity of treadmill (KPH) 16.74 17.74 18.74 19.74 13.0 VCL -1 -1 (ml-kg -min ) 55.38±2.4 61.23±2.12 62.86±1.98 66.08±1.78 69.80 vo2 79 88 90 95 100 (percent MAX) ExCCL (ml-kg -min ) 13.96^1.08 18.83±3.14 23.43±2.26 24.74^1.64 26.57 ExCCL z (percent MAX) 53 71 88 93 100 Blood lactate (mM/L) 5.096 -8.261 11.927 14.053 — Heart Rate (b.p.m.) 168 180 187 184 185 94.31±9.27 (7:30 min. only) Ve (STPD) 76.01±3.44 107.28±9.92 114.51- 118.71 height (kg.) 67.5 67.5 67.1 66.7 67.10 71 Subject: LH VARIART.ES v tam-1 Vtam Vtam+1 v tam+2 MAX Velocity of treadmill (KPH) 15.94 16.94 17.94 18.94 14.0 V02 -1 -1 (ml-kg -min ) 51.29-1.5 57.45-.52 64.66^.62 66.9-1.65 67.01 vo2 (percent MAX) 76 86 96 100 100 ExC02 (ml-kg-1-min"1) 13.02±.76 15.73±.34 15.24^1.09 20.7±2.08 26.63 ExC02 (percent MAX) 49 59 57 78 100 Blood lactate (rrM/L) 1.479 2.493 4.570 9.263 Heart Rate (b.p .m.) 150 161 167 V (STPD) e 78.6±2.17 93.70-1.47 107.44-3.56 125.03-8.15 130.84 Weight (kg.) 71.0 70.2 70.9 71.2 72.0 72 Subject: JT VARIARTiES V . tam-1 Vtam Vtam+1 V tam+2 MAX Velocity of teeadmill (KPH) 15.94 16.94 17.94 18.94 13.5 V02 -1 -1 (ml-kg -min ) 51.52^1.32 55 .98-1.04 60.12-2.84 57.42^1.32 64.11 vo2 (percent MAX) 80 87 94 90 100 ExC02 (ira-kg^-min-1) 9.96-1.04 14 .11-.66 15.85-.41 22.9-.80 26.77 ExC02 (percent MAX) 37 53 59 85 100 Blood lactate (mM/L) 2.053 3.397 4.191 6.978 Heart Rate (b.p.m.) 164 164 170 176 V (STPD) e 73.24^3.9,1 88 .44^4.12 89.13^3.12 111.57-6.36 126.48 Weight (kg.) 68.0 67.5 68.2 67.6 68.5 73 Subject: JH V7ARIART.ES Vtam-1 Vtam V tam+1 V tam+2 MAX Velocity of treadmill (KPH) 17.55 18.55 19.55 20.55 14.5 V02 54.18±.95 61.48±.81 62.36^1.42 62.09±1.24 -1 -1 (ml-kg -min ) 67.47 VO (percent MAX) 80 91 92 92 100 ExC02 (ml-kg^-niin-1) 9.75±.51 14.95±.93 21.77^1.89 24.3±1.12 35.71 ExC02 27 42 61 68 100 (percent MAX) Blood lactate (mM/L) 1.747 3.837 8.077 8.945 Heart Rate (b.p.m.) 168 180 187 191 200 V (STPD) e 75.09*1.93 87.74±1.44 104.95±5.07 107.10±3.6 128.40 Weight (kg.) 70.1 70.5 70.0 69.6 70.5 74 Subject: SP VARIABLES Vtam-1 Vtam V tam+1 V tam+2 MAX Velocity of treadmill (KPH) 16.74 17.74 18.74 19.74 14.5 VCL -1 -1 (ml'kg -10111 ) 53.7±.48 59.63-1.33 61 .09-1.31 66.87^2.04 72.42 vo2 (percent MAX) 74 82 84 92 100 ExCCL (ml-kg -min ) LI.62-.85 12.60-.7 15 .37^1.68 18.53-1.01 26.42 ExC02 (percent MAX) 44 48 58 70 100 Blood lactate (mM/L) 2.774 2.908 4.277 9.385 Heart Rate (b.p .m.) 165 164 173 180 V (STPD) e 79.05-1.51 89.73^1.66 94 .80-1.85 111.85^-3.70 136.50 Weight (kg.) 68.1 68.5 67.5 67.9 68.5 ANACIOUIC Tlli'.tjJilOLO CUKVE Excess C02 (.til/ky) vs ri'-lii ( tin) & ol'RGO (npii) Excess C02 (ml/kg) NW il 1 2 3 4 5 (. 7 1 J 1U Li 12 13 14 ID lf> 17 lrt 19 2J 5 6 7 U 9 10 11 • 12 1J 14 15 (minutes) •;H>KE.J ('jiiii Ul ANAEROBIC THRESHOLD CURVE Excess C02 (ml/kg) vs TIME (rain) & SPEED (mph) Excess C02 (ml/kg) 28.00 25.20 22.40 19.60 16.80 14.00 11.20 8.4 0 5.60 2.80 0.00 ** * *• 1-0 1 2 3 4 5 6 7 8 9 1 0 11 12 13 14 15 16 17 18 19 20 5 6 7 8 9 10 11 12 13 14 15 TIME (minutes) LJJ SPEED (mph) CTl 77 «- 3 LO O r^- — co in rg. r-> ANAEROBIC THRESHOLD CURVE Excess C02 (ml/kg) vs TIME (min) & SPEED (mph) Excess C02 (ml/kg) 38.00 34.20 30.40 26.60 22.80 19.00 15.20 11.40. 7. 60-3.80 0.00 * * * * * * * * **• » ** 5 1 6 3 7 5 I 7 ? 9 " 11 12 " 14 15 16 17 18 19 20 6 7 8 9 10 11 12 13 14 15 JH 11 12 TIME (minutes) SPEED (mph) 80 JOHN M. BUCHANAN FITNESS & RESEARCH CENTRE Informed Consent: You will perform a graded exercise test on a motor-driven treadmill. The purpose of this test is to examine the response of your heart and lungs to exercise. The test consists of running at one or more levels of difficulty. Your electro-cardiogram will be monitored throughout the exercise and recovery periods. Blood samples will be taken by.way of a venous puncture. It is expected that you will complete the exercise test without complications. Because of the very uncommon, unpredictable response of some individuals to exercise, unforseen difficulties may arise which would necessitate treatment. Complications have been few during exercise tests and these usually clear quickly with little or no treatment. You are asked to report any unusual symptoms during the test. We may stop the test at any time because of signs of fatigue or you may stop when you wish to because of personal feelings of fatigue or discomfort. Every effort will be made to conduct the test in such a way as to minimize discomfort and risk. However, there exists the possibility of potential risks such as; abnormal blood pressure, fainting, disorders of heart beat and very rare instances of heart attack. You will also perform tests of lung capacity and body composition. In signing this consent form you.state that you have read and understand the description of the tests and their complications. You enter the battery of tests willingly, but you may withdraw or refuse to participate at any time. Finally, all data collected about you will be kept in strictest confidence. CONSENT I have read the above comments and understand the explanation and I wish to proceed with the tests. DATE: SUBJECT: Signature WITNESS: 

Cite

Citation Scheme:

        

Citations by CSL (citeproc-js)

Usage Statistics

Share

Embed

Customize your widget with the following options, then copy and paste the code below into the HTML of your page to embed this item in your website.
                        
                            <div id="ubcOpenCollectionsWidgetDisplay">
                            <script id="ubcOpenCollectionsWidget"
                            src="{[{embed.src}]}"
                            data-item="{[{embed.item}]}"
                            data-collection="{[{embed.collection}]}"
                            data-metadata="{[{embed.showMetadata}]}"
                            data-width="{[{embed.width}]}"
                            async >
                            </script>
                            </div>
                        
                    
IIIF logo Our image viewer uses the IIIF 2.0 standard. To load this item in other compatible viewers, use this url:
http://iiif.library.ubc.ca/presentation/dsp.831.1-0077391/manifest

Comment

Related Items