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Effect of voluntary hyperventilation on venous blood lactate during recovery from submaximal exercise Vickery, N.N. 1976

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EFFECT OF VOLUNTARY HYPERVENTILATION ON VENOUS BLOOD LACTATE DURING RECOVERY FROM SUBMAXIMAL EXERCISE BY N.H. VICKERY B.A. (University of B.C.) B.Ed. (Dalhousie University) . THESIS SUBMITTED IN PARTIAL FULFILLMENT OF REQUIREMENTS FOR THE DEGREE OF MASTER OF PHYSICAL EDUCATION In the School of Physical Education and Recreation We accept this thesis as conforming . to the required standard University of British Columbia September, 1973 0 N.H. Vickery, 1976 In p resent ing t h i s t h e s i s in p a r t i a l f u l f i l m e n t o f the requirements fo r an advanced degree at the U n i v e r s i t y of B r i t i s h Columbia, I agree that the L i b r a r y s h a l l make i t f r e e l y a v a i l a b l e fo r reference and study. I f u r t h e r agree tha t permiss ion fo r e x t e n s i v e copying of t h i s t h e s i s f o r s c h o l a r l y purposes may be granted by the Head of my Department or by h i s r e p r e s e n t a t i v e s . It i s understood that copying or p u b l i c a t i o n o f t h i s t h e s i s f o r f i n a n c i a l ga in s h a l l not be a l lowed without my w r i t t e n p e r m i s s i o n . a Depa rtment The U n i v e r s i t y of B r i t i s h Columbia 2075 Wesbrook Place Vancouver, Canada V6T 1W5 -6 i ABSTRACT The purpose of t h i s study was to determine whether a specified hypocapnia (27 mm Hg — end t i d a l PCOg) induced by voluntary overbreathing would affect venous blood lactate decay, during recovery from submaximal exercise i n humans. Eight students (male and female) volunteered f o r the 10-day study. Four students underwent experimental condition (A^) f i r s t and four underwent experimental condition (A2) f i r s t . The experimental^condition (Ag) involved a four minute period of underbreathing after a four minute period of submaximal exercise on a bicycle ergometer. Experimental condition (A^) involved a four minute period of overbreathing, immediately following a four minute period of submaximal exercise (7O-8C70 of maximum). Three venous blood samples, f o r lactate analysis were drawn from the antecubital v e i n , one just p r i o r to exercise and two at the 2nd and 4th minute, post exercise. Simultaneous micro^amples were obtained f o r pH determinations. Heart rate and respiratory values ( i n f r a red analyzer) were continuously monitored. S i g n i f i c a n t l y lower recovery lactate values at two and four minutes were observed during overbreathing and while pH and heart rate were higher during^overbreathing, they were not s i g n i f i c a n t l y changed by these t r e a t -ment conditions at the .05 l e v e l . i i ACKNOWLEDGEMENTS The author would l i k e to express h i s sincere gratitude to Dr. John G r i f f i t h f o r his permission to use the Vancouver General Hospital Blood Gas Lab f a c i l i t i e s , I would also l i k e to thank the members of my committee, Dr, S, R, Brown, Dr, R, Schutz, Dr, D, R. Jones and p a r t i c u l a r l y , Dr. K.D. Coutts. i i i TABLE OF CONTENTS Chapter Page I Statement of the Problem ••••••••••••••••••••••••••••••• 1 Introduction,•••••••••••••••••••••••••••••••••••••• 1 Purpose of Study........ ••••• 2 D e l i m i t a t i o n s . . 2 D e f i n i t i o n s . • • • • • • • • • • • • 2 Assumptions & Limitations.......................... 3 H y p o t h e s i s . 3 Significance of the Study... ••••••• ••••• 3 I I Review of the Literature................................ 4 Introduction.•••••••••••••••••••••••••••••••••••••• 4 Early and More Generalized Studies................. :h 4 E x t r a c e l l u l a r Consequences of Hyperventilation................................... 7 Carbon Dioxide Stores.............................. 12 Summary.,..••••••••••••••••••••••••••••••••»••••••• 14 I I I Methods and P r o c e d u r e s . . . . . . . . . . . . . . . . . . . . . . 1 6 S t a t i s t i c a l Analyses and Experimental D e s i g n . . 1 9 IV Results and Discussion....................... 21 Results.••.••••••••••••••••••••••••••«••••..••.......... 21 Lactate C e l l M e a n s . , , • • • • • • • 21 ANOVA - Lactate 24 pH C e l l Means • •••••• 26 ANOVA - pH 28 Heart Rate C e l l Means 29 ANOVA - Heart Rate • 31 Discussion.,.•••••.••••••.•.••••••••••••••*»«••......... 32 V Summary.••••••••••••«••,,,,,,,,,•••««,,«,,««•••••••••••• 37 Conclusions. •••••••••••••••••••••••••••••••••.*• •••••••• 38" REFERENCES 39 APPENDIX A.... 44 Raw Scores,•••••••••••••••••»•••••....»»••».,„,,,,,, 44 LIST OF TABLES Table Page I Acid-base Changes Accompanying Hyperventilation i n D o g s . . • • • • • • • • • • 11 I I Effects of HV at PCO «= 30mm Hg.. 15 I I I Schematic Representation of Experimental Design.•••••••••••••••••••••••••••••••••••••••••••••• 20 IV Venous Blood Lactate C e l l M e a n s . • • • • • • • • • • • 21 V ANOVA Summary - Blood Lactate....... 24 VI C e l l Means for pH Values...... • • ••• 26 VII pH ANOVA Summary • • 28 VIII Heart Rate C e l l Means • 29 IX ANOVA Summary - Heart Rate ••• 31 0 LIST OF FIGURES Figure Page I Lactate Decay Values — Individual Subjects •• • • 22-23 I I Mean Lactate Decay Values During Overbreathing and U n d e r b r e a t h i n g . , , . • • • • • « • . 2 5 I I I Mean pH Values During Overbreathing and U n c e r b r e a t h i n g . . . . , . . « . , . , , , , . . 2 7 IV Graph of Heart Rates During Cnrerbreathing and Underbreathing Over the Four Minute Recovery Period.....................•••••••••••••••••• 30 1 CHAPTER I Statement*of the Problem Introduction The general purpose of this study was to investigate the effects of voluntary hyperventilation (HV) during recovery from exercise on certain relevant physiological variables, e.g. lactate, end tidal PC02» pH and heart rate. Although studies of HV upon the concentration of blood lactate, have been done under resting conditions, there has not previously been any study that compares blood lactate concentrations during recovery from exercise under hyperventilation conditions and under hypoventilation conditions. The majority of studies (Axelrod, 196l; Boucot, 1956; Eichenholz, 1965} Eldridge, 1965; Elkington, 1955; Takano, 1966) of HV during testing conditions, have indicated only a slight rise in blood lactate (3 to 7 mg$). During exercise, blood lactate rises to a level commensurate with intensity of work and falls relatively rapidly during recovery. Altered breathing patterns (different from normal) during recovery may affect lactate removal. The question arises as to whether or not the post exercise blood lactate levels will drop when subjects alter breathing^patterns during a recovery period when lactate levels are already elevated. 2 Purpose of Study The s p e c i f i c purpose of t h i s study was to determine whether two breathing patterns which produce two levels of end t i d a l PCCv, have different effects on venous blood lactate removal during recovery from submaximal exercise i n the normal human subject. Delimitations i? This study was delimited i n the following ways: (1) The physiological variables under investigation were: (a) end t i d a l PC0 2 (b) heart rate (c) venous blood lactates and pH. Blood lactate and pH were sampled at three s p e c i f i c times : (a) just previous to exercise (b) at the 2nd and 4th recovery minutes. (2) The exercise was a 4 minute period of work on the bicycle ergometer at 70-80$ maximum. (3) Subjects were young (18-30 yrs.) human males and females. Definitions Overbreathing: operationally defined f o r t h i s study to indicate the the breathing pattern (rapid deep breaths) necessary to produce an end t i d a l PC0 o of 25 mm Hg. 3 Underbreathing: operationally defined to indicate the breathing pattern (shallow slow breaths) necessary to produce an end t i d a l PCC^ of 45 mm Hg, Assumptions and l i m i t a t i o n s This study was l i m i t e d by one of the procedures of t h i s experiment. The fact that only two recovery lactate values were obtained, reduces the information about the lactate decay over the 4 minutes. More values with the use of an indwelling catheter would have allowed a more sophisticated exponential decay p l o t . Hypothesis Venous blood*lactate levels and/or decay rates may be altered by two d i f f e r e n t breathing patterns; overbreathing, underbreathing, during an exercise recovery period. Significance of the Study The primary value of t h i s study was i t s further elucidation of COg disposal mechanisms and venous blood lactate decay rates, as a part of the recovery processes. I t was unique i n that a l i n k between blood la c t a t e catabolism and hypocapnia during recovery was investigated. I t also suggests the possible p r a c t i c a l value of rapid and deeps breathing to f a c i l i t a t e recovery from a b r i e f exercise bout. 4 CHAPTER I I Review of the Literature Introduction Although the general subject of t h i s review i s the physiological phenomena associated with hyperventilation, primary attention i s directed toward the effects of transient (4-24 mins.) periods of HV on acid-base balance i n the blood. HV, which produces a depression of the normal blood COg tension and a subsequent r i s e i n pH, also produces effects not ea s i l y predicted. Besides the disturbance of acid-base balance, many other changes occur, such as an a l t e r a t i o n of blood volume, changes i n urine composition and volume, c i r c u l a t o r y changes and a d e s t a b i l i z i n g effect i n nerve and muscle. Research i n the respiratory a l k a l o s i s area has been la r g e l y confined to an examination of the reasons f o r blood acid-base changes during passive HV. The effects of voluntary HV before, during or after exercise have, according to Brown f (1959» not yet received proper investigation. Early and More Generalized Studies Some attention should, at the outset, be directed toward the early and more generalized HV studies. Several early works, Anrep (1923), C a j o r i (1923), C o l l i p (1920), Davies (1920), Grant (1920), Haggard (1920), H i l l (1908), Talbott (1938) and Sutton (1909), reported a pronounced f a l l 5 in PaCOg and an increase in pH up to 7.8. Himwich (1932) found that overventilation (50$ PC02 change) led to small increases in lactic acid as a means of offsetting alkalosis and could be said to be a protective device involving a complex of physiological changes* Talbott (38) reviewed two types of alkalosis, respiratory and metabolic. Respiratory alkalosis resulted in increases in fixed acids, but he did not test specifically for blood lactates. A mild metabolic acidosis was thus superimposed on the respiratory alkalosis. Investigations by Brassfield (41) and Chepper and Shock (42) of changes in venous blood CC^ tension and pH during forced breathing have demonstrated a quick rise in pH beginning within 5 to 20 seconds and continuing for two to three minutes. After this, i t increased more slowly reaching a maximum in ten to fifteen minutes. These researchers found pH would return to normal in about 5 minutes after hyperventilation was discontinued. Elkington (54) summarized the general order of events when humans are exposed to respiratory acid-base disturbances. A major part of the immediate buffering in the extra-cellular fluid is met by exchanges of hydrogen for sodium across the cell boundaries in body tissues. The progression of events, in the immediate defence of normality of body fluids during hyperventilation i s : 6 (1) the physico-chemical mechanism involved i n the action of the buffer systems of the body, (2) the bicarbonate-carbonic acid system of the rest of the extra c e l l u l a r f l u i d s , and (3) the organic phosphates and proteins of tissue c e l l s and some of the bone s a l t s . Besides the chemical action of these buffers, certainophysiological mechanisms aid i n t h i s homeostatic regulation: (1) regulation of respiratory minute volume so as to achieve a more normal l e v e l of CC^ pressure i n body f l u i d s , and (2) changes i n c e l l u l a r metabolism such as an increase i n the rate of formation of organic acids (e.g. blood l a c t a t e ) . Elkington further noted that part of the c e l l u l a r buffering i n respiratory a l k a l o s i s consisted of a release of hydrogen ions with an undetermined anion. Although not i d e n t i f i e d i n his experiments, the anion was thought to be lactate since a s l i g h t increase i n e x t r a c e l l u l a r l a c t i c acid had previously been reported by Anrep ( 2 3 ) , Nims (42) and Stanbury ( 0 5 ) . Balke (58) i n experiments with airforcement) found a marked increase i n hypocapnic tolerance and an improvement i n psychomotor performance at low P „ C 0 o (15.5mm Hg) after regular exposure to hypocapnia. During voluntary HV at a l t i t u d e , he found some individuals achieved the lowest values of alveolar tension (7mm Hg at v e n t i l a t i o n rates 7 to 8 times 7 normal) one can obtain, by conscious maximal ventilation efforts. However, only minor symptoms of hypocapnia were observed at altitude probably due to some counterbalancing effects of hypoxia. Increases in venous blood lactate were slight ( l to 6 mg$). A 5 to 10$ increase of oxygen carrying capacity was recorded, but this change may have been due to a decrease in plasma volume. Extracellular Consequences of Hyperventilation There are a very large number of studies which have sought to precisely explain the extracellular changes resulting from hypocapnia. Of this group of investigations, only a few have used voluntarily hyperventilating subjects and only one (Buhlmann, 70) examined the effects of HV while the subjects were exercising. Giesbisch (54), using normal dogs, pointed out that changes in blood lactate have been repeatedly observed in respiratory alkalosis, but the precise origin of these changes is not known. Lactate production varied inversely with P C0o which may indicate a direct effect of COg partial pressure on lactate metabolism. Boucot (56) said that hyperventilation is associated with a glycolytic response that will account for the observed changes in plasma lactate. He found that only after the f a l l of arterial plasma COg exceeded 5 mM/l, did the lactate increase. This increase was thought to be cellular in origin 8 Roberts (56) noted a small lactate increase (along with two other anions, chlorides and ketones) in respiratory alkalosis. The lactic acid increase was said to be a result^ of breakdown of glycogen and other products of carbohydrate metabolism. The body converts the bicarbonate to C0 2 by titration which in turn is excreted by the lungs. She notes that the carbonic acid fraction of the plasma is ex-pressed as the partial pressure of dissolved C0 2 . Loss of carbonic acid (lungs) without equal losses in bicarbonate alters the normal 20:1 ratio and the pH will increase. "Metabolic compensation occurs rapidly, leading to a decrease in bicarbonate (represents the major fraction of total C0 2) as well as carbonic acid." Huckabee (58) in experiments with healthy men, found that blood lactate can be increased by methods that would not be expected to produce hypoxia (eg., hyperventilation). He concluded that the pro-duction of lactate in man has no necessary significance with respect to hypoxia of the tissues. 3 Papadopoulos (59) deliberately hyperventilated twenty male and female patients for up to four hours, taking arterial samples at 10 minutes, 1 hr., 2 hrs., 3 hrs., and4;4 hours. Increases in blood lactate up to 9 mg$ (maximum C0 2 experiments produce values ranging from 125-150 mg$) were recorded, but were not considered to produce a degree of metabolic acidosis of any clinical significance. Subjects who voluntarily hyperventilated to a PC0 9 of 20 mm Hg, showed increases in 9 blood lactate from 1 - 2m Eq./l. Corrected bicarbonate values and blood buffer-base values indicated only small increases in fixed acids. Papadopoulos speculated that the increases in fixed acids was the result of compensatory mechanisms, in response to pH elevation. Axelrod (6l) found that in ambulatory male human subjects, HV produced a small rise in blood lactate. During control periods, mean arterial plasma lactate was 8.3 mg/lOOml and the mean venous level 9.4 mg/lOOml. Maximum arterial plasma lactate levels were 5.6 - 11.4 mgfo greater than the control values and the venous maximums were 9 - l6f?ng$ greater. Severe exercise produces values of the order of 125 mg$. Axelrod surmised that HV produces a change in inter-mediary metabolism. Eichenholz (62) in a study of the progression of the true bicarbonate deficit brought on by a severe reduction of PC02 and the rate of lactic acid in the production of this deficit, concluded that the rise in this acid is precipitated by the reduction of PC02 and accounts for the appearance of the true bicarbonate deficit after sixty minutes. He did not speculate on the enzymatic reaction responsible for the rise in lactate. Takano (68) examined cellular as well as extracellular changes during 4 hours passive HV of dogs. She was primarily concerned with blood lactate change and its causative factors during HV. Although she did not investigate whether alkalization of cell pH activates 10 metabolic production of lactate, she speculated that intracellular alkalosis may cause a small increase in blood lactate. Zborowska (67) also examined the reasons for blood lactate changes during four hours of passive HV, but made different conclusions. He felt that the source of lactate was probably from increased blood cell glycolysis. He stated that since Mno oxygen debt was contracted, that hypoxia could be excluded as a primary source of lactate." Eldridge (67) determined arterial lactates at various levels of hypocapnia in humans during voluntary HV. The maximum individual lactate rise in any one subject was only 1.87 mM/l, at sixty minutes. The mean pH increased to 7.62 after one hour, then showed no further change. Engle (1971) (Table l) carried out experiments on anesthetized ventilated dogs to examine short term blood acid-base responses. Engle stated that "although a l l investigators are in agreement that hyperventilation elicits an increase in blood lactate, a detailed examination of the literature reveals a striking variability as to duration and amount of hypocapnia hyperlactaemia elicited by acute experimental HV." The results of his studies present a more detailed description of acid-base changes over a shorter time span. 11 TABLE I Effect of Hyperventilation on PC02, pH, Venous Blood Lactate and HCO~ (Dogs) e PC02 / I T (Units) (mmHg) 7?2o3 LA(Mg.#) (mVa./l) -17 42.6 12.2 18.6 Normal r8 45.2 7.249 11.0 19.1 Ventilation -2 46.8 7.247 12.4 19.7 (44.9) 7.253 12.0 19.1 +5 21.1 7.508 18.1 16.2 Hyper- +10 18.7 7.540 19.8 15.4 ventilation +15 16.9 7.547 20.0 14.2 +55 14.5 7.551 25.1 12.3 Engle cites the following reasons for lactate increase during hypocapnia. Circulation factors may be of some consequence, but there may be a more direct influence of pH upon the rate of glycolytic lactate formation i n tissues and red blood c e l l s . Buhlmann (70) examined the effects of hyperventilation and hypo-volemia i n competitive sport at medium altitude. This was the only reviewed study which investigated blood lactate changes during exercise accompanied by voluntary HV. Blood volume, arterial blood gasses, blood lactate and pulse rate were recorded i n 14 male athletes during strenuous physical exercise on a bicycle ergometer at normal and reduced oxygen tensions. Voluntary HV during exercise i n hypoxia (equal to an altitude of 2000m) resulted i n a decrease i n blood volume, 18% greater than with normal ventilation and normoxia. Buhlmann's findings, 12 although during exercise, are similar to Takanos' (68) with respect to the greater effect on lactates of hypocapnia with hypoxia than without. Aside from the typical arterial blood gas changes, both Buhlmann (70) and Straub (69) found an increase in pulse rate, a drop in skin-temperatur©, an increase in hematocrit and a 5*2% increase in serum protein with HV. The relationship between hyperventilation-hypocapnia and blood lactate production is s t i l l poorly understood. Most studies show that lactate increases at rest are very small and not progressive even when P C0o levels are very low. Zborowska (67), Buhlmann (70), Guest (63) and Murphy (65) generally concluded that on the basis of in vitro experiments, the low PC02 or alkaline pH stimulated blood cell glygolysis and could account for most of the lactate produced. Carbon Dioxide Stores Vance (1959) discussed the adjustment of carbon dioxide stores during voluntary HV by three trained male physicians. He attempted to determine how much C 0 2 can be eliminated by HV, where i t comes from, and in what manner elimination proceeds. Subjects hyperventilated (50$ max.) for one hour. The output of C02 stores was i n i t i a l l y (5 min.) at a high rate but decreased thereafter. From . 5 to 2 .5 liters of C 0 2 stores were eliminated, which represented a reduction of C 0 2 in the lungs by one-third (50 mis), in the blood by one-sixth (500 mis), and the remainder coming from other tissues. Excess oxygen uptake was also measured. The rate of 0 2 uptake increased immediately with HV/ but returned to near resting values after ten minutes. Tomashefski (59) observed COg and acid-base transients during voluntary HV by healthy U.S. Airforce men. A mean pH of 7.60 was recorded when subjects hyperventilated to 20mm Hg for 12 minutes.1 Elimination of C0 2 stores was said to come largely from: (1) alveolar air, (2) lung parenchyma, and (3) blood. After 3 minutes, C0o largely came from blood and tissues. 14 SUMMARY For many years attention has been focused on the state*of the COg system as an indicator of the acid«*ase condition of the blood. The acid-base response to HV- produced-hypocapnia was stated. Very small lactate increases were seen and generally ascribed to the stimulating effect of low PCOg and/or high pH on blood cell glycolysis. Table II (Elkington, J.R., 1955) is presented as being fairly re-presentative of findings on the effects of respiratory alkalosis on selected acid^base parameters in humans at rest. TABLE II E f f e c t of Hyperventilation at PC0 2 3 0 mm Hg For 3 0 Minutes Time of Hv Basal PC0 2 mm Hg. 43.5 pH 7.40 Lactate mg.% 9.2 change from basal Pyruvate mmoles/ .103 l i t e r of H 20 Plasma (HC03") 25.9 m E q . / l i t e r Corrected (HCOj") 25.7 m E q . / l i t e r V e n t i l a t i o n , l i t e r s / 6.2 min. (BTPS) 2 Min 31 7.51 14.4 + 4.1 .111 23.5 25.2 11. 3 20 Min. 3 0 Min. 30 7.50 16.0 + 5.9 . 116 23.6 25 11.3 30 7.52 17.2 + 9.8 .119 23.7 25.4 11.7 16 CHAPTER I I I Methods and Procedures Eight healthy male and female students (21-30 yrs.) of the University of B r i t i s h Columbia, volunteered f o r t h i s ten day study which began i n May, 1972. P r i o r to the f i r s t treatment condition, a l l subjects underwent Astrand's (1971) bicycle ergometer test for the prediction of maximum CO,, • On the basis of the individual's oxygen uptake-heart rate relationship, a submaximal work-load (70-80$ of maximum) i n terms of heart rate (150 approx.) was calculated, which would produce a s i g n i f i c a n t lactate increase. Subjects reported f o r t h e i r f i r s t t e s t session early i n t h e i r day and p r i o r to any (except f o r normal movement) physical a c t i v i t y . At minus l 6 minutes, subjects started a 15 minute rest period. At minus 1 minute, pretest blood samples were drawn (right antecubital v e i n ) . Blood was deproteinized immediately with 10$ t r i c h l o r o a c e t i c acid and then centrifuged. Supernatant was then pipetted-off and stored i n a lak temperature freezer. Duplicate sets of blood samples were processed. Lactate analysis was done, according to a method by Bochringer, within twenty four hours. pH determination, using micro blood samples drawn simultaneously from the finger t i p , were completed almost immediately (3 min.) using a Micro Astrup Radiometer. Subjects began exercising on a Monark bicycle ergometer as soon 17 as ECG and infra-red C02 - 0 2 analyzer instruments were fitted. Workload (3-5 kilopbunds) and pedal frequency (50rpm.) was set as exercise began at time 0. Experimental (A^) test subjects received overbreathing instructions just prior to exercise. Exercise was terminated at plus 4 minutes and subjects remained seated on the bicycle for the i n i t i a l 4 minutes of the recovery period. Upon cess-ation of the exercise, 4 of the 8 subjects overbres&ed so that their end tidal PC0o readings, which were visually represented on the I infra-red C02 analyzer recorder, read no higher than 25 mm Hg. and no lower than 23 mm Hg. Subjects maintained overbreathing for four minutes, attempting to keep P C0o indicator needle at the prescribed a ^ I i level. Blood samples were drawn (venoject needles and 8 ml. vacuum tubes) for lactate and pH (fingertip lance and capillary tube) deter-minations, at the 2nd and 4th minute — post exercise. These 4 subjects terminated this experimental session at the 4th minute of recovery and were scheduled to return before seven days had elapsed. During the second experimental (Ag) session recovery period, subjects were instructed to ventilate so that their P C0o readings remained at an aimed-for normal resting level of 45 mm Hg. The other 4 subjects were treated identically, except the order of the two experimental (A^ and A 2) testing sessions was reversed. Mean end tidal PC02 levels actually obtained during overbreathing was 27 mm Hg and during underbreathing or control was 49 mm Hg. 18 Subjects experienced some d i f f i c u l t y in accurately maintaining P C 0 2 targets set down. They would consistently undersoot or overshoot the mark. The range for experimental (A 2 ) condition was 45-55 mm hg and for the experimental (A 1 ) condition was 24-30 mm Hg. 19 S t a t i s t i c a l Analysis and Experimental Design Decay rates f o r venous blood l a c t a t e s , f o r the i n i t i a l four minutes of recovery were of primary i n t e r e s t . Recovery lactates and pH's were s t a t i s t i c a l l y compared under treatment conditions. A repeated measures ANOVA for a 2 x 2 design, shown i n Table I I I , was carried out using the Biomed Computer Programs, with 2 treatments (A^ = Overbreathing)(A 2 = Underbreathing) and 2 times (B^ = 2 mins.) ( B 2 = h mins.). Inherent i n t h i s design are two contrasts which w i l l indicate: (1) (a) Whether there i s a s t a t i s t i c a l difference between underbreathing and overbreathing conditions at 2 minutes into recovery i . e . , tests i f A x Bj - A 2 B 1 = 0 (b) Whether there i s a s t a t i s t i c a l difference between underbreathing and overbreathing conditions at 4 minutes into recovery i e . , tests i f A x B 2 - A 2 B 2 = 0 (2) Whether there i s a difference i n slope (rate of lactate decay) from the second minute to the fourth minute of recovery, between underbreathing and overbreathing conditions i . e . , tests i f ( A ^ - A J 3 - ) = ( A ^ - A 2 B 2) 20 TABLE II I A Schematic Representation of the Experimental Design Overbreathing CA-,) Underbreathing (A ?) 2 Min.(B 1) 4 Min.(B 2) 2 Min. (Bp 4 Min.(B2) s l X l l X12 X13 X14 S2 X21 X22 X23 X24 S 3 X31 X32 X33 X34 S4 X41 X42 X43 X44 S5 X51 X52 X53 X54 S6 X61 X62 X63 X64 S7 X71 X72 X73 X74 S8 X81 X82 X83 X84 21 CHAPTER IV Results and Discussion Results The c e l l and marginal means of the venous blood lactate as deter-mined f o r the four blood sampling periods are presented i n Table IV. TABLE IV Venous Blood Lactate C e l l Means B(Time) 2 Min. (B 1) 4 Min. (B 2) Over (A 1) 52.50mg$ 38.86mg$ 45.68 A(Treatment) Under (A 2) 64.32mg$ 50.64mg$ 57.48 58.41 44.75 51.58 grand mean Two and four minute lactate decay values f o r underbreathing and overbreathing conditions are presented f o r each i n d i v i d u a l i n Figures I and f o r the group i n Figure I I . 22 2 min. 4 min. 2min. F I G U R E I . L a c t a t e D o c a y V a l u e s -I n d i v i d u a l S u b j e c t s 23 2 min. 4nr»in. 2min. 4 min. FIGURli I . Lactate Decay Values -Individual Subjects 24 Table V presents an ANOVA lactate summary. It i s a 2 x 2 f a c t o r i a l design with, subjects repeated oyer conditions. TABLE V ANOVA Summary - Venous Blood Lactate Source df Mean Square F P Subjects 7 768.55 A( treatment) 1 1113.68 6.036 <,05 SA 7 184.50 B time 1 1492.77 36.19 <,05 SB 7 41.24 AB 1 .0041 < 1.0V >,05 SAB _7 31 36.18 F.01; 1, 7 = 12.25 F.05; 1, 7 = 5.59 25 1001 49_mra Hg _A2" 50 80r 40 60l 40F ®r6 27^7 mm Hg . _ . A s 30 P C O 2 mm Hg 420 201 10 1 B 1 2 Min. B 2 4 Min = FIGURE I I . Mean Lactate Decay Values During Overbreathing and Underbreathing The c e l l and marginal means for pH values are presented in Table VI. TABLE VI C e l l Means for pH Values B (A,) 2 Min. (Bp 4 Min.(B 2) Overventilation 7.27987 7.33737 7.3086 A CA2) Unde r v e n t i l a t i o n 7.25675 7.30900 7.2828 7.26831 7.3231 7.340 7.320 7 : 3 0 0 7.280 7.260 7.240 7.2201 7.2001 B 1 2 Min. B 2 4 Min, FIGURE I I I . Mean pH Values During Overbreathing and Underbreathing pH values were examined using the same 2 x 2 f a c t o r i a l design. These results are presented in Table VII. TABLE VII ANOVA Summary - pH Values Source df Mean Square Subjects 7 A(treatment) 1 SA 7 B(time) 1 SB 7 AB 1 SAB 7 3T . 262 . 530 .954 .241 . 008 . 055.-.128 .556 29. 25 <1.0 >.05 <.05 >.05 F.01; 1, 7 = 12.25 ; F.05; 1, 7 = 5.59 The c e l l and marginal means f o r heart rate values are presented i n Table VIII. TABLE VIII C e l l Means for Heart Rate Values B (Time) 0 Min. 2 Min.CB,) 3 Min. 4 Min. CB7) Overbreathing (A-^ ) Underbreathing (A~) 161 137 160 128 105 95 99 72 160.8 132.8 102.5 84.1 30 170 •M Pi O 160 150 140 130 120 110 100 90 80 70 \ \ A, ^ 4 2 Time 4 - Minutes FIGURE IV. Graph of Heart Rates During Overbreathing and Underbreathing Over the Four Minute Recovery Period H e a r t r a t e r e s u l t s are p r e s e n t e d i n the ANOVA summary i n T a b l e IX. TABLE IX ANOVA Summary - H e a r t Rate Source df Mean Square S u b j e c t s 7 A ( t r e a t m e n t ) 1 SA 7 B (t i m e ) 3 SB 21 AB 3 SAB 21 63 668.46 1396.89 1061.03 18277.18 52.68 344.7 278.05 1.32 346.93 1.24 >.05 <.05 >.05 32 DISCUSSION Treatment Effect (Lactate) The i n i t i a l two minute comparison of means revealed a 12 mg$ lactate difference, precisely the same as the subsequent 4 minute com-parison of the lactate values. However, lactate values during (overbreathing) were lower. I t would thus appear that overbreathing during recovery may s i g n i f i c a n t l y affect venous blood l a c t a t e l e v e l s early i n the recovery period. The ANOVA summary (Table V) confirmed that the A^ effect was s i g n i f i c a n t at the .05 l e v e l . Figure IV graphically depicts the mean A^ and A 2 decay slopes. The fact that they are v i r t u a l l y p a r a l l e l (on a l i n e a r plot) i l l u s t r a t e s the s i m i l a r i t y of decay patterns i n the recovery period. Time Effect (B) Lactate The s i g n i f i c a n t ( .05,level) decrease i n blood lactate over the 4 minute recovery period was expected. I n i t i a l decreases i n blood l a c t a t e , p a r t i c u l a r l y a f t e r short periods ( l to 4 niin.) of heavy work ( above 75$ of max.), have been reported (Astrand, 1969) to be more dramatic early i n the recovery period. During severe work Astrand noted decreases i n venous blood l a c t a t e of the order of 30-40 mg$ by the 6th minute of recovery from severe exercise (bicycle ergometer). The mean decrement (14 mg$) from 2 to 4 min. i n the recovery period 33 was e s s e n t i a l l y the same f o r both experimental c o n d i t i o n s . Th i s decrement would have probably been more s u b s t a n t i a l with a heav ier work l o a d . pH The A 1 Treatment E f f e c t on pH was not s i g n i f i c a n t (Table V I I ) , accord ing to the ANOVA summary. Overbreathing appears not to produce a s i g n i f i c a n t upward change i n pH. I t should be noted however, that s i g n i f i c a n c e was o n l y narrowly missed wi th an obtained F o f 5*562, on ly s l i g h t l y lower than the requ i red F . In each case , (Table VI) at 2 min. and 4 m i n . , the pH values were h igher dur ing overbreath ing (A^) than dur ing underbreathing ( A 2 ) . There was v i r t u a l l y no d i f f e r e n c e (2 min. - . 0 2 3 , 4 min. - . 0 2 8 ) between the A^ and A 2 v a l u e s . F igure V g r a p h i c a l l y shows the mean A.^  and A 2 pH s lopes from 2 to 4 niinutes i n t o recovery . The over v e n t i l a t i o n s lope (A^) i s on ly s l i g h t l y steeper than the A 2 s l o p e . The AB e f f e c t ( i n t e r a c t i o n ) was not evident here and d i d not ga in s i g n i f i c a n c e . The B or Time E f f e c t was expected to be s i g n i f i c a n t . An inc rease of pH dur ing recovery has been found by many i n v e s t i g a t o r s . L a c t a t e accumulation and removal has been found to be the most important f a c t o r f o r a change i n pH (Pernow, 1965). There i s a l i n e a r r e l a t i o n between inc rease of pH and decrease of l a c t a t e . In view of the s i g n i f i c a n t decrease i n l a c t a t e over time and t h i s h igh c o r r e l a t i o n between venous l a c t a t e and pH, one would expect a s i m i l a r change i n pH over t i m e . 34 The ANOVA summary (Table VII) did show a s i g n i f i c a n t (.05 l e v e l ) time effect on pH. The mean pH increase (7.2683 to 7.3231) was .0548. Heart Rate An examination of heart rate c e l l means (Table VIII) shows that the heart rates were consistently higher during over v e n t i l a t i o n (A^) than during underventilation ( A 2 ) . Although the heart rates were not s i g n i f i c a n t l y higher, t h i s observation does agree with observations made elsewhere. Voluntary HV during exercise and at rest usually leads to higher pulse rates (A.A. Buhlmann, 1969). The ANOVA Summary (Table IX) confirmed that the A effect was not s i g n i f i c a n t . On the other hand, the B effect (time) was highly s i g n i f i c a n t . C e l l means for A^ and A 2 over the recovery periods a l l decreased sub-s t a n t i a l l y . The A^ decrement was 66 beats (l6l to 95) while the A 2 drop was 88 beats (160 to 72). General Discussion There appears, according -to the measurements taken, to be l i t t l e to substantiate any claim, that departures from normal breathing during the immediate post-exercise period would aid i n recovery. The results seem to indicate that over or underbreathing during recovery from sub maximal exercise, makes l i t t l e difference. 35 Some differences from normal were obtained i n the values of the three variables (pH, lactate and heart rate) under examination, but there are a number of possible reasons why these occurred. Although both (2 and 4 minute) lactate values were lower during overbreathing, i t i s quite possible that these values are misleading. In the f i r s t place, when one examines the i n d i v i d u a l values (Figure I I I ) f o r l a c t a t e , there can be found to be considerable differences from i n d i v i d u a l to i n d i v i d u a l . For example, l a c t a t e values f o r subject 2 showed very large differences ( 53 mg$ at 2 mins.) during over and under-breathing, whereas the mean difference was only 12 mg$. I f the data f o r t h i s subject had not been included i n the s t a t i s t i c a l analysis, the results would not have been s i g n i f i c a n t . Secondly, subjects 4» 5» 7, and 8 had v i r t u a l l y i d e n t i c a l values f o r both treatment conditions. Thus one, or possibly two (subject l ) subjects, accounted f o r p r a c t i c a l l y al l , the observed differences. Other factors also make these lactate results rather tenuous. For example pH results were not s i g n i f i c a n t and since pH and lactate are usually highly correlated, i t may be that the lactate values do not r e f l e c t actual l e v e l s . Another factor arises from the fact that values derived from venous arm samples, may not be i n d i c a t i v e of lactate changes i n the venous blood of working legs. J o r f e l d t (1970) found that during submaximal work, there was considerable 36 v a r i a t i o n i n venous blood lactate (5.7 to 8.5 mg$) when sampled simult-aneously at various s i t e s i n the body. Variation of t h i s kind, as reported by J o r f e l d t and others, suggests further possible sources of error i n the measurement of l a c t a t e . These factors, i . e . v a r i a b i l i t y of i n d i v i d u a l lactate values, lack of significance of pH r e s u l t s , v a r i a b i l i t y of blood l a c t a t e with the sampling s i t e , and the lack of reaffirmation of lactate values i n the pH r e s u l t s , make the lac t a t e results open to some question. 37 CHAPTER V Summary and Conclusions Summary The purpose of t h i s study was to determine whether a specified hypocapnia (27 mm Hg), induced by voluntary overbreathing would affect venous blood lactate decay, during recovery from sub maximal exercise i n humans. The study was conducted over a ten-day period on eight Univ-e r s i t y of B r i t i s h Columbia students, 18-30 years o l d . A l l subjects under-went two sub maximal four minute bicycle ergometer r i d e s . On the basis of the subjects, oxygen uptake-heart rate relationship, a submaximal workload (75%) i n terms of heart rate was calculated to produce a s i g -n i f i c a n t l a c t a t e increase. Experimental conditions A 1 and A 2 were a l -ternated with successive subjects. One experimental condition involved a 4 minute period of underbreathing a f t e r the 4 minute bicycle r i d e and the other experimental condition involved a 4 minute period of over-breathing a f t e r exercise. Venous blood l a c t a t e and pH were measured i n two samples taken during the recovery period. Heart rates and end t i d a l PC0 2 l e v e l s were continuously monitored. Recovery lactates and pH's were s t a t i s t i c a l l y compared under the two experimental (A and A Q) conditions, using a 2 x 2 repeated measures 38 ANOVA. The results of the comparisons showed s i g n i f i c a n t l y lower lactate values during overbreathing. However, the v a l i d i t y of t h i s result was shown to open to some question. Furthermore, i t was concluded that the value of overbreathing as an aid i n recovery was questionable at best. Conclusions Two breathing patterns which produced low levels of end t i d a l PC0 2 had di f f e r e n t effects on venous blood lactate removal during recovery from submaximal exercise i n the normal human subject. (1) S i g n i f i c a n t l y lower recovery lactate values were observed during hypocapnia at each (2 and 4 min.) sampling time. (2) The preceding hypocapnia effect which apparently produced the i n i t i a l (2 min.) decrement i n l a c t a t e , did not produce an i n -creasing difference i n time. (3) pH and Heart Rate were not s i g n i f i c a n t l y changed by the hypo-capnia induced by overbreathing. (4) Lactate, pH and heart rate a l l changed s i g n i f i c a n t l y during the 4 minute recovery period. 39 REFERENCES > Adler, S. Roy, A. Relman, A.S. Intracellular acid-base regulation. J . of Clin. Invest., 44:8, 1965 Adler, S. Intracellular acid-base regulation. J . Cl i n . Invest., 44:21, 1965 Anrep, G.V. The concentration of la c t i c acid i n blood i n experimental alkalemia and acidemia. J . of Physiol. 58:244, 1923 Astrand, P.O. Textbook of Work Physiology. Charles C. Thomas, Springfield, 111. 1969 Axelrod, D.R. Organic acids and calcium i n hyperventilation. J . of Appl. Physiol. 16:709-12, 1961 Balke, B. Adaptive responses to hyperventilation. J. of Appl. Phys. 12:269, 1958 Bjontorp, P. et a l . Effects of physical training on exercise blood flow and enzymatic activity i n skeletal muscle. Cardiovascular  Research, 4:418-22, 1970 Boehringer, C.F, Mannheim Biochemisch Abteilung, Fibel, 1956 Boucot, N.B. dal. Extrarenal buffering of acute respiratory alkalosis. J . Physiol, London, 132:63, 1956. Brassfield, C.R. et a l . Correlation of the pH of ar t e r i a l blood and urine as affected by changes i n pulmonary ventilation. Amer. J . of Physiol., 132:272, 1941. Brown, E.B. J r . , Hyperventilation. Physiol. Rev. 33:445, 1953. Buhlmann, A.A. Hyperventilation and hypovolemia i n competitive sport at medium altitude. Schw. Med. Wo. 99:1886, 1969. Cajori, F.A. et a l . The effect of the application of external heat on acid-base balance. J . of B i o l . Chem. 57:217, 1923. Carlsten, A. et a l . Myocardial metabolism of glucose, la c t i c acid, amino acids and fatty acids i n healthy human individuals at rest and different work loads. Scand. J . of Cl i n . Lab. Invest.. 13:418, 1961 Collip, J.B. The effect of prolonged hyperapnia on C 0 2 combining power of the plasma, the C 0 2 tension of the alveolar a i r and the excretion of acid, basic phosphate and ammonia by the kidney. Amer. J . Physiol. 51:568, 1920 Cori, C.F. Regulation of enzyme activity i n muscle during work. In, Enzymes, Units of Biological Structure and Function, edit, by O.H. Gaebler. N.Y.: Academic, p. 573-83, 1956. Davenport, H.W. A.B.C. of Acid-Base Chemistry. Chicago, Univ. of Chicago Press, 1958. Davies, H.W. et a l . Regulation of the bloods alk a l i n i t y . J . Physiol. 54:32, 1920. Depocas, R. Rates of formation and oxidation of la c t i c acid. Canadian J. of Physiol, and Pharmac. 47:603, 1969. Eichenholz, A. Respiratory alkalosis. Archwes. of Internal  Med. 116:699, 1965. Eldridge, F. Effect of respiratory alkalosis on blood lactate i n humans. J . of Appl. Phys. 22/3:46l, 1967. Elkington, J.R. et a l . Effects i n man of acute experimental res-piratory alkalosis and acidosis on Ionic transfer i n t o t a l body flu i d s . J . of C l i n . Invest. 3 4 : l 6 7 l , 1955. Engel, K. Effects of acute respiratory alkalosis and acidosis on l a c t i c acid concentration. J . C l i n . Lab. Invest. 20:179 , 1967. Farhi, L.E. Dynamics of changes i n C0„ stores. Anaesth. 21:604, I 9 6 0 . ^ Fenn, W.O. Physiological observations on hyperventilation at altitude. J . Appl. Phys. 1:773-89, 1949. Fowle, A.S.E. The immediate C0„ storage capacity of man. Clin . S c i . 27:41-9, 1964. Gevers, W. and Dowdle, E., The effect of pH on glycolysis i n Vitor.- C l i n . S c i . 25:343-9, 1963. Giebisch, G. et a l . The extrarenal response to acute acid-base disturbances of respiratory origin. J . Cl i n . Invest. 34:221, 1955. Grant, S.B. Forced respiration and experimental production of tetany. Amer. J . of Physiol. 52:209, 1920. Haggard, H.W. Alteration of the CCL ratio (HgCO^NaHCO-) i n blood during elevation of bhe body temperature. J . of B i o l . Chem. 44:131, 1920. Harris, P. The regional metabolism of lactate and pyruvate during exercise i n patients with rheumatic heart disease. C l i n . S c i . 23:545-560, 1962. Hastings, A.B. COp and pH as regulators of metabolism. Advances i n Enzyme Regulation. 3:147-159, 1965. Hermansen, L. and Jan-Bjc/rn, Osnes. Acid-base balance after maximal exercise of short duration. J . of Appl. Phys. 32/1:59-64, 1972. H i l l , A.V. Influence of the external medium on the internal pH of muscle. Proc. Royal Society. B 144:1-22, 1955. Himwich, H.E. Respiratory alkalosis. Yale Journal of Biology  and Medicine. 4:259, 1932. Holloszy, J.O. Biochemical adaptations i n muscle. J . of B i o l . Chem. 242/9:2278-2282, 1967. Huckabee, W.E. Relationships of pyruvate and lactate during anaerobic metabolism effects of hyperventilation. J . of C l i n . Invest. 37:244, 1958. Jorfeldt, L. Metabolism of L(+)-lactate i n human skeletal muscle during exercise. Acta Physiologica .Scand. Supp. 338:66-99, 1970. Karlsson, M. and Bjorntor, P. Deterniination of succinic oxidase activity i n human skeletal muscle. Scand. J . C l i n . Invest. 26:145, 1970. Keul, J . The substrate supply of human skeletal muscle at rest, during and after work. Experiments. 23:974-979, 1964. Krebs, H. S i r . The Croonian lecture: Gluconeogehesis. Annals  N.Y. Academy of Sciences. 159:545-564, 1964. Loewen, H. Hyperventilation and the postponement of fatugue. Unpublished Masters Thesis, University of B r i t i s h Columbia, Vancouver, Br i t i s h Columbia, Canada. Margaria, R. Contracting and paying the oxygen debt. Amer. J .  of Physiology. 106:689, 1964. Papadopoulos, C.N. et a l . The metabolic acidosis of hyper-ventilation by controlled respiration. Anesthesiology. 20:156, 1959. Pernow, B. and J . Wahren, Lactate and pyruvate formation and oxygen u t i l i z a t i o n i n the human forearm muscles during work of high intensity and varying duration. Acta. Phyasiol. Scand. 56:267, 1962. Roberts, K.E. et a l . Respiratory alkalosis. Annals, New York  Academy of Sciences. 66:955f 1957. Robin, E.D. Fundamental determinant of COg-HCO^  activities i n biological systems. J . C l i n . Invest. 44:1091, 1965. Roughton, M. Hypoxia and disturbances of C02» Handbook of Physiology: Respiration I I , Chapt. 37, 985-1002. 1964. S a i k i , H. Lactic acid production i n submaximal work. Arbeitsphysiol. 24:57-61, 1967. Stanbury, S.W. et a l . The extrarenal buffering of acute res-piratory alkalosis. J . of Physiol., London. 132:63, 1956. Straub, P.W. and Buhlmann, A.A. Hyperventilation and hypovolemia during exercise at altitude. The Lancet. May 16, 1970. Sutton, H. Heat and hyperventilation. J . of Path, and Bact. 13:62, 1909. Takano, N. Blood lactate accumulation and i t s causative factors during passive hyperventilation i n dogs. Japan J. Physiol. 16/5:481, 1966. Talbott, J.H. et a l . Acid-base balance of the blood i n a patient with hysterical hyperventilation. Arch. Neurol, and Psychiat. 39:973, 1938. Tobin. R.B. In vivo influences of H+ on lactate and pyruvate i n the blood. Amer. J . Physiol. 207:601-605, 1964. Tomashefski, J . and Wilkes, S.S. Mech. of hyperventilation i n man. J. Aviation Med. 25:265, 1954. Vance, J.W. Adjustment of Stores of C02 during voluntary hyperventilation. Diseases of the Chest. 37:304, I960. Waddell, W.J. et a l . Intracellular pH. Physiol. Rev. 49:285-324, 1969. Winters, R.W. Terminology of acid-base disorders. Ann. N.Y.  Acad. Sciences. 133:1, 1965. Zborowska-Sluis, D.T. Hyperlactatemia of hyperventilation. J . of Appl. Physiol. 22:746, 1967. 44 APPENDIX A MR SCORES Lactate CMgl) PH Heart Rate Over Under Over Under Over Under Recovery 1 44.75 60.38 7.260 7.283 158 161 Recovery 2 15.05 51. 75 7.370 7.371 144 140 108 108 88 80 Recovery 1 53.73 102.00 7.262 7.239 161 180 Recovery 2 43.90 71.98 7.289 7.271 140 150 119 130 95 106 Recovery 1 38.10 51.75 7.280 7.241 160 166 Recovery 2 17.59 27.66 7.301 7.262 132 133 100 99 77 77 Recovery 1 59.28 59.47 7.292 7. 272 155 155 Recovery 2 53.72 57.11 7.350 7.302 110 115 85 80 70 76 Recovery 1 48.46 49.49 7.338 7.235 165 141 Recovery 2 31.90 38.93 7.354 7.289 140 90 100 81 Recovery 1 71.20 85.90 7.236 7. 205 164 155 Recovery 2 67.46 72.70 7.315 7.293 142 130 108 99 91 82 Recovery 1 55.5Q 55.60 7.299 7.283 161 161 Recovery 2 40.70 44. 3Q 7.358 7.318 146 140 118 100 90 85 Recovery 1 49.00 50.00 7.272 7.296 165 165 Recovery 2 40 .60 40. 7Q 7.362 7.366 143 131 106 100 90 77 


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