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The effects of carbon dioxide upon recovery after submaximal exercise Lee, Jim H. (James Henry) 1974

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THE EFFECTS OF CARBON DIOXIDE UPON RECOVERY AFTER SUBMAXIMAL EXERCISE by JAMES HENRY LEE B.Sc.(PE), University of Guelph, 1973 A THESIS SUBMITTED IN PARTIAL FULFILLMENT OF THE 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 THE UNIVERSITY OF BRITISH COLUMBIA November, 197U In presenting 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 of the requirements f o 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 f o r reference and study. I f u r t h e r agree that permission for extensive 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 representatives. It i s understood that copying or p u b l i c a t i o n of t h i s t h e s i s f o r f i n a n c i a l gain s h a l l not be allowed without my w r i t t e n permission. James H. Lee Department of P h y s i c a l E d u c a t i o n and R e c r e a t i o n The U n i v e r s i t y of B r i t i s h Columbia Vancouver 8, Canada D a t e January 28, 1975. i i ABSTRACT Nine male P h y s i c a l Education students were s e l e c t e d to t e s t the hypothesis t h a t a d d i t i o n of CCv> to the i n s p i r e d a i r during recovery w i l l cause s i g n i f i c a n t increases i n v e n t i l a t i o n above c o n t r o l c o n d i t i o n s and t h a t recovery from submaximal e x e r c i s e w i l l be enhanced by the a d d i t i o n of 2 . 7 8 / 0 or 5 > . 8 0 $ CO2 to room a i r . The e x e r c i s e was administered f o r s i x minutes a t a xrorkload predetermined to e l i c i t 7%% of h i s maximal oxygen uptake. The dependent v a r i a b l e s (heart r a t e , v e n t i l a t i o n , oxygen uptake, and carbon dio x i d e e l i m i n a t i o n ) were subjected to a one way a n a l y s i s of var i a n c e and s i g n i f i c a n t F r a t i o s evaluated using Dunnett's Test. V e n t i l a t i o n i s i n c r e a s e d s i g n i f i c a n t l y (pC.05-) above c o n t r o l values w i t h the a d d i t i o n of %.Q0% CO2 t o room a i r during recovery however, there i s no s i g n i f i c a n t increase i n oxygen uptake. The a d d i t i o n o f 2 . 7 8 $ CO2 to room a i r during recovery does not s i g n i f i c a n t l y ( p } . 0 5 > ) increase v e n t i l a t i o n ; there i s however a s i g n i f i c a n t ( p ^ . 0 5 ) increase i n oxygen uptake i n the f i r s t 3 0 seconds of recovery. N e i t h e r treatment e f f e c t causes s i g n i f i c a n t changes i n heart r a t e . The a d d i t i o n of $.80% CC>2 to the i n s p i r e d a i r s i g n i f i c a n t l y ( p < . 0 ^ ) reduces carbon d i o x i d e e l i m i n a t i o n . In k s u b j e c t s , the e f f e c t produced a carbon d i o x i d e uptake a t c e r t a i n time i n t e r v a l s . The a d d i t i o n of 2,7$% CO^ to the i n s p i r e d a i r caused a s i g n i f i c a n t (p^.O^) r e d u c t i o n of carbon dioxide e l i m i n a t i o n i n the f i r s t minute of recovery. Approved i i i TABLE OF CONTENTS Page ABSTRACT i i LIST OF TABLES v LIST OF FIGURES v i ACKNOWLEDGEMENT v i i Chapter 1. INTRODUCTION 1 Introductory Statement . 1 Statement of the Problem 2 J u s t i f i c a t i o n of the Problem . 2 Hypothesis 2 Rationale 3 D e f i n i t i o n s 3 Delimitations . . . h Limitations k 2. REVIEW OF LITERATURE 5 D i r e c t l y Related L i t e r a t u r e 5 I n d i r e c t l y Related L i t e r a t u r e . . . 11 3. PROCEDURES ,c Ik Subjects lU Experimental Period . Ik T r a i n i n g of Assistants . . . » lU Pre Testing 16 Chapter Page Apparatus 16 Research Design 19 Measurement at Exercise 19 S t a t i s t i c a l Analysis 22 U. RESULTS AND DISCUSSION 23 Discussion 31 5". SUMMARY AND CONCLUSIONS 39 Conclusions IjO Recommendations to Further Research . U l BIBLIOGRAPHY ,c U2 APPENDIX 1. SUBJECT INFORMATION AND INSTRUCTIONS h5 2. PHOTOGRAPHS OF EQUIPMENT H6 3. COMPUTER PROGRAM FOR TRANSFORMATION OF RAW DATA . . . h9 U. DEPENDENT VARIABLES DURING RECOVERY 50 5 . MEAN VALUES OF ALL DATA 59 V LIST OF FIGURES Figure Page 1. Schematic of P r i n c i p l e Responses to CO2 13 2. Schematic Diagram of Apparatus 18 3 . Mean Heart Rate Values 28 h. Mean V e n t i l a t i o n Values 29 5". Mean V C 0 2 Values 30 6. Mean V 0 2 Values 31 7. V E / P A C 0 Relationship During Recovery 33 v i LIST OF TABLES Table Page 1. Subject Data 15 2. Scope and Reasons f o r Missing Data 20 3. ANOVA Table F i r s t Two Minutes of Recovery 24 i i . ANOVA Table Treatments A and C 25 5. Mean Differences f o r Dunnett's Test 26 6. Slopes and Intercepts of Vg/P^QQ Relationship . . . . 3^ 2 v i i ACKNOWLEDGEMENTS The author would like to acknowledge the aid of several individuals. Mr. Dave McGinn provided countless hours of assistance in the labora-tory. Mr. Dave Goodman designed the computer program for the transfor-mation of the raw data. The author would also like to thank the members of the thesis committee for their aid and advice. 1 Chapter 1 INTRODUCTION INTRODUCTORY STATEMENT The f i r s t studies on the effects of the addition of carbon dioxide to the inspired air were undertaken nearly 100 years ago; these numerous studies served to help elucidate the nature of the control of respira-tion (28). Both Dripps and Comroe (11) and Neilsen and Smith (29) showed that the addition of carbon dioxide to the inspired a i r increased the ventilation. Neilsen and Smith (29) determined that this response occurred at alveolar CO2 levels above 31»5" mm Hg. and rose in a linear fashion. During exercise however, other factors served to influence this response to carbon dioxide (3). Body temperature, blood lactate, pH, and hypoxia tend to alter the sensitivity of the central chemoreceptors (32), pro-ducing a response to CO2 different than the 0.58 l/min. change in venti-lation per mm Hg increase i n alveolar CO2 (12) found at rest. In adding sufficient CO2 to the inspired air to bring alveolar CO2 to resting levels during recovery, Bannister et al.(3) noted that the ventilation was raised above the levels found i n the hyperpnea of exercise. Reynolds (31) administered varying concentrations (3, 6, and 1%) of CO2 i n ambient air for 2$ minutes i n resting subjects and noted increases in t i d a l volume, frequency and minute volume proportional to the increased C02« I t i s the intention of this study to determine the effects of adding CO2 to inspired a i r on recovery after submaximal exercise. 2 STATEMENT OF THE PROBLEM The purpose of t h i s study i s to investigate the e f f e c t s of two con-centrations of CO2 i n the i n s p i r e d a i r upon heart rate, minute v e n t i -l a t i o n , oxygen uptake, and carbon dioxide e l i m i n a t i o n during recovery a f t e r submaximal exercise. JUSTIFICATION OF THE PROBLEM Responses to CO2 at r e s t or during exercise appear to be w e l l documented (3, 11, 13j 16, 29); however, the v a r i e t y of f a c t o r s a f f e c -t i n g the responses to CO2 during recovery have served to obscure these responses. Bannisters' work (3) on recovery indicates that there w i l l be increases i n v e n t i l a t i o n with the ad d i t i o n of CO2 to the i n s p i r e d a i r during recovery. I t i s hoped that t h i s i n v e s t i g a t i o n w i l l serve the following two purposes: (1) to i d e n t i f y the nature and p h y s i o l o g i c a l implications of the response to CO2 during recovery. (2) to stimulate f u r t h e r research i n t o the use o f CO2 enriched a i r as an ergogenic a i d during recovery. HYPOTHESES (1) The addi t i o n of CO2 to the i n s p i r e d a i r during recovery causes s i g -n i f i c a n t increases i n v e n t i l a t i o n above the con t r o l conditions. (2) Recovery from submaximal exercise, as r e f l e c t e d by a decreased heart rate and increased oxygen uptake, i s enhanced by the addition of C 0 2 to the i n s p i r e d a i r . 3 RATIONALE The addition of COg to the inspired air will act as a stimulus to respiration thus enhancing the recovery after exercise. DEFINITIONS For purposes of clarification, the following definitions and abbre-viations were considered applicable throughout this study. (1) Alveolar CO2 (Op): The partial pressure of C 0 2 ( 0 2 ) in the alveolar air, abbreviated P^ QQ (P^Q )• (2) Average percent CO? (Op): The fractional concentration of C0 o ( 0 o ) in the expired air, abbreviated F„nr, (F„. ). (3) Carbon dioxide elimination; The volume of CO,, exhaled from the lungs in a one minute period as determined by measurement and analysis of the expired air with correction for any inspired C 0 2 , abbreviated VCOg. (I4.) Maximum workload; The workload at which a subject will exhibit his maximal oxygen uptake as estimated by the Astrand nomogram. {$) Minute ventilation; The volume of air expired in one minute determined by the product of the average tidal volume and respiratory frequency for that minute, abbreviated MV. (6) Oxygen uptake; The volume of oxygen removed by the blood from alveolar air in one minute, abbreviated ¥ 0 2 . (7) Submaximal exercise; Work performed on the bicycle ergometer at a workload which would e l i c i t an oxygen uptake of 7$% of the subjects maximum. (8) Tidal volume; The volume of air expired in one breath, deter-mined as the area under the curve produced by the flowmeter times the k correction factor for that sample DELIMITATIONS This investigation was restricted to the following dependent v a r i -ables: heart rate, minute volume, oxygen uptake and carbon dioxide elimination. The subjects ranged i n age from 18 to 23 (N a 9) and were healthy, male Physical Education students. The three treatments were: (1) 2.78$ C0 2, 21,$% 0 2, balance N g (2) $,B0% C0 2, 20.8$ 0 2, balance N 2 (3) ambient a i r LIMITATIONS This investigation was restricted by the size and nature of the sample. The quality of the data obtained was limited by the equipment and test procedures. 5 Chapter 2 REVIEW OF LITERATURE DIRECTLY RELATED LITERATURE Studies of the effects of C0 2 upon the ventilation were initiated nearly 100 years ago, however, the knowledge of these effects is s t i l l incomplete. Meischer (28) noted that the addition of the same molecular weight of carbon dioxide changed the ventilation more than did the addi-tion of oxygen to the inspired air. Haldane and Priestly (20) noted the changes in alveolar air with changes in ambient C02» A change of 0.2$ in alveolar air CO2 caused an increase in ventilation of about 100$. After these observations, most attention was focused upon the effects of oxygen inhalation (19). Advancement in technology allowed analysis of expired and alveolar air and more attention was focused upon the seeming waste product of respiration, carbon dioxide. Barcroft and Margaria (h) noted that the hyperpnea following inhalation of CO^  was less than that produced by severe exercise. Their conclusion that the small changes in arterial SPCOg during exercise could not be an explanation for the hyperp-nea of exercise x-ras confirmed (11) later. Dripps and Comroe's (11) investigation was intended to determine the effects of higher concentration of C02 upon respiration and circulation. Earlier, these results had been "recorded incompletely and only upon small groups" (11 :h$)» Although expired gas composition was not determined, they provided valid data of the effects of higher concentrations of 00^ upon the rate, depth, and minute volume of respiration with a large group (N= l|B). By administering 7.6$ C09 in oxygen, the minute volume increased to a mean of 51.5" L/min. and with 10.k% CO^  to a mean value of 76.3 L/min. from a control of 8 L/min. It should be noted that these determinations were made with CO2 i n 0^ rather than i n ambient a i r . There was a large subject variation i n the response that could not be explained. Gray (17) formulated the f i r s t theory of the control of respiration by oxygen and carbon dioxide. His multiple factor theory predicted that the chemical stimuli i n the arterial blood acted i n an independent and additive way. Neilsen and Smith (29) agreed with Gray (17) that P 0 2 can exert effects independent of PCO^  or H+, but disagreed that the level of stimuli would be an algebraic summation of the independent stimuli. Their graph of alveolar P C 0 - versus ventilation at different P i s s t i l l widely 2 accepted (2 :236). The investigators were the f i r s t to use the term "the threshold value of C 0 2 " (29:295). A point i s reached under dif f e r -ing hypoxic - hyperoxic conditions at which adding CO^  to the inspired air causes ventilation to increase rapidly from a plateau value. From this point the ventilation increases rapidly for a given increase i n P A C 0 * A t a n a l v e o l a r P 0 2 o f 37 J™1 Hg. the threshold value of COg appears to be about 30 mm Hg.; at hi mm Hg. P^ , the value i s about 31.5 mm Hg. Under normal conditions (P a 109 mm Hg.) the threshold AO 2 stimulus was found by extrapolation to be 31.5 mm Hg. (29:298). The threshold level under hyperoxic conditions (P = 168 mm Hg.) was found A U 2 by extrapolation to be 31•5 mm Hg. The authors could not determine how the increased sensitivity to CO2 i n the hypoxic state came about. Grodins (18) applied engineering techniques to the regulation of respiration and formulated linear equations for a closed loop system. 7 He postulated that intracellular CCv, concentration in the tissue is depen-dent upon respiration and vice versa. The terra "feedback regulating system" was used to describe this process (18:236). Tenney (36) was concerned with the ventilatory response to C02 in-patients with emphysema. He eliminated the hypoxic drive by adding 0 2 to the inspired air and found a varying response to C0 2 between normal sub-jects and patients with emphysema. The apparent effect was a decreased response to C0 2. This was due to the hypoxic drive playing a large part in the patients resting ventilation so that any increase in ventilation caused by another stimulus would increase P„„ and thus actually diminish A0 2 J the partial effect of the increased P„„rt . e AC02 Bannister et al . ( 3 ) examined several facets of the problem. Although mainly concerned with the hyperpnea of exercise, the role of CCv, as a stimulus to respiration was also discussed. In adding C02 to the inspired air during recovery, they found "the expected changes" (3 :112). How-ever, since this was not a major thrust of the paper, they did not elabor-ate further. During exercise, the respiration was controlled through multiple factors including hypoxia and a lowering of the threshold of the respiratory center to C02 as a result of changes in H+ concentration and body temperature. These account for an increase in the ventilatory response to arterial C02. F.N. Craig (8) attempted to f i t an equation to ventilatory response during exercise. While not specifically mentioning the terms H> concen-tration or body temperature, his term work rate is analagous to these. He found that there appeared to be a simple increment of factors. As either work rate or P^ QQ increased, the minute ventilation was des-cribed by a term of the product of these two factors divided by term also containing these two factors, so that the net effect is for one factor to reduce the effect of the other. Joels and Neil (23) felt that the factors of P 0 2 and P C 0 2 were not additive (8) but that the combination of anoxia and hypercapnia exerted a greater than additive effect on the chemoreceptor response. Lloyd et al.(25) examined the results of Neilsen and Smith in a more detailed fashion. They found that the intercept of the MV/P line with the P . P N axis was independent of PCL and that the slope of the line 2 varied inversely with P 0 2 . This supported the work of Neilsen and Smith (29) and Bannister (3) that the threshold of P C 0 2 was unchanged by either P 0 2 or exercise. They also concluded that at normal P 0 2 there was an hypoxic stimulus affecting ventilation. Clark and Godfrey (7) found that the M V / P ^ Q line intercepted the P C 0 2 axis at Ul)..7 mm Hg. at rest but that exercise decreased the slope of this line. The intercept was not decreased significantly by the exercise. R. E. Button et al . ( 1 2 ) found greater increases in ventilation per mm Hg. P^QQ with intermittent administration of 20$ C 0 2 as compared to continuous administration of 3% C 0 2 . For continuous administration this was an increase in MV of 0.58 L/min. per increase of 1 mm Hg. in P^QQ * They concluded that the chemoreceptors are stimulated by intermittent oscillations in P A R V I as well as mean levels. Some of the changes in A00 2 ventilation found in exercise may be due to the rate of change of arterial P C 0 2 . This finding supports the work of Riley et al.(33). They found higher ventilation with a corresponding lower mean arterial ?C0^ in inter-mittent administration of 20% GO^ than steady 5% in air. 9 Edelman et al . ( 1 3 ) administered single breaths of 6 to 20$ COg i n ambient a i r and suggested that the peripheral chemoreceptors were respon-sible for approximately one-third of the over-all steady state ventilatory response to hypercapnia. When hypercapnia i s potentiated by hypoxia, the stimulus interaction occurs primarily at the central chemoreceptors. The hypoxia tended to increase the slope of the Wj/P^^ l i n e . J. W. Riedstra (32) produced an extensive report of the influence of PCOg on ventilation. His COg response curves resembled those of Neilsen and Smith (29), however, the point of threshold stimulation occurs at a PAC0 °^ ^ ^ ^ * i^®? 6 1 1 0^ 1 1* °£ Pu2* ^ e attributed this to the anes-thesia used in his experiments. In hyperoxia (arterial PO2 = 500 mm Hg.) MV increases linearly with carbon dioxide pressure over the whole range from 30 - 60 mm Hg. due to a purely central effect. The increase of ventilation i n normal and hypoxic ranges with an increase i n a r t e r i a l PCO2 i s less below art e r i a l PC02 of I4S mm Hg. than i n hyperoxia. This phenomenon occurs because the c r i t i c a l oxygen tension decreases with increase of PCO2 i n the PGO2 range below LjB mm Hg. However since the slope of the MV/P^Q lines are the same below this l e v e l , the central effect of PC02 i s independent of the oxygen tension. At P A C 0 i n excess of I18 mm Hg., the peripheral CO,, receptors come into play. As Neilsen and Smith (29) found, the increase in slope of the MV/P n line corresponds to an increase in arterial C0„ tension increas-AOr J2 ing with decrease in P . This i s the result of several factors. An Q 2 increase i n P A C Q increases the c r i t i c a l level for C0 2 since the p e r i -pheral influence overrides the decreasing central influence. The increase i n a r t e r i a l C0 2 pressure is the higher as oxygen tension i s 10 lower. Leigh (2li), i n a series of animal experiments, reported results con-sistent with the belief that the peripheral chemoreflex response to COg depends on P0 9, being greater at low P and less at high P . N . c A0 2 A U 2 R. 5. Gabel (16) tested carotid body sensitivity i n humans. He found highest minute ventilations by administering 1$% COg i n Ng, followed by 5% COg i n Ng. The increases occurred within about 6 seconds and were greatest in the second or third breath. W. J. Reynolds (31) administered varying P A C Q for 25 minutes and found a rapid increase in t i d a l volume to a plateau value, with a gra-dual increase of respiratory frequency. Schaeffer et al.(35) found increased minute volume, t i d a l volume (but a decreased, rate) and P^ QQ with administration of 1.5$ C0 2 i n ambient air for a period of 2x2 days. However, there was no difference i n oxygen uptake. Lopez-Majano (26) reported wide subject variation i n the response to COg as did Farber and Bedell (lU). Farber and Bedell (in) determined that the ventilatory response to COg was not an index to the overall responsiveness of the respiratory control system. Variation did appear to be present i n the ventilatory response as opposed to the neurogenic response. In summary, an increase i n P^ QQ represents a stimulation leading to an increased ventilation mediated primarily through the medullary chemosensitive receptors (2 :232). As long as COg i s being inhaled, the ventilation remains elevated since a reduced ventilation would once more increase P^ QQ above normal levels of lj.0 mm Hg. (2 :232). The rapidly changing conditions of recovery from exercise w i l l alter the response of 11 the central chemoreceptors to inspired CCv, (3 :110). INDIRECTLY RELATED LITERATURE Neilsen and Smith (29) f e l t that the 'COg threshold' found i n their experiments was most probably the threshold for CO^ i n the respiratory center. However, i t would appear that H+- i s responsible for observed effects since increasing arterial PCOg with maintenance of H+" did not increase ventilation (32). Similar results have been shown by Hornbein and Ross (21), as long as adequate time was allowed for ion equilibrium. Peripheral C0 2 chemoreceptors would only appear to be important under hypoxic conditions (2 :232). Hypercapnia potentiates the effects of hypoxia, possibly by a change in the intracellular H+ concentration or a reduction i n the blood flow to the area xrtiere the chemoreceptors are located (32:u20). Generally, alveolar PCOg equals art e r i a l PCOg (l5:8U5) although the equilibrium of COg with the blood buffer system doesn't occur u n t i l blood has passed through the capillary. The carbon dioxide carrying power of the blood thus coincides with the buffering power (3U:797). The concen-tration of dissolved CCv, i n ar t e r i a l plasma i s 1.2 mmoles/L and intra-cellular f l u i d i s 1.5 mmoles/L (27:106). The respiration thus acts to maintain these levels i n homeostasis. When ar t e r i a l PCOg i s increased to 50 mm Hg., the H concentration i s raised to I4.8 mmoles/L from the normal 38 mmoles/L thus increasing the stimulus to ventilation (27:108). The medullary respiratory center i s also affected by changes i n the R> con-centration of cerebrospinal f l u i d (CSF). Changes in the pH of the CSF are less than those i n the blood with the addition of G0o to the inspired 1 2 a i r (30:62). The a c i d o s i s caused by increased a r t e r i a l PCO^ increases the c a p i l -l a r y permeability (6 :U7) and acts generally on vascular smooth muscle to cause r e l a x a t i o n or v a s o d i l a t i o n (22:3uO). As the pH of the blood decreases to 6.9, most blood vessels are f u l l y d i l a t e d (5). Therefore, except i n the lungs, the d i r e c t action of carbon dioxide i s to decrease p e r i p h e r a l vascular r e s i s t a n c e . As P A r, n i s increased to about k$ mm Hg. there i s a small increase AGOg i n cardiac output, however t h i s i s dependent upon the p o s i t i o n of the body. Low concentrations of COg have no e f f e c t on cardiac output when the subject i s standing, however when supine a 6% COg mixture causes a 10$ increase i n cardiac output ( 1 ) . Tenney and Lamb (37) b e l i e v e that t h i s may be due to the increased oxygen consumption. However, carbon dioxide does not profoundly a f f e c t the c i r c u l a t i o n j the changes found i n the c i r c u l a t i o n are probably induced to maintain tissue POg at a normal l e v e l during the hyperventilation (37)• Thus a r t e r i a l POg w i l l have an overriding e f f e c t c r e a t i n g stimulatory or depressant actions as the need a r i s e s . Increased tissue PCOg may a l s o have pronounced metabolic e f f e c t s . In s k e l e t a l muscle the e f f e c t s of COg are thought to depress metabolism (37:1001), while i n b r a i n t i s s u e increased PCOg r e s u l t s i n increased aerobic g l y c o l y s i s or oxygen consumption (8:330). Similar r e s u l t s are found i n other t i s s u e (37)• Tenney's shematic diagram (Figure l ) provides a good summary of response to C0 9. 13 F I G U R E 1 Schematic of Principle Responses to CO2 lactic acid production buffers HCO3 -PCO. H chemoreceptors brain s tem ACH AC.H-ase heart & bloo,d vessels vent i lat ion : / adrenal cortex iver hypothalamus | [corticosteroids epinephrine norepinephri ne autonomic nervous system 'stimulatory effects depressant effects ' a f * e r Tenney (37) Ik Chapter 3 PROCEDURES SUBJECTS Nine male subjects, aged 19 to 23 were selected from volunteer Physical Education students at the University of B r i t i s h Columbia. A l l subjects were classified healthy, x-jith no previous history of cardio-respiratory abnormalities and ranged in level of training from average to high. Subject information i s provided in Table 1. A l l subjects were familiarized with the ergometer and breathing apparatus before testing. A l l were properly informed of the nature of the experiment (Appendix 1). A Protocol for Human Experimentation was approved by the proper authorities. A l l subjects also signed a release form. EXPERIMENTAL PERIOD The treatments were administered during the period January 28 to March l£, 19lh» The treatments were administered according to a 3 x 3 Latin Square design repeated three times. Subjects were assigned numbers according to order of i n i t i a l involvement. A l l testing was performed i n the UBC Human Performance Laboratory. TRAINING OF ASSISTANTS I n i t i a l l y , two assistants were trained to help during the testing. Later, two other assistants were also trained to aid in test administra-tion. 1 5 TABLE 1 Subject Data Subject Number In i t i a l s Age (yrs.) Height (ins.) Weight (lbs.) MVOo (L/min):, 1 D.L. 19 71.7 160 3.2ii 2 P.W. 21 67.0 130 2.90 3 R.M. 22 70.0 iho 3.70 h D.L. 22 71.0 165 2.70 5 M.H. 22 72.5 185 3.25 6 M.L. 21 68.5 180 h.iil 7 J.I. 22 69.0 175 h.h3 8 G r . C . 23 72.0 170 3.10 9 J.M. 23 68.0 157 2.90 f 21.9 70.0 162 3.40 16 PRE-TESTTNG Each subject was given a submaximal t e s t o f c a r d i o r e s p i r a t o r y f i t -ness (2 :6l7) t o determine maximal oxygen uptake. An equation^ was used to determine the workload a t which each s u b j e c t would x-rork. This was to ensure t h a t each subject would be working a t the same r e l a t i v e work l e v e l (approximately 75$ of the su b j e c t ' s maximum), re g a r d l e s s of l e v e l o f f i t n e s s s Thessubject workloads ranged from 650 kgm/min t o 1200 kgm/min w h i l e steady s t a t e heart r a t e s during e x e r c i s e ranged from 138 t o 160. Subject estimated maximum oxygen uptakes ranged from 2.1 l/min to I t . l l/min. APPARATUS The data was obtained by u t i l i z a t i o n of the f o l l o w i n g equipment. p The s u b j e c t breathed through a high flow v a l v e from a metal mixing chamber. Test gases, obtained commercially-^ according t o s p e c i f i c a t i o n s , were introduced through 3/l6" (ID) diameter t u b i n g and h u m i d i f i e d and s t o r e d i n a m e t e o r o l o g i c a l b a l l o o n . The ambient a i r (Treatment C) was drawn d i r e c t l y through a three way v a l v e . E x p i r e d a i r was passed through 30 mm. diameter tubing to a f l o w -meter.^- Changes i n e l e c t r i c a l r e s i s t a n c e were r e f l e c t e d by v a r y i n g Workload - (.75 x MV0 2) 0.3 ( 2 075 ^Quinton Instruments Co. In c . , Milwaukee, Wisconsin, U.S.A. 3union Carbide, Linde D i v i s i o n . ^ J . Langham Thompson L t d . , Bushey Heath Herts, England. 17 voltages v i a a bridge c i r c u i t and voltage supply (1.5- v . ) . DC voltage was ampl i f i e d by a Sanborn 35>0-2700 C a m p l i f i e r ^ and recorded on a Sanborn 7700 recorder.^ A sample of expired a i r was analyzed f o r % COg and % 0 2 v i a a small port i n the breathing valve and 3/l6" diameter tubing by a Godart Capno-graph? and a Westinghouse Pulmonary Function Monitor.^ The gas percen-tages were recorded on a Riken Denshi 2 channel recorder.^ C a l i b r a t i o n of the e l e c t r o n i c analyzers was accomplished by the tes t gases which were v e r i f i e d on a Micro Schollander Gas Analyzer.-^ Heart rate was recorded by a three lead ECG on a Sanborn ECG Amp l i f i e r and the Sanborn 7700 recorder. The subject exercised on a Monark b i c y c l e ergometer.x-'- A schematic diagram i s presented i n Figure 2 and photographs i n Appendix 2. The dependent v a r i a b l e s were c a l c u l a t e d by a s p e c i a l l y written com-puter program.-^ (Appendix 3) at the Computer Center, U3B.C. In those instances where the i n h a l a t i o n of the tes t gas had to be terminated e a r l y due to subject discomfort, the l a s t reading was taken as the f i n a l minute. The subject was then switched to the i n h a l a t i o n of ambient a i r and the f i n a l recording made one minute a f t e r the switch. ^Hewlett-Packard, Waltham D i v i s i o n , Massachusetts, U.S.A. 6 I b i d . ^Godart/Statham NY, Holland. ^Westinghouse E l e c t r i c Corporation, Pittsburgh, Pa., U.S.A. ^Riken Denshi Ltd., Japan. 1 0 0 t t o K. Hebel S c i e n t i f i c Instruments, Rutledge, P.A., U.S.A. •^Hewlett-Packard Ltd., op c i t Written by Mr. D. Goodman, School of Ph y s i c a l Education and Recrea-t i o n , U.B.C. 1 8 FIGURE 2 S c h e m a t i c Diagram of Apparatus 1 subject 2 mix i ng chamber 3 meteor log ica l -balloon 4 tes t gas 5 v a l ve 6 35 m m tubing 7 breath ing valve 8 3/161' tub ing 9 pressure transducer 10 capnograph 1 1 C>2 monitor 12 recorder 13 3 0 m m tubing 14 f l o w m e t e r 15 ECG preamplif ier 16 r e c o r d e r 1 9 A summary of the tests that were terminated prematurely i s pre-sented i n Table 2 . Two subjects experienced nausea, dizziness and head-aches. These te s t s were terminated when the subject i n d i c a t e d t h a t he could not to l e r a t e the t e s t gas any longer. Subjects 1 and 7 were switched from the i n h a l a t i o n of Test gas B when they appeared to be laboring with h y p e r v e n t i l a t i o n . The remainder of the data was removed when values obtained were s i g n i f i c a n t l y lower than those expected at r e s t . RESEARCH DESIGN The independent v a r i a b l e s were the concentration of carbon dioxide i n the i n s p i r e d a i r during recovery. The three l e v e l s of t h i s indepen-dent variable were: Level 1 ( Treatment A ) 2 . 7 8 $ C0 2 21.$% 0 2 bal. N 2 2 ( Treatment B ) 5 . 8 0 $ C0 2 2 0 . 8 $ 0 2 b a l . N 2 3 ( Treatment C ) ambient a i r The other independent variable was the time during recovery when the recovery observations were made. The dependent v a r i a b l e s were heart r a t e , minute v e n t i l a t i o n , oxygen uptake and carbon dioxide e l i m i n a t i o n . These v a r i a b l e s were used to determine the e f f e c t s of carbon dioxide during recovery. The experimental design was a 3 (Treatment ) X 1 2 (Time) f a c t o r i a l with repeated measures on both f a c t o r s . MEASUREMENT AT EXERCISE Just p r i o r to each session, the barometric pressure and ambient TABLE 2 Scope and Reasons for Missing Data Subject Treatment Time Interval Dependent Reason for Missing Missing Variables Data 1 B 12 - 18 A l l Hyperventilation 3 B 16 - 18 A l l Subject Discomfort h B 15 - 18 A l l Subject Discomfort h G 10 - 18 vo 2 Uninterpretable Data 5 C 15 - 18 vo 2 Uninterpretable Data 7 B i i - 18 A l l Hyperventilation 7 C 10 - 12 VO 2 Uninterpretable Data 9 C 16 - 18 VO o Uninterpretable Data 2 1 temperature were recorded. The laboratory temperature ranged from 20° to 23°C. A l l subjects were at l e a s t three hours postabsorptive. Each session, the subject warmed up on the ergometer f o r 3 to 5> minutes. The subject then dismounted and had the electrodes a f f i x e d . He then remounted the ergometer and rest e d while the head harness and valve were placed into p o s i t i o n . The equipment was allowed to s t a b i -l i z e and a one minute recording made. The subject then began exe r c i s i n g at 5>0 rpm at the predetermined workload. At the conclusion of the s i x minute exercise bout, the subject was switched to the i n h a l a t i o n of the t e s t gas. The subject remained seated on the ergometer f o r a 10 minute recovery period. At the end of 10 minutes, the subject was switched back to the i n s p i r a t i o n of room a i r fo r one minute. The dependent v a r i a b l e s were recorded a t one minute i n t e r v a l s except f o r the f i r s t two minutes of recovery which were recorded at 30 second i n t e r v a l s . The expired a i r was analyzed continuously but was c a l c u l a t e d as the average of four breaths during that minute. VO2 and VCO2 were c a l c u l a t e d ^ by a computer program f o r each of the time i n t e r v a l s . 1 . F T V0 ? = T x f „ (((100 - F F - F F ) JE'02 ) - F "TOO" (52 C02 (100 - F T T ~ J" *J02) i02 1C02 VCOp ~ T x f ( F F - F j ) "TOO" C02 C02 A l l notations as i n ( 2:631 ) STATISTICAL ANALYSIS The nature of the data i s such that a multivariate a n a l y s i s of variance i s the proper procedure for s t a t i s t i c a l a n a l y s i s ; t h i s was planned on o r i g i n a l l y . However, missing data i n Treatment B ( Table 2 ) precluded the use of t h i s procedure, as MANOVA procedures are i n v a l i -dated with missing data. An analysis of variance f o r f a c t o r i a l design was performed on Treatments A and C f o r the 12 observations i n the 10 minute recovery period, r e s u l t i n g i n a 2 x 12 ANOVA with repeated measures on the second f a c t o r . Since a l l data was complete i n the f i r s t two minutes ( h observa-t i o n s ) of recovery, another ANOVA was performed on Treatments A, B and C f o r the f i r s t two minutes thus giving a 3 x 1» a n a l y s i s . In both analyse separate operations were performed on each of the dependent v a r i a b l e s . In order to show that the v e n t i l a t o r y response to i n s p i r e d COg changes during the recovery period ( 1.5, 3, 5j 1, 8, and 10 minutes ) the mean v e n t i l a t i o n and corresponding mean F-^Q^ f o r each of the three treatments at that time were determined. A l i n e a r regression by the l e a s t squares method using the observations f o r each of the three treatments was performed by the UCLA BMD:05R program. This procedure grouped the data of the 3 treatments at each time i n t e r v a l and produced a l i n e a r r e l a t i o n s h i p between the FJ-QQ and MV at each observation during the recovery p e r i o d . The slopes and intercepts were then determined and com-pared with values from the l i t e r a t u r e . The f i r s t hypothesis (that C0 2 w i l l increase the v e n t i l a t i o n ) was t e s t e d by Analyses 1 and 2 on the dependent va r i a b l e minute v e n t i l a t i o n , The second hypothesis was tested by the evaluation of the r e s u l t s of both analyses on a l l v a r i a b l e s . 23 Chapter k RESULTS AND DISCUSSION The dependent variables (heart r a t e , minute v e n t i l a t i o n , oxygen uptake and carbon dioxide elimination) f o r each subject are presented i n Appendix 3 . Mean values of each of the dependent variables are found i n Appendix%. Graphical representation of t h i s data i s found i n Figures 3 through 6. Inspection of Figure 3 indicates that heart rate increases during the exercise to a mean value o f about lh% bpm. During recovery, the heart rate decreases r a p i d l y i n the f i r s t three minutes with no s i g n i f i -cant (p.>.03>) differences between the treatments. The heart rate then l e v e l s o f f gradually i n a l l treatments s i m i l a r to the expected changes (2). V e n t i l a t i o n increases during the exercise to a l e v e l of about 60 l/min. (Figure U). V e n t i l a t i o n then declines r a p i d l y during the f i r s t two minutes of recovery with a l l treatment conditions. The ana l y s i s of variance (Table h) reveals that there i s a s i g n i f i c a n t (p<£05") treatment e f f e c t during the f i r s t two minutes of recovery. Dunnett's Test (Table 5) reveals minute v e n t i l a t i o n was s i g n i f i c a n t l y (p<Co05) greater under Treatment B than under c o n t r o l conditions a t each 30 second i n t e r v a l i n the f i r s t two minutes. The v e n t i l a t i o n under Treatment A was greater than the c o n t r o l at a l l observations, but t h i s difference was not s i g -n i f i c a n t (p>.0f>). The analysis of variance f o r the e n t i r e recovery pe r i o d under Treatments A and C shows a s i g n i f i c a n t (p^.05") treatment e f f e c t (Table k). 2k TABLE 3 ANOVA Table First Two Minutes of Recovery-Minute Ventilation Source df SS F F at p • Treatment 2 12778.9 2lu52 3.63 Linear 1 2898.5 11.12 4.49 Quadratic 1 9880.U 286.29 h.k9 Trials 3 4260.9 41.15 3.01 Linear 1 U232.9 122.65 4.26 Quadratic 1 9.9 0.28 4.26 Cubic 1 18.1 0.52 4.26 Heart Rate Treatment 2 575.6 2.11 3.63 Linear 1 U60.1 3.37 4.49 Quadratic 1 115.5 O.84 4.49 Trials 3 11932.7 142.58 3.01 Linear 1 11334.5 406.29 4.26 Quadratic 1 597.3 21.41 l i . 26 Cubic 1 .9 0.32 4.26 Oxygen Uptake Treatment 2 3.6 6.02 3.63 Linear 1 3.2 11.42 4.49 Quadratic 1 0.3 1.0U 4.49 Trials 3 21.8 66.70 3.01 Linear 1 18.9 173.80 4.26 Quadratic 1. 2.7 24.78 4.26 Cubic 1 .1 1.52 4.26 Carbon Dioxide Elimination Treatment 2 3.6 30.38 3.63 Linear 1 3.2 4.81 4.U9 Quadratic 1 0.3 0.55 4.49 Trials 3 21.8 35.53 3.01 Linear 1 18.9 102.86 4.26 Quadratic 1 2.7 3.71 4.26 Cubic 1 0.1 0.01 4.26 .05 25 TABLE k ANOVA Table Treatments A and C Minute Ventilation Source df SS F F at p = .05 Treatment 1 61*77.1 3U.61 5.32 Trials 11 1837.6 37.52 1.99 Oxygen Uptake Treatment 1 5.U 9.15 5.32 Trials 11 31.9 53.77 1.99 Heart Rate Treatment 1 682.5 3.79 5.32 Trials 11 33859.5 117.5U 1.99 Carbon Dioxide Elimination Treatment 1 0.6 17.31 5.32 Trials 11 30.3 1*6.79 1.99 2 6 Table 5 Mean Differences for Dunnett's Test Variable Time A-C B-C Dunnett's Critical Difference at p».05 Minute 0:30 12.03 21.35 15.66 Ventilation 1:00 11.98 26.59 15.66 1:30 13.66 31.28 15.66 2:00 11.35 27.32 15.66 Oxygen 0:30 0.62 0.08 o .5 l Uptake 1:00 0.39 0.06 0.51 1:30 0.33 O.lit 0.51 2:00 0.26 0.08 o .5 l Carbon 0:30 0.35 1.14 o.$5 Dioxide 1:00 0.2k 0.79 0.55 Elimination 1:30 0.15 0.58 0.35 2:00 O.lli 0.53 0.35 27 Oxygen uptake (Figure 6) increases to a l e v e l of about 2 l/min. during the exercise period. Treatment C shows a r a p i d decrease i n oxygen uptake i n the f i r s t 90 seconds of recovery and s t a b i l i z e s atcabout 0.3 l/min. Treatment A increases i n i t i a l l y with recovery about 0.2 l/min. and then declines exponentially to l e v e l at O.u l/min. Treatment B declines exponentially to 0.3 l/min. An inspection of Table k reveals a s i g n i f i c a n t (p-^05) treatment e f f e c t i n the f i r s t two minutes. The only s i g n i f i c a n t (p-^05) d i f f e r e n c e i s found i n the f i r s t 30 seconds between Treatment A and the c o n t r o l (Table 5 ) . Treatments A and B have l a r g e r oxygen uptakes than the c o n t r o l condition, but these differences are not s i g n i f i c a n t . The analysis of variance f o r the e n t i r e recovery p e r i o d shows a s i g n i f i c a n t (p<^.05) treatment e f f e c t . Carbon dioxide e l i m i n a t i o n increases to a l e v e l of about 2.5 l/min. during exercise. Treatments A and C decline exponentially to a l e v e l of about 0.3 l/min. Carbon dioxide e l i m i n a t i o n under Treatment B decreases to a greater extent and plateaus at 0.1 l/min. There i s a s i g n i f i c a n t (p<»05) treatment e f f e c t between the three treatments during the f i r s t two minutes of recovery. Treatment B has a s i g n i f i c a n t l y greater carbon diox-ide e l i m i n a t i o n than the c o n t r o l f o r each observation i n the f i r s t two minutes. The carbon dioxide e l i m i n a t i o n under Treatment A i s s i g n i f i c a n t l y greater than the c o n t r o l f o r the f i r s t minute only. Four subjects had a net carbon dioxide uptake i n at l e a s t one obser-vatio n under Treatment B. This accounts f o r the low mean l e v e l of carbon dioxide e l i m i n a t i o n . In order to determine the v e n t i l a t o r y response to i n s p i r e d COg at various stages i n the recovery, the v e n t i l a t i o n and the corresponding 2 8 F IGURE 3 Mean H e a r t Rate Va lues 180 r 160 140 HR 120 (bts/min) 100 S O +1 + o t reatment A + B x C o + + J 1 [ — ( I i i I i I I l i I I ' I I j I 5 10 15 20 TIM E (mi n.) 2 9 F I G U R E 4 Mean V e n t i l a t i o n Values 6 0 r 50 o o x 4 0 V r + 30 ( l/min) 20 treatment + + o - + o A • B * C ° 10 0 o o I i I I 1 1 I I: I — i | I i i i i I 10 15 2 0 T I M E (mi n.) 30 F I G U R E 5 M e a n V C O „ Values 3-0 r 2.5 o x + v c o 2.0 2 1,5 o + (l/min) 1.0 0.5 f-j i f i o + o X X o + treatment A + B « C o X * * X J I I I t I I I ' t J L 10 15 20 TIME (min) 3 1 3.0, 2.5 2,0 VO. F I G U R E 6 Mean VO-2 V a l u e s + + 1 ,5-( l/min) 1.0 X-c t r e a t m e nt A + B * C o 0.5 + + o + X O + + e ! o J _ l L _ J t I I L J 1 I L 10 15 20 TIME (mi n.) 3 2 inspired COg were determined at various stages in the recovery. The times used were . . 5 , 1.5, 3 , 5, 7,' 8 and 10 minutes of recovery. A linear regression by the least squares method using the observations for each of the three treatments was performed by the UCLA BMD;05R program processed on an IBM 370-f5 Computer located at the UBC Computing Center. The results of the procedure are indicated i n Figure 7. The slopes and inter-cepts are given i n Table 6. I n i t i a l l y , the slope of the MV/PCOg rela-tionship increases, but after 2 minutes of recovery, decreases. The intercept i s quite low i n i t i a l l y (about 5 mm Hg.) but then increases to 21 mm Hg. with no change in the intercept after 3 minutes of recovery. The subject workloads ranged from 650 kgm/min to 1200 kgm/min while steady state heart rates ranged from 138 to 160. Subject estimated maxi-mum oxygen uptakes ranged from 2.1 l/min to h l/min. Mean steady state oxygen uptake was approximately 2 l/min. The ventilation developed as a response to this workload was about 60 l/min, DISCUSSION The steady state exercise heart rates are in the range expected from a workload designed to e l i c i t work of about 75$ of the subject's maximum. The mean plateau value of oxygen uptake was within range of the expected value. The procedure employed for obtaining the same relative exercise stress i n a sample with a wide range of fitness levels would appear to be valid. This procedure may be appropriate for use i n studies where level of fitness w i l l alter the response to a particular testing situation. The 7g developed as a response to the particular workload would appear to be low i n view of the heart rate of l l i 5 beats per minute. 35 FIGURE 7 V E / ' = ' E C O Relationship During Recovery i J 1 1 I L 2 0 40 6 0 VENTILATION ( l/min) 34 T a b l e 6 • S l o p e s a n d I n t e r c e p t s o f ^M^GO R e l a t i o n s h i p * 2 T i m e S c o p e I n t e r c e p t :30 1 . 4 2 m m H g 1:30 1.8 15.9 m m H g 3:00 1.9 21.4 m m H g 5:00 1.5 21.4 m m H g 7:00 1.2 21.4 m m H g 8:00 1.2 21.4 m m H g 10:00 1.1 21.4 m m H g 3 5 Astrand (2) presents fi g u r e s which show a v e n t i l a t i o n range of 80 - 100 l/min. at t h i s workload. Since the e r r o r i s not random, the v e n t i l a t i o n c a l i b r a t i n g f a c t o r may be i n e r r o r . In s p ite of the large differences i n v e n t i l a t i o n between the e x p e r i -mental treatments and the c o n t r o l , the difference i n oxygen uptake i s not s i g n i f i c a n t . Since oxygen uptake i s the product of v e n t i l a t i o n and per-cent oxygen extracted, there must be a difference i n oxygen e x t r a c t i o n . Once the percent oxygen extracted has reached a steady state d u r i n g recovery, nearly twice as much oxygen (2% vs. h%) i s extracted under con-t r o l conditions as under Treatment A. The percent oxygen extracted under Treatment B i s only about 1.5$. Recovery from exercise of the same r e l a t i v e stress should require the repayment of a s i m i l a r oxygen debt. Although the difference i s not s i g n i f i c a n t , Treatment A does increase oxygen uptake through the recovery period (Figure 5 ) . This difference i s approximately 0.2 l/min. a t the end of recovery. This difference would appear to be p h y s i o l o g i c a l l y s i g n i f i c a n t since the oxygen uptake at r e s t i s normally 0.25 l/min. (2:28U). The wide subject v a r i a t i o n i n the response to COg noted here and i n other studies (11, 26) i s probably the cause of the high c r i t i c a l difference (0.515 l/min.) required f o r s i g -n i f i c a n c e i n Dunnett's Test. Thus, the v e n t i l a t i o n produced as a r e s u l t of Treatment A appears s u f f i c i e n t to increase the oxygen uptake despite the decreased percent oxygen extracted. I f v e n t i l a t i o n was the only f a c t o r involved i n increasing oxygen uptake, Treatment B should produce the greatest changes i n oxygen uptake. There i s no tested difference i n oxygen uptake betweennTreatment B and the 3 6 group (Figure 5). Inhalation of 5.8$ CO i n a i r at r e s t w i l l increase P_, to about 2 AC02 1*8 mm Hg. (31). The PCOg of mixed venous blood at r e s t i s normally 1x6 mm Hg. (2). Thus i n s p i r a t i o n of 5.8$ COg w i l l elevate the PCOg of pulmonary blood and cause a COg uptake (10:228). A f t e r exercise the PCOg of mixed venous blood w i l l be close to the l e v e l s found at r e s t (2:228). This increase i n a r t e r i a l PCOg from 1*0 mm Hg. (2:226) to 1*8 mm Hg. i s respon-s i b l e f o r the large increase i n v e n t i l a t i o n , e s p e c i a l l y since the p e r i -pheral chemoreceptors are stimulated by l e v e l s of PCOg above 1*8 mm Hg. (32). The e f f e c t of t h i s s h i f t i s profound. The net e f f e c t w i l l be to i n h i b i t the absorption of oxygen from the a l v e o l a r a i r . The increase i n blood a c i d i t y w i l l cause changes i n the oxygen-hemoglobin d i s s o c i a t i o n curve (10) to decrease the percentage of oxygen saturation. This w i l l i n turn create hypoxic conditions which f u r t h e r stimulate the v e n t i l a t i o n . Thus despite the rather large differences i n v e n t i l a t i o n between the co n t r o l and Treatment B, the difference i n oxygen uptake i s minimal. The r e l a t i o n s h i p between alveolar COg and v e n t i l a t i o n has been thoroughly investigated. Clark and Godfrey (7) asserted that exercise decreased the slope of th i s r e l a t i o n s h i p , but there appears to be no e f f e c t upon the i n t e r c e p t (25). The slopes and intercepts (Figure 7) obtained i n t h i s study indicate that the in t e r c e p t i s decreased at the onset of recovery and gradually increases to a steady state value. The slope of the r e l a t i o n s h i p increases i n the f i r s t three minutes o f reco-very and then decreases. Neilsen and Smith (29) noted that the ^ .intercept was 31.5 mm Hg. at r e s t . The differ e n c e between the value and the r e s u l t s 37 i n the present study i s due to the use of mixed expired a i r rather than true a l v e o l a r a i r . In t h i s study, the apparatus was such that an analysis of a l v e o l a r a i r was impossible to a s c e r t a i n . The length of the tubing and the number of valves caused considerable mixing within the expired and i n s p i r e d samples. In a d d i t i o n , the number of observations used to obtain the r e l a t i o n s h i p between minute v e n t i l a t i o n and P A p n i s small (3), thus the 'threshold value of CO^' i s d i f f i c u l t to a s c e r t a i n . Comroe (10) dismisses the concept of 'threshold value of C0 2' as a c a l c u l a t i o n to "make some r e s p i r a t o r y p h y s i o l o g i s t s happy" (10:68). I f the PCOg of the cerebrospinal f l u i d i s a stronger stimulus to r e s p i r a t i o n than a r t e r i a l PCO^, these c a l c u l a t i o n s are meaningless, since some time i s required f o r the former to r i s e i n response to an elevated a r t e r i a l P C O 2 . In spite of the differences i n the methodology used to obtain the r e l a t i o n s h i p s , i t i s i n t e r e s t i n g to note the changes i n th i s r e l a t i o n s h i p with the process of recovery observed i n t h i s study. A f t e r f i v e minutes of recovery, there i s l i t t l e change i n the r e l a t i o n s h i p . This would sug-gest that the recovery processes which influence the v e n t i l a t o r y response to i n s p i r e d 60 2 have s t a b i l i z e d . The response to C0 2 i n i t i a l l y ( f i r s t 30 seconds of recovery) i s s i m i l a r to steady state response i n terms of the changes i n v e n t i l a t i o n per mm Hg. i n P^ QQ . This response i s displaced along the v e n t i l a t i o n axis so that the response occurs at a much higher v e n t i l a t i o n i n i t i a l l y . As the recovery proceeds, the i n t e r c e p t increases (or the v e n t i l a t o r y response begins at a lower v e n t i l a t i o n ) . The v e n t i l a t o r y response how-ever, increases so that there i s a much greater change i n v e n t i l a t i o n per mm Hg. increase i n P . F AC0 2 38 Comroe suggests that the perip h e r a l chemoreceptors play an impor-tant r o l e i n determining the v e n t i l a t o r y response to carbon dioxide only when the c e n t r a l chemoreceptors are depressed or when the action of the pe r i p h e r a l chemoreceptors i s potentiated by an hypoxic condition (10:63). The peak response to i n s p i r e d COg occurs a f t e r the PCOg of the cerebrospinal f l u i d has matched that of a r t e r i a l PCO2. This response takes several minutes, thus o f f e r i n g one explanation f o r the delay i n obtaining the peak response r a t e . There i s however, a r e f l e x response to r a p i d large increases i n i n s p i r e d COg mediated through the pe r i p h e r a l chemoreceptors. This r e f l e x i s demonstrated i n the increase i n v e n t i l a t i o n i n the f i r s t 30 seconds of recovery with administration of $.Q0% COg. Astrand (2) presents a graph which demonstrates that blood l a c t a t e reaches peak values some two to four minutes a f t e r the cessation of exercise. Since blood l a c t a t e i s one of the determinants of the response to COg (10:62) the s l i g h t delay i n obtaining the maximum response to the i n s p i r e d CO2 i s not unexpected. These findings suggest that due to a v a r i e t y of f a c t o r s , the maxi-mum r e s p i r a t o r y response to i n s p i r e d CO2 occurs 2 - h minutes a f t e r administration of the gas. There i s however, an immediate r e f l e x response to large increases i n i n s p i r e d COg. These findings are substantiated i n t h i s study. Recovery i s an estimate of the return of the body functions to pre-exercise l e v e l s . However, not a l l measures of body functions return to pre-exercise l e v e l s at the same rate or manner. Perhaps the best e s t i -mate of recovery i s a subjective one based upon i n t e r p r e t a t i o n of a l l a v a i l a b l e data. 39 Chapter 5 SUMMARY AND CONCLUSIONS Nine male Ph y s i c a l Education students, aged 19 to 23 years, were selected to t e s t the following hypothesis: 1 Addition of COg to the i n s p i r e d a i r during recovery causes s i g -n i f i c a n t increases i n v e n t i l a t i o n above c o n t r o l conditions. 2 Recovery from submaximal exercise i s enhanced by the addi t i o n of COg to the i n s p i r e d a i r during recovery as determined by the dependent v a r i a b l e s heart r a t e , minute v e n t i l a t i o n , oxygen uptake and carbon dioxide e l i m i n a t i o n . The subjects were administered two experimental (2.78$ COg i n room a i r and 5.80$ COg i n room a i r ) and one c o n t r o l (room a i r ) treatment. Assignment of treatment order was provided by a L a t i n Square Design. The experimental design was a 3 (Treatment) by 12 (Time) f a c t o r i a l . Inspired a i r f o r the experimental treatments was supplied by pre-analyzed standard tanks. Heart rate was determined by a three lead ECG and a Sanborn Amplifier and Recorder. Expired volume was determined by a Langham Thompson flowmeter and the Sanborn Amplifier and Recorder. Analysis of the expired a i r was provided by a Godart Capnograph and Westinghouse Pulmonary Function Monitor and connected to a Riken Denshi Recorder. A l l t e s t i n g was performed i n the UBC Exercise Physiology Laboratory. The subjects exercised on a Monark b i c y c l e ergometer at a workload predetermined to e l i c i t 75$ of his maximal oxygen uptake. A l l subjects exercised at 50 rpm f o r s i x minutes. The responses during the recovery period were determined at one minute intervals with 3 0 second intervals in the first two minutes of recovery. Dependent variables were calculated by a specially written computer program-*- at the UBC Computing Center. The program UBC Simcort was used for in i t i a l data inspection. The dependent variables were subjected to a one way analysis of variance and significant F ratios evaluated using Dunnett's Test. The results indicate that ventilation increased significantly ( p ^ . 0 5 ) above control values with the addition of 5 . 8 0 $ COg to room air . Addi-tion of 2.79% COg to room air also increases the ventilation during the recovery period, but not significantly ( p ^ . 0 5 ) . . Despite the rather large increase in ventilation with the 'addition of S> .80$ COg to the inspired air, there was no significant (p^.05-) increase in oxygen uptake. The addition of 2.79% COg to the inspired air did however, increase oxygen uptake in the f irst 3 0 seconds of recovery. The addition of $.80$ to the inspired air significantly ( p < . 0 £ ) reduces carbon dioxide elimination. In 1| subjects, the effect produced a carbon dioxide uptake at certain time intervals. This was postulated to be due to the elevation of alveolar PCOg above that of venous PCOg. The addition of 2.79$ COg to the inspired air caused a significant reduction of carbon dioxide.elimination only in the f irst minute of recovery. CONCLUSIONS 1) The addition of 5 > . 8 $ carbon dioxide to the inspired air during ^Program written by Mr. D. Goodman, School of Physical Education and Recreation, U.B.C. the recovery phase a f t e r submaximal exercise causes a s i g n i f i c a n t increase i n the v e n t i l a t i o n over control values. 2) The addi t i o n of 5.8$ or 2.79$ COg to the i n s p i r e d a i r during recovery has no e f f e c t upon heart r a t e . 3) There i s a s i g n i f i c a n t (p<\05) increase i n oxygen uptake during the f i r s t 30 seconds of recovery with the addition of 2.79$ CCv, to the in s p i r e d a i r . It) The addition of 5.8$ GGg causes a s i g n i f i c a n t (p<.05) decrease i n COg elimination during the f i r s t 30 seconds of recovery. RECOMMENDATIONS TO FURTHER RESEARCH In order to further investigate the e f f e c t s of carbon dioxide upon recovery, a more encompassing approach should be used. There are several avenues of approach: 1 ) Varying the concentration of carbon dioxide i n the i n s p i r e d a i r . 2) Concomitantly varying the concentration of oxygen i n the i n s p i r e d a i r . 3) Varying the time and length of administration of carbon dioxide and/or oxygen. In a d d i t i o n , future i n v e s t i g a t i o n s should include blood gas analysis to a i d i n determining the mechanisms of the e f f e c t s of carbon dioxide upon recovery. REFERENCES CITED 1. Asmussen, E. "CO2 Breathing and Output of the Heart," Acta Physiologica Skand., VI (19k3), 176. " 2. Astrand, P.O. and K. Rodahl, Textbook of Work Physiology. New York: McGraw-Hill, 1970. 3. Bannister, R.G. et a l , "The Carbon Dioxide Stimulus to Breathing i n Severe Exercise," J . of Physiology, London, CXXV (1951*), 90-117. U. B a r c r o f t , J . and R. Margaria, "Some E f f e c t s of Carbonic A c i d on the Character of Human Respiration," J . of Physiology, LXXII (1931), 175-185. . 5. Brickner, E.W. et a l , "Mesenteric Blood Flow as Influenced by Progressive Hypercapnia," Amer. J . of Physiology, CLXXXIV (1956), 275-281. 6. Chambers, R. and B.W. Zweifach, " I n t r a c e l l u l a r Cement and C a p i l l a r y Per-meability," P h y s i o l o g i c a l Revue XXVII (19U7), it36-i+63» 7. Clark, T.J. and S. Godfrey, "The Effec't of COg on V e n t i l a t i o n and Breath Holding During Exercise.and While Breathxng Through an Added Resis-tance," J . of Physiology, London, CCIV (1969), $51-5^6. 8. Craig, F.N., "The E f f e c t of Carbon Dioxide Tension on the Metabolism of Cerebral Cortex and Medulla Oblongata," J . of Gen. Physiology, XXVII (19liU), 325-338. 9. Craig, F.N. et a l , "Exhausting Work Limited by External Resistance and Inhalation of Carbon Dioxide," J . of Applied Physiology, XXIX (1970), 8U7-851. 10. Comroe, J.H., Physiology of Respiration. Chicago: Yearbook Medical Publishers, 1970. 11. Dripps, R.D. and J.H. Comroe, "The Respiratory and C i r c u l a t o r y Response of Normal Man to Inhalation of 7.6 and 10.1; Percent COg With a Comparison of the Maximum V e n t i l a t i o n Produced by Severe Muscular Exercise, Inhalation of COg and Maximal Voluntary Hyperventilation," Amer. J . of Physiology, CXLLX (I9u7), U3. 12. Dutton, R.E. et a l , " V e n t i l a t o r y Response to Intermittent Inspired Car-bon Dioxide," J . of Applied Physiology, XIX (1963), 931-936. 13. Edelman, N.H. et a l , " V e n t i l a t o r y Responses to Transient Hypoxia and Hypercapnia i n Man," Respiration Physiology, XVII (1973), 302-315. l U . Farber, J.P. and G.N. B e d e l l , "Responsiveness of Breathing Control Centers to Carbon Dioxide and Neurogenic S t i m u l i , " Respiration Physiology, 43 XIX (1973), 88-96. 15". Forster, R.E., "Diffusion of Gases," i n W.O. Fenn and H. Rahn (eds.), Handbook of Physiology, sec. 3, Respiration, Vol. 11, p. 839, Washington: American Physiological Society, 196U. 16. Gabel, R.S. et a l , "Vital Capacity Breaths of $% or \ % C02 i n Np of 0 2 to Test Carotid.Chemosensitivity," Respiration Physiology, XVII (1972), 195-208. 17. Gray, J.S., Pulmonary Ventilation and Its Physiological Regulation. Springfield: CC. Thomas, 1950. . 18. Grodins, F.S., "Analysis of Factors Concerned i n Regulation of Breathing i n Exercise," Physiological Revue, XXX (1950), 220-239. 19. Haldane, J.S. and M. Poulton, "The Effects of Want of Oxygen on Respira-tion," J. of Physiology, XXXVII (1908), 37. 20. Haldane, J.S. and J.G. Priestly, "The Regulation of the Lung Ventila-tion," J. of Physiology, XXXII (1905), 225-266. 21. Hornbien, T.F. and A. Roos, "Specificity of H. Ion Concentration as a Carotid Chemoreceptor Stimulus," J. of Applied Physiology, XVIII (1963), 580-58U. . 22. Itami, S., "The Action of Carbon Dioxide on the Vascular System," J. of Physiology, London, XLV (1912) 338-344. 23. Joels, N. and Ne i l , E., "The Influence of Anoxia and Hypercapnia, Separately and in Combination on Chemoreceptor Impulse Discharge," J. of Physiology, CLV (1961), 2u. Leigh, J., "Dependence of Peripheral Chemoreflex Response to C0p i n Man on P02," J. of Physiology, London, CCXXV (1972), 63P-65P. 25. Lloy-d, B.B. et a l , "The Relation Between Alveolar Oxygen Pressure and the Respiratory Response to C0p in Man," Quart. J. of Exper. Physio- logy, XLIII (1958), 43. 26. Lopez-Majano, V., "Correlation Between Predicted and Measured C02 Ten-sion," Respiration, XXVIII (1971), 31-35. 27. Masoro, E.J. and P.D. Stegel, Acid-Base Regulation: Its Physiology and Pathophysiology. Philadelphia: W.B. Saunders Co., 1971. 28. Meischer, R., Arch, f. Physiolgie 1885, 355. 29. Neilsen, M. and H. Smith, "Studies on the Regulation of Respiration i n Acute Hypoxia," Acta Physiologica Skand. XXIV (1952), 293. 30. Paul, H.G. et a l , "Chronic Derangement of Cerebrospinal Fluid Acid-Base Components i n Man," J. of Applied Physiology XVII (1962), 993-99&* 31. Reynolds, W.J., "Dynamic Ventilatory Response to Hypercapnia and Hypoxia i n the Human." Unpublished.Doctor's dissertation, University of Mississippi, 1972. 32. Riedstra, J.W., "Influence of Central and Peripheral PC02 (pH) on the Ventilatory Response to Hypoxic Chemoreceptor Stimulation," Acta  Physiologica Pharmacologica Neerlandica, XII ( 1 9 6 3 ) , I4.O7. 33. Riley, P. et a l , "Pulmonary Arterial PCO? and Ventilation i n Man," Federation Proceedings, XX (1961), n31» 3u. Roughton, F.J.W., "Transport of Oxygen and Carbon Dioxide," i n W.O. Fenn and H. Rahn (Eds.), Handbook of Physiology, sec. 3, Respiration, . vol. 11, p. 767, Washington: American Physiological Society, 1961a. 3 5 . Schaefer, K.E. et a l , "Respiratory Acclimatization to Carbon Dioxide," J. of Applied Physiology, XVIII (1963), 1071-1078. 36. Tenney, S.M., "Ventilatory Response to Carbon Dioxide i n Pulmonary Emphysema," J. of Applied Physiology, VI (19510, ll77. 37. Tenney, S.M. and T.W. Lamb, "Physiological Consequences of Hypoventi-lation and Hyperventilation" i n W.O. Fenn and H. Rahn (eds.), Handbook of Physiology, sec. 3, Respiration, Vol. 11, p. 9 7 9 , Washington: American Physiological Society, 1 9 6 U . Appendix l SUBJECT INFORMATION AND INSTRUCTIONS While the exact nature of t h i s study cannot be revealed t o you a t t h i s time, I am required to inform you of some pertinent d e t a i l s . You t r i l l be asked i n i t i a l l y to perform an estimation of maximal oxygen intake using procedures o u t l i n e d by Astrand. You 1*111 then be f a m i l i a r i z e d with the re s t of the equipment to be used. This equipment w i l l be used to determine your responses (heart r a t e , v e n t i l a t o r y rate and volume) to a pre set exercise l o a d . This t e s t i n g session w i l l c o n s i s t of a warm-up, r e s t , 6 minute exercise period and a 10 minute recovery period. There w i l l be 3 sessions. None of the information thus obtained w i l l be i d e n t i f i e d as belong-ing to you, but w i l l be pooled with r e s u l t s obtained from other subjects. I, the undersigned, have read and understand the above information. NAME DATE k9 Appendix ~5 COMPUTER PROGRAM FOR TRANSFORMATION OF RAW DATA 1 C 2 C PROGRAM TO READ IN JIM'S DATA AND TRANSFORM IT 3 C k DIMENSION X(l8) 5 WRITE (6,la) 5.25 DO 10 1-1,1000 6 READ(5,H, END-99) (X ( j ) , J-1,13) 7 X ( l l i ) = x(U)*x(5>x(6) 8 X(l5) = ( 1 0 O . - X ( l l ) r X ( 1 2 ) ) * ( X ( 7 ) / ( 1 0 O . - X ( 7 ) - X ( 8 ) ) ) - X ( l l ) 8.25 Z=X(7)-X(9) 9 x(i6) = (x( iu)/ioo.)*x(i5) 10 X (17) = (X(12)-X(8))*(X(lU)AOO.) 10.25 IF (Z .LE. .01) GO TO 88 11 X(18) = (X(10)-x(8))/(x(7)-X(9)) 11.25 GO TO 77 11.5 88 X(18) = 0.0 12 77 WRITE(6.12) (X(J), J=l,l8) 13 WRITE(7,15) X(13), X(lU), X(l6), X(17), X(18) lU WRITE(8,12) (X(J), J=1,18) 15 10 CONTINUE 16 11 FORMAT(F1.0,2F2.0,lX,2F6.2,F6.0,6F6.1,F6.0) 17 15 FORMAT(1 >,5F8.3) 17.25 12 FORMAT(>,18F7.2) 18 Ik F0RMAT(!1',2X'SUBJ TREAT TIME AREA CORFAC, 19 91X,'FREQ. INSP02 INSC02 EXPOS . EXP002 ET02 ETC02', 20 92X,!HR EXVOL TR02 V02 VC02 PC') 21 99 STOP 22 END 23 $DATA 2k ISTOP 25 $END 5 0 APPENDIX , 4 DEPENDENT VARIABLES DURING RECOVERY SUBJECT TR. TIME HR :30 132 1:00 120 1:30 108 2:00 100 3:00 96 4:00 96 5:00 96 6:00 92 7:00 92 8:00 92 9:00 96 10:00 9k :30 iko 1:00 118 1:30 iiU 2:00 108 3:00 108 :30 136 1:00 104 1:30 104 2:00 10k 3:00 102 4:00 100 5:00 98 6:00 92 7:00 9k 8:00 96 9:00 94 10:00 94 MV V0 2 vco2 U8.070 2.265 1.154 43.263 1.471 1.082 39.330 0.949 0.7U7 28.230 0.472 0.508 33.212 0.811 0.598 32.119 O.803 0.514 26.744 0.600 0.428 22.942 0.485 0.367 11.624 0.239 0.209 6.817 O.I4O 0.123 14.202 0.296 O.24I 12.236 0.217 0.232 97.538 2.U39 0.195 73.U16 0.918 0.073 71.318 0.709 0.071 80.758 O.803 O.081 71.318 0.729 0.010 32.100 1.539 1.701 27.392 0.91U 1.260 17.976 0.595 0.845 I4.466 0.479 0.680 11.984 0.455 0.515 13.696 0.527 0.562 9.587 0.U07 0.431 9.587 0.330 0.403 8.218 0.362 0.362 6.677 0.253 0.287 7.233 0.273 0.318 6.677 0.255 0.280 51 SUBJECT TR. TIME HR :30 136 1:00 128 1:30 116 2:00 116 3:00 108 4:00 96 5:00 ioU 6:00 100 7:00 96 8:00 96 9:00 98 10:00 100 :30 11*0 1:00 132 1:30 128 2:0 0 130 3:00 128 it: 00 12U 5:00 116 6:00 94 7:00 112 8:00 116 9:00 9k 10:00 98 :30 lUo 1:00 116 1:30 112 2:00 108 3:00 116 4:00 100 5:00 92 6:00 92 7:00 104 8:00 88 9:00 92 10:00 90 MV vo2 vco2 5l.i;80 2.206 1.544 38.739 l.itll 1.162 25.740 O.768 0.669 25.740 0.724 0.592 23.166 0.586 0.556 20.592 0.600 0.494 23.166 0.695 0.486 20.592 0.538 0.432 16.731 0.437 0.351 13.814 0.379 0.290 14.801 0.319 0.281 13.728 0.349 0.261 40.296 1.207 O.846 35.040 0.516 0.561 1|2.0U8 0.290 0.505 28.382 0.195 o.3ia 42.O48 0.325 0.378 26.017 0.194 0.260 28.908 0.186 0.260 22.338 O.I44 0.201 23.652 0.122 0.213 26.017 0.108 0.208 23.652 0.092 0.213 23.652 0.092 0.213 36.372 1.060 1.110 22.516 .670 1.040 22.516 0.670 0.750 20.264 0.700 0.940 25.980 1.280 0.940 23.382 1.290 0.890 13.856 0.790 0.610 7.794 O.38O 0.360 6.495 0.370 0.260 12.990 0.711 0.590 6.495 0.350 0.290 12.990 0.350 0.560 5 2 SUBJECT TR. TIME HR 130, 101* 1:00 92 1:30 80 2:00 80 3:00 78 1*:00 Ik 5:00 72 6:00 72 7:00 66 8:00 68 9:00 68 10:00 72 :30 112 1:00 100 1:30 9k 2:Q0 88 3:00 81* 1*:00 81* 5:00 82 6:00 81* 7:00 82 :30 116 1:00 10l* 1:30 Six 2:00 81* 3:00 76 1*:00 72 5:00 76 6:00 69 7:00 7U 8:00 78 9:00 76 10:00 68 MV vo2 7C02 1*7.739 1.936 1.381* 39.k$S 1.020 0.868 1*7.821* 0.91*3 l.OOi* 30.71*1* 0.905 0.707 30.7U* 0.71*2 0.581* 23.570 0.623 0.1*71 20.621* 0.619 0.1*33 19.780 0.1*90 0.356 20.1*96 0.1*60 0.328 18.788 0.1*53 0.357 21.350 0.1*79 0.31*2 15.030 0.1*01 0.286 65.208 0.192 1.109 71QOl*2 0.158 1.066 70.1*85 0.1*97 1.128 38.610 0.332 0.579 1*8.01*8 0.229 0.721 39.61*0 0.189 0.595 1*0.151* 0.21*3 0.602 33.1*62 0.203 0.502 36.808 0.223 0.552 27.019 0.572 1.321* 29.877 0.181 1.315 25.893 0.185 1.036 20.781* 0.227 0.831 16.627 O.198 0.682 17.320 0.172 0.675 16.627 0.203 0.665 11.258 0.185 0.1*81* 11*. 51*9 0.210 0.597 10.132 0.215 0.1*1*6 10.132 0.205 0.1*36 10.695 0.233 0.1*1*9 5 3 SUBJECT TR. TIME HR :30 136 1:00 12k 1:30 112 2:00 108 3:00 104 it: 00 100 5:00 104 6:00 100 7:00 96 8:00 98 9:00 96 10:00 98 :30 124 1:00 116 1:30 106 2:00 104 3:00 98 4:00 98 5:00 9k 6:00 96 :30 124 1:90 120 2:3'0 116 2:00 102 3:00 104 4:00 100 5:00 112 6:00 10k 7:00 102 8:00 100 9:00 100 10:00 98 MV vo2 vco2 46.374 1.841 1.484 34.640 0.950 1.039 24.248 0.599 0.630 19.485 0.443 0.468 18.186 0.i4l0 0.364 20.784 O.U36 0.436 16.887 0.338 0.338 14.635 0.255 0.293 16.887 0.343 0.321 15.761 0.295 0.315 10.761 0.320 0.299 12.990 0.247 0.247 38.192 I . 2J4 . 6 0.611 36.U56 0.660 0.474 4I.664 0.493 0.333 38.192 0.365 0.267 38.192 0.376 0.229 38.192 0.348 0.153 31.248 0.276 0.156 32.810 0.299 0.131 34.320 2.130 1.956 18.447 0.865 1.051 9.438 0.328 0.519 8.580 0.205 0.455 7.500 0.0 o.koo .6.692 0.0 0.335 6.700 0.0 0.340 6.864 0.0 0.343 5.148 0.0 0.257 5.148 0.0 0.257 U.290 0.0 0.21a 4.290 0.0 0.21a SUBJECT TR. TIME HR 5 A :30 120 1:00 116 1:30 102; 2:00 92 3:00 100 1*:00 90 5:00 88 6:00 92 7:00 92 8:00 92 9:00 92 10:00 89 :30 128 1:00 121* 1:30 120 2:00 112 3:00 108 4:00 112 5:00 108 6:00 10l* 7:00 10l* 8:00 106 9:00 101* 10:00 101* :30 136 1:00 12l* 1:30 116 2:00 112 3:00 112 U i O O 108 5:00 112 6:00 108 7:00 101* 8:00 100 9:00 100 10:00 96 MV vo2 vco2 51.000 2.578 1.071 1*6.920 1.266 0.81*5 33.660 0.761* 0.505 30.600 0.9kh o .55i 25.500 0.791* 0.1*33 30.600 0.953 0.520 25.500 0.859 0.1*33 26.775 0.875 0.1*28 18.700 0.555 0.21*3 2l*.310 0.802 0.365 2i*.310 0.857 0.389 9.91*5 0.312 0.159 55.078 1.861* 0.386 56.290 1.032 0.169 56.290 0.632 0.056 2j2.088 0.1*72 0.01*2 60.620 0.775 0.000 57.372 0.61*1* 0.057 51.960 0.1*79 -0.052 32.865 0.318 0.066 31*. 2 9l* 0.297 0.031* 34.291* 0.351 0.000 30.007 0.260 0.030 31.176 0.327 -0.631 1*8.30i* l . i oa 2.171* 13.020 0.283 0.51*7 13.020 0.211 0.573 11.978 0.000 0.1*91 13.541 0.000 0.51*2 16.666 0.271 0.650 8.680 0.000 0.321 9.982 0.197 0.399 8.680 0.000 0.31*7 9.982 0.000 0.1*09 7.812 0.000 0.320 7.812 0.000 0.312 55 SUBJECT TR. TIME HR :30 112 1:00 100 1:30 88 2:00 88 3:00 84 4:00 80 5:00 84 6:00 80 7:00 76 8:00 70 9:00 72 10:00 76 :30 112 1:00 100 1:30 88 2:0,0 90 3:00 72 4:00 76 5:00 80 6:00 88 7:00 .80 8:00 84 9:00 84 10:00 80 :30 136 1:00 116 1:30 100 2:Q0 92 3:00 86 4:00 92 5:00 88 6:00 80 7:00 86 8:00 .86 9:00 84 10:00 72 MV vo2 vco2 37.928 2.247 1.176 31.032 0.758 0.838 34.480 0.631 0.896 28.446 0.472 0.65U 23.274 0.316 0.465 15.861 0.150 0.333 19.826 0.391 O.4I6 13.792 0.290 0.290 15.861 0.292 0.333 12.068 0.319 O.24I 10.344 0.337 0.217 10.344 0.37U 0.228 54.823 1.904 0.713 43.100 O.884 0.388 37.066 O.78I 0.259 29.653 0.511 0.208 31.032 0.503 0.186 24.826 O.346 0.124 22.757 0.272 • 0.068 25.601 0.248 0.051 23.274 0.367 0.070 22.412 0.217 0.0li5 20.688 0.221 0.062 17.930 0.214 0.054 24.248 1.520 1.091 38.IO4 1.616 1.905 32.908 I.I48 I.48I 19.052 0.665 0.857 12.470 0.476 0.524 8.443 0.338 0.338 4.330 0.000 0.182 4.330 0.195 0.173 4.330 0.231 0.182 4.330 0.217 0.195 4.330 0.193 0.182 4.330 0.222 0.173 5 6 SUBJECT TR. TIME HR 7 C :30 120 1:00 10U 1:30 101* 2:00 100 3:00 96 1*:00 100 5:00 96 6:00 88 7 :00 88 8 :00 78 9 :00 78 10:00 78 :30 136 1:0,0 121; 1:30 116 2:0:0 112 :30 132 1:0.0 121; 1:30 108 2:00 io l * 3:00 98 1*:00 92 5:00 92 6:00 92 7:00 92 8:00 96 9 :00 92 10:00 88 MV v o 2 v c o 2 76.339 1.636 1.832 67.731; 1.577 1.1*90 75.1146 1.521; 1.1*28 5u.l87 1.293 1.081* 51.120 1.022 1.022 51.120 0.796 0 .665 1;3.963 1.111 0.659 33.739 0.988 0.61*1 30.672 0.907 0.552 27.605 0.922 0.1*97 37.1*88 1.022 0.637 30.672 0.91*6 0.552 102.102 1.322 0.1*08 81.853 0.828 0.1*09 86.1*86 0.836 0.173 86.1*86 0.591 0.259 $h.99% 0.922 2.035 67.893 0 .713 2.173 47.821; 0 .137 1.769 39.967 0.000 1.1*79 25.361; 0.000 1.01*0 17.080 0.000 0 .717 17.080 0.365 0.581 17.080 0.1*17 0.51*7 15.372 0.1*17 0 .553 10.21*8 0.281 0.359 10.21*8 0.299 0.389 8.198 0.268 0.320 57 SUBJECT TR. TIME HR :;30 144 1:00 124 1:30 108 2:00 102 3:00 98 4:00 100 5:00 96 6:00 96 7:00 94 8:00 96 9:00 90 10:00 90 :30 132 1:00 128 1:30 116 2:00 108 3:00 98 4:00 100 5:00 100 6:00 100 7:00 98 8:00 98 9:00 98 10:00 94 :30 152 1:00 116 1:30 108 2:00 104 3:00 100 4:00 98 5:00 9k 6:00 92 7:00 90 8:00 88 9:00 84 10:00 88 MV vo2 vco2 47.410 1.578 1.944 37.928 0.889 1.327 27.929 0.627 0.950 31.032 0.652 0.931 34.135 0.581 0.888 34.135 0.590 0.853 17.240 0.333 O.U65 19.826 0.419 0.496 18.102 0.326 O.489 13.792 0.235 0.359 18.964 0.317 0.512 17.240 0.288 0.465 43.452 1.956 0.956 53.676 1.363 1.020 48.564 0.990 0.680 35.443 O.687 O.46I 25.049 0.543 0.351 32.717 0.653 O.36O 35.443 0.742 0.425 28.627 0.542 0.286 21.811 0.447 0.196 25.347 0.494 0.203 25.347 0.501 0.177 23.856 o.ii35 0.191 $2.$39 2 . i a i 2.942 20.171 0.716 1.150 17.8U3 0.562 O.946 15.516 0.473 0.807 17.240 0.513 0.862 15.171 O.4O2 0.728 11.206 0.399 0.583 7.758 0.192 O.388 8.620 O.246 0.388 8.620 0.257 0.431 8.620 0.282 O.U57 6.896 0.205 0.345 SUBJECT TR. TIME HR :30 10U 1:00 96 1:30 88 2:00 80 3:00 88 lx:00 92 5:00 92 6:00 92 7:00 72 8:00 76 9:00 74 10:00 68 :30 108 1:00 92 1:30 80 2:00 76 3:00 88 lx:00 76 5:00 76 6:00 61* 7:00 80 8:00 72 9:00 80 10:00 88 :30 12k 1:00 10k 2:30 9k 2:00 92 3:00 82 4:00 81* 5:00 80 6:00 88 7:00 80 8:00 80 9:00 78 10:00 78 MV v o 2 v c o 2 42.800 1.925 1.156 30.816 0.687 0.61x7 17.805 0.229 0.320 18.918 0.219 0.3U1 15.750 0.1+81 0.299 15.750 0.353 0.252 13.696 0.374 0.233 13.696 0.377 0.219 13.011 0.381 0.21*7 13.696 O.387 0.21*7 13.696 O.387 0.247 10.957 0.310 0.197 36.380 1.247 O.364 51.360 0.716 0.257 30.816 0.092 0.092 31.501 0.0 0.095 29 .4U6 0.239 0.088 27*73U 0.225 0.083 27.392 0.160 0.055 26.194 0.220 0.052 30.816 0.180 0.062 27.392 0.097 0.027 24.653 0.112 0.o!t9 28.248 0.093 0.056 30.960 1.047 1.517 25.5U2 0.498 1.0l*7 15.82U 0.221 0.601 1U.620 0.178 0.585 13.760 0.168 0.550 13.846 0.169 0.554 13.760 0.175 0.523 12.384 0.157 0.1*71 13.760 0.179 0.509 13.760 0.000 0.523 12.040 0.000 0.1x82 13.760 0.000 0.1*82 59 Appendix | MEAN VALUES OF ALL DATA Treatment A Exercise Recovery Time Heart Rate V e n t i l a t i o n v o 2 VC0„ 2 1:00 127.33 36.51 1.57 1.67 2:00 137.33 42.21 1.60 1.93 3:00 140.00 49.61 1.75 2.33 4:00 142.67 55.21 1.73 2.45 5:00 I48.OO 60.73 I.87 2.58 6:00 I46.22 57.01 I.84 2.37 :30 123.11 49.90 2.02 1.U2 1:00 111.56 41.17 1.11 1.03 1:30 100.89 36.24 0.78 0.79 2:00 96.22 29.71 0.68 0.65 3:00 94.67 28.34 O.64 0.58 4:00 92.00 27.17 0.59 0.50 5:00 92.44 23.07 0.59 0.43 6:00 90.22 20.64 0.52 0.39 7:00 85.78 18.01 O.44 0.34 8:00 85.11 16.29 0.44 0.31 9:00 84.89 18.99 O.48 0.35 10:;00 85.00 14.79 0.38 0.29 6 0 Treatment B Time Heart Rate V e n t i l a t i o n vo2 vco2 1:00 125.56 34.53 1.39 1.59 2:00 134.67 46.01 1.69 2.05 3:00 137.11 51.79 1.85 2.2U 4:00 139.56 55.8U 1.90 2.39 5:00 140.44 56.63 1.93 2.ijl 6:00 143.33 56.03 1.93 2.30 :30 125.78 59.23 1.49 0.62 1:00 114.89 55.80 0.79 0.49 1:30 106.89 53.86 0.59 0.37 2:00 103.11 45.68 0.49 0.26 3:00 98.00 43.22 O.46 0.28 4:00 95.71 35.21 0.37 0.23 5:00 93.71 33.98 0.34 0.22 6:00 90.00 28.84 0.28 0.18 7:00 92.67 28.14; 0.27 0.18 8:00 95.20 27.09 0.25 0.12 9:00 92.00 2U.87 O.24 0.11 10:00 92.80 24.97 0.23 0.10 61 Treatment C Exercise Recovery Time Heart Rate Ventilation vo2 vco2 1:00 131.56 39.05 1.55 1.79 2:00 11*0.56 51.42 2.00 2.27 3:00 lkh.Uk 53.71* 2.07 2.38 1*:00 lii7.ll 61.38 2.36 2.67 5:00 1U9.11 61.81 2.22 2.65 6:00 153.56 60.52 2.52 2.61* :30 132.89 37.87 1.1*0 1.76 1:00 11U.22 29.22 0.72 1.28 1:30 10U.67 22.58 0.1*5 0.95 2:00 100.22 18.36 0.1*2 0.79 3:00 97.33 16.05 0.52 0.67 1*:00 9U.00 11*. 70 o.l*5 0.61 5:00 93.78 11.31 0.39 0.1*7 6:00 90.78 9.67 0.26 0.1*0 7:00 91.78 9.1*6 0.29 0.38 8:00 90.22 9.10 0.32 0.39 9:00 88.89 7.91 0.27 0.31* 10:00 85.78 8,1*1 0.26 0.35 

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