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The relationship between excess CO2 and blood lactate in elite cyclists Anderson, Gregory Steven 1988

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THE RELATIONSHIP BETWEEN EXCESS C02 AND BLOOD LACTATE IN ELITE CYCLISTS by GREGORY STEVEN ANDERSON B„P.E., U n i v e r s i t y of B r i t i s h Columbia, 1985 A THESIS SUBMITTED IN PARTIAL FULFILLMENT OF THE REQUIREMENTS FOR THE DEGREE OF MASTER OF PHYSICAL EDUCATION i n FACULTY OF GRADUATE STUDIES School o f P h y s i c a l E ducation and Recreation We accept t h i s t h e s i s as conforming to the r e q u i r e d standards THE UNIVERSITY OF BRITISH COLUMBIA Ju l y , 1988. (cjGregory Steven Anderson, 198Q In presenting this thesis in partial fulfilment of the requirements for an advanced degree at the University of British Columbia, I agree that the Library shall make it freely available for reference and study. I further agree that permission for extensive copying of this thesis for scholarly purposes may be granted by the head of my department or by his or her representatives. It is understood that copying or publication of this thesis for financial gain shall not be allowed without my written permission. Department of P fH^ fS fC^L EbU.CfiTlfit<] The University of British Columbia 1956 Main Mall Vancouver, Canada V6T 1Y3 DE-6(3/81) ABSTRACT. T h i s study examined the r e l a t i o n s h i p between e x p i r e d non- m e t a b o l i c COS (EXC02) and the accumulation of blood l a c t a t e , while emphasis was placed on the v e n t i l a t o r y (EXC02 and VE/VO-2) and l a c t a t e t h r e s h o l d r e l a t i o n s h i p . Twenty-one e l i t e c y c l i s t s (15 males, 6 females) performed a p r o g r e s s i v e i n t e n s i t y b i c y c l e ergometer t e s t (PIT) d u r i n g which v e n t i l a t o r y parameters were monitored o n - l i n e at 15 second i n t e r v a l s , and blood l a c t a t e sampling occured on each minute. Threshold v a l u e s were determined f o r each o f the t h r e e i n d i c e s ; excess C02 (EXTT), VE/V02 (WTT), and blood l a c t a t e (LATT). The t h r e e t h r e s h o l d v a l u e s (EXTT, WTT, LATT) a l l c o r r e l a t e d s i g n i f i c a n t l y (P<8.881> when each was expressed as an a b s o l u t e VQ2 (I/min). A s i g n i f i c a n t RM ANOVA <F=S.41, P<8. 881) and post hoc c o r r e l a t e d t - t e s t s demonstrated s i g n i f i c a n t d i f e r e n c e s between the EIXTT and LATT (P<8.881) and the EXTT and WTT v a l u e s <P<8.8£5>. The LATT occured at an average blood l a c t a t e c o n c e n t r a t i o n of 3.35 mmol/1, while the mean e x p i r e d excess C02 volume at the EXTT was 14.84 ml/kg/min. Over an 11 minute range a c r o s s the t h r e s h o l d v a l u e s (EXTT and LATT), which were used as r e l a t i v e p o i n t s of r e f e r e n c e , the e x p i r e d EXC02 volume (ml/kg/min) and blood l a c t a t e c o n c e n t r a t i o n (mmol/1) c o r r e l a t e d s i g n i f i c a n t l y <r=8. 69, P<8. 881). Higher i n d i v i d u a l c o r r e l a t i o n s over the s a m e p e r i o d o f time <r=8.8£ - ©.96, P <8.©81) s t r e s s the i n d i v i d u a l nature o f t h i s r e l a t i o n s h i p . E x p i r e d EXCO£ volume appeared t o t r a c k blood l a c t a t e l e v e l s over t h i s 11 minute p e r i o d when the s i g n i f i c a n t t h r e s h o l d d i f f e r e n c e <1.35 min. ) was taken i n t o c o n s i d e r a t i o n . These r e s u l t s i n d i c a t e a s t r o n g r e l a t i o n s h i p between the t h r e e t h r e s h o l d values, although changes and e x p i r e d EXCO£ precede changes i n blood l a c t a t e c o n c e n t r a t i o n and the v e n t i l a t o r y e q u i v e l a n t <VE/VQ£). Although changes i n e x p i r e d EXCO£ volume appear t o t r a c k changes i n blood l a c t a t e c o n c e n t r a t i o n , blood l a c t a t e c o n c e n t r a t i o n can not be a c c u r a t e l y p r e d i c t e d from e x p i r e d EXCO£ volume as the nature o f t h i s r e l a t i o n s h i p v a r i e s between i n d i v i d u a l s and. appears t o be i n f l u e n c e d by gender. - i v - T A B L E OF CONTENTS Abstract . ... i i L i s t of Figures v i i L i s t of Tables ....... v i i Acknowledgment . . .'....... v i i i CHAPTER ONE ; INTRODUCTION TO THE PROBLEM. Trit reduction ........ ...... .... "... ....... . .... . ... 2. Statement of the Problem 4. J u s t i f i c a t i o n ..... ...... .'......... .•............ 5. D e f i n i t i o n s ... ... .......... .......... ...... ........ ........ ...... 6. Hypothesis ... ......... ..... . . ... ..... . ........ ..... ....... .. 7. Rat ionale . . . ...... . .... . ........................ ... ... 8. CHAPTER TWO ; S E L E C T I V E L I T E R A T U R E REVIEW. Introduction ... ......... ... .......... ... . . .,. 12. Models of Transition ..... .... . ...... . . ........ ... . . . . .... . . 13. Single Breakaway 13.. Double Breakaway 14. Exponential .....16. Thresholds 17. L a c t a t e Threshold . 19. .1 T i s s u e 02 Supply 21. .2 P r o d u c t i o n vs. Removal £2. .3 Muscle F i b e r Recruitment £3. .4 F a t i g u e £4. V e n t i l a t o r y T hreshold £4. .1 Vent i l a t o r y C o n t r o l £5. .2 VC02, RQ, and Excess COS £7. .3 Comparing Noninvasive Measures ..38. .4 Excess C02 and Performance 32. P r o t o c o l s ' for' E l u c i d a t ing T r a n s i t i o n ............34. Conclusions:. ....... ... ................... ...... ...... ..... .37. CHAPTER THREE. ; METHODS AND PROCEDURES. S u b j e c t s .40. Test ing Procedures and P r o t o c o l 40. Experimental. Design and Data Analysis- . .42. CHAPTER FOUR ; RESULTS AND DISCUSSION. R e s u l t s . ..• 44. D i s c u s s i o n 50. CHAPTER FIVE: ; SUMMARY AND CONCLUSIONS. Summary . .57. Cone 1 us ions 59. - v i - BIBLIOGRAPHY 60. APPENDIX 68. A. Observer Threshold Values 69. B. EXC02 74. C. EXC02 and Blood L a c t a t e 76. D. Threshold Curve Samples 78. E. Pre/Post Threshold Graphs 88. - v i i - LIST OF FIGURES Chpt. 4. F i g u r e 1. LATT vs. EXTT (r) 4®. F i g u r e s . LATT vs. WTT (r) 40. F i g u r e 3. EXTT vs. WAT (r) 41. F i g u r e 4. L a c t a t e vs. E x p i r e d EXC02 (r) .......43. LIST OF TABLES Chpt. 3. Table 1. The P r o g r e s s i v e Loading Scheme ........... 36. Chpt. 4. Table 1. D e s c r i p t i v e Subject Data 39. Table 2. A Threshold C o r r e l a t i o n Matrix 39. Table 3. ANOVA and Post Hoc Cornparisions .......... 42. Chpt. 5. Table 1. Summary of Hypotheses .....52. - v i i i - ACKNOWLEDGEMENT I would l i k e t o thank Dr. E.C.Rhodes f o r h i s guidance and d i r e c t i o n throughout t h i s p r o j e c t ; h i s su g g e s t i o n s were w e l l r e c i e v e d . I would a l s o l i k e t o thank Dr. G. Ma.theson f o r h i s suggestions and e d i t t i n g o f the i n i t i a l p r o p o s a l ; my committee f o r t h e i r s u g g e s t i o n s and d i r e c t i o n ; and my f r i e n d s f o r t h e i r many o p i n i o n s . I would l i k e t o thank my f i a n c e , S h e r r i Watts, f o r her patience, computer e x p e r t i s e , and continued support through the many t r y i n g moments; my brother, C l a y t o n Anderson, f o r being h i m s e l f - the best o f b i g b r o t h e r s ; and our parents f o r t h e i r love,, support, and understanding. - ] - CHAPTER ONE INTRODUCTION AND STATEMENT OF THE PROBLEM INTRODUCTION As e a r l y as 1930 W. H. Qwles r e c o g n i z e d t h a t t h e r e was a c r i t i c a l e x e r c i s e i n t e n s i t y l e v e l above which the working muscles produced l a c t i c a c i d . Owles a l s o observed t h a t accompanying an accumulation of blood l a c t a t e was an i n c r e a s e i n COS e x c r e t i o n and v e n t i l a t i o n . H a r r i s o n and P i l c h e r <1930) reasoned t h a t the excess COS being produced was the r e s u l t o f b i c a r b o n a t e b u f f e r i n g of a c i d s being produced d u r i n g a n a e r o b i c metabolism. Recent s t u d i e s suggest t h a t as much as 3Qi% of the hydrogen i o n produced d u r i n g a n a e r o b i c metabolism i s i n f a c t immediately b u f f e r e d by the b i c a r b o n a t e system (Wasserman e t . a l , 1986). In 1964 Wasserman and Whipp r e c o g n i z e d t h a t the onset o f blood l a c t a t e accumulation c o r r e l a t e d h i g h l y with break p o i n t s i n v e n t i l a t i o n (VE), carbon d i o x i d e e x c r e t i o n (VCOS), and the r e s p i r a t o r y exchange r a t i o (R), parameters which c o u l d be monitored n o n i n v a s i v e l y . It was suggested t h a t the i n i t i a l onset of blood l a c t a t e accumulation r e f l e c t e d a s h i f t from a e r o b i c t o a n a e r o b i c metabolism, a s h i f t i n the use o f energy pathways, and t h a t t h i s p o i n t o f t r a n s i t i o n c o u l d be a c c u r a t e l y determined through the n o n i n v a s i v e measures i n v e s t i g a t e d . It was at t h i s time t h a t they d e f i n e d t h a t p o i n t immediately preceding the n o n - l i n e a r i n c r e a s e i n VE, VCOS, or the sudden i n c r e a s e i n R as the "anaerobic t h r e s h o l d . " T h i s " t h r e s h o l d " p o i n t appears t o r e p r e s e n t a c r i t i c a l i n t e n s i t y above which endurance performance i s s e v e r e l y l i m i t e d (Rhodes et a l , 1981) and i s p o s t u l a t e d t o r e p r e s e n t a t r a n s i t i o n point i n energy metabolism: a t r a n s i t i o n t h r e s h o l d . S i n c e i t s time o f c o n c e p t i o n the "anaerobic t h r e s h o l d " (AT) has been put t o many uses. In the past t h i s ' t r a n s i t i o n t h r e s h o l d ' has been used c l i n i c a l l y i n a s s e s s i n g e x e r c i s e t o l e r a n c e (Wasserman e t . a l , 1964), i n e x e r c i s e p r e s c r i p t i o n (Davis e t . a l , 1981, Tanaka e t . a l , 1981), t o c h a r a c t e r i z e endurance a t h l e t e s (Rusko e t . a l , 1980), and t o p r e d i c t endurance performance (Rhodes et a l , 1981). The AT has been d e s c r i b e d as a key parameter which d e f i n e s the a b i l i t y t o m a i n t a i n h i g h - i n t e n s i t y e x e r c i s e (Whipp e t . a l , 1981), yet the concept of the AT i s s t i l l extremely c o n t r o v e r s i a l . Although t h e r e does appear t o be a " c r i t i c a l i n t e n s i t y " above which endurance performance i s s e v e r e l y l i m i t e d , and t h i s i n t e n s i t y i s concomitant with an i n c r e a s e i n blood l a c t a t e accumulation, VC02, EXC02, VE, VE/V02, and R, t h e r e i s no c o n c l u s i v e evidence s u p p o r t i n g the t h e o r y o f the a n a e r o b i c t h r e s h o l d . It appears i t i s i n the mechanisms o f such i n c r e a s e s , the nomenclature, and the o r i g i n a l assumptions t h a t the e x p l a n a t i o n f o r the AT i s f a i l i n g . Many o f the o r i g i n a l i d e a s and assumptions of the AT are being c h a l l e n g e d . It was o r i g i n a l l y surmised t h a t the l a c t a t e t h r e s h o l d and v e n t i l a t o r y t h r e s h o l d were synonymous (Wasserman et a l , 1964), and b e l i e v e d t h a t o n l y under hypoxic c o n d i t i o n s do the t i s s u e s produce l a c t i c a c i d (Margaria et a l , 1933). The - 4 - appearance o f l a c t a t e i n the bloodstream was thought t o r e f l e c t the p r o d u c t i o n of l a c t i c a c i d w i t h i n the muscle c e l l , yet t h i s i d e a i s being c h a l l e n g e d by many i n v e s t i g a t o r s who are f i n d i n g l a c t a t e t o be r e l e a s e d under what they b e l i e v e t o be adequate t i s s u e oxygenation (Connett et a l , 1984, J o b s i s et a l , 1958), and f i n d i n g t h a t the l a c t a t e and v e n t i l a t o r y t h r e s h o l d s can be uncoupled (Segal et a l , 1979). Other i n v e s t i g a t o r s b e l i e v e t h a t blood, l a c t a t e l e v e l s do not a c c u r a t e l y r e p r e s e n t the c e l l u l a r l a c t a t e p r o d u c t i o n or c o n c e n t r a t i o n . I n v e s t i g a t o r s are f i n d i n g t h a t a c o n s i d e r a b l e p o r t i o n o f the l a c t a t e formed w i t h i n the muscle may be o x i d i z e d w i t h i n the a c t i v e muscle t i s s u e (Brooks, 1986), and t h a t a t r a n s l o c a t i o n h inderance t o the- l a c t a t e molecule may be present (Stainsby, 1986). These f i n d i n g s suggest t h a t the appearance of blood l a c t a t e may be delayed, not r e p r e s e n t i n g an i n c r e a s e d r e l i a n c e on a n a e r o b i c energy p r o d u c t i o n o r the c e l l u l a r l a c t a t e c o n c e n t r a t i o n . The r e l a t i o n s h i p between blood l a c t a t e accumulation and EXC02, or non-metabolic COS CVC02 - (RQ x V02)3, has not yet been determined, although e a r l y r e s e a r c h by CIode, C l a r k and Campbell (1961) and I s s e k u t z and Rodahl (1961) r e p o r t e d high c o r r e l a t i o n s between the l a c t a t e t h r e s h o l d and EXC02. The e a r l i e r i n v e s t i g a t i o n s suggest t h a t EXC02 permits changes i n blood l a c t a t e c o n c e n t r a t i o n t o be d e t e c t e d with r e a s o n a b l e accuracy. W.E. Hearst (1982, unpublished t h e s i s ) found t h a t EXC02 c o r r e l a t e d h i g h l y with blood l a c t a t e at f o u r s p e c i f i c running speeds (r=8.89). It has been p o s t u l a t e d t h a t e x p i r e d EXC02 volume may r e f l e c t i n t r a c e l l u l a r p r o d u c t i o n o f l a c t i c a c i d . Recent s t u d i e s suggest that as much as 9$ - 94* of the l a c t i c a c i d produced i s immediately b u f f e r e d by the b i c a r b o n a t e b u f f e r i n g system (Wasserman et a l , 1986). EXC02 i s then produced d u r i n g p e r i o d s when the r a t e of l a c t i c a c i d i s i n c r e a s i n g , such as i n a p r o g r e s s i v e i n t e n s i t y t e s t . T h i s study w i l l examine the r e l a t i o n s h i p between EXC02 and blood l a c t a t e at a l l p o i n t s d u r i n g a p r o g r e s s i v e i n t e n s i t y t e s t w h i l e examining the r e l a t i o n s h i p between the EXC02, blood l a c t a t e , and the VE/V02 t h r e s h o l d s , t h e i r e q u a l i t y or d i f f e r e n c e , and the c o n s i s t e n c y o f any d i s c r e p a n c i e s which may occur. T h i s i n v e s t i g a t i o n w i l l , i n part, examine the concepts o f both l a c t a t e and v e n t i l a t o r y t h r e s h o l d e q u a l i t y , and the r e f l e c t i o n o f c e l l u l a r l a c t a t e p r o d u c t i o n by blood l a c t a t e accumulation. jysiiEiQaiiQN The use of- the AT has become widespread i n the f i e l d o f e x e r c i s e p h y s i o l o g y as i s thought t o r e f l e c t one's a e r o b i c work c a p a c i t y . T h i s t r a n s i t i o n t h r e s h o l d (TT) r e p r e s e n t s t h a t c r i t i c a l i n t e n s i t y above which work c a p a c i t y i s s e v e r e l y l i m i t e d . Examination o f n o n i n v a s i v e measures at the TT a l l o w s one t o examine the person's a b i l i t y t o t r a n s p o r t oxygen to, e x t r a c t and u t i l i z e oxygen i n the working muscle mass. The work i n t e n s i t y at the TT i s thought t o r e p r e s e n t a person's endurance c a p a c i t y , and EXCD2 has been c o r r e l a t e d h i g h l y with marathon performance times. The mechanisms u n d e r l y i n g the TT are a l s o mechanisms which w i l l l i m i t a e r o b i c performance and induce f a t i g u e . Determining the TT a c c u r a t e l y a l l o w s one t o study l i m i t i n g f a c t o r s i n a p a t i e n t and a t h l e t i c p o p u l a t i o n , determine a e r o b i c c a p a c i t y , monitor t r a i n i n g a d a p t a t i o n s , and p r e s c r i b e e x e r c i s e t h a t w i l l s t r e s s the d e s i r e d energy systems. Most r e s e a r c h e r s opt t o use n o n i n v a s i v e v e n t i l a t o r y and/or gas exchange v a r i a b l e s i n d e t e c t i n g the TT. Although some r e s e a r c h e r s have claimed t o have v a l i d a t e d the use o f n o n i n v a s i v e measures and have found them t o be r e l i a b l e i n d i c e s (Powers e t . a l . 1984, C a i o z z o e t . a l . 1982, D a v i s et . a l . 1976), many r e s e a r c h e r s s t i l l q u e s t i o n the p r a c t i c e (Simon e t . a l . 1983, Hughes e t . a l . 1982, Hagberd e t . a l . 1982). Research on the t o p i c has f a i l e d t o i n v e s t i g a t e the r e l a t i o n s h i p between blood l a c t a t e accumulation and the n o n i n v a s i v e v e n t i l a t o r y and gas exchange v a r i a b l e s at p o i n t s o t h e r than those o f the t h r e s h o l d o r "breakaway" p o i n t s . The d i s c u s s i o n o f EXC02 has been r e s t r i c t e d t o the r e l a t i o n s h i p between EXC02 and performance (Volkov et a l , 1974, Rhodes e t . a l , 1984, Hearst, 1982 unpublished t h e s i s ) . T h i s study i s j u s t i f i e d i n t h a t i t examines the r e l a t i o n s h i p between EXC02 and blood l a c t a t e at a l l p o i n t s d u r i n g a p r o g r e s s i v e i n t e n s i t y t e s t . T h i s study w i l l a l s o examine the r e l a t i o n s h i p between the l a c t a t e and v e n t i l a t o r y t h r e s h o l d s , t h e i r e q u a l i t y or d i f f e r e n c e , and the c o n s i s t e n c y o f any d i s c r e p a n c i e s which may occur. DEFINITIONS T r a n s i t i o n T h r e s h o l d (TT) - t h a t p o i n t where the a e r o b i c - 7 - energy pathways can no longer m a i n t a i n the t i s s u e s m e t a b o l i c l e v e l and the i n c r e a s i n g demands of the t i s s u e s are met through an i n c r e a s e d r e l i a n c e on a n a e r o b i c metabolism, with l a c t a t e accumulation exceding i t s removal. L a c t a t e Threshold. (LATT) - t h a t work r a t e j u s t below the point at which t h e r e i s an abrupt i n c r e a s e i n venous blood l a c t a t e ; t h at work r a t e below the breakaway poin t on the l a c t a t e / t i m e curve. V e n t i l a t o r y T h r e s h o l d (VT) - t h a t work r a t e j u s t below the poin t where t h e r e i s a non l i n e a r i n c r e a s e i n EXC02 (EXTT), and an abrupt i n c r e a s e i n the r a t i o VE/V02 (VVTT). Excess C0£ (EXC02) - the nonmetabolic C0£ produced through the b u f f e r i n g o f a c i d s by the b i c a r b o n a t e b u f f e r i n g system. EXCO£ can be c a l c u l a t e d by comparing the C0£ produced and the 02 consumed. It i s commonly c a l c u l a t e d by the f o l l o w i n g e q u a t i o n : EXC02 - VC02 - ( r e s t i n g RQ x V02) HYPOJHESIS 1. t h e r e w i l l be a s i g n i f i c a n t c o r r e l a t i o n between EXTT and LATT. 2. t h e r e w i l l be a s i g n i f i c a n t d i f f e r e n c e between EXTT and LATT. 3. EXC02 l e v e l s w i l l p a r a l l e l blood l a c t a t e l e v e l s through a l l s t a g e s o f the p r o g r e s s i v e i n t e n s i t y t e s t . SECONDARY HYPOTHESIS w i l l be a s i g n i f i c a r i t c o r r e l a t i o n between EXTT and w i l l be a s i g n i f i c a n t d i f f e r e n c e between EXTT and w i l l be a s i g n i f i c a n t c o r r e l a t i o n between WTT and w i l l be a s i g n i f i c a n t d i f f e r e n c e between WTT and Approximately 90 - 94% o f the hydrogen i o n produced i n the working muscle mass from the d i s s o c i a t i o n o f l a c t i c a c i d w i l l be b u f f e r e d immediately by the b i c a r b o n a t e system producing non-metabolic (excess) C02 and water (Wasserman e t . a l . 1986). EXC02 w i l l be generated as long as the r a t e o f l a c t i c a c i d p r o d u c t i o n i s i n c r e a s i n g as t h e r e will., be a d d i t i o n a l hydrogen ion t o b u f f e r (Wasserman e t . a l . 1986). In a p r o g r e s s i v e i n t e n s i t y t e s t (PIT) with i n c r e a s i n g workloads l a c t i c a c i d p r o d u c t i o n w i l l c o n t i n u e t o r i s e , s l o w l y at f i r s t and then r a p i d l y i n a c u r v i l i n e a r f a s h i o n throughout the d u r a t i o n o f the t e s t producing a r e l a t i v e i n c r e a s e i n EXC02. The hydrogen i o n and COS produced w i t h i n the muscle r e a d i l y move a c r o s s the muscle membrane i n t o the blood stream, enhanced by the presence of c a r b o n i c anhydrase i n the c a p i l l a r y 1. t h e r e WTT. 2. t h e r e WTT. 3. t h e r e LATT. 4. there- LATT. RATIONALE eridothel i a l c e l l s . The l a c t a t e molecule i s not, however, r e a d i l y d i f f u s a b l e a c r o s s the muscle membrane (Stainsby 1386) and may be removed by the o x i d a i t v e f i b e r s w i t h i n the a c t i v e muscle bed (Brooks 1986). Because of l a c t a t e ' s delayed r e l e a s e i n t o the blood stream EXC02 w i l l precede the accumulation of l a c t a t e i n the blood and may o f f e r a more a c c u r a t e p r e d i c t i o n o f c e l l u l a r l a c t a t e p r o d u c t i o n and accumulation (Issekutz and Rodahl 1961). The v e n t i l a t o r y parameters most o f t e n used i n the d e t e r m i n a t i o n of the t r a n s i t i o n t h r e s h o l d , VE and VE/VOS, are d i r e c t l y l i n k e d t o the p r o d u c t i o n and r e l e a s e of C02 and H+ from the a c t i v e muscle mass. The prime d r i v i n g f o r c e s f o r i n c r e a s e s i n v e n t i l a t i o n are an i n c r e a s e i n the PCOS and decrease i n the pH of the blood. Because the r e l e a s e of COS and H+ p r o v i d e the d r i v i n g f o r c e f o r v e n t i l a t i o n , i n c r e a s e s i n e x p i r e d COS w i l l precede an i n c r e a s e i n v e n t i l a t i o n with the VE and VE/VOS t h r e s h o l d p o i n t s o v e r e s t i m a t i n g the onset of a n a e r o b i c metabolism and l a c t a t e accumulation w i t h i n the working muscle mass. DELIMITATIONS T h i s study i s d e l i m i t e d by: a) T h i s s u b j e c t sample s i z e (N=21). b) The sample type, c o n s i s t i n g of e l i t e c y c l i s t s . c) The sampling r a t e of COS (15 s i n t e r v a l s ) and blood l a c t a t e (1 min. i n t e r v a l s ) . — US — LIMITATIONS T h i s study's r e s u l t s are l i m i t e d by: a) Data c o l l e c t i o n c a p a b i l i t i e s o f the Beckmari M e t a b o l i c Measurement Cart and i n t e r f a c e d Hewlett Packard Data A c q u i s i t i o n system. b> The i n d i v i d u a l ' s m e t a b o l i c response t o the p r o t o c o l . c) The blood l a c t a t e sampling and measurement technique. d> The d e t e r m i n a t i o n o f the t r a n s i t i o n t h r e s h o l d through v i s u a l , i n s p e c t i o n . CHAPTER TWO SELECTIVE REVIEW THE LITERATURE - 1 2 - A CRITICAL REVIEW OF BLOOD LACTATE AND VENTILATORY METHODS OF DETECTING THE TRANSITION THRESHOLD INIBODUCTigN fls early as 1930 W. H. Owles recognized that there was a c r i t i c a l exercise i n t e n s i t y level above which the working muscles produced l a c t i c acid. Accompanying an accumulation of blood lac t a t e Owles observed an increase in C02 excretion and v e n t i l a t i o n . Harrison and Pilcher (1930) reasoned that the excess C02. being produced: was a re s u l t of bicarbonate buffering of a c i d s being produced during anaerobic metabolism. This c r i t i c a l i n t ensity, dubbed the 'anaerobic threshold' by Wasserman and Whipp in 1964, appears to represent a work in t e n s i t y above which endurance performance i s severely limited, and i s postulated to represent a t r a n s i t i o n point i n energy metabolism — a ' t r a n s i t i o n threshold*. Physical exercise requires a balance between the production and: consumption of energy within the working musculature. The coupling of these two elements depends on the in d i v i d u a l ' s limited response of the cardiovascular and respiratory systems to exercise. There seems to be a ' c r i t i c a l i n tensity' above which the cardiovascular and/or respiratory response i s of an i n s u f f i c i e n t magnitude, f a i l i n g to supply the energy demanded through the aerobic pathways, and work capacity i s severely limited (Knuttgen, 1962). Work performed below t h i s c r i t i c a l i n t e n s i t y may be performed for i n d e f i n i t e durations as the energy required for muscular contraction i s being supplied - 13 - predominately through unlimited aerobic energy sources while waste products are being adequately removed. Work i n t e n s i t i e s above t h i s c r i t i c a l i n t e n s i t y r e s u l t i n rapid fatigue due to a r e l i a n c e on limited anaerobic energy sources and an accumulation of i n h i b i t o r y waste products. The; determination of t h i s t r a n s i t i o n point has been the subject of many investigations and has found mixed reviews. The object of t h i s review w i l l be to present previous research findings pertaining to the aerobic-anaerobic t r a n s i t i o n , the accumulation of blood and muscle lactate, and the subsequent release, of non—metabolic carbon dioxide.. Emphasis w i l l be placed on the determination of the c r i t i c a l i n t e n s i t y at which there i s a sharp increase i n i n t r a c e l l u l a r l a c t i c acid formation. .Kg MQDELS_QF_TRflNSITION The. concept: of a c r i t i c a l i n t e n s i t y above which there i s an increase i n blood lactate was introduced i n the early 1900's by Christiansen et al. (1914) and l a t e r by Owles (1938). It was also recognized at t h i s time that changes in v e n t i l a t i o n accompanied t h i s phenomena (Douglas, 1927). It was long believed that these changes were associated with a r e l a t i v e shortage of oxygen at th& muscular level ( H i l l et a l , 1924) which lead to the concept of the "anaerobic threshold" forwarded by Wasserman and Mcllroy (1964) (Davis, 1985). In more recent years the concept of a t r a n s i t i o n threshold has been under close scrutiny and the controversy around the concept has lead to the formulation of three separate models of aerobic-anaerobic t r a n s i t i o n . — 14 - l t l SINGLE_BRE9KaWBY_M0D^ The: c l a s s i c a l , model of aerobic-anaerobic t r a n s i t i o n during progressive i n t e n s i t y t e s t i n g i s the s i n g l e breakaway model stemming from early work which i d e n t i f y a " c r i t i c a l i n t e n s i t y " above which there was an accumulation of blood lactate. Margaria and colleagues (1933 and others) greatly influenced the i n i t i a l model in that they established the idea that l a c t i c acid was formed and blood l a c t a t e accumulated during times of lo c a l muscle hypoxia: at the onset, of exercise, and during times of oxygen d e f i c i t . , (fin idea: questioned to date, f i r s t refuted by Hubbard, 1973) In 1964 Wasserman and Mcllroy introduced the term "anaerobic threshold" to denote that work rate at which the t i s s u e s oxygen supply f i r s t f e l l below demand and the "excess" energy needs were supported through anaerobic metabolism. They f i r s t defined t h i s point as that point: immediately preceding a disproportional increase i n plasma lactate l e v e l s above res t i n g lev«?ls. They also suggested that t h i s point could be determined by decreases in blood bicarbonate or pH, or an abrupt increase? i n the respiratory exchange r a t i o (R). It was Wasserman and colleagues that l a t e r further investigated and refined the non-invasive v e n t i l a t o r y measures of the anaerobic threshold. They more recently supported the. s i n g l e threshold phenomena by employing a. log—log transformation of lactate concentration and V 0 2 (Beaver et a l , 1985). 1.2 D0UBLE_BREaK9WQY_MgDEL A three phase, double breakaway model was forwarded by Kindermann, Simon and Keul (1979) i n response to reported threshold lacta t e values of both 2 and 4 mrnol/1. These authors found that exercise could be maintained at high load i n t e n s i t i e s , producing a. steady-state lactat e concentration of approximately 4 mmol/1, for prolonged durations. These authors suggested that the anaerobic threshold proposed by Wasserman et a l (1964),. which occured in the range of 2 mmol of lactat e per l i t e r of blood volume, r e f l e c t e d the upper l i m i t of exclusive aerobic metabolism, and suggested that t h i s 'threshold' should be refered to as the * aerobic threshold'., In t h e i r framework the. 1 aerobics-anaerobic t r a n s i t i o n ' period occured between blood lactate; concentrations of 2 and 4 mmol/l,» and that a blood lactate, concentration of 4- mmol/1 represented the true * anaerobic threshold' - a: value above which lactate production exceeds- i t s removal and endurance exercise i s severely limited. The: model and terminology proposed by Kindermann et al. (1979) wasr further developed by Skinner and McLe11an i n 1981. These- authors, drawing information from past: research a r t i c l e s , attempted to explain each stage of the three phase double breakaway model and the physiological mechanisms underlying the events; which occured. Skinner and McLellan (1981) described the i n i t i a l phase, the aerobic phase, as being predominantly aerobic with a heavy r e l i a n c e on type I (ST or SO) muscle f i b e r s and free f a t t y acids <FFA) as the metabolic substrate. The aerobic threshold, following, leads into the aerobic-anaerobic t r a n s i t i o n phase which involves the recruitment of type I l a (FOG) f i b e r s and the appearance o f l a c t a t e i n the blood. L a c t i c a c i d i n t u r n d ecreases blood and i n t r a c e l l u l a r pH and causes an i n c r e a s e i n excess C02, v e n t i l a t i o n (VE), R and a d i s p r o p o r t i o n a l i n c r e a s e i n VE/V02., There i s an i n c r e a s e i n the f r a c t i o n a l c o n c e n t r a t i o n o f e x p i r e d 02 (Fe02) and a continued r i s e i n the f r a c t i o n a l c o n c e n t r a t i o n o f e x p i r e d C02 <FeC02). The a e r o b i c - a n a e r o b i c t r a n s i t i o n phase ends at the an a e r o b i c t h r e s h o l d where l a c t a t e production- e q u a l s i t s removal c a p a c i t y . The a n a e r o b i c phase, the t h i r d phase, f o l l o w s . T h i s phase i n v o l v e s the r e c r u i t m e n t o f type, l i b - (FG) f i b e r s with a r a p i d r i s e i n l a c t i c a c i d production.; L a c t a t e p r o d u c t i o n exceeds i t s removal with a r a p i d i n c r e a s e i n blood l a c t a t e and VE, and a decrease i n FeC02. 1^3___EXP0NENTIftL_M0DEL The e x p o n e n t i a l model d e s c r i b e d by Yeh et a l (1983) and Hagan and Smith (1984) has had b r e i f appearances i n the l i t e r a t u r e s i n c e i t was f i r s t d e s c r i b e d by J e r v e l l i n 1929... Hughson et, a l (1987) found: that, blood l a c t a t e c o n c e n t r a t i o n i n c r e a s e d as a conti n u o u s f u n c t i o n d u r i n g p r o g r e s s i v e e x e r c i s e . In c o n t r a s t i n g the conti n u o u s f u n c t i o n model and the s i n g l e breakaway model (the l o g - l o g model o f t h r e s h o l d determination) d e s c r i b e d by Beaver et a l (1985) Hughson et a l (1987) found t h a t the mean square e r r o r was approximately 3.5 times l a r g e r (P,0.001) when the s i n g l e breakaway model was used as compared t o the continuous f u n c t i o n p l u s constant model they employed. The authors suggested that a l a c t a t e s l o p e index would be a p r e f e r e d i n d i c a t o r o f ' f i t n e s s ' r e p l a c i n g the p r e v i o u s l y a p p l i e d t h r e s h o l d concept. T h e i r model suggests that t h e r e i s no "breakaway" point at which there i s an increased r e l i a n c e on anaerobic metabolism, but that there i s an exponential increase in the production of energy through the anaerobic energy pathways from the onset of incremental exercise. In t h i s model a l l parameters - blood lactate, VE, VCO£,. and R - are thought to increase in a c u r v i l i n e a r fashion from the onset of incremental exercise. This model challenges the very exsistence of c r i t i c a l i n t e n s i t i e s , lactate and v e n t i l a t o r y thresholds, upholding a b e l i e f that anaerobic energy sources supply an ever increasing proportion of the : t o t a l energy expenditure from the onset of incremental exercise. 2^®_ THRESHOLDS During the t r a n s i t i o n from aerobic to anaerobic metabolism an abrupt increase in blood lactate concentration, expired COS (VC02), and v e n t i l a t i o n may be observed, and have been reported throughout the last century. The c r i t i c a l i n t e n s i t y at which t h i s t r a n s i t i o n occurs has been widely researched appearing i n the l i t e r a t u r e under a wide var i e t y of nomenclature. This ' t r a n s i t i o n threshold' has been refered to as the 'anaerobic threshold' (Wasserman et a l , 1964) r the 'aerobic threshold' (Kindermann et a l , 1979), and the 'aerobic—anaerobic threshold' by Mader et a l <1976> (Jacobs, 1986). This t r a n s i t i o n threshold represents a combination of both a lact a t e and a v e n t i l a t o r y "threshold." The. use of the t r a n s i t i o n , or 'anaerobic' threshold has become widespread i n the f i e l d of sport science and exercise - 18 - physiology. The t r a n s i t i o n threshold represents that c r i t i c a l i n t e n s i t y above which work capacity i s severely limited. Examination of the t r a n s i t i o n threshold has enabled investigators to examine a person's a b i l i t y to transport oxygen to, extract and u t i l i z e , oxygen in the working muscle mass. The work i n t e n s i t y at the t r a n s i t i o n threshold i s thought to be representative of a person's endurance capacity (Rusko et a l , 1980), and has been correlated highly with marathon performance times (Rhodes et a l , 1981). The proposed mechanisms underlying the t r a n s i t i o n threshold are mechanisms which l i m i t aerobic performance. and induce fatigue. Determining the t r a n s i t i o n threshold accurately would allow investigators to study l i m i t i n g factors i n both patient and a t h l e t i c populations (Wasserman et al,. 1964), determine aerobic capacity ( F a r r e l l et a l , 1979), monitor t r a i n i n g adaptations (Ready et al,, 198£), and prescribe exercise which w i l l s t r e s s the desired energy systems (Davis et a l , 1981; Tanaka et a l , 1981; Kinderman et a l , 1979). The 'anaerobic threshold' has been described as a key parameter which defines the a b i l i t y to maintain high-intensity exercise (Whipp et a l , 1981), yet the concept of the 'anaerobic threshold', or any combination of the lactate and v e n t i l a t o r y thresholds, remains extremely co n t r o v e r s i a l . It appears i t i s i n the mechanisms of such increases, the nomenclature, and the o r i g i n a l assumptions that the t r a n s i t i o n threshold i s f a i l i n g . Many of the o r i g i n a l ideas and assumptions of the 'anaerobic threshold' are being challenged. It was o r i g i n a l l y surmised that the lactate threshold and v e n t i l a t o r y threshold were synonymous - 19 - (Wasserman et a l , 1964), and b e l i e v e d t h a t o n l y under hypoxic c o n d i t i o n s d i d the t i s s u e s produce l a c t i c a c i d (Margaria et a l , 1933). The appearance o f l a c t a t e i n the blood stream was thought t o r e f l e c t the p r o d u c t i o n o f l a c t i c a c i d w i t h i n the muscle c e l l . These i d e a s are being c h a l l e n g e d by i n v e s t i g a t o r s who are f i n d i n g l a c t a t e t o be r e l e a s e d under what they b e l i e v e t o be adequate t i s s u e oxygenation (Connett et a l , 1984; J o b i s et a l , 1968), and f i n d i n g t h a t the l a c t a t e and v e n t i l a t o r y t h r e s h o l d s can be uncoupled (Segal et a l , 1979). Other i n v e s t i g a t o r s are f i n d i n g t h a t blood l a c t a t e l e v e l s do not a c c u r a t e l y r e p r e s e n t the c e l l u l a r l a c t a t e p r o d u c t i o n or c o n c e n t r a t i o n . I n v e s t i g a t o r s are f i n d i n g t h a t a c o n s i d e r a b l e p o r t i o n o f the l a c t a t e formed w i t h i n the muscle may be o x i d i z e d w i t h i n the a c t i v e muscle t i s s u e s (Brooks, 1986), and t h a t a t r a n s l o c a t i o n hinderance t o the l a c t a t e molecule may be present (Stainsby, 1986). These f i n d i n g s suggest t h a t the appearance o f blood l a c t a t e may be delayed, not r e p r e s e n t i n g an i n c r e a s e d r e l i a n c e on the a n a e r o b i c energy p r o d u c t i o n or the c e l l u l a r l a c t a t e c o n c e n t r a t i o n . 2^1 LACTATE_THJESHOLD Almost a l l t i s s u e s o f the body can produce l a c t i c a c i d , but the best example i s the e x e r c i s i n g s k e l e t a l muscle. L a c t a t e i s produced i n o r d e r t o supplement a e r o b i c energy supply. The presence o f l a c t a t e i n the blood stream i s b e l i e v e d t o r e p r e s e n t an i n c r e a s e d r e l i a n c e on g l y c o l y t i c pathways of energy p r o d u c t i o n (Jones et a l , 1981). Pyruvate i s the key i n t e r m e d i a r y ( J o b i s et a l , 1968; Wasserman et a l , 1986). An imbalance between pyruvate fo r m a t i o n and i t s o x i d a t i o n i n the Krebs c y c l e w i l l cause pyruvate accumulation and i t s subsequent c o n v e r s i o n t o l a c t a t e . The c o n v e r s i o n o f pyruvate t o l a c t i c a c i d a l l o w s the o x i d a t i o n o f NftDH and the c o n t i n u a t i o n o f g l y c o l y s i s (Stainsby, 1986; Jones, 1980). L a c t i c a c i d w i l l immediately d i s s o c i a t e i n the p h y s i o l o g i c a l pH range <pKa=3.9) forming two l a c t a t e and two hydrogen ions. The l a c t a t e which i s formed may then be t r a n s p o r t e d t o, and taken up by o t h e r t i s s u e s with adequate oxygen supply - and u t i l i z e d as a source o f f u e l (Brooks, 1986; Sta i n s b y , 1986). The l a c t a t e t h r e s h o l d , r e p r e s e n t i n g the a e r o b i c - a n a e r o b i c t r a n s i t i o n t h r e s h o l d , has been observed s i n c e the e a r l y 190011 s and has been d e f i n e d i n many ways s i n c e i t s i n t r o d u c t i o n . The l a c t a t e t h r e s h o l d has been set as an a b s o l u t e blood l a c t a t e c o n c e n t r a t i o n such as 2rnM (Hughson et a l , 1982) o r 4mM ( S j o d i n et a l , 1981; Kinderman et a l , 1979), at the i n i t i a l i n c r e a s e i n blood l a c t a t e above r e s t i n g l e v e l s (Wasserman et a l , 1973; Davis et a l , 1976), at t h a t p o i n t where t h e r e i s an abrupt i n c r e a s e i n l a c t a t e accumulation (flunola et a l , 1984), at t h a t p o i n t where t h e r e i s a s y s t e m a t i c i n c r e a s e i n blood l a c t a t e c o n c e n t r a t i o n (Ciaozzo et a l , 1982), o r at a set s l o p e v a l u e such as 51 o r 45 degrees (Jones et a l , 1982). Brooks (1985) d e f i n e d the l a c t a t e t h r e s h o l d as t h a t workload at which t h e r e was an abrupt i n c r e a s e i n , o r d i s p r o p o r t i o n a l l y high, n o n - l i n e a r i n c r e a s e i n blood l a c t a t e c o n c e n t r a t i o n . Davis (1986) d e f i n e d the l a c t a t e t h r e s h o l d as that workload immediately preceding a o r o q r e s s i v e i n c r e a s e i n blood l a c t a t e c o n c e n t r a t i o n . It aooears t h a t the l a t e r d e f i n i t i o n s best apply as account f o r i n t e r - s u b j e c t v a r i a b i l i t y , although may be c r i t i c i z e d as having a wide margin of i n t e r - o b s e r v e r e r r o r i n t h r e s h o l d d e t e r m i n a t i o n . fit the onset o f a p r o g r e s s i v e i n t e n s i t y t e s t t h e r e i s a s l i g h t i n i t i a l i n c r e a s e i n blood l a c t a t e (Brooks, 1986) which should not be mistaken as the t r a n s i t i o n t h r e s h o l d . T h i s l e v e l w i l l be maintained, o r i n c r e a s e very l i t t l e , uo t o a c r i t i c a l workload which v a r i e s between i n d i v i d u a l s . fit t h i s c r i t i c a l p oint t h e r e w i l l be a d i s p r o p o r t i o n a l or abrupt i n c r e a s e i n the blood l a c t a t e c o n c e n t r a t i o n . During p r o g r e s s i v e i n c r e a s e s i n i n t e n s i t y of e x e r c i s e a stage i s reached at which t h e r e i s an ever i n c r e a s i n g r e l i a n c e on a n a e r o b i c metabolism and the r e l e a s e o f l a c t a t e i n t o the blood (Davis et a l , 1983). ft gradual i n c r e a s e i n blood l a c t a t e may be noted p r i o r t o an abrupt i n c r e a s e i n blood l a c t a t e which o c c u r s at a p o i n t r e p r e s e n t i n g the l a c t a t e t h r e s h o l d (Davis et a l , 1983; Brooks, 1985; Wasserman, 1986). iiliA_IAssue_0£_Supj3^ It was i n i t i a l l y b e l i e v e d t h a t l a c t a t e was produced d u r i n g p e r i o d s o f i n s u f f i c i e n t oxygen supply ( H i l l et a l , 1924; Margaria et a l , 1933). I f t h e r e i s an i n a p p r o p r i a t e response to the l e v e l o f muscular a c t i v i t y by e i t h e r the c a r d i o v a s c u l a r o r r e s p i r a t o r y system and the oxygen supply o f the muscle i s not met, the d e f i c i t i n energy demand i s met through a n a e r o b i c energy p r o d u c t i o n ( f l l p e r t , 1965; Jones, 1980) with the breakdown of glucose and/or glycogen ending with the f o r m a t i o n o f l a c t i c a c i d . D i l l et a l (1932) warned, however, t h a t the accumulation of l a c t i c a c i d alone was i n c o n c l u s i v e evidence of an oxygen d e f i c i t ( G o l l n i c k , 1986). Research has taken many d i r e c t i o n s i n the quest f o r c o n c l u s i v e evidence s u p p o r t i n g e i t h e r adequate o r inadequate oxygen supply. J o b i s and S t a i n s b y (1968) looked toward NftD/NftDH l e v e l s f o r an answer and concluded t h a t the high NftD l e v e l s d u r i n g l a c t i c a c i d f o r m a t i o n i n d i c a t e d adequate oxygen supply. Graham (1978), however, found no r e l a t i o n s h i p between NftD c o n c e n t r a t i o n and blood l a c t a t e l e v e l s . S t a i n s b y l a t e r concluded (1986) t h a t l a c t a t e p r o d u c t i o n without hypoxia was r e l a t e d t o the more r a p i d a c t i v a t i o n o f g l y c o l y s i s over o x i d a t i v e p h o s p h o r y l a t i o n . H o l l o s z y (1976) looked a t changes i n blood l a c t a t e l e v e l s and oxygen u t i l i z a t i o n at subrnaximal workloads i n o r d e r t o determine the presence o r absence o f l o c a l t i s s u e hypoxia. H o l l o s z y found t h a t a f t e r t r a i n i n g t h e r e was a lower blood l a c t a t e content at the same subrnaximal workload w h i l e the oxygen u t i l i z a t i o n d i d not change. It was concluded t h a t muscle hypoxia c o u l d not be present as changes i n blood l a c t a t e c o u l d not be a t t r i b u t e d t o i n c r e a s e s i n vTJ£. Davis (1985) suggested t h a t t h i s was a c o r r e c t assumption f o r subrnaximal workloads where adequate oxygen supply i s undisputed but d i d not however r e v e a l i n f o r m a t i o n r e g a r d i n g oxygen supply above the anaerobic t h r e s h o l d . Much c o n t r o v e r s y s t i l l e x s i s t s around the h y p o t h e s i s t h a t hypoxic c o n d i t i o n s are present when l a c t i c a c i d i s being produced i n the working t i s s u e s . Recent a r t i c l e s by Brooks (1985) , Davis (1985), G o l l n i c k et a l (1986), and Wasserman et a l (1986) r e i t t e r a t e the concern. P r o d u c t i o n of l a c t a t e does augment the c e l l u l a r supply of ATP, but Brooks (1985) and S o l l n i c k et a l (1986) are f i r m b e l i e v e r s t h a t t h i s o c c u r s i n the presence or absence of adequate oxygen supply while Wasserman and c o l l e a g u e s (1986) are f i r m b e l i e v e r s t h a t l a c t a t e accumulation i s oxygen dependent and r e q u i r e s a change i n the redox s t a t e of the c e l l . 2s.la.2_L.act at e_ Product ign_ys. Removal Cohen et a l (1976) suggested t h a t l a c t a t e accumulation was not o n l y due t o l o c a l t i s s u e hypoxia but t o an imbalance between the r a t e of l a c t a t e p r o d u c t i o n and i t s removal. The f a t e of the l a c t a t e molecule has been a t o p i c o f i n v e s t i g a t i o n s i n c e the e a r l y 1900's. Recent r e s e a r c h suggests t h a t as much as 75% o f the l a c t a t e produced i s removed w i t h i n the working muscle mass (Brooks, 1986; Hermansen et a l , 1976). E a r l i e r r e s e a r c h found that the l a c t a t e r e l e a s e d i n t o the blood stream c o u l d be removed by w e l l oxygenated s k e l e t a l muscle ( J o r f e l d t , 1970), by the l i v e r ( C o r i and C o r i , 1929) o r kidney (Yudkin et a l , 1975) v i a gluconeogenesis, by the heart (Car1sten, 1961), o r the b r a i n ( B e l c a s t r o et a l , 1975). Recognizing the importance of the l i v e r i n the removal of blood l a c t a t e Donovan and Brooks (1983) suggested t h a t reduced h e p a t i c blood flow, and hence h e p a t i c c l e a r a n c e of l a c t a t e , may play an important r o l e i n the l a c t a t e t h r e s h o l d . Whichever mechanisms l i m i t l a c t a t e removal, the consequence o f an imbalance between l a c t a t e p r o d u c t i o n and i t s removal i s an i n c r e a s e i n both muscle and blood l a c t a t e l e v e l s (Skinner et a l , 1981; Brooks, 1985; Davis, 1985: Wasserman, 1986), both having major p h y s i o l o g i c a l i m p l i c a t i o n s . - £4 - Muscle f i b e r type and f i b e r type recruitment patterns may be important factors which contribute to the lactate threshold (Skinner et a l , 1981). J o r f e l d t (1970) suggested that type II f i b e r s are net producers of lactate while type I f i b e r s are net consumers, therefore lactate accumulation would depend on muscle f i b e r type and recruitment patterns. Type II f i b e r s have an abundance of M-LDH which favors the reduction of pyruvate to lactate (Sjodin, 1976) and are more l i k e l y to become hypoxic as have a low c a p i l l a r y density, mitochondrial concentration and rate of oxidative phosphorylation (Tesch et a l , 1981). Type I f i b e r s favor the oxidation of lactate to pyruvate having an abundance of H-LDH (Sjodin, 1976). Graham (1978) found tyoe I f i b e r s to have three times the amount of lactate as compared to type II f i b e r s . £iljL^_L3£ti2_Bel^ _ 3 n d_Fat2gue L a c t i c acid produced during anaerobic g l y c o l y s i s immediately dis s o c i a t e s producing two hydrogen ions and two lactate molecules. The hydrogen ion liberated from l a c t i c acid formation i s predominately buffered by the bicarbonate buffering system, while the lactate molecule i s an important form of stored fuel for energy production, and supplies precursors for blood glucose (Cori et a l , 19£9; Brooks, 1986). If, however, the biDroducts of l a c t i c acid are allowed to accumulate within the working t i s s u e there w i l l be a rapid onset of fatigue. Increased lactate •reduction w i l l cause increased H+ release and a subseauent decrease in muscle and blood pH (Wenger et a l , 1976). ft decrease i n muscle and blood pH w i l l l i m i t the p r o d u c t i o n o f energy through a n a e r o b i c g l y c o l y s i s through the i n h i b i t i o n o f the r a t e l i m i t i n g enzymes P F K (phospho-fructokinase) (Danforth, 1965), and phosphorylase (Hultman et a l , 198©). ft decreased c e l l u l a r DH may a l s o cause f a t i g u e by a l t e r i n g membrane p e r m e a b i l i t y (Wenger et a l , 1976) o r i n t e r f e r i n g with t h e Ca++ b i n d i n g at the actomyosin b i n d i n g s i t e s (Wenger et a l , 1976). Increased l a c t a t e p r o d u c t i o n may p l a y a r o l e i n i m p a i r i n g the a e r o b i c energy supply by i n h i b i t i n g FFft m o b i l i z a t i o n from the adipose t i s s u e , l i m i t i n g t he su p p l y o f f u e l f o r a e r o b i c energy p r o d u c t i o n ( I s s e k u t z et a l , 1962). _E_TI_aTgRY_THRESHOLpS Noninvasive measures o f the onset o f m e t a b o l i c a c i d o s i s , the t r a n s i t i o n t h r e s h o l d , have allowed wide use o f the concept. The refinement o f n o n i n v a s i v e measures t o determine the t r a n s i t i o n t h r e s h o l d has been an ongoing process s i n c e the 1931a's when Owles (1932) r e c o g n i z e d t h a t e x p i r e d volume (Ve) and volume o f e x p i r e d C02 (VC02) i n c r e a s e d d i s p r o p o r t i o n a l l y above a c r i t i c a l i n t e n s i t y at which plasma l a c t a t e began t o r i s e . T u r r e l l and Robinson (1942) b e l i e v e d t h a t the i n c r e a s e i n C02 p r o d u c t i o n was the r e s u l t o f b i c a r b o n a t e b u f f e r i n g o f the m e t a b o l i c a c i d s being produced (ft.), with the r a p i d d i s s o c i a t i o n o f the newly formed c a r b o n i c a c i d (B. ) : ft. HLa +• NaHC03 = NaLa + H2C03 ( c a r b o n i c a c i d ) B. H2C03 = H20 + C02 The i n c r e a s e d C02 pro d u c t i o n , an a s s o c i a t e d f a l l i n blood b i c a r b o n a t e , and a r i s e i n a r t e r i a l DH are now b e l i e v e d t o be prime s t i m u l a t o r s of v e n t i l a t i o n , a c c o u n t i n g f o r the r i s e i n e x p i r e d volume observed by Owles i n 1932. 2 i . 2 i . l _ Vent 2 l at ory_Cont roi_ Under normal c o n d i t i o n s changes i n m e t a b o l i c demand are met with changes i n minute v e n t i l a t i o n o f a magnitude which w i l l m a i n t a i n the a r t e r i a l oxygen and carbon d i o x i d e p a r t i a l p r e s s u r e s at r e l a t i v e l y constant v a l u e s . Changes i n the r a t e and depth o f b r e a t h i n g are made i n o r d e r t o a l l o w a matching o f a v e o l a r v e n t i l a t i o n t o blood p e r f u s i o n , and a l l o w f o r the c o r r e c t i o n o f venous P02 <Sutton et a l , 1979). T h i s v e n t i l a t o r y c o n t r o l i s accomplished through the c e n t r a l nervous system. Input t o the c e n t r a l nervous system through neurogenic and humoral s t i m u l i a l l o w s e n s i t i v e c o n t r o l of the v e n t i l a t o r y response. fit the onset o f e x e r c i s e v e n t i l a t i o n i n c r e a s e s on the f i r s t f u l l r e s p i r a t o r y c y c l e due t o a neurogenic component i n v o l v i n g c e r e b r a l i r r a d i a t i o n and r e f l e x i v e s t i m u l i from mechanoreceptors i n the limbs (Powers et a l , 1985). Humoral s t i m u l i work above t h i s i n i t i a l i n c r e a s e and a l l o w s e n s i t i v e r e s D i r a t o r y c o n t r o l e n s u r i n g a p p r o p r i a t e a v e o l a r v e n t i l a t i o n . The humoral s t i m u l i , P02, PC02, and pH, cause a gradual i n c r e a s e i n r e s o i r a t i o n although t h e i r exact v a l u e s do not i n c r e a s e s i g n i f i c a n t l y ; the v e n t i l a t o r y response prevents wide f l u c t u a t i o n s i n the humoral v a r i a b l e s from o c c u r i n g . It appears v e n t i l a t i o n i s more c l o s e l y l i n k e d t o C02 output than any o t h e r v a r i a b l e (Sutton et a l , 1979, Wasserman et a l , 1975). A r t e r i a l PC02 i s r e g u l a t e d by v e n t i l a t i o n , with v e n t i l a t i o n i n c r e a s i n g i n p r o p o r t i o n t o C02 p r o d u c t i o n (Swanson, 1977), a f a c t t h a t has lead some t o b e l i e v e that PC02 i s not a primary r e g u l a t i n g f a c t o r (Asmussen, 1983). The C02 p r o d u c t i o n w i l l i n c r e a s e d u r i n g e x e r c i s e due t o a e r o b i c metabolism of f a t s and c a r b o h y d r a t e s up t o the "anaerobic t h r e s h o l d " a f t e r which an a d d i t i o n a l C02 load w i l l be i n t r o d u c e d due t o the p r o d u c t i o n and b u f f e r i n g o f l a c t i c a c i d by b i c a r b o n a t e . Up t o the "anaerobic t h r e s h o l d " v e n t i l a t i o n w i l l i n c r e a s e i n p r o p o r t i o n t o the i n c r e a s e s i n C02 p r o d u c t i o n , however, above t h i s p o i n t i n c r e a s e s i n v e n t i l a t i o n above those r e s p o n s i b l e f o r PaCD2 compensation do not a l l o w f o r the complete compensation f o r the pursuing l a c t i c a c i d o s i s (Wasserman et a l , 1975). The hydrogen i o n e n t e r i n g the blood stream w i l l have an a d d i t i o n a l independent v e n t i l a t o r y s t i m u l u s s t i m u l a t i n g the c e n t r a l chemoreceptors (Sutton et a l , 1979), and v e n t i l a t i o n i n c r e a s e s i n an attempt t o lower the hydrogen i o n content o f the blood. Hyperpnea w i l l d r i v e PaC02 lower than normal c o n s t r a i n i n g the b u f f e r i n g c a p a c i t y of the blood, and pH w i l l drop (Whipp et a l , 1980). Increased C02 p r o d u c t i o n at high i n t e n s i t y e x e r c i s e lead r e s e a r c h e r s t o look toward the r e s p i r a t o r y Quotient (VC02/V02) t o answer q u e s t i o n s i n r e g a r d s t o e x e r c i s e c a p a c i t y and accumulation o f l a c t a t e i n the bloodstream. Balke et a l (1954) observed comparible i n c r e a s e s i n VCQ2 and V02 UP t o a s p e c i f i c p o i n t at which VCD2 exceded V02. They took t h i s p o i n t , wnere R was g r e a t e r than 1.0, as i n d i c a t i n g the upper l i m i t s of a e r o P i c metabolism. In 1961 and 1962 Issekutz and Rodahl i n v e s t i g a t e d changes i n RQ and r e l a t e d them back t o a e r o b i c work c a p a c i t y and maxV02. They concluded that changes i n RQ best r e p r e s e n t e d the degree t o which a n a e r o b i c g l y c o l y s i s p a r t i c i p a t e d i n the t o t a l p r o d u c t i o n o f energy - i t s c o n t r i b u t i o n t o the t o t a l energy expenditure. They c o n s i d e r e d changes i n RQ above 8.75 t o be an index o f inadequate oxygen supply t o the working musculature, which was l a t e r supported by Naimark et a l (1964). Wasserman and M c l l r o y (1964) concluded t h a t the t h r e s h o l d o f ana e r o b i c metabolism c o u l d be observed without i n v a s i v e measures or maximal e f f o r t i n c a r d i a c p a t i e n t s when R was measured c o n t i n u o u s l y d u r i n g a p r o g r e s s i v e i n t e n s i t y t e s t , r e p r e s e n t e d by an abrupt i n c r e a s e i n R. The nomenclature, t h r e s h o l d o f an a e r o b i c metabolism, was soon known and r e f e r e d t o as the "anaerobic t h r e s h o l d . " Wasserman and c o l l e a g u e s (Naimark et a l , 1964) found chances i n R at d i f f e r e n t workloads t o r e f l e c t the balance between oxygen supply and oxygen demand at the l e v e l o f the working musculature. They r e c o g n i z e d t h a t R r o s e a p p r e c i a b l y at the onset o f blood l a c t a t e accumulation, and t h a t the f a l l i n blood b i c a r b o n a t e was h i g h l y c o r r e l a t e d with thp p r o d u c t i o n o f non-metabolic COS (r = 8.98). Issekutz and Rodahl (1961) had suggested t h a t the p r o d u c t i o n and displacement of b i c a r b o n a t e (nonmetabolic) C02 r e f l e c t s a n a e r o b i c metabolism more c l o s e l y than blood l a c t a t e due t o i t s r a p i d d i f f u s i o n from the muscle c e l l . Using a r e s t i n g RQ between 8.78 and 8.88 thev c a l c u l a t e d the nonmetabolic CQ2, Excess C02 = VC02 - (RQrest * V02) which h i p h l y c o r r e l a t e d (r = 0.9S) with changes i n blood l a c t a t e l e v e l s , and i n c r e a s e d i n p r o p o r t i o n t o i n c r e a s e s i n v e n t i l a t i o n . The r e s u l t s i n d i c a t e d that v e n t i l a t i o n was h i p h l y i n f l u e n c e d by the accumulation o f m e t a b o l i c a c i d s and the p r o d u c t i o n of excess COS (Iss e k u t z et a l , 1961). Using h e a l t h y t r a i n e d and u n t r a i n e d males Bouhuys et a l (1966) c o u l d not d u p l i c a t e the e x c e l l e n t c o r r e l a t i o n s found by Issekutz and Rodahl i n 1961. T h e i r i n v e s t i g a t i o n found that the i n c r e a s e i n l a c t i c a c i d was of a g r e a t e r magnitude than the decrease i n standard bicarbonate, with the d i f f e r e n c e s being i n t e n s i f i e d with i n c r e a s i n g workload. They concluded t h a t i n c r e a s e s i n both R and excess COS were a s s o c i a t e d with i n c r e a s e s i n l a c t i c a c i d accumulation (r = 0.6SS and r = 0.796) but the r e v e r s e was not always t r u e . They suggested t h a t R and excess COS o n l y provided a rough e s t i m a t i o n o f the degree of e x e r c i s e induced a c i d o s i s w h i l e d i r e c t l a c t a t e d e t e r m i n a t i o n was s t i l l p r e f e r a b l e . It had been suggested that v e n t l a t o r y and gas exchange v a r i a b l e s measured i n volumes ( i e . VCOS and Ve) r a t h e r than those presented as r a t i o s ( i e . R and Ve/VOS) would be more p r o p o r t i o n a l t o blood l a c t a t e l e v e l s (Nairnark et a l , 1364, and Wasserman et a l , 1964). Clode and Campbell (1969) provided s u p p o r t i n g evidence f o r t h i s h y p o t h e s i s when i n v e s t i g a t i n g COS balance i n the body and found that blood l a c t a t e c o u l d be estimated a c c u r a t e l y by VCOS when changes i n t i s s u e PCOS are taken i n t o c o n s i d e r a t i o n . They concluded that using a COS ba l a n c i n g t echnique changes i n blood l a c t a t e c o n c e n t r a t i o n c o u l d - 30 - be estimated with r e a s o n a b l e accuracy. 2_2_3_Comj3ar_I'_^ In 1973 Wasserman et a l d e f i n e d the a n a e r o b i c t h r e s h o l d as "the l e v e l o f work or 02 consumption j u s t below t h a t at which m e t a b o l i c a c i d o s i s and t h e a s s o c i a t e d changes i n gas exchange occur <pg- 236)." In comparing n o n i n v a s s i v e gas exchange v a r i a b l e s using b r e a t h - t o - b r e a t h gas a n a l y s i s d u r i n g incremental e x e r c i s e these i n v e s t i g a t o r s found t h a t the t r a n s i t i o n t h r e s h o l d c o u l d be determined as t h a t work r a t e o r V02 immediately preceding a n o n l i n e a r i n c r e a s e i n Ve or VCG2, an i n c r e a s e i n R, o r t h a t point where e n d - t i d a l 02 i n c r e a s e s without a c o r r e s p o n d i n g decrease i n e n d - t i d a l C02. Of t h e s e measures R was found t o be the l e a s t s e n s i t i v e as the m e t a b o l i c RQ i n c r e a s e s d u r i n g incremental t e s t s at i n c r e a s e d workloads producing i n c r e a s i n g amounts of m e t a b o l i c C02. The m e t a b o l i c p r o d u c t i o n o f C02 i s much g r e a t e r than the p r o d u c t i o n of excess C02 i n normal s u b j e c t s with changes i n R being overshadowed. J.ft. Davis et a l <1976) i n v e s t i g a t e d the v a l i d i t y and f e a s a b i l i t y o f using n o n i n v a s i v e l a b o r a t o r y measures i n the d e t e c t i o n o f the 'anaerobic t h r e s h o l d * i n t h r e e modes o f e x e r c i s e . fts Wasserman et a l (1973) these i n v e s t i g a t o r s found R t o be the l e a s t s e n s i t i v e measure. Using Ve alone t o p r e d i c t the l a c t a t e t h r e s h o l d p o i n t produced a c o r r e l a t i o n c o e f f i c i e n t o f 0.88, and when a l l gas parameters were usee i n c o r r e l a t i n g both l a c t a t e and gas a n a l y s i s t r a n s i t i o n t h r e s h o l d s a c o r r e l a t i o n c o e f f i c i e n t o f 0.95 was found. They suggested t h a t the major l i m i t a t i o n i n d e t e c t inn the t r a n s i t i o n t h r e s h o l d from chances i n - 31 - gas exchange v a r i a b l e s i s the s u d e c t i v e d e t e r m i n a t i o n of tne t h r e s h o l d point from a time-based Dlot, although Questioned the use o f i n c r e a s e d blood l a c t a t e l e v e l s above r e s t i n g v a l u e s as the c r i t e r i o n measure, being an i n d i r e c t index of muscle l a c t i c a c i d p r o d u c t i o n . The common v e n t i l a t o r y and gas exchange measures used i n 'anaerobic t h r e s h o l d ' d e t e c t i o n were s t u d i e d i n 198£ by C a i o z z o et a l t o determine which i n d i c e s provided the most a c c u r a t e and r e l i a b l e d e t e r m i n a t i o n of the l a c t a t e t r a n s i t i o n t h r e s h o l d . The i n v e s t i g a t o r s used f o u r s e p a r a t e n o n i n v a s i v e measures (Ve, VCO£, R, and Ve/VO£) t o determine the v e n t i l a t o r y t h r e s h o l d p o i n t and each was c o r r e l a t e d t o the c r i t e r i o n measure, the l a c t a t e t h r e s h o l d . It was found t h a t ve/VO£ provided the h i g h e s t c o r r e l a t i o n ( r - 0; 93, P < 0.001) and provided the best t e s t - r e t e s t c o r r e l a t i o n <r = 0.93, P < 0.001). R was the l e a s t s e n s i t i v e measure <r = 0.39) w h i l e VC02 and Ve appeared t o p r o v i d e e x c e l l e n t p r e d i c t i o n s of the l a c t a t e t h r e s h o l d (r = 0.83, r — 0.88). M u l t i p l e c o r r e l a t i o n a l a n a l y s i s d i d not s i g n i f i c a n t l y improve the t h r e s h o l d d e t e c t i o n over Ve/VO£ va l u e s , w h i l e the t h r e s h o l d p o i n t s expressed as a %v"Q£max produced lower c o r r e l a t i o n c o e f f i c i e n t s than d i d e x p r e s s i n g the t h r e s h o l d p o i n t as an a b s o l u t e V0£ (1/min). Powers et a l (1984) were not a b l e t o reproduce the high c o r r e l a t i o n s found e a r l i e r and concluded t h a t the l a c t a t e t h r e s h o l d can not be a c c u r a t e l y determined by nas exchange i n d i c e s i n a l l s u b j e c t s . Using a s l i g h t l y d i f f e r e n t p r o t o c o l , with work increments o f t h r e e minutes, and a blood l a c t a t e sampling r a t e of once every t h r e e minutes ( t h e i r c r i t e r i o n r e f e r e n c e ) , these i n v e s t i g a t o r s found a noor c o r r e l a t i o n (r = 0.63) between the t r a n s i t i o n t h r e s h o l d when determined through Ve/VO£ and through blood l a c t a t e . £_ Non-Met abol_ ic_ C O£_and_Perf orioa^ce Approximately 90 - 94 % o f the hydogen i o n produced w i t h i n the working muscle mass from the d i s s o c i a t i o n of l a c t i c a c i d w i l l be immediately b u f f e r e d by the b i c a r b o n a t e b u f f e r i n g system producing non-metabolic (excess) CD£ and water (Wasserman et a l , 1986). Excess C0£ (EXCO£) w i l l be generated as long as the r a t e of l a c t i c a c i d p r o d u c t i o n i s i n c r e a s i n g as t h e r e w i l l be a d d i t i o n a l hydrogen i o n t o b u f f e r (Wasserman et a l , 1936). In a p r o g r e s s i v e i n t e n s i t y t e s t (PIT) with i n c r e a s i n g workloads l a c t i c a c i d p r o d u c t i o n w i l l c o n t i n u e t o r i s e , s l o w l y at f i r s t and then r a p i d l y a f t e r the t r a n s i t i o n t h r e s h o l d i n a c u r v i l i n e a r f a s h i o n producing a r e l a t i v e i n c r e a s e i n excess C0£ LEXC02 = VCO£ - (RQrest * VO£)D. The r e l a t i o n s h i p between blood l a c t a t e accumulation and EXCO£ has not yet been determined, although e a r l y r e s e a r c h by Clode, C l a r k and Campbell (1961) and Issekutz and Rodahl (1961) r e p o r t e d high c o r r e l a t i o n s between the l a c t a t e t h r e s h o l d and EXCQ£. These e a r l i e r i n v e s t i g a t i o n s suggest t h a t the c a l c u l a t i o n of EXCO£ permits changes i n blood l a c t a t e t o be d e t e c t e d with r e a s o n a b l e accuracy. The hydrogen i o n and C0£ produced w i t h i n the muscle c e l l r e a d i l y d i f f u s e a c r o s s the muscle memnrane i n t o the blood stream, enhanced by the presence of c a r b o n i c anhycrase i n the c a p i l l a r y e n d o t h e l i a l c e l l s . The l a c t a t e molecule, however, may be removed by the o x i d a t i v e f i b e r s w i t h i n the a c t i v e muscle bed (Brooks, 1986) and has a t r a n s l o c a t i o n hinderance (Stainsby, 1986) t o movement a c r o s s the c e l l membrane. Because of these mechanisms i n c r e a s e s i n e x p i r e d EXCO£ may be d e t e c t e d b e f o r e a s i g n i f i c a n t r i s e i n blood l a c t a t e i s d e t e c t e d ; EXCO£ may o f f e r a more a c c u r a t e p r e d i c t i o n of c e l l u l a r l a c t a t e p r o d u c t i o n and accumulation ( I s s e k u t z et a l , 1961). In 1975 Volkov et a l suggested t h a t the measurement o f excess C0£ d u r i n g a maximal oxygen consumption t e s t a l l o w s a c c u r a t e n o n i n v a s i v e d e t e r m i n a t i o n of a s u b j e c t ' s a n a e r o b i c power. The i n v e s t i g a t o r s thought t h a t the excess C0£ index i s d i r e c t l y r e l a t e d t o the magnitude of l a c t a t e p r o d u c t i o n through the g l y c o l y t i c pathways and the organism's b u f f e r i n g c a p a c i t y . They found t h a t t h e r e i s a c o n s i s t e n t i n c r e a s e i n excess COS when a c r i t i c a l i n t e n s i t y , or the t h r e s h o l d o f a n a e r o b i c metabolism, i s surpassed, and t h a t t h i s t r a n s i t i o n t h r e s h o l d point depends on the s u b j e c t ' s s t a t e o f t r a i n i n g . In 1981 Rhodes and McKenzie found t h a t the running speed at which a breakaway poin t i n e x p i r e d EXCO£ occured c o u l d be used t o p r e d i c t marathon running performance. These authors found a h i g h l y s i g n i f i c a n t c o r r e l a t i o n <r=.94, P<3.81) between p r e d i c t e d and a c t u a l marathon times s u g g e s t i n g t h a t the r a p i d i n c r e a s e i n e x p i r e d EXCD£ may be an i n d i c a t i o n o f the c r i t i c a l i n t e n s i t y at which the onset o f a n a e r o b i s i s o c c u r s . These r e s u l t s were supported by Hearst (198£, unpublished t h e s i s ) who found t h a t e x p i r e d EXCO£ c o r r e l a t e d h i g h l y (r=.89) with blood l a c t a t e accumulation at f o u r s p e c i f i c running speeds. - 34 - 3__ £SQIS£QL§_FOR_£LyCID@IING_TR U n d e r l y i n g i n v e s t i g a t i o n s o f the t r a n s i t i o n t h r e s h o l d a r e p r o g r e s s i v e i n t e n s i t y t e s t s (PIT). In 1975 Wasserman and w n i p p d e s c r i b e d the responses one c o u l d expect t o o b t a i n when using d i f f e r e n t f o r c i n g f u n c t i o n s . In gene r a l , at work r a t e s Delow the t r a n s i t i o n t h r e s h o l d mean a r t e r i a l pH and PC02 are maintained by i n c r e a s e s i n a l v e o l a r v e n t i l a t i o n which are p r o p o r t i o n a l t o the i n c r e a s e s i n C02 pr o d u c t i o n . Pit work r a t e s above the t r a n s i t i o n t h r e s h o l d the compensation f o r m e t a b o l i c a c i d o s i s i s accomplished through a d i s p r o p r t i o n a l l y high i n c r e a s e s i n v e n t i l a t i o n over those mediated by i n c r e a s e d C02 p r o d u c t i o n c a u s i n g a r t e r i a l PC02 t o f a l l w h i l e pH remains unchanged, fit even g r e a t e r work r a t e s yet (80% max +) i n c r e a s e s i n v e n t i l a t i o n are unable t o compensate f o r i n c r e a s e s i n blood pH due t o the l o s s o f blood b i c a r b o n a t e and blood pH f a l l s . (Wasst=rman and Whipp, 1975) During a p r o g r e s s i v e i n t e n s i t y t e s t with i - 4 minute increments the f o l l o w i n g t r e n d s may be observed: 1. VQ2 i n c r e a s e s l i n e a r l y throughout the t e s t u n t i l a maximal v a l u e i s reached at which V02 w i l l p l a t e a u . 2. Ve and VC02 w i l l i n c r e a s e l i n e a r l y with V02 up t o a c r i t i c a l i n t e n s i t y , the an a e r o b i c t h r e s h o l d , at whicn l a c t i c a c i d i s produced causing VC02 t o i n c r e a s e f a s t e r than V02. 3. Ve w i l l i n c r e a s e i n p r o p o r t i o n t o VC02, t h e r e f o r e i n c r e a s e s i n Ve equal i n c r e a s e s i n VC02 whicn are both g r e a t e r than i n c r e a s e s i n V02. 4. R i n c r e a s e s s i n c e i n c r e a s e s i n VC02 are o r e a t e r than i n c r e a s e s i n V0£. The d i f f e r e n c e between the two d i f f e r e n t f o r c i n g f u n c t i o n s , 1 or 4 minutes, i s t h a t w h i l e using 1 minute increments e n d - t i d a l P02 w i l l i n c r e a s e at the a n a e r o b i c t h r e s h o l d w h i l e e n d - t i d a l PCO£ remains constant, w h i l e using 4 minute increments e n d - t i d a l P0£ i n c r e a s e s at the a n a e r o b i c t h r e s h o l d w h i l e e n d - t i d a l PC02 decreases. (Wasserman and Whipp, 1975) Wasserman and Whipp (1975) concluded t h a t p r o g r e s s i v e i n t e n s i t y t e s t s using one minute increments had s e v e r a l advantages over using f o u r minute increments when n o n i n v a s i v e d e t e r m i n a t i o n of the 'anaerobic t h r e s h o l d ' was a major o b j e c t i v e . T h i s c o n c l u s i o n was based on f i v e major p o i n t s : 1. 1 minute increments allowed a more s p e c i f i c d e f i n i t i o n of the a n a e r o b i c t h r e s h o l d . 2. the t e s t i s much s h o r t e r . 3. l a c t a t e v a l u e s do not reach such high v a l u e s a l l o w i n g q u i c k e r r e c o v e r y from e x h a u s t i v e e x e r c i s e . 4. i s e a s i e r t o reach and determine the maxVO£ i f so d e s i r e d . 5. the 'anaerobic t h r e s h o l d ' can be expressed as e i t h e r a V0£ or work r a t e without l a r g e e r r o r s i n e s t i m a t i o n . It appears t h a t the t r a n s i t i o n t h r e s h o l d can be d i s c e r n e d r e a d i l y from t e s t s using 1 or 4 minute workload increments, o r v a l u e s inbetween, as long as one r e c o g n i z e s t h a t d i f f e r e n t responses occur. S i m i l a r t r a n s i t i o n t h r e s h o l d v a l u e s have been r e p o r t e d d u r i n g t e s t s using 1 and 4 minute workload increments (Wasserman et a l , 1975: Yoshida, 1935). M c L e l l a n (1987) a t t r i b u t e s much of the c o n f l i c t i n g data t o methodological e r r o r s i n t h r e s h o l d d e t e c t i o n , using changes i n v e n t i l a t o r y ana pas exchange parameters observed i n a ' f a s t ' increment t e s t t o determine the a n a e r o b i c t h r e s h o l d d u r i n g a 'slow' increment t e s t and v i s a - v e r s a . - 37 - 4..0 CONCLUSIONS Amidst the c o n t r o v e r s y surrounding the e q u a l i t y and cause- a n d - e f f e c t r e l a t i o n s h i p o f the v e n t i l a t o r y and l a c t a t e t r a n s i t i o n t h r e s h o l d s t h e r e are s t i l l many f i r m b e l i e v e r s i n the phenomena (McLellan, 1987; Wasserman et a l , 1986; Davis, 1985). Many r e v i e w e r s (Hughson et a l , 1987; Brooks, i985; S t a i n s b y 1985), however, s t i l l q u e s t i o n the r e l a t i o n s h i p . It a D o e a r s t h a t t h e r e i s i n c o n c l u s i v e evidence s u p p o r t i n g e i t h e r p o s i t i o n , i n a l a r g e part due t o an i n s u f f i c i e n t method o f deter m i n i n g i n t r a c e l l u l a r events, s u g g e s t i n g a need f o r f u r t h e r r e s e a r c h i n the a r e a u t i l i z i n g some o f the new t e c h n o l o g i e s . 38 - CHAPTER T H R E E METHOD AND PROCEDURES - 40 - _iIHQDS_BNO_ERQQiDyRES S u b j e c t s Twenty-one national team c y c l i s t s (15 males arid fa females) p a r t i c i p a t e d i n the study. The subjects were tested over'a tnree day period just p r i o r to the national team time t r i a l s : a l l subjects were in a highly trained state. The suojects were asked to r e f r a i n from heavy exercise £4 hours ori o r to the test and perform on an empty stomach. Test_ng_Procedures The baseline measures of height and weinht were taken ori o r to t e s t i n g . Testing was performed at U. B. C. in the J . tt. Buchanan Fitness and Research Center. Subjects were asked to warm up 15 minutes pr i o r to Peine tested, and were allowed only a limited war roup with the testing apparatus in place. The test protocol consisted of a continuous progressive i n t e n s i t y test on a Monarch stationary b i c y c l e . Foilowinn a two minute warmup at a work rate of 58 or 188w (female/male) tne c y c l i s t s pedalled against an i n i t i a l resistance of 180 or 158w (female/male) with increases of £5W every second minute (figure 1.0). ft cadence of 98 rpm was maintained throughout tne t e s t . The test was terminated upon v o l i t i o n a l fat icue: that point where the athlete was unaole to maintain or regain tns 98 RPM frequency. — 41 T a b l e 1. 0 Th s i v s l o a d i n g s e n erne. stage *• i rne w o r k r a t e (w) frequency < rn i n) ma i e female (RPM) wmuD 0 - 2 100 58 i 2 - 4 150 108 98 2 4 - 6 175 125 98 3 6 - a 283 158 93 4 a - 10 225 175 93 5 10 - 12 258 230 33 S 12 - 14 275 225 98 7 14 — 16 380 253 98 e t c . T e s t i n g measures i n c l u d e d V02, VE, VC02, R. EXC02, aiood l a c t a t e and HR. R e s p i r a t o r y gas exchange v a r i a a i e s were monitored o n l i n e using a Beckman M e t a b o l i c Cart i n t e r e f a c e d with a Hewlett Packard Data A c q u i s i t i o n System. V a r i a b l e s were determined or c a l c u l a t e d over 15 second time i n t e r v a l s . HR was monitored i n the l a s t 18 seconds of eacn minute through the use of a t h r e e lead V5 EC3 r e c o r d i n g . Blood samples were ta;<en v i a f i n g e r t i o v e n o u s sampling at minute i n t e r v a l s throughout the d u r a t i o n o f the p r o c r e s s i v e i n t e n s i t y t e s t . The blood samples were taken. immediately rseamolysed using c o o l e d P e r c h l o r i c a c i d , and analysed. T o t a l blood l a c t a t e was determined using a Kontron Med ica1 L a c t a t e A n a l y z e r S43. The breakaway t h r e s h o l d p o i n t s w e r e D e t e r m i n e d ay t n r e e indepencant o a s e r v e r s through v i s u a l i n s p e c t ion of tne EXTT, WTT and LftTT curves. b a c h set of curves w e r e analysed s e p a r a t e l y w h i l e the s u b j e c t s i d e n t i t y was w i t h h e l d . The proposed areakaway p o i n t s , or t r a n s i t i o n t h r e s h o l d s , were t h e n d i s c u s s e d by the group of t h r e e o b s e r v e r s and an exact brsaxaway point was agreed upon. There were t h r e e dependent v a r i a a l e s (blood l a c t a t e . EXC02 and VE/VD2) and one independant v a r i a a l e ( p r o g r e s s i v e i n t e n s i t y t e s t ) . P) r e g r e s s i o n a n a l y s i s was performed comparing EXTT and LftTT, EXTT and WTT, LftTT and WTT. C o r r e l a t i o n c o e f f i c i e n t s and an r * v a l u e were o a t a i n e d f o r the data. S i g n i f i c a n t d i f f e r e n c e s were determined using a repeated measures ftiMOVft. ft s i g n i f i c a n t F v a l u e was f u r t h e r i n v e s t i p a t e d using post hoc procedures. The decree t o which the curves p a r a l l e l e d each other w a s i n v e s t i g a t e d by graphing average a b s o l u t e EXCG2 and l a c t a t e v a l u e s f o r f i v e minutes pre a n d post t h r e s h o l d . ft c o r r e l a t i o n c o e f f i c i e n t was determined f o r a l l . data p o i n t s pre/post t h r e s h o l d . CHAPTER FOUR RESULTS AND DISCUSSION - 44 - B l i y L I i Twenty-one Canad i am National c a l i p e r c y c l i s t s p a r t i c i D a t e d i n t h i s study just p r i o r to the Canadian National team time t r i a l s . The d e s c r i p t i v e subject data i s presented in Taole 1. TABLE 1. Descriptive subject data for a l l subjects grouped, males and females GROUP : : N = £1 MALE FEMALE : n = 15 . n = 6. : Ape (yr). : £3.19 + : 3. 34 ; £3. £6 + £3.00 + : : £.79 . 1.95 " : Wei qht ~ <kp>. : 70.10 + : 8.46 : 73.57 + 61.43 + : 7.30 3. 34 : Height : 175.5 + : 1.57 • 177.9 + 169.6 + : : 6. 90 . 1.59 : MaxVO£ : 63.41 + : 65.38 + 58.50 + : JaU*B_*i0iDl _ 5 _ 3 i 5_8 ._ 5_jt \_ Aerobic - anaerobic t r a n s i t i o n threshold values were determined by using each of three sing l e indices (ie. LATT - blood lactate, EXTT - excess CC£, and WTT - the v e n t i l a t o r y equivalent for V0£, VE/VO£). The mean threshold V0£ values (+S.D.) for each method of AT detection, reported in I/min, were 3.65 + 0.57, 3.46 + 0. 6£, and 3.53 + ©.51 for each of LATT, EXTT, and WTT respectively. Table £ presents a c o r r e l a t i o n matrix for the reported indices. Diagrams 1 throuch 3 TABLE. 2. A c o r r e l a t i o n matrix between absolute VOc AnT values as determined throuch d i f f e r e n t method* LATT EX s T W T T LATT 1.3 EXTT 3. 95 * . 1.0 WTT : 0.91 * 0. 9£ * i . 0 * s i o n i f i c a n t at s-'<3.00: represent plots comparing the three indices anc report the repression ecuat ions. The highest c o r r e l a t i o n set ween t r a n s i t i o n thresholds determined through d i f f e r e n t methods was found between LATT and EXTT (r = 8. 95, ?<8.881). The lowest c o r r e l a t i o n between two measures was found Petween LATT and WTT (r = 12.91, P<8. 881). 4. 5: 4. £: X 3.9! T T 3. 6: m 3. 3: i / 3. 0: k g £.7: / m £.4; i n ... • E I G U R E_1_ LATT <mmoi/i) vs £XTT (mi/kc/min) fi = £1 R = 8.95 P(R)<8.881 X = 8. 8Sl3*Y + .6653 £.4 3.8 3. 6 4. £ LATT (rnmol/1) 4. 8 E I S U _ E _ £ _ i_ATT (rnmoi/I) vs WTT <V£/vu£) H = £1 R = 8.91 P(R) <8.881 X = 1.8£5b*Y - .0£9 £. 4 £.8 £. 8 • 3. 6 4. 4 LATT <mmol/l) - 4to - EI§yEI_3s_ EXTT (ml/ka/'min) vs WTT (VE/V02) N = £1 5? = 8.92 P < R) <8. 881 Y = .?462*X + .9974 2. 8 >. 8 3.6 4.4 EXTT <ml/kn/min> The equality of the three t r a n s i t i o n threshold V02 values (I/rnin) was determined through the use of a repeated measures ANOVA which revealed a s i g n i f i c a n t difference oe-cween c e i l means (F = 8.41, P<8.881). Post hoc cornoar i s i o n s revealed s i g n i f i c a n t differences between LATT and EXTT means (t = 4.287, P<8.881) and between EXTT and WTT means (t = 2.212, P<8.825), but a nonsignificant difference between the LATT and WTT means <see TABLE 3). There was a general trend for the EX i'7 to preceded the WTT, which preceded the LATT. Although the trends for the WTT were inconsistent, the trend for the EXTT to precede The L A T T held true in 19 of 21 subjects. As V02 (1/rnin) and time are l i n e a r l y related differences - 47 - between V02 means represent differences between tne means when represented as a time (minutes). The mean times (min) at which the t r a n s i t i o n thresholds occured were approximately 12 + 3 minutes (LATT), 10.5 + 3 minutes (EXTT), and 11.5 ± £.5 minutes (WTT). Using correlated t-Tests s i g n i f i c a n t differences were found between both LATT and EXTT means (t = 5.81. P<8.881) and EXTT and WTT means (t = £ . 8 8 , P, 8.858). The blood lactate t r a n s i t i o n threshold (LATT) was s i g n i f i c a n t l y delayed, as compared to the ve n t i l a t o r y t r a n s i t i o n threshold detected through the increased release of EXCO£ in expired a i r , with an average time delay of 1.4 minutes. TABLE_3_ RM ANOVA and Post Hoc comparisions of the threshold V0£ values (1/min) as detected through di f f e r e n t means TT . POST HOC CORRELATED T-TESTS. N . MEAN VQ2 INDEX LATT . EXTT . WTT (1/min) LATT — t = 4 . £ 9 . t = 1.33 £1 . 3.65 +8.57 . EXTT . P (8.881 . . t =£. £1 £1 . 3. 46 +8. 63 . WTT . P>8. 85* . P <8. 8£5 . — £1 . 3.58 +8.51 ,. ANOVA .F=8.41 . P<8. 881 . df * nonsignificant difference Individual subjects were compared over a r e l a t i v e period of time pre and post thresholds, using the EXCO£ and blood lactate threshold points as r e l a t i v e points of comparision. This procedure also allowed for the s i g n i f i c a n t time delay in the appearance of blood lactate to be accounted f o r . The subject's expired EXC02 volume and blood lactate concent rat i ons were compared over a f i v e minute pre threshold and f i v e minute post threshold period, for a t o t a l of eleven minutes. Apsolute values - 43 - of l a c t a t e (rnmoi/I) arid excess CG2 (ml/kc/rsin) c o r r a l atsc s i g n i f icarit l y (r = 8. 69, P <0. 801) (see DI AGRA*! 4) over t h i s 1: minute ranee- With an r * of 0.48, approximately 58?C of the v a r i a n c e i n blood l a c t a t e l e v e l s can be accounted f o r by cnances i n e x p i r e d excess C02 when using the TT as a r e l a t i v e point f o r ccrnparision. I n d i v i d u a l c o r r e l a t i o n s over ztis same time p e r i o d produced h i g h l y s i g n i f i c a n t c o r r e l a t i o n s (ranging from .82 t o .95, P<8.881), with approximately 88 - 98'/. of the v a r i a t i o n i n blood l a c t a t e being accounted f o r through changes i n EXCQ2. The i n f l u e n c e s o f both i n d i v i d u a l d i f f e r e n c e s and gender d i f f e r e n c e s rnay account f o r the lower grouped c o r r e l a t i o n o b t a i n e d . F IGURE_4_ L a c t a t e (mrnol/1) vs e x p i r e d excess C02 (ml/kg) over an 11 minute range (5 min. pre & post AT) using the AT as a r e l a t i v e point o f r e f e r e n c e n = £24 R = 8.69 P<8.881 X = .4391*Y - 1.7895 L A C T A T E (rnmol/1) - 43 - Changes i n EXC02 appear to t r a c k changes i n piood l a c t a t e l e v e l s when the t h r e s h o l d s are used as r e l a t i v e p o i n t s , although the nature of t h i s r e l a t i o n s h i p v a r i e s between i n d i v i d u a l s and gender. Both average male and female l a c t a t e v a l u e s were s i m i l a r pre t h r e s h o l d a f t e r which the female's blood l a c t a t e and EXC02 i n c r e a s e d at an i n c r e a s e d r a t e over the male's. The s i g n i f i c a n t i n d i v i d u a l c o r r e l a t i o n s of blood l a c t a t e and EXC02 over t h i s p e r i o d of time suggest the two are i n t e r r e l a t e d . DISCUSSION While p r e v i o u s s t u d i e s (Caiozzo et a i , 1932; Davis et a l , 1376; Wasserman et a l , 1973; Wasserman et a l , 1364) have demonstrated a r e l a t i o n s h i p between v e n t i l a t o r y and blood l a c t a t e t h r e s h o l d s , and e a r l i e r s t u d i e s have suggested t h a t EXC02 may r e f l e c t changes i n blood l a c t a t e (Issekutz et a l , 1351; Clode et a l , 1361), the exact r e l a t i o n s h i p between excess, non-metabolic C02 and blood l a c t a t e accumulation has yet t o be e l u c i d a t e d . The purpose of t h i s study was t o determine the r e l a t i o n s h i p between blood l a c t a t e and EXC02 throughout a p r o g r e s s i v e i n t e n s i t y t e s t i n twenty-one e l i t e l e v e l c y c l i s t s , w h i l e p a r t i c u l a r emphasis was placed on the r e l a t i o n s h i p between the blood l a c t a t e and the v e n t i l a t o r y (EXCD2, and VE/V02) t h r e s h o l d s . Although many s t u d i e s have examined the a e r o b i c - a n a e r o b i c t r a n s i t i o n t h r e s h o l d u t i l i z i n g a b i c y c l e e r g © m e t e r p r o g r e s s i v e i n t e n s i t y t e s t , an e x t e n s i v e review of the l i t e r a t u r e has not r e v e a l e d any p r e v i o u s s t u d i e s i n v e s t i g a t i n g these s p e c i f i c v e n t i l a t o r y measures or u t i l i z i n g such an e l i t e l e v e l s u b j e c t pool. The r e s u l t s o f t h i s study demonstrated s i g n i f i c a n t c o r r e l a t i o n s between each of the t h r e e i n d i c e s used i n determining the t r a n s i t i o n t h r e s h o l d (EXCQ2, VE/VQ2, and blood l a c t a t e ) . ft c o r r e l a t i o n of r=0.91 was found between the l a c t a t e and VE/VC2 t h r e s h o l d s , c o n s i s t e n t with e a r l i e r f i n d i n g s ' (Caiozzo et a i , 1932; Davis st a l , 1376; Wasserman et a l , 1 9 7 3 ). These p r e v i o u s authors have suggested that VE/VQ2 may o f f e r tins most s e n s i t i v e measure of the l a c t a t e t h r e s h o l d . T h i s study found the EXC02 t h r e s h o l d t o c o r r e l a t e best with the l a c t a t e t h r e s h o l d (r=8.95), although the EXCDS t h r e s h o l d d i d not r e p r e s e n t the a c t u a l occurance of the l a c t a t e t h r e s n o l d . ft s i g n i f i c a n t (P<8.881) d i f f e r e n c e was found between the average EXCD2 and l a c t a t e t h r e s h o l d s , r e p r e s e n t e d by a 1.35 minute time delay i n the appearance of blood l a c t a t e . fts the VE/V02 t h r e s h o l d point d i d not s i g n i f i c a n t l y d i f f e r from the l a c t a t e t h r e s h o l d p o i n t (P>8. 85), VE/V02 may be u t i l i z e d , as pre v i o u s r e s e a r c h e r s have suggested, t o r e f l e c t the point at which t h e r e i s an abrupt i n c r e a s e i n blood l a c t a t e (Caiozzo et a l , 1982; Davis et a l , 1976; Wasserman et a l , 1973). S t u d i e s which have used blood l a c t a t e as t h e i r c r i t e r i o n measure must be i n t e r p r e t e d with c a u t i o n . Recent s t u d i e s have suggested that blood l a c t a t e may not r e f l e c t i n t r a c e l l u l a r l a c t a t e p r o d u c t i o n o r c o n c e n t r a t i o n (Stainsby, 1986; Brooks, 1936). Although. VE/V02 and blood l a c t a t e have been found t o breakaway at s i m i l a r p o i n t s , these s i m i l a r i t i e s may i n no way r e f l e c t the accumulation o f i n t r a c e l l u l a r l a c t a t e . In t h i s study the n o n - s i g n i f i c a n t VE/VQ2 and l a c t a t e t u r n p o i n t d i f f e r e n c e may be due t o the e r r a t i c VE/V02 and l a c t a t e t u r n p o i n t r e l a t i o n s h i p . In 13 of 21 cases the VE/V02 t u r n p o i n t was equal t o or preceded the l a c t a t e t u r n p o i n t , while i n 8 of 21 cases the VE/V02 t u r n p o i n t occured a f t e r the l a c t a t e t u r n p o i n t (a range of 3 min. pre t o 2 min. post l a c t a t e t u r n p o i n t ) . Although the average VE/V02 t u r n p o i n t was not s i g n i f i c a n t l y d i f f e r e n t from the average lactate turnpoint, the wide range of VE/V02 turnpoint values, spanning the lactate turnpoint, may be largely responsible for t h i s finding.. EXC02 tumpoints were found to be more consistently related to the lactate tumpoints, preceding the lactate turnpoint i n 19 of £1 cases. Not only were the EXC02 and lactate turnpoints s i g n i f i c a n t l y correlated (r=i2. 95) a s i g n i f i c a n t difference was found between them (P<0.f2(21). This data suggests that EXC02 di f f u s e s across the muscle membrane more r e a d i l y than the lactate molecule i s released from within the c e l l , supporting evidence of a translocation mechanism (Stainsby, 1988). This hypothesis i s further supported by the r e s u l t s documented by Caiozzo et a l (1982) who found the VCD2 turnpoint was scual to, or preceded the lactate turnpoint in 13 of lb subjects, although the s i g n i f i c a n c e of such a difference was not investigated. The mean absolute lactate value was found to. be 3.35 mmol/1 (+0.829), occur ing over a 1.72 - 5.30 rnmol/1 range. These r e s u l t s would suggest that individual differences must be recognized (Stegrnann et a l , 1981), and that individual determination of the lactate threshold at a set value of 2 or 4 mmol/1 (Kindermann et a l , 1979; Sjodin et a l , 1981) i s not possible, being subject to large factors of error. The r e l a t i o n s h i p between blood lactate and EXC02 was investigated over an eleven minute range (5 min. pre and post turnpoint) in the present study. In order to compare subjects the EXC02 and lactate tumpoints were used as r e l a t i v e points for comparision. when the two curves were compared in t h i s manner i t was found that changes in EXCOS cl o s e l y tracked changes i n blood lactate, although the r e i a t ionshin was d i f f e r e n t for both males and females. Approximately 5054 of the variance i n blood lactate concentration could bs accounted for by changes in expired excess COS when using the turnpoint5 as r e l a t i v e points of reference (r=0. 69, P<3.081). Individual c o r r e l a t i o n s over the same period of time ranged from'0.82 to 3.96 (P<0.081). This data i s in agreement with the e a r l i e r findings of Bouhuys et a l (1966) who found a c o r r e l a t i o n c o e f f i c i e n t of r=8.80 between changes in blood lactate concentration and changes i n excess COS, although the grouped c o r r e l a t i o n i s much lower than those r e s u l t s found by Issekutz and Rodahl (r=0. 92,. 1961). The lower c o r r e l a t i o n c o e f f i c i e n t found for the group in t h i s study was largely influenced by the combination of the two sexes (male r=8.7£,. female r=8.73), while Bouhuys et a l (1966) found age to be an influencing factor. The r e f l e c t i o n of i n t r a c e l l u l a r lactate concentrations by pooled venous blood lactate l e v e l s must be acknowledged as a source of error (Brooks, 1986), while the C02 storage capacity of the ind i v i d u a l must also be acknowledged (Clode et a i , 19S7>. Previous studies have suggested however, that the use of a CDS balancing technique does allow changes in blood lactate to be determined with reasonable accuracy (Clode et a l , 1969; Clode et a l , 1967; Bouhuys et a l , 1966; Issekutz et a l , 1961). This study suggests that expired EXC02 may be r e f l e c t i n g i n t r a c e l l u l a r lactate production, as suggested by Volkov et ai (1975). The s i g n i f i c a n t differance between an increase in expired EX-COS and - 5 4 - blood l a c t a t e accumulation may r e f l e c t the delayed r e l e a s e o f l a c t a t e i n t o the blood stream, while EXC02 i s f r e e l y d i f f u s a b l e a c r o s s the c e l l membrane a t r a n s l o c a t i o n hinderance may prevent the r a p i d d i f f u s i o n o f l a c t a t e a c r o s s the c e l l membrane as suggested by S t a i n s b y (1986). Although the blood t r a n s i t time t o the c o l l e c t i o n s i t e must be c o n s i d e r e d as c o n t r i b u t i n g t o the delay, d u r i n g s t r e n o u s e x e r c i s e the t r a n s i t time i s decreased and would o n l y account f o r a very s m a l l p o r t i o n o f the observed d i f f e r e n c e . The average excess. COS t h r e h o l d v a l u e was 14.04 ml/kg/min (+2.7S). The mean a b s o l u t e l a c t a t e c o n c e n t r a t i o n at the t h r e s h o l d point was 3.35 mmol/1 (+0.8S9), i n c l o s e agreement with Hearst (198S unpublished d a t a ) . The wide range of t h r e s h o l d values, 1.7S - 5.3® mmol/1, suggests t h a t t h i s p o i n t i s h i g h l y dependent upon the i n d i v i d u a l and the s e t t i n g o f predetermined t h r e s h o l d v a l u e s would not al l o w f o r t h i s i n t e r - i n d i v i d u a l v a r i a t i o n . P r e v i o u s s t u d i e s i n v e s t i g a t i n g the r e l a t i o n s h i p between EXCOS p r o d u c t i o n and performance (Hearst, unpublished 198S; Rhodes et a l , 1981; Volkov et a l , 1975) have found t h a t a s i g n i f i c a n t r e l a t i o n s h i p does e x s i s t between these two v a r i a b l e s . The p r e v i o u s s t u d i e s have suggested that the index o f EXCOS i s d i r e c t l y r e l a t e d t o the magnitude of l a c t i c a c i d p r o d u c t i o n through the g l y c o l y t i c pathways and the organism's b u f f e r i n g c a p a c i t y . The EXCOS t u r n a o i n t may r e p r e s e n t the onset of m e t a b o l i c a c i d o s i s , as suggested by the r e l a t i o n s h i p between the t u r n p o i n t and performance v a r i a b l e s , w h i l e the r e l a t i o n s h i p between m e t a b o l i c a c i d o s i s and f a t i g u e has been w e l l documented (w'enger et a l , 1975). VE/V02 t h r e s h o l d p o i n t s are harder t o c i s c e m than those t h r e s h o l d p o i n t s i n the e x p i r e d EXC02 and Plood l a c t a t e accumulation. The VE/V02 t h r e s h o l d p o i n t s do, however, allow trie blood l a c t a t e t h r e s h o l d p o i n t s t o be p r e d i c t e d with a high degree o f accuracy. EXC02 may o f f e r a v a l u a b l e n o n i n v a s i v e method of determining the point where i n t r a c e l l u l a r l a c t a t e p r o d u c t i o n and consumption are unbalanced and the r a p i d onset o f met a b o l i c a c i d o s i s occurs. F u r t h e r i n v e s t i g a t i o n i n t o the r e l a t i o n s h i p between i n t r a - c e l 1 u l a r l a c t i c a c i d p r o d u c t i o n and the r e l e a s e o f EXC02 may all o w performance v a r i a b l e s t o be determined with g r e a t e r c a r e and accuracy. New r e s e a r c h t e c h n o l o g i e s w i l l a l l o w t h i s r e l a t i o n s h i p t o be b e t t e r documented i n the f u t u r e . - 5 6 - C H A P T E R F I V E : SUMMARY AND C O N C L U S I O N S - 57 - SUMMARY Sig n i f i c a n t c o r r e l a t i o n s were found between the threshold points as determined through three independent indices (blood lactate, excess C02, and the r a t i o VE/V02). The best c o r r e l a t i o n between any two of the threshold points was found between the threshold points as determined through the blood lactate index and the excess C02 index (r=0.95). ft c o r r e l a t i o n was found of r=®.9i between the threshold points as determined through the blood lactate index and the VE/V02 index, while a c o r r e l a t i o n of r=0.92 was found between the VE/V02 index and the excess C02 index. A s i g n i f i c a n t F r a t i o was found when comparing the threshold points as determined through the three independent indices (F=8.41, P<0.001). Post hoc te s t s revealed a s i g n i f i c a n t difference between the threshold points as determined through blood lactate and through excess C02 (P<0.001), and between the excess CD2 index and the VE/V02 index (P<0.025). There was no s i g n i f i c a n t difference found between the blood lactate and VE/V02 indices (P>0.05). The mean absolute lactate concentration at the threshold point was 3.35 mrnol/1 (+0.829), while the range of threshold values varied from 1.72 -5.30 mmol/1. The average excess C02 threshold value was 14.04 ml/kg/rnin (+2.72). Blood lactate concentration correlated s i g n i f i c a n t l y (r=0.69, P<0.001) with expired excess C02 volume over an 11 - 5-3 - minute range across the threshold points. Higher <©.S2 - ®«3S) c o r r e l a t i o n c o e f f i c i e n t s obtained for each individual express the independent nature of the r e l a t i o n s h i p between EXCQ2 and blood lactate. Excess C02 volume appeared to track blood lactate l e v e l s throughout the progressive i n t e n s i t y test, although excess CG2 volume increased at a s i g n i f i c a n t l y lower level (P<0.001) than did blood lactate, with an average time delay i n the appearance of blood lactate of 1.35 minutes (V02 difference of 0.133 l/min>. The r e l a t i o n s h i p between expired excess CQ2 volume and blood lactate concentration appeared to be sex dependant. The females (n=6) had a lower excess C02 volume for each unit of lactate concentration as compared to the males (n=15). When compared on a r e l a t i v e scale, with the zero point at the threshold point as determined through each of the two indices, the r e l a t i o n s h i p between blood lactate concentration and excess C02 volume can be visua l i z e d . T a b l e 1. Hypotheses: v a r i a b l e s s__. c o r r e l a t i o n s__. d i f f e r e n c e : si_./non : P : si_./non « P s LATT vs EXA7 : s i g n i f i c a n t :P<0. 001: s i g n i f i c a n t :P<0. 001: EXTT vs WTT : sig n i ficant :P<0. 001: s i gni f i c a n t :P<0. 025: WTT vs LATT : s i g n i f i c a n t :P<0.001: non-signif. :P>0. 050: Changes in expired excess C02 volume appear to track changes i n blood lactate concentration (r=0.63) when the two variables are put on a r e l a t i v e scale (accounting for the s i g n i f i c a n t time difference between the two threshold points), aithougn there i s a wide var iat ion -.between indivi d u a l s i n the exact nature of t h i s r e l a t i o n s h i p ie. blood lactate can not be predicted from excess QQS^ilh-lCE^2'D§ihlE-^££lJ'£^£li - 59 - CONCLUSIONS 1. There i s a strong r e l a t i o n s h i p (r=0.31 - 0.95) between the t r a n s i t i o n thresholds as determined through the three indices. £. Changes i n expired excess C0£ volume precede changes in blood lactate concentration and the ve n t i l a t o r y equivalent (VE/VO£). 3. Changes in expired excess C0£ volume appear to track changes in blood lactate concentration <r=8.69, P<0.001), although the exact nature of t h i s r e l a t i o n s h i p depends on the individual and appears to be influeced by gender. 4. Blood lactate concentration can not be accurately predicted from expired excess C0£ volume. 5. Further investigation i s required to determine the re l a t i o n s h i p between i n t r a - c e l 1 u l a r lactate concentration and expired excess C0£ volume. 6. The blood lactate concentration at the t r a n s i t i o n threshold may vary widely between ind i v i d u a l s (3.35 mmol/1 +0.8£3), and should not be set at a predetermined value. 7. Changes i n blood lactate concentration may not be r e f l e c t i n g changes in i n t r a - c e l l u l a r lactate concentration, with blood lactate thresholds not r e f l e c t i n g the rapid onset of metabolic acidosis. Excess C0£ may r e f l e c t increased i n t r a - c e l l u l a r lactate production with greater accuracy, making studies using blood lactate threshold points as t h e i r c r i t e r i o n reference suspect to wide margins of error. - SiZi - BIBLIOGRAPHY - 61 - REFERENCES ftlpert, N. R. Lactate production and removal and the regulation of metabolism. AnnaJ,s___Y^_Acad__S^ii 11.9(3): 995 1011, ~ 1965. Asmussen, E. Control of v e n t i l a t i o n in exercise. Ex.. Spt__Sc_ i - Rey_ 11: 24 - 54, 1.983. Aunola, S., and H. Rusko.- Reproducibility of aerobic and anaerobic thresholds in 20-50 year old men. Eur_ J__ApDjI_ Et3__i_i_ 53: 260 - 266, 1984.. Beaver, W. L. , K.. Wasserman, and B.J. 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The c o n t r i b u t i o n o f t h e k i d n e y t o t h e removal o f a l a c t i c a c i d : l o a d under normal a c i d o t i c c o n d i t i o n s i n t h e c o n s c i o u s r a t . C l i n . S c i . _£2l____§!_i_ed._ 48: 1.21 — 131, 1975. - 68 - APPENDIX P, - 6 9 - LACTATE THRESHOLDS: A SUMMARY OF OBSERVER ESTIMATES EXPRESSED IN MINUTES N=21 # I. 2 3 4 5 6 7 a 9 10 11 12: 13 14 15 16 17 18 19 2© 21 OBSERVER #1 #2 #3 13.0 13.0 13.0 18.5 18.0 18.0 10.5 10.0 10.0 15.5 15.5 15.0 14.0 14.5 10.5 10.5 10.5 13. 0 13. 0 15.5 13.5 14.5 16.5 16.5 17.0 7.0 7.5 14.5 14.5 14.5 12.5 12.5 12.5 11.5 12.0 11.5 10.0 10.5 11.0 11.0 10.5 9.0 9.0 10.0 10.0 10.0 10.0 8. 5 9. 5 12.0 12.0 12.5 9.0 9.0 10.0 10.0 10.0 10.0 ACCEPTED VALUE (MIN) 13. 0 18. 0 10. 0 15.5 14.5 10. 5 13. 0 15. 0 16. 5 7. 5 14.5 12.5 11.5 10. 5 10. 5 9.0 10. 0 10.0 12. 0 9. 0 10. 0 RANGE WIDTH 0. 0 0.5 0. 5 0.5, 0. 5 0.0 0. 0 2.-0 0. 5 0. 5 0. 0 0. 0 0. 0 0. 5 0. 5 0. 5 0. 5 0. 0 0. 5 1. 0 _____ AVERAGE <0.5 - 70 - EXC02 THRESHOLDS: A SUMMARY OF OBSERVER ESTIMATES EXPRESSED IN MINUTES OBSERVER #1 #2 #3 11.0 11.5 9.5 ia.5 i a . 0 ia.0 9. 0 9. 0 8. 5 12.0 12.0 12.0 11.5 ll.,5 11.5 10.5 10.5 10.5 12.5 12.5 12.5 14. 0 14. 5 12. 5 15.0 15.0 15.0 5.0 5.0 4.5 13.0- 13.0 12.5 11.5 12.0 11..0 10. 0 10. 0 10.0 10.5 10.0 9.0 9.0 5.0 5.0 9.0 9.0 9. 0 9.0 10.0 9.0 3. 0 8.0 9.5 10.0 9. 0 5.0 9. 0 9.0 9. 0 8. 0 9. 5 ACCEPTED VALUE (MIN) 11.0 18.0 9. 0 12.0 11.5 10.5 12.5 14.5 15.0 5.0 13.0 11.5 10.0 10.0 9. 0 5. 0 9. 0 9. 0 9. 5 8. 0 10. 0 RANGE WIDTH 2. 0 0. 5 0. 5 0. 0 0. 0 0.0 0. 0 2.0 0. 0 0. 5 0. 5 1 . 0 0. 0 0. 5 0. 0 0. 0 0. 0 0. 0 1.0 0. O _____ AVERAGE <0. 5 - 71 - VE/VG2 THRESHOLDS: A SUMMARY OF OBSERVER ESTIMATES EXPRESSED IN MINUTES N=21 # 1 2. 3 4 5. 6 7 a 9 10 11 12 13 14 15 16 17 ia 19 20 £1 OBSERVER #1 #2 #3 12.0 12.0 11.5 18.5 18."5 18.5 9.0 9.0 13.0 13.0 12.5 1.1.5 12.0 11.5 12.5 13.0 12.5 12.0 13.0 12.5 12.0 12.0 11.5 15..5 15.0 14.5 7.0 7.0 7.0 12.5. 13.0 13.0 13.5 15.5 10.0 9.5 9.5 9. iZ 9. 0 11.0 11.5 6.0 9.0 11.5 11.5 9.0 8.0 8.0 12.0 11.5 9. 0 11.5 11.0 11.0 11.0 10.0 18.0 12.0 10.0 10.0 9.5 ACCEPTED VALUE (MIN) 12. 0 18. 5 9.0 13.0 11.5 12. 5 12.5 12.0 14. 5 7. 0 13. 0 13. 5 9. 5 9. 0 11.5 9.0 8. 5 11.5 11.0 18. 0 10. 8 RANGE WIDTH 8. 5 8. 8 0. 8 0. 5 0.5 0.5 1.0 0.5 1.0 8. 8 0. 5 2. 5 0. 5 2. 5 0. 5 3. 8 1. 8 8. 5 8. 8 2. 8 AVERftGE <i.8 - 72 - APPENDIX B - 73 - ) — i i 1 1 1 1 1 1 T r Workload or time - 74 APPENDIX - 75 - E x C 0 2 and blood lactate Workload or time - 76 APPENDIX - 77 - 8L000 LACTATE (mmol/l) - 78 - BLOOD LACTATE (mmol/l) TIME (min)  oo i c E CI O U X u E X C E S S C 0 2 PROFILE MALE #6 "1 I I I I I 1 1 1 1 1 1 1 r 10 11 12 13 14 15 16 17 18 19 20 21 22 23 24 TIME (min) E X C E S S C 0 2 PROFILE MALE #12 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 1fl 19 20 21 2? 23 24 25 TIME (min) - 83 - V E / V 0 2 (l/min/ml)   - 86 - APPENDIX E AVERAGE EXC02 VALUES PRE AND POST THRESHOLD 24 -j 23 - 22 - 00 CO \ O £ E u A V E R A G E LACTATE V A L U E S PRE AND POST THRESHOLD • OVERALL LA AV. TIME (min pre/poat threahold) +-.. MALE LA AV. O FEMALE LA AV.

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