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The effect of induced alkalosis and acidosis on blood lactate appearance and performance capacity during… Brien, Donald Michael 1987

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THE EFFECT OF INDUCED ALKALOSIS AND ACIDOSIS BLOOD LACTATE APPEARANCE AND PERFORMANCE CAPACITY DURING SIMULATED ROVING by DONALD MICHAEL BRIEN B. Phys. Ed., Dalhousie U n i v e r s i t y , 1982 A THESIS SUBMITTED IN PARTIAL FULFILLMENT OF THE REQUIREMENTS FOR THE DEGREE OF MASTER OF PHYSICAL EDUCTION i n THE FACULTY OF GRADUATE STUDIES School of P h y s i c a l E d u c a t i o n We accept t h i s t h e s i s as conforming to the r e q u i r e d standard THE UNIVERSITY OF BRITISH COLUMBIA A p r i l , 1987 © Donald Michael B r i e n , 1987 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. Donald M. Brien Department of PHYSICAL EDUCATION The University of British Columbia 1956 Main Mall Vancouver, Canada V6T 1Y3 Date A p r i l 10,1987  DE-6(3/81) ABSTRACT In order t o t e s t the e f f e c t of a r t i f i c i a l l y induced a l k a l o s i s and a c i d o s i s on the appearance of blood l a c t a t e and work production, s i x w e l l - t r a i n e d oarsmen <age= 23.8 ±2.5 wt.= 82.0 ±7.5kg.) were t e s t e d on three separate o c c a s i o n s a f t e r i n g e s t i o n of 0.3 gm/kg body wt. ITH4C1 ( a c i d o s i s ) , M;aHC03 ( a l k a l o s i s ) or a placebo ( c o n t r o l ) . Blood was taken from a forearm v e i n immediately p r i o r t o e x e r c i s e f o r d e t e r m i n a t i o n of pH and bic a r b o n a t e (HC03). One hour f o l l o w i n g the i n g e s t i o n p e r i o d , s u b j e c t s rowed on a s t a t i o n a r y ergometer at a pre-determined sub-maximal r a t e f o r 4 minutes, then underwent an immediate t r a n s i t i o n t o a maximal e f f o r t f o r 2 minutes. Blood samples from an i n d w e l l i n g c a t h e t e r p l a c e d i n the c e p h a l i c v e i n were taken at r e s t and every 30 seconds throughout the 6 minute e x e r c i s e t e s t , and every 3 minutes d u r i n g a 30 minute p a s s i v e r e c o v e r y p e r i o d . P r e - e x e r c i s e blood v a l u e s demonstrated s i g n i f i c a n t d i f f e r e n c e s (p<0.01) i n pH and HC03 i n a l l three c o n d i t i o n s . Work outputs were unchanged i n the submaximal t e s t and i n the maximal t e s t (p>0.05), although a t r e n d toward decreased p r o d u c t i o n was ev i d e n t i n the a c i d o t i c c o n d i t i o n . A n a l y s i s of e x e r c i s e blood samples u s i n g ANOVA with repeated measures r e v e a l e d t h a t the l i n e a r i n c r e a s e i n blood l a c t a t e concentration(CBLA]) d u r i n g c o n t r o l was s i g n i f i c a n t l y g r e a t e r than a c i d o s i s (p<0.01), although CBLa] d u r i n g a l k a l o s i s were c o n s i s t a n t l y e l e v a t e d above c o n t r o l there was no s i g n i f i c a n t d i f f e r e n c e i n the l i n e a r t r e n d (p>0.05). During recovery, there was no s i g n i f i c a n t d i f f e r e n c e i n the r a t e of l a c t a t e disapperance amongst the three c o n d i t i o n s . It was concluded t h a t under t h i s p r o t o c o l a r t i f i c i a l m a n i p u l a t i o n of the acid-base s t a t u s of the blood does not s i g n i f i c a n t l y i n f l u e n c e work p r o d u c t i o n d e s p i t e s i g n i f i c a n t l y reduced CBLa] d u r i n g a c i d o s i s . The i n a b i l i t y of these pH changes t o a l t e r e x e r c i s e performance emphasizes the r e l a t i v e importance of the i n t r a c e l l u l a r and the e x t r a c e l l u l a r b u f f e r systems i n w e l l t r a i n e d a t h l e t e s . i i i TABLE OF CONTENTS A b s t r a c t i i L i s t of Ta b l e s v L i s t of F i g u r e s v i Acknowledgement v i i I. INTRODUCTION 1 II. METHODS 5 S u b j e c t s 5 Pre-Experimental Procedures 5 Experimental Procedures 6 L a c t a t e C o n c e n t r a t i o n Determination 8 S t a t i s t i c a l A n a l y s i s 8 I I I . RESULTS 10 P r e - e x e r c i s e Blood Values 10 Work Output and Performance 11 E x e r c i s e Blood L a c t a t e C o n c e n t r a t i o n s 12 Recovery L a c t a t e C o n c e n t r a t i o n s 12 IV. DISCUSSION 19 V. REFERENCES 30 APPENDIX A: REVIEW OF LITERATURE 34 APPENDIX B: PRE-EXERCISE BLOOD pH AND BICARBONATE VALUES ' 67 APPENDIX C: WORK OUTPUTS AND POWER OUTPUTS FOR EXERCISE TESTS 69 APPENDIX D: EXERCISE BLOOD LACTATE CONCENTRATIONS 71 APPENDIX E: RECOVERY BLOOD LACTATE CONCENTRATIONS 73 i v LIST QF TABLES 1. P r e - e x e r c i s e Blood Values 14 2, Work Output and Power P r o d u c t i o n During Ergometric Rowing 15 v LIST OF FIGURES 1. Mean Power P r o d u c t i o n For Each Minute During Ergometric Rowing In A c i d o s i s , A l k a l o s i s and C o n t r o l C o n d i t i o n s 16 2. Mean Blood L a c t a t e Values During Ergometric Rowing In A c i d o s i s , A l k a l o s i s and C o n t r o l C o n d i t i o n s 17 3. Mean Blood L a c t a t e Values During S t a t i o n a r y Recovery i n A c i d o s i s , A l k a l o s i s and C o n t r o l C o n d i t i o n s 18 v i Acknowledgement Perhaps those most worthy of acknowledgement are the s u b j e c t s . I t r u l y a p p r e c i a t e the time and energy they o f f e r e d and hope they gained from the experiance, I would a l s o l i k e t o thank my committee members Dr. Coutt.s, Dr. Rhodes and Dr. Taunton f o r t h e i r feedback and c o o p e r a t i o n . I am p a r t i c u l a r l y g r a t e f u l t o Dr. McKenzie f o r h i s input, guidance and encouragement throughout t h i s work and my Master's degree. Furthermore, I would l i k e t o thank Dr. Schutz f o r h i s s t a t i s t i c a l e x p e r t i s e and Dr. Parkhouse, Dr. Matheson, Walter M a r t i n d a l e and a l l o t h e r s i n v o l v e d i n data c o l l e c t i o n and a n a l y s i s . F i n a l l y I would l i k e t o acknowledge the s i g n i f i c a n t c o n t r i b u t i o n made by my wife Robbie. v i i I INTRODUCTION During i n t e n s e e x e r c i s e , anaerobic g l y c o l y s i s i s a c t i v a t e d t o meet engery demands t h a t exceed the c a p a c i t y of a e r o b i c metabolism (Stainsby, 1986). T h i s augmented c e l l u l a r s u pply of ATP r e s u l t s i n the accumulation of l a c t a t e and a concomitant r i s e i n hydrogen i o n c o n c e n t r a t i o n <[H+3). It i s t h e o r i z e d t h a t decrements i n pH a s s o c i a t e d with l a c t a t e p r o d u c t i o n i n h i b i t s both the c o n t r a c t i l e and energy producing processes of the muscle ( G o l l n i c k et a l . , 1986). In order to maintain or i n c r e a s e maximal e x e r c i s e i n t e n s i t y the need t o produce l a c t a t e i s e s s e n t i a l t o s a t i s f y the energy requirements. However, the adverse e f f e c t s a s s o c i a t e d with l a c t a t e p r o d u c t i o n e v e n t u a l l y l i m i t s e x e r c i s e performance c a p a b i l i t i e s . It i s t h e r e f o r e , e s s e n t i a l t o sequester the H+ i n c r e a s e w i t h i n the muscle by i n t r a c e l l u l a r b u f f e r systems or t r a n s p o r t the H+ out of the working muscle t o d e l a y the development of i t s d e t r i m e n t a l e f f e c t s . S e v e r a l s t u d i e s have demonstrated t h a t e x t r a c e l l u l a r pH i n f l u e n c e s the r a t e of l a c t a t e e f f l u x from the muscle(Mainwood and Vorsley-Brown 1975; Sea,1984). Hirche et a l . , (1975) found t h a t l a c t a t e e f f l u x was three times hig h e r d u r i n g a l k a l o s i s (high e x t r a c e l l u l a r b i c a r b o n a t e c o n c e n t r a t i o n ) than d u r i n g a c i d o s i s (low e x t r a c e l l u l a r pH) i n blood p e r f u s e d working dog gastrocnemius. As the s t a t u s of the e x t r a c e l l u l a r f l u i d s appears to p l a y a key r o l e i n determining the r a t e of proton e f f l u x , 1 and a decrease i n i n t r a c e l l u l a r pH has been i m p l i c a t e d as a l i m i t i n g f a c t o r d u r i n g maximal e x e r c i s e , an i n c r e a s e d b u f f e r i n g c a p a c i t y of the blood should manifest i t s e l f i n an improvement i n performance d u r i n g anaerobic e x e r c i s e ( C a s t e l l i n i and Somero, 1981). In an e f f o r t t o i n v e s t i g a t e the i n f l u e n c e of H+ on muscle f a t i g u e and e x e r c i s e performance c a p a c i t y , a r t i f i c i a l acid-base changes of the e x t r a c e l l u l a r f l u i d s have been induced by i n g e s t i o n or i n f u s i o n of sodium b i c a r b o n a t e <HaHC03) and ammonium c h l o r i d e (NH4C1). E a r l y r e s e a r c h e r s (Dennig et a l . , 1931; D i l l e t a l . , 1932; and Dorow et a l . , 1940) noted t h a t a r t i f i c i a l a c i d i f i c a t i o n a c h eived by HH4C1 i n g e s t i o n r e s u l t e d i n e a r l i e r e x h a u s t i o n than t h a t encountered d u r i n g normal c o n d i t i o n s . A s t a t e of a l k a l o s i s was a l s o e s t a b l i s h e d by HaHC03 i n g e s t i o n which r e s u l t e d i n an i n c r e a s e d performance c a p a c i t y and h i g h e r blood l a c t a t e c o n c e n t r a t i o n s CBLal. Based on these i n i t i a l f i n d i n g s subsequent s t u d i e s have demonstrated i n c o n s i s t a n t r e s u l t s (Johnson and Black, 1953; Margaria et a l . , 1971; Simmons and Hardt, 1973). More rec e n t i n v e s t i g a t i o n s t h a t use s p e c i f i c a n aerobic e x e r c i s e t a s k s and maximal t o l e r a b l e treatment dosages have demonstrated a s i g n i f i c a n t ergogenic e f f e c t with NaHC03 i n g e s t i o n CInbar et a l . , 1983; Wilkes et a l . , 1983; C o s t i l l et a l . , 1984; and McKenzie et a l . , 1986) while o t h e r s have r e p o r t e d t h a t induced a l k a l o s i s had no ergogenic b e n e f i t <Kindermann et a l . , 1977; Katz e t a l . , 1984). 2 A study by Jones et a l . , (1977) demonstrated that r e l a t i v e l y modest changes i n blood pH through NH4C1 and NaHCQ3 i n g e s t i o n s u b s t a n t i a l l y i n f l u e n c e d plasma l a c t a t e and performance time. A l a t e r study by the same i n v e s t i g a t o r s (Sutton et a l . , 1981) confirmed these r e s u l t s , d etermining t h a t e x e r c i s e time t o exhaustion was longest i n a l k a l o s i s and s h o r t e s t a f t e r NH4C1 a d m i n i s t r a t i o n . Corresponding plasma l a c t a t e c o n c e n t r a t i o n s were s i g n i f i c a n t l y h igher at submaximal work r a t e s and at exhaustion d u r i n g a l k a l o s i s , as compared t o a c i d o s i s . Examining the i n t e r n a l muscle compartment by needle biopsy these i n v e s t i g a t o r s were a b l e t o conclude t h a t the lower plasma l a c t a t e c o n c e n t r a t i o n s d u r i n g e x e r c i s e i n a c i d o s i s appeared t o be due to an i n h i b i t i o n of muscle g l y c o l y s i s combined with a r e d u c t i o n i n l a c t a t e e f f l u x . Muscle sampling was a l s o conducted by C o s t i l l et a l . , (1984) who observed a 42% improvement i n performance f o l l o w i n g NaHC03 treatment. A hig h e r muscle pH and a g r e a t e r drop i n blood pH immediately before the l a s t bout of i n t e r m i t t a n t e x e r c i s e support the concept t h a t an i n c r e a s e i n b u f f e r p o t e n t i a l of the e x t r a c e l l u l a r f l u i d s r e s u l t s i n a g r e a t e r e f f l u x of H+ from the muscle. The ergogenic p o t e n t i a l of NaHC03 " l o a d i n g " and the examination of the l i m i t i n g f a c t o r s of maximal e x e r c i s e i n normal h e a l t h y s u b j e c t s appear t o be a main concern of s e v e r a l r e s e a r c h papers. Few i n v e s t i g a t o r s have i n c l u d e d h i g h l y t r a i n e d a t h l e t e s d u r i n g t h e i r s p o r t s p e c i f i c e x e r c i s e task. As t r a i n i n g - i n d u c e d a d a p t i v e changes are r e s p o n s i b l e f o r a s p e c i f i c enhancement i n performance ( G o l l n i c k and Hermansen, 1973; Parkhouse et a l . , 1983) i n d u c i n g a l k a l o s i s 3 and a c i d o s i s and monitoring t h i s i n f l u e n c e throughout e x e r c i s e w i l l a l l o w a comparable d e r t e r m i n a t i o n of how t r a i n e d s u b j e c t s respond t o s h i f t s i n the acid-base s t a t u s of the blood. Futhermore i t may be p o s s i b l e t o i d e n t i f y the mechanisms r e s p o n s i b l e f o r the enhanced performance c a p a c i t y demonstrated by w e l l t r a i n e d a t h l e t e s . The purpose of t h i s i n v e s t i g a t i o n was to t e s t the hypotheses t h a t o r a l l y induced a c i d o s i s and a l k a l o s i s i n h i g h l y t r a i n e d s u b j e c t s w i l l i n f l u e n c e the appearance of blood l a c t a t e d u r i n g i n t e n s e e x e r c i s e and d u r i n g p a s s i v e recovery, and t h a t t h i s a cid-base d i s t u r b a n c e w i l l a l s o e f f e c t e x e r c i s e performance c a p a c i t y . More s p e c i f i c a l l y the hypotheses of t h i s i n v e s t i g a t i o n are: 1) During submaximal work, blood l a c t a t e c o n c e n t r a t i o n s w i l l be e l e v a t e d above c o n t r o l l e v e l s d u r i n g induced a l k a l o s i s ; 2) d u r i n g submaximal work, blood l a c t a t e c o n c e n t r a t i o n s d u r i n g induced a c i d o s i s w i l l be lower than c o n t r o l values; 3 ) d u r i n g maximal e x e r c i s e , work output c a p a c i t y w i l l be enhanced d u r i n g a l k a l o s i s and decreased d u r i n g a c i d o s i s compared to c o n t r o l , and 4) the r a t e of l a c t a t e disappearance i n p a s s i v e recovery, w i l l be h i g h e r i n a c i d o s i s and lower i n a l k a l o s i s compared to c o n t r o l i n t r a i n e d s u b j e c t s , 4 II METHODS Subj e c t s S i x oarsmen, a l l members of the N a t i o n a l Rowing team, three of which were members of the 1984 Olympic team <age=23.8±2.5 y r s ; height=187.2±4.4 cm; weight= 82.0±7.5 kg.) v o l u n t e e r e d f o r t h i s study. A l l s u b j e c t s were c u r r e n t l y f a l l o w i n g a s y s t e m a t i c d a i l y t r a i n i n g program. T e s t i n g took p l a c e i n the winter months as not to i n t e r f e r e with t r a i n i n g and r a c i n g d u r i n g the summer c o m p e t i t i o n season. A l l s u b j e c t s were very experianced with ergometric rawing as i t i s an important t r a i n i n g and mon i t o r i n g device. P e r m i s s i o n t o do t h i s r e s e a r c h was o b t a i n e d from the C l i n i c a l S c r e e n i n g Committee f o r Research and Other S t u d i e s i n v o l v i n g Human Su b j e c t s . W r i t t e n consent was obt a i n e d from each s u b j e c t a f t e r they were informed of the procedures and p o s s i b l e r i s k s i n v o l v e d i n t h i s study. A l l s u b j e c t s were ab l e t o complete the e n t i r e study. Pre-Experimental Procedures As blood l a c t a t e v a l u e s were t o be examined under t h r e e treatment c o n d i t i o n s a primary concern was t h a t the s u b j e c t s e x e r c i s e d at the same submaximal work r a t e d u r i n g the f i r s t f o u r minutes of the e x e r c i s e t e s t . Approximately f i v e days p r i o r t o experimental t e s t i n g each s u b j e c t r e p o r t e d to the l a b t o s u b j e c t i v e l y determine a submaximal 4 minute work r a t e based on p r e v i o u s maximal r a t e s o b t a i n e d over a 6 minute t e s t . Work output and s t r o k e r a t e was re c o r d e d every 5 30 seconds. A l l e x e r c i s e t e s t s were performed on a G j e s s i n g rowing ergometer ( G j e s s i n g Ergorow, Bergen, Norway) c o n s i d e r e d t o be the most a c c u r a t e l a b o r a t o r y t o o l which s i m u l a t e s the a c t u a l mechanics and p h y s i o l o g i c a l respones of on-the-water rowing (Hagerman et al.,1979). A s i x minute e x e r c i s e bout was chosen as i t s i m u l a t e s a 2000 meter race i n an e i g h t oared s h e l l . Experimental Procedures During t h i s t e s t the s u b j e c t s rowed at a submaximal r a t e f o r 4 minutes and then underwent an immediate t r a n s i t i o n t o a maximal e f f o r t f o r the l a s t 2 minutes. The s u b j e c t s underwent three separate experimental e x e r c i s e t e s t s w i t h i n a 2 week p e r i o d . S u b j e c t s were asked t o r e f r a i n from t r a i n i n g 24 hours before each t e s t i n g s e s s i o n . On t e s t i n g day, 3 hours p r i o r t o the e x e r c i s e t e s t body weight was measured and s u b j e c t s were a d m i n i s t e r e d e i t h e r NH4C1 ( a c i d o s i s ) , NaHC03 ( a l k a l o s i s ) , or a placebo ( c o n t r o l ) amounting to a t o t a l dose of 0.3g/kg body weight. The placebo a d m i n i s t e r e d was l a c t u l o s e , a substance used as a f i l l e r i n p r e s c r i p t i o n c a p s u l e s t h a t i s not absorbed i n t o the systemic c i r c u l a t i o n . The c a p s u l e s were i n g e s t e d over a 2 hour p e r i o d ending one hour before e x e r c i s e t e s t i n g began. Approximately 500 ml of water was consumed a l o n g with the c a p s u l e s t o a i d i n g e s t i o n . The order of t e s t i n g was randomly a s s i g n e d and the experiment was conducted i n a double b l i n d manner. To determine whether a s i g n i f i c a n t change had o c c u r r e d i n p r e - e x e r c i s e acid-base s t a t u s (one hour f o l l o w i n g 6 the i n g e s t i o n period) a p r e - e x e r c i s e blood sample was taken from a forearm v e i n and immediately analysed i n d u p l i c a t e f o r pH and bi c a r b o n a t e determination, on a Corning 175 Automated Blood Gas Analyser. F o l l o w i n g t h i s sample, a 20 guage t e f l o n c a t h e t e r was i n s e r t e d under s t e r i l e c o n d i t i o n s i n t o the c e p h a l i c v e i n of the l e f t arm. 100 cm. of I.V. t u b i n g was used t o connect a 20 cc. s y r i n g e f i l l e d with normal s a l i n e t o the c a t h e t e r . A f t e r a s t a n d a r d i z e d warm-up s u b j e c t s performed the 6 minute e x e r c i s e t e s t . I n f u s i o n of normal s a l i n e was used to keep the c e p h a l i c v e i n patent, and to c l e a r the draw tube of the p r e v i o u s sample. T h i s sampling technique p r o v i d e d a r e l i a b l e a c c e s s t o an u n r e s t r i c t e d flow of bloo d without i n t e r f e r i n g with the rowing movement. The preplanned submaximal work r a t e was v i s u a l l y d i s p l a y e d i n f r o n t of the s u b j e c t s . Work output and s t r o k e r a t e were monitored every 30 seconds t o i n s u r e t h a t the submaximal r a t e was maintained. The s u b j e c t s were always i n f u l l view of the work r a t e i n d i c a t o r and c o n t i n u a l l y n o t i f i e d of the e l a p s e d time. At f o u r minutes s u b j e c t s were i n s t r u c t e d t o row a t the hi g h e s t work r a t e p a s s i b l e f a r the f i n a l 2 minutes. A 30 minute p a s s i v e r e c o v e r y p e r i o d f o l l o w e d the e x e r c i s e t e s t . In t o t a l , twenty three, 1-1.5 ml venous blood samples were taken d u r i n g each experimental t r i a l . Beginning with the r e s t i n g sample, samples were drawn every 30 seconds d u r i n g the 6 minute e x e r c i s e t e s t , and at 1,3,6,9,12,15,18,21 25, and 30 minutes p o s t - e x e r i c e . Each sample was drawn 7 through the draw tube i n t o a s t e r i l e 3 cc. s y r i n g e . Samples were immediately p l a c e d i n a pre-marked t r e a t e d v a c u t a i n e r tube c o n t a i n i n g 17.5 mg. sodium f l u o r i d e and 14 mg. potassium o x a l a t e which i n h i b i t s g l y c o l y s i s i n the r e d blood c e l l . During the e x e r c i s e and r e c o v e r y p e r i o d samples were s t o r e d i n i c e . L a c t a t e C o n c e n t r a t i o n Determination A f t e r samples were c o l l e c t e d they were c e n t r i f u g e d at 7, 000/rpm f o r 10 minutes i n a r e f r i d g e r a t e d c e n t r i f u g e . At t h i s time, the supernatant was s e p a r a t e d from the packed c e l l s by m i c r o - p i p e t t i n g , and p l a c e d i n premarked storage tubes. The packed r e d blood c e l l s were d i s c a r d e d and the supernatant was f r o z e n at -20 C. A f t e r a l l s u b j e c t s had completed a l l t h r e e treatment c o n d i t i o n s , the samples were thawed and analyzed e n z y m a t i c a l l y f o r l a c t a t e c o n c e n t r a t i o n a c c o r d i n g t o the methods of Bergmeyer <1974) and M c G r a i l et a l . , (1978). L a c t a t e c o n c e n t r a t i o n d e t e r m i n a t i o n was made with the Pye Unicam SP8-400 U.V. spectrophotometer. S t a t i s t i c a l A n a l y s i s The s t a t i s t i c a l a n a l y s i s used to i n v e s t i g a t e the e f f e c t of a r t i f i c i a l l y induced a l k a l o s i s and a c i d o s i s on blood l a c t a t e appearance was a two-way a n a l y s i s of v a r i a n c e with repeated measures and t r e n d a n a l y s i s a v a i l a b l e from the BMDP2V computer program (Dixon, 1981). T h i s a n a l y s i s was f a l l o w e d with a preplanned nonorthogonal comparion to r e v e a l s p e c i f i c d i f f e r e n c e s between treatment groups. E x e r c i s e b l o o d l a c t a t e c o n c e n t r a t i o n s and r e c o v e r y c o n c e n t r a t i o n s were 8 analyzed s e p a r a t e l y , and s t a t i s t i c a l s i g n i f i c a n c e was accepted at the p=0.01 l e v e l f o r a l l t e s t s of s i g n i f i c a n c e . Work output d u r i n g the 4 minute submaximal t e s t and the 2 minute maximal t e s t were a l s o c o n s i d e r e d s e p a r a t e l y . A one-way ANOVA model was used t o t e s t s i g n i f i c a n c e at the 0.05 l e v e l of p r o b a b i l i t y . A s i m i l a r a n a l y s i s was done f o r p r e - e x e r c i s e r e s t i n g blood pH and bicarbo n a t e v a l u e s with s t a t i s t i c a l s i g n i f i c a n c e accepted at p=0.01. When a s i g n i f i c a n t F r a t i o was acheived a post hoc S c h e f f e t e s t was used t o a s c e r t a i n where d i f f e r e n c e occurred. 9 P r e - E x e r c i s e Blood Values A n a l y s i s of the post-treatment blood sample taken one hour f o l l o w i n g the i n g e s t i o n p e r i o d r e v e a l e d t h a t a s i g n i f i c a n t a c i d o s i s <p<0.01> had been acheived f o l l o w i n g the i n g e s t i o n of NH4C1 and a s i g n i f i c a n t a l k a l o s i s <p<0.01) was observed f o l l o w i n g NaHCQ3 a d m i n i s t r a t i o n (Table #1). Values reco r d e d f o l l o w i n g the placebo treatment of l a c t u l o s e were c o n s i d e r e d t o be c o n t r o l and were found t o be i n the normal r e s t i n g range (Keele e t a l . , 1982). F o l l o w i n g NH4C1 a d m i n i s t r a t i o n blood pH and standard [HC03] was s i g n i f i c a n t l y decreased from c o n t o l v a l u e s of 7.34±0.03 and 24.9±1.1 mmol/1 r e s p e c t i v e l y t o 7.22±0.04 and 18.6±1.6 mmol/1. These blood v a l u e s were s i g n i f c a n t l y e l e v a t e d t o 7.40±0.03 and 31.5±2.3 mmol/1 one hour a f t e r NaHC03 intake. S h i f t s of s i m i l a r magnitude are r e p o r t e d by Jones et a l . , (1977),Wilkes et a l . , (1983) and McKenzie et a l . , (1986). Blood l a c t a t e c o n c e n t r a t i o n of the r e s t i n g samples taken immediately p r i o r t o warm-up was on the average h i g h e s t d u r i n g a l k a l o s i s 1.5±1.1 and lowest d u r i n g a c i d o s i s , 0.6 ±0.15 mmol/1. The c o n t r o l r e s t i n g blood l a c t a t e c o n c e n t r a t i o n was 1.0±.39 mmol/1 which i s c o n s i d e r e d normal ( G o l l n i c k et a l . , 1986). In g e n e r a l s u b j e c t s r e p o r t e d o n l y minimal g a s t r o i n t e s t i n a l d i s c o m f o r t s d u r i n g and f o l l o w i n g the i n g e s t i o n p e r i o d . On one o c c a s s i o n a s u b j e c t developed an 10 upset stomach and severe cramps a f t e r t a k i n g s e v e r a l c a p s u l e s at one time and was unable t o e x e r c i s e . Vork Output and Performance Table #2 p r e s e n t s work output and power p r o d u c t i o n d u r i n g the f o u r minute submaximal t e s t and the two minute maximal t e s t . There i s no s i g n i f i c a n t d i f f e r e n c e i n work output d u r i n g the f o u r minute submaximal p o r t i o n of the t e s t <p>0.05) with a work output of 83.5±4.6 KJ f o r c o n t r o l , and 83.5 ±4.4 KJ f o r a l k a l o s i s and 81.0±4.7 KJ d u r i n g a c i d o s i s . Therefore, as i n s t r u c t e d s u b j e c t s were ab l e t o repeat the pre-determined submaximal work r a t e d u r i n g each of the three treatment c o n d i t i o n s . The mean submaximal work output i s s l i g h t l y lower d u r i n g a c i d o s i s . Work done d u r i n g the maximal t e s t was a l s o not s i g n f i c a n t l y changed (p>0.05),with 42.0±2.0 KJ d u r i n g c o n t r o l compared t o 41.9±3.7 KJ d u r i n g a l k a l o s i s , a n d 38.3±4.7 KJ f o l l o w i n g NH4C1 i n g e s t i o n . Work output d u r i n g the submaximal and maximal t e s t was lowest d u r i n g a c i d o s i s i n a l l but one subj e c t . Power p r o d u c t i o n has been i n c l u d e d t o compare the work r a t e between the submaximal and maximal t e s t of the three experimental conditons. During a c i d o s i s power p r o d u c t i o n was lower d u r i n g the maximal t e s t d e c r e a s i n g from 337.4 W i n the submaximal t e s t t o 318.8 W d u r i n g the f i n a l 2 minutes. There was on l y a n e g l i g i b l e i n c r e a s e i n power d u r i n g the maximal t e s t i n a l k a l o s i s (349.2W) and c o n t r o l (350.0W) compared t o the submaximal r a t e of 348.0 W. 11 C o n s i d e r i n g the s m a l l changes t h e r e i s no s i g n i f i c a n t d i f f e r e n c e i n power p r o d u c t i o n (p>0.05) between the submaximal and maximal t e s t i n a l l three treatment c o n d i t i o n s as presented i n F i g u r e #1. E x e r c i s e Blood L a c t a t e C o n c e n t r a t i o n s F i g u r e #2 p r e s e n t s the mean s e r i a l blood l a c t a t e c o n c e n t r a t i o n s of the three experimental c o n d i t i o n s , d u r i n g the s i x minute e x e r c i s e bout. At the f o u r minute mark (end of the submaximal t e s t ) of the e x e r c i s e bout, the work output i s equal under each treatment c o n d i t i o n . A blood l a c t a t e c o n c e n t r a t i o n of 14.9 mmol/1 occured at t h i s time i n a l k a l o s i s , a c o n c e n t r a t i o n of 13.7 mmol/1 was measured i n the c o n t r o l c o n d i t i o n , and the lowest c o n c e n t r a t i o n , 10,3 mmol/1 was ev i d e n t d u r i n g a c i d o s i s . A s i m i l a r t r e n d f a l l o w e d at the end of the maximal t e s t (6 minutes) with a peak l a c t a t e c o n c e n t r a t i o n of 20.2 mmol/1 i n a l k a l o s i s , compared t o 17.9 mmol/1 i n c o n t r o l , and 12.4 mmol/1 c o n c e n t r a t i o n i n a c i d o s i s . A n a l y s i s of the mean s e r i a l b l o o d l a c t a t e c o n c e n t r a t i o n s determined t h a t , the 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 d u r i n g c o n t r o l was s i g n i f i c a n t l y g r e a t e r than a c i d o s i s (p<0.01). Although l a c t a t e c o n c e n t r a t i o n s d u r i n g a k l a l o s i s were c o n s i s t e n t l y e l e v a t e d above c o n t r o l , t h e r e was no s i g n i f i c a n t d i f f e r e n c e i n the t r e n d of the a l k a l o s i s and c o n t r o l values. Blood l a c t a t e c o n c e n t r a t i o n d u r i n g the s i x minute e x e r c i s e t e s t were s i g n i f i c a n t l y h i g h e r i n a l k a l o s i s compared t o a c i d o s i s (p<0.01). 12 Recovery L a c t a t e Concentrat i o n F i g u r e #3 p r e s e n t s the mean s e r i a l b l o o d l a c t a t e c o n c e n t r a t i o n of the three experimental c o n d i t i o n s d u r i n g a 30 minute p a s s i v e r e c o v e r y p e r i o d . There was no s i g n i f i c a n t d i f f e r e n c e i n the decrease of bloo d l a c t a t e c o n c e n t r a t i o n s between the a c i d o t i c , a l k a l o t i c and c o n t r o l c o n d i t i o n s . Blood sampling 1 minute p o s t - e x e r c i s e , r e v e a l s a notable decrease i n blood l a c t a t e c o n c e n t r a t i o n from the samples taken a t the c e s s a t i o n of e x e r c i s e , i n each of the treatment c o n d i t i o n s . Within 1 minute p o s t - e x e r c i s e blood l a c t a t e c o n c e n t r a t i o n decreased by 1.2 mmol/1 d u r i n g a c i d o s i s s i m i l a r 1.3 mmol/1 d u r i n g a l k a l o s i s and by 2.8 mmol/1 i n c o n t r o l . Blood l a c t a t e c o n c e n t r a t i o n 30 minutes p o s t - e x e r c i s e were s u b s t a n i a l l y e l e v a t e d above r e s t i n g v a l u e s with mean v a l u e s of 10.3 mmol/1, 8.6 mmol/1 and 4.7 mmol/1 f o r a l k a l o s i s , c o n t r o l and a c i d o s i s r e s p e c t i v e l y , 13 T a b l e I. P r e - e x e r c i s e b l o o d v a l u e s (Mean ±SD)  pH S t a n d a r d HCO3 (mmol /1) ACIDOSIS 7 .22 ± 0 . 0 4 * 1 8 . 6 ± 1 . 6 * ALKALOSIS 7 . 4 0 ± 0 . 0 3 * 3 1 . 5 ± 2 . 3 * CONTROL 7 .34 ± 0 . 0 3 * 2 4 . 9 ±1 .1 * P r e - e x e r c i e v a l u e s s i g n i f i c a n t l y d i f f e r e n t t h a n c o n t r o l ( p - ^ O . O l ) . 14 T a b l e I I . Work o u t p u t and power p r o d u c t i o n d u r i n g e r g o m e t r i c r ow ing (Mean ±SD) .  WORK ( K J ) POWER (W) T r e a t m e n t Submaximal 0 - 4 m i n . Ra te Maximal Ra te 4 - 6 m i n . Submaximal Ra te 0 - 4 m i n . Maximal Ra te 4 - 6 m i n . ACIDOSIS 8 1 . 0 ±4 .7 3 8 . 3 ± 4 . 7 3 3 7 . 4 ± 1 9 . 6 3 1 8 . 8 ± 3 9 . 2 ALKALOSIS 8 3 . 5 ± 4 . 4 4 1 . 9 ± 3 . 7 3 4 8 . 0 ±18 .3 3 4 9 . 2 ± 3 0 . 8 CONTROL 8 3 . 5 ± 4 . 6 4 2 . 0 ± 2 . 0 3 4 8 . 0 ±19 .2 3 5 0 . 0 ±16.7 15 Figure 1: Mean power production for each minute during ergometric rowing in acidosis, alkalosis and control conditions. 0 1 2 3 4 5 6 7 Exercise time (minutes) Figure 2: Mean (±S.E.M.) blood lactate values during ergometric rowing in acidosis, alkalosis, and control conditions 24 , j Rest .5 1.0 1.5 2.0 2.5 3.0 3.5 4.0 4.5 5.0 5.5 6.0 Exercise time (minutes) 17 Figure 3 : Mean (±S.E.M.) blood lactate values during stationary recovery in acidosis, alkalosis, and control conditions l J L . 1 i 1 « « » « « 0 3 6 9 12 15 18 21 24 27 30 Recovery time (minute) 18 IV DISCUSSION In the present study h i g h l y t r a i n e d oarsmen were s t u d i e d d u r i n g ergometric rowing t o i n v e s t i g a t e the i n f l u e n c e of a r t i f i c i a l l y - i n d u c e d acid-base d i s t u r b a n c e s on the appearance of l a c t a t e i n the blood, and the r o l e these induced changes p l a y i n performance c a p a c i t y . The e x e r c i s e t e s t was designed t o a l l o w f o r comparison of CBLa] at i d e n t i c a l submaximal work r a t e s and a maximal e f f o r t under c o n d i t i o n s of a l k a l o s i s , a c i d o s i s and c o n t r o l . With t h i s p r o t o c o l , the extent t o which changes i n e x t r a c e l l u l a r pH and CHC03] i n f l u e n c e l a c t a t e e f f l u x from the muscle, and the consequence t h i s has on performance c a p a b i l i t i e s can be considered. R e s u l t s from t h i s study demonstrate t h a t work output remained unchanged from c o n t r o l , f o l l o w i n g i n g e s t i o n a maximal t o l e r a b l e dose <0.3g/kg body weight) of NH4C1 ( a c i d o s i s ) and NaHC03 ( a l k a l o s i s ) , d u r i n g a 4 minute submaximal e x e r c i s e bout, immediately f o l l o w e d by a 2 minute maximal t e s t . These r e s u l t s c o n t r a d i c t f i n d i n g s by Jones et a l . , (1977) and Sutton et a l . , (1981) who have shown t h a t s i m i l a r p r e - e x e r c i s e acid-base changes s i g n i f i c a n t l y e f f e c t e x e r c i s e performance. These authors have r e p o r t e d t h a t time t o e x h austion was longest a f t e r a l k a l i n i z a t i o n (p<0.05) and s h o r t e s t f o l l o w i n g NH4C1 i n g e s t i o n (p<0.05) i n comparison t o c o n t r o l p e r i o d . The r e s u l t s of the i n i t i a l i n v e s t i g a t i o n s which induced a r t i f i c a l a c i d o s i s and a l k a l o s i s by Denning et a l . , (1931) and D i l l e t a l . , (1932) concur with the f i n d i n g s , o f Jones and Sutton, however, these e a r l i e r r e s u l t s and s e v e r a l 19 subsequent s t u d i e s which o n l y induced a l k a l o s i s (Johnson and Black, 1953; Margaria et a l . , 1971 and Simmons and Hardt, 1973) are somewhat c o n f l i c t i n g and i n c o n c l u s i v e . In these s t u d i e s i t i s u n l i k e l y t h a t the treatment dosage was adequate enough to produce a s u b s t a n i a l change i n b l o o d pH. In a l l cases the treatment dosage was l e s s than 20% of t h a t employed i n the present study. Furthermore, i n some i n s t a n c e s the e x e r c i s e t a s k was s t r i c t l y a e r o b i c i n nature, which o n l y e l i c i t e d minimal i n c r e a s e s i n [ BLa] , t h e r e f o r e not adequately t e s t i n g the e f f e c t of changes i n e x t r a c e l l u l a r pH on l a c t i c a c i d accumulation. S e v e r a l , more re c e n t s t u d i e s t h a t have c o n t r o l l e d f o r these e r r o r s have demonstrated s i g n i f i c a n t e rgogenic b e n e f i t s with NaHC03 i n g e s t i o n (Inbar e t a l . , 1983; Wilkes et a l . , 1983; MacLaren and Morgen 1985; McKenzie et a l . , 1986). Although a e r o b i c energy sources c o n t r i b u t e s i g n i f i c a n t l y t o the energy demands of the e x e r c i s e t e s t used i n the present study, i t i s u n l i k e l y t h a t the t a s k i s i n s u f f i c i e n t t o adequately examine the a b i l i t y of the a t h l e t e s t o accumulate l a c t i c a c i d at a h i g h r a t e . D e s c r i p t i v e s t u d i e s on rowing and e l i t e rowers i n d i c a t e t h a t t h i s a c t i v i t y provokes extremely h i g h a e r o b i c and anaerobic respones throughout the e x e r c i s e bout. These a t h l e t e s f u n c t i o n at a very h i g h percentage of t h e i r maximal a e r o b i c c a p a c i t y and i n doing so they develop an immediate s i g n i f i c a n t a n aerobic response which must be t o l e r a t e d f o r the remainder of the event (Hagerman e t a l , , 1979; Koutedakis and Sharp, 1985). The t r e n d of s e r i a l blood l a c t a t e v a l u e s 20 and peak [ BLa] d u r i n g c o n t r o l c o n d i t i o n s i n t h i s study-compare f a v o u r a b l y with those of other e r g o m e t r i c rawing s t u d i e s (Hagerman et a l . , 1979; McKenzie and Rhodes, 1982). The Peak [BLa3 of 20.2 mmol/1 witnessed i n the present study d u r i n g a l k a l o s i s are s l i g h t l y h i g h e r than the c o n t r o l v a l u e s of 17.9 mmol/1 which are s i g n i f i c a n t l y e l e v a t e d above the peak [BLa] a s s o c i a t e d with a c i d o s i s <12.4 mmol/1). The peak v a l u e s d u r i n g the a l k a l o t i c c o n d i t i o n are comparable t o the most extreme l e v e l s of l a c t a t e appearance r e p o r t e d i n the l i t e r a t u r e (Kindermann and Keul 1977; McCartney et a l . , 1986). Even though the f i r s t f o u r minutes of the e x e r c i s e t e s t was to be a submaximal t e s t and the l a s t 2 minutes were to be a maximal e f f o r t , examination of power p r o d u c t i o n (Figure #1) i n d i c a t e s t h a t work r a t e was v i r t u a l l y unchanged between these two p o r t i o n s of the t e s t . T h i s i n d i c a t e s t h a t they were working at a near maximal r a t e throughout the s i x minute t e s t . There does appear t o be a t r e n d of decreased work output d u r i n g a c i d o s i s . However, t h i s d i f f e r e n c e was not s i g n i f i c a n t . During t e s t i n g i t was apparant t h a t the s u b j e c t s were e x p e r i e n c i n g some d i f f i c u l t y and i n c r e a s e d d i s c o m f o r t i n t r y i n g t o maintain the pre-determined pace d u r i n g a c i d o s i s . The r e s u l t s observed d u r i n g the a l k a l o t i c c o n d i t o n of t h i s study are i n agreement with work by Kindermann et a l . , (1977) and Katz et a l . , (1984). In the Kindermann study NaHC03 and T r i s - b u f f e r were a d m i n i s t e r e d by infus.ion t o 21 normal h e a l t h y males u n t i l pH v a l u e s g r e a t e r than 7.5 were obtained. A f t e r b u f f e r i n f u s i o n run time <400m) and maximal [BLa] remained unchanged from c o n t r o l . A c c o r d i n g to Katz et a l . , (1984) c y c l i n g time to e x h a u s t i o n (approximately 100s) d i d not d i f f e r s i g n i f i c a n t l y between induced a l k a l o s i s <0.2g NaHC03/kg body weight) and a placebo CNaCL). An a n a l y s i s of v a r i a n c e with repeated measures over time was performed, i n order t o e v a l u a t e any d i f f e r e n c e s i n l a c t a t e appearance between the t h r e e experimental conditons, d u r i n g the e x e r c i s e t e s t . T h i s s t a t i s t i c a l a n a l y s i s of blood l a c t a t e t r e n d s d u r i n g the e x e r c i s e t e s t r e v e a l e d s i g n i f i c a n t l y decreased CBLa] d u r i n g a c i d o s i s . Whereas CBLa] f o l l o w i n g HaHC03 a d m i n s t r a t i o n tended to be e l e v a t e d above c o n t r o l v a l u e s throughout e x e r c i s e , these v a l u e s were not s i g n i f i c a n t l y d i f f e r e n t <p>0.05). Data from s e v e r a l animal s t u d i e s have e s t a b l i s h e d t h a t the e x t r a c e l l u l a r pH i s an important determinant i n the r a t e of l a c t a t e and H+ e f f l u x from the muscle. Mainwood and Worsley-Brown (1975) found t h a t e f f l u x of l a c t a t e from i s o l a t e d f r o g muscle i s f a c i l i t a t e d by i n c r e a s i n g the EHC03] of the p e r f u s i n g f l u i d . T h i s was a l s o a s s o c i a t e d with improved muscle f u n c t i o n . S i m i l a r l y Hirche e t a l . , (1975) determined t h a t l a c t a t e permeation was n e a r l y t h r e e times h i g h e r d u r i n g a s t a t e of induced a l k a l o s i s compared to a c i d o s i s i n e l e c t r i c a l l y s t i m u l a t e d i s o l a t e d b l o o d p e r f u s e d dog gastrocnemius. 22 These o b s e r v a t i o n s from animal s t u d i e s are supported by human i n v e s t i g a t i o n s . Jones et a l . , (1977) and Sutton et a l . , <1981) r e p o r t e d t h a t a f t e r NAHC03 treatment there were h i g h e r l a c t a t e l e v e l s i n the b l o o d at two submaximal work r a t e s (66% and 95% V02 max) than t h e r e was a f t e r STH4C1 a d m i n i s t r a t i o n . Through needle b i o p s y Sutton and c o l l e a g u e s <1981) c o u l d d i r e c t l y compare s e v e r a l g l y c o l y t i c i n t e r m e d i a t e c o n c e n t r a t i o n s amongst the t h r e e experimental c o n d i t i o n s . It was determined t h a t a r e d u c t i o n i n glycogen u t i l i z a t i o n a s s o c i a t e d with lower CBLa] i n a c i d o s i s , appeared to be due t o an i n h i b i t o n of muscle g l y c o l y s i s at the l e v e l of phosphofructokinase,combined with a r e d u c t i o n i n l a c t a t e e f f l u x . A more r e c e n t study by C o s t i l l et a l . , (1984) a l s o i n c l u d e d muscle sampling f o r muscle pH determination. F o l l o w i n g f o u r 1-minute c y c l i n g bouts at 100% V02 max, the f i f t h bout t o exhaustion i n an a l k a l o t i c c o n d i t o n (0.2g NaHC03/kg body weight) was 42% longer (p<0.01) than c o n t r o l t r i a l s . A h i g h e r muscle pH immediately before the f i f t h c y l c i n g bout, and a g r e a t e r drop i n blood [HC03] d u r i n g the repeated bouts supports the concept of a g r e a t e r e f f l u x of H+ from the muscle, due t o the i n c r e a s e d b u f f e r p o t e n t i a l of the e x t r a c e l l u l a r f l u i d . D e spite the s i g n i f i c a n t d i f f e r e n c e s observed i n blood and muscle pH and blood CHC03], th e r e was no d i f f e r e n c e between mean bloo d and muscle l a c t a t e v a l u e s between the NaHC03 t r i a l s and placebo (NaCl) t r i a l s . T h i s f e a t u r e of blood l a c t a t e i s c o n s i s t a n t with f i n d i n g s i n the present study; however, other s t u d i e s have demonstrated 23 i n c r e a s e d e f f l u x r a t e s of both H+ and l a c t a t e with i n c r e a s e s i n e x t r a c e l l u l a r [HC03] (Jones et a l . , 1977, Wilkes et a l . , 1983). The e f f l u x of l a c t a t e and H+ from the muscle t o the blood i s c o n s i d e r e d t o occur at s i m i l a r r a t e s i n man ( S a l h i n et a l . , 1976; S a l h i n et a l . , 1978) and i n v i t r o (Seo, 1984). On the c o n t r a r y e a r l i e r i n v e s t i g a t i o n i n man r e p o r t e d a s l i g h t l y h i g h e r i n c r e a s e i n base d e f i c i t than c o u l d be accounted f o r by l a c t a t e accumulation (Bouhuys e t a l . , 1966; Osnes and Hermansen, 1972). S i m i l a r f i n d i n g s are r e p o r t e d by Benade and H e i s l e r (1978) u s i n g the i s o l a t e d r a t diaphragm and f r o g s a r t o r i u s muscle. S a l h i n et a l . , (1978) has observed an excess accumulation of H+ d u r i n g the e a r l y p a r t of recovery. The a c t u a l mechanism f o r H+ and l a c t a t e t r a n s p o r t through the muscle c e l l i s complex and somewhat unclear. However, i t i s suggested t h a t d e s p i t e i t s pKa of 3.9, the u n d i s s o c a t e d molecule, l a c t i c a c i d , i s expected to be the major permeating s p i e c e s i n v i v o (Reybroack et a l . , 1975; Hultman and S a l h i n , 1980). There i s i n c r e a s i n g evidence t h a t i n t r a c e l l u l a r pH i s a l i m i t i n g f a c t o r d u r i n g maximal e x e r c i s e (Hultman and S a h l i n , 1980) and the pH s t a t u s of e x t r a c e l l u l a r f l u i d p l a y s a key r o l e i n determining i n t r a c e l l u l a r pH balance (Mainwood and Renaud, 1986). However, based on the r e s u l t s of t h i s present study the r o l e t h a t induced p r e - e x e r c i s e acid-base changes p l a y i n performance c a p a c i t y i s questionnable. There are a number of f a c t o r s i n t h i s experiment t h a t may account f o r the unchanged performance response under the a l k a l o t i c 24 and a c i d o t i c treatment c o n d i t i o n s . The major b u f f e r i n g components of human s k e l e t a l muscle are the b i c a r b o n a t e b u f f e r system, c r e a t i n e phosphate u t i l i z a t i o n , i n o r g a n i c phosphates, protein-bound h i s t i d i n e r e s i d u e s , and the h i s t i d i n e - c o n t a i n i n g d i p e p t i d e s c a r n o s i n e and a n s e r i n e (Hultman and S a h l i n , 1980). Parkhouse e t a l . , (1983) found c a r n o s i n e l e v e l s i n the vastus l a t e r a l i s muscle to be e l e v a t e d i n h i g h l y t r a i n e d 800 meter runners and rowers, compared t o marathon runners and u n t r a i n e d s u b j e c t s . Therefore, i t was concluded t h a t the c a p a c i t y of the s k e l e t a l muscle to b u f f e r r e s u l t a n t pH decrements a s s o c i a t e d with maximal e x e r c i s e may be enhanced, e n a b l i n g these t r a i n e d a t h l e t e s to s u s t a i n a naerobic work f o r an extended time before the onset of f a t i g u e . Another concern i s the r e s u l t s of animal l a c t a t e t r a c e r s t u d i e s t h a t have documented i n c r e a s e d m e tabolic c l e a r a n c e r a t e s ( i n c r e a s e d l a c t a t e removal, r e l a t i v e t o [BLa]) with endurance t r a i n i n g (Donovan and Brooks, 1983). T h i s a d a p t a t i o n permits lower l a c t a t e l e v e l s i n t r a i n e d i n d i v i d u a l s d u r i n g e x e r c i s e a t a g i v e n work r a t e s i n c e l a c t a t e p r o d u c t i o n i s balanced by an i n c r e a s e d r a t e of removal. As the primary metabolic f a t e of l a c t a t e and H+ i s t h a t of o x i d a t i o n , t h i s improved removal of l a c t i c a c i d w i l l serve t o suppress the f a l l of muscular pH d u r i n g e x e r c i s e . T h i s p o t e n t i a l f o r an enhanced i n t r a c e l l u l a r b u f f e r c a p a c i t y and a i n c r e a s e d r a t e of l a c t a t e c l e a r a n c e , c o u l d have a f f o r d e d the h i g h l y t r a i n e d s u b j e c t s i n the 2 5 present study an enhanced a b i l i t y t o d e a l with the i n h i b i t o r y e f f e c t s of maximal e x e r c i s e . Therefore, a l t e r a t i o n s i n the r a t e of l a c t a t e and H+ e f f l u x p r o v i d e d by pH changes i n the blood are perhaps not a dominant l i m i t i n g f a c t o r , a s maybe the case with u n t r a i n e d s u b j e c t s . T h i s may e x p l a i n why the s i g n i f i c a n t l y reduced blood l a c t a t e v a l u e s d u r i n g a c i d o s i s i n t h i s study were a s s o c i a t e d with a r e l a t i v e l y unchanged work r a t e while the l i t e r a t u r e r e p o r t s decreased performance with decreased CBLa] with u n t r a i n e d s u b j e c t s (Jones et a l . , 1977, Sutton et a l , , 1981). These ada p t i v e mechanisms may a l s o o f f e r a p l a u s i b l e e x p l a n a t i o n of why NaHC03 i n g e s t i o n d i d not produce an ergogenic e f f e c t d e s p i t e s l i g h t l y i n c r e a s e d [BLa]. The i n f l u e n c e of the e x t r a c e l l u l a r b u f f e r c a p a c i t y and the e f f e c t induced pH changes have on "whole-body b u f f e r i n g " must be kept i n p e r s p e c t i v e . It i s important t o c o n s i d e r t h a t the i n t r a c e l l u l a r b u f f e r mechanism r e p r e s e n t s 35 l i t e r s i n bulk compared t o the volume of the bloo d which i s about 5 l i t e r s (Keele et a l . , 1982). It has been suggested, t h a t s k e l e t a l muscle must be the most important determinant of o v e r a l l b u f f e r i n g c a p a c i t y by v i t u r e of i t s high mass, i t s range f o r metabolic a c t i v i t y and i t s hi g h anaerobic c a p a c i t y ( H e i s l e r and P i i p e r , 1972). On t h i s premise these a d a p t i v e changes of the muscle a s s o c i a t e d with a e r o b i c and anaerobic t r a i n i n g are v a l i d c o n s i d e r a t i o n s . F i n d i n g s of t h i s present study are not i n agreement with those of Wilkes et a l . , (1983) and McKenzie et a l . , 26 (1986) who r e p o r t ergogenic b e n e f i t s (p<0.05) i n moderatley t r a i n e d s u b j e c t s with induced metabolic a l k a l o s i s . A c c o r d i n g t o Wilkes f o l l o w i n g NaHC03 i n g e s t i o n (0.3g/kg body weight) the mean 800 meter r a c i n g time (N=6) was 2,9 seconds f a s t e r (p<0.05) than a c o n t r o l and placebo time of 2:05.8 and 2:05.1 r e s p e c t i v e l y . It i s q u e s t i o n a b l e whether the l e v e l of t r a i n i n g i n these s u b j e c t s i s comparable t o t h a t of the oarsmen i n the present study. It i s g e n e r a l l y accepted t h a t the c e l l membrane i s r e l a t i v e l y impermeable t o HC03 and there i s no s i g n i f i c a n t change i n muscle pH a f t e r i n g e s t i o n of HaHCQ3 (Robin, 1961; C o s t i l l e t a l . , 1984). T h i s concept i s debatable as s t u d i e s u s i n g animal p r e p e r a t i o n s have found some d i s c r e p a n c i e s (Adler e t a l . , 1965; Hirche et a l . , 1975). The p o s s i b i l i t y t h a t a d m i n i s t r a t i o n of NaHC03 does not i n f l u e n c e i n t r a c e l l u l a r acid-base balance may e x p l a i n why power output was not i n c r e a s e d d u r i n g a l k a l o s i s i n t h i s present study. A s i m i l a r assumption i s made by Katz et a l . , (1984). A subsequent study by C o s t i l l et a l . , (1984) d i r e c t l y determined t h a t muscle pH was unchanged f o l l o w i n g I$raHCQ3 i n g e s t i o n and r e p o r t e d an ergogenic b e n e f i t with repeated bouts of maximal e x e r c i s e . During r e c o v e r y the present data demonstrates t h a t b l o o d l a c t a t e v a l u e s g r a d u a l l y d e c l i n e toward r e s t i n g values, CBLa3 observed at one minute p o s t - e x e r c i s e were s l i g h t l y lower (1.2-2. 8mmol/l) than samples at the c e s s a t i o n of 27 e x e r c i s e . It i s r e p o r t e d t h a t f o l l o w i n g heavy e x e r c i s e CBLa3 c o n t i n u e s t o r i s e r e a c h i n g a peak approximately 5 minutes a f t e r the t e r m i n a t i o n of e x e r c i s e C G o l l n i c k et a l . , 1986). A p a s s i b l e e x p l a n a t i o n i s t h a t these h i g h l y t r a i n e d a t h l e t e are able t o o x i d i z e l a c t i c a c i d w i t h i n the s k e l e t a l muscle ( G o l l n i c k and Hermansen, 1973). It i s g e n e r a l l y accepted t h a t the use of a c t i v e r e c o v e r y f o l l o w i n g e x e r c i s e r e s u l t s i n a much higher r a t e of l a c t a t e r e d u c t i o n than complete r e s t (Bonen and B e l c a s t r o , 1976) which was the p r o t o c o l used i n the present study. Few human i n v e s t i g a t i o n s have ce n t e r e d on the e f f e c t s of pH changes on blood l a c t a t e appearance d u r i n g recovery. In the present study i t was noted t h a t t h e r e were no s i g n i f i c a n t d i f f e r e n c e s i n the decrease of CBLa] between the a c i d o t i c , a l k a l o t i c and c o n t r o l c o n d i t i o n s . Mainwood and Cechetto <1980) provide evidence which suggests t h a t an in c r e a s e i n e x t e r n a l b i c a r b o n a t e can a c c e l e r a t e the r e c o v e r y from f a t i g u e i n i s o l a t e d r a t diaphragm muscle. It was a l s o noted t h a t when e x t r a c e l l u l a r pH was h e l d at a low l e v e l , r e c o v e r y from f a t i q u e was suppressed. F o l l o w i n g a maximal c y c l i n g bout of about 1.5 min Katz et a l . , <1984) observed t h a t [BLa] cont i n u e d t o i n c r e a s e and reached a peak at 7-9 minutes p o s t - e x e r c i s e , i n both a c o n t r o l and a l k a l i n e c o n d i t i o n . At t h i s time [BLa] was s i g n i f i c a n t l y h i g h e r i n the a l k a l o t i c group u n t i l 20 minutes p o s t - e x e r c i s e . As blood l a c t a t e l e v e l s r e p r e s e n t a balance between l a c t a t e e n t r y and l a c t a t e removal i t c o u l d be hyp o t h e s i z e d t h a t the enhanced 28 r a t e of l a c t a t e removal through o x i d a t i o n , by these h i g h l y t r a i n e d s u b j e c t s may be a more important determinant i n blood l a c t a t e disappearance than e x t r a c e l l u l a r acid-base s t a t u s . In summary g i v e n the c o n d i t i o n s of t h i s i n v e s t i g a t i o n , i t i s concluded t h a t i n g e s t i o n of NH4C1 p r i o r t o i n t e n s e e x e r c i s e causes a s i g n i f i c a n t r e d u c t i o n i n blood l a c t a t e appearance d u r i n g the e x e r c i s e bout, i n r e l a t i o n t o c o n t r o l values. F o l l o w i n g NaHC03 i n g e s t i o n b l o o d l a c t a t e c o n c e n t r a t i o n s though s l i g h t l y e l e v a t e d , are not s i g n i f i c a n t l y d i f f e r e n t from c o n t r o l v a l u e s d u r i n g e x e r c i s e . Despite s i g n i f i c a n t s h i f t s i n p r e - e x e r c i s e pH and standar d CHC03] a f t e r NH4C1 and HaHC03 a d m i n i s t r a t i o n , submaximal respones and maximal work output c a p a c i t y are v i r t u a l l y unchanged. The t r e n d of blood l a c t a t e disappearance d u r i n g a 30 minute s t a t i o n a r y r e c o v e r y p e r i o d a l s o d i d not s i g n i f i c a n t l y d i f f e r between a l k a l o t i c , treatments, a c i d o t i c treatments, and c o n t r o l . 29 V REFERENCES Adler, S., Roy A., Relman, A.S. I n t r a c e l l u l a r acid-base r e g u l a t i o n . 1. 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L a c t i c a c i d removal and heart r a t e f r e q u e n c i e s d u r i n g r e c o v e r y a f t e r strenuous rowing e x e r c i s e . B r i t . J. S p o r t s Med. , 19(4): 199-202, 1985. Mainwood, G.V., and Cechetto, D. The e f f e c t of bi c a r b o n a t e c o n c e n t r a t i o n on f a t i q u e and recover y i n i s o l a t e d r a t diaphragm muscle. Can. J. P h y s i o l . Pharmacol.,58: 624-632, 1980. Mainwood, G. W. , and Vorsley-Brown, P. The e f f e c t of e x t r a c e l l u l a r pH and b u f f e r c o n c e n t r a t i o n on e f f l u x of l a c t a t e from f r o g s a r t o r i u s muscle. J. Ph y s i o l . , ( L o n d . ) 250: 1-22, 1975. Margaria, R., Aghemo, P., and S a s s i , G. E f f e c t of a l k a l o s i s on performance and l a c t a t e f ormation i n supramaximal e x e r c i s e . Int. Z. Angew. P h y s i o l . 29: 215-223, 1971. McCartney, W., S p r i e t , L.L., Heigenhauser, G.J., Kowalchuk, J.M., Sutton, J.R., and Jones, N.L. Muscle power and metabolism i n maximal i n t e r m i t t e n t e x e r c i s e . J. Appl.  P h y s i o l . , 60(4): 1164-1169, 1986. MacLaren, D.P.M., and Morgan, G.D. E f f e c t s of sodium bicarb o n a t e i n g e s t i o n on maximal e x e r c i s e . Proceedings  of the N u t r i t i o n S o c i e t y , 44, 26A, 1985. McGrail . J.C., Bonen, A., and B e l c a s t r o , A.N. Dependance of l a c t a t e removal on muscle metabolism i n man. Eur. J. Appl. P h y s i o l . , 39: 89-97,1978. McKenzie, D.C. Coutts, K., S t i r l i n g , D., Hoeben, H.H., and Kuzara, G. Maximal work p r o d u c t i o n f o l l o w i n g two l e v e l s of a r t i f i c a l l y induced metabolic a l k a l o s i s . J.  Sp o r t s S c i . , 4: 35-38, 1986. McKenzie, D.C., and Rhodes, E.C. C a r d i o r e s p i r a t o r y and metabolic respones t o e x e r c i s e on a rowing ergometer. Aus. J• S p o r t s Med., 14(1): 21-23, 1982. Osnes, J.B., and Hermansen, D. Acid-base balance a f t e r maximal e x e r c i s e of s h o r t d u r a t i o n . J. Appl. P h y s i o l . 32: 59-63, 1972. Parkhouse, ¥.S., and McKenzie, D.C. P o s s i b l e c o n t r i b u t i o n of s k e l e t a l muscle b u f f e r s t o enhanced anaerobic performance:a b r i e f review. Med. S c i . S p o r t s E x e r c i s e . , 6 (4): 328-338, 1984. 32 Parkhouse, W.S,, McKenzie, D.C, Hochachka, et a l . The r e l a t i o n s h i p between c a r n o s i n e l e v e l s , b u f f e r i n g c a p a c i t y , f i b e r types and anaerobic c a p a c i t y i n e l i t e a t h l e t e s . In: Bi o c h e m i s t r y of E x e r c i s e , H. Knuttgen, J. Vogel, and J. Poortmans (Eds.). Champaign IL: Human K i n e t i c s P u b l i s h e r s , 1983, pp. 275-278. Reybroack, T., Heigenhauser, G. J . , and Faulkner, J.A. L i m i t a t i o n t o maximum oxygen uptake d u r i n g arm, l e g and combined arm-leg ergometry. J.Appl. P h y s i o l . , 38: 774-779, 1975. Robin, E. D. Of men and mitochondria: i n t r a c e l l u l a r and s u b c e l l u l a r acid-base r e l a t i o n s h i p s . H. Engl• J. Med., 265: 780-785, 1961. S a h l i n , K., A l v e s t r a n d , A., Brandt, R., and Hultman, E. Acid-base balance i n bloo d d u r i n g exhaustive b i c y c l e e x e r c i s e and f o l l o w i n g the re c o v e r y p e r i o d . Acta P h y s i o l . Scand., 104: 370-372, 1978. S a h l i n , K., H a r r i s , R.C. Ny l i n d , B., and Hultman, E. L a c t a t e content and pH i n muscle samples o b t a i n e d a f t e r dynamic e x e r c i s e . P f l u g e r s Arch., 367: 143-149, 1976. Seo, Y. E f f e c t s of e x t r a c e l l u l a r pH on l a c t a t e e f f l u x from f r o g s a r t o r i u s muscle. Am. J. P h y s i o l . , 2 4 7 ( C e l l P h y s i o l . 16): C175-C181, 1984. Simmons, R.W., and Hardt, T.A. The e f f e c t of a l k a l i i n g e s t i o n on performance of t r a i n e d swimmers. J. Spor t s  Med. P h y s i c a l F i t . , 13: 159-63, 1973. Stainsby, W. N. Bioch e m i c a l and p h y s i o l o g i c a l bases f o r l a c t a t e p r o d u c t i o n . Med. S c i . Sp o r t s Exerc., 18(3): 341-343, 1986. Sutton, J.R., Jones, N.L., and Toews, C.J. E f f e c t of pH on muscle g l y c o l y s i s d u r i n g e x e r c i s e . C l i n . S c i . , 61: 331-338, 1981. Wilkes, D., Gledhi11,U., and Smyth, R. The e f f e c t of acute induced metabolic a l k a l o s i s on 800m r a c i n g time. Med. S c i . S p o r t s Exerc,, 15: 277-280, 1983. 33 APPENDIX A Review of L i t e r a t u r e 34 Review of L i t e r a t u r e I n t r o d u c t i o n During heavy e x e r c i s e the r a p i d f o r m a t i o n and accumulation of l a c t a t e and hydrogen ions<H+)during anaerobic g l y c o l y s i s produces s e v e r a l d e l e t e r i o u s e f f e c t s on energy metabolism and muscle f u n c t i o n (Hultman and S a l h i n , 1980; Sutton et a l , 1981). It i s t h e r e f o r e e s s e n t i a l t o sequester t h i s proton accumulation w i t h i n the muscle or t r a n s p o r t the H+ out of the working muscle, i f e x e r c i s e i s t o continue. The removal of l a c t a t e from the muscle has been assumed t o be a simple process of d i f f u s i o n CMargaria et a l . , 1963). Muscle samples ob t a i n e d by percutaneous biopsy have i n d i c a t e d t h a t a s u b s t a n t i a l c o n c e n t r a t i o n g r a d i e n t can e x i s t between l a c t a t e i n the muscle and l a c t a t e i n the blood a f t e r strenuous e x e r c i s e (Diamant e t a l . , 1965). Futhermore J o r f e l d t e t a l . , (1978) observed t h a t e x e r c i s i n g s k e l e t a l muscle e x h i b i t s a s a t u r a t i o n i n the l a c t a t e t r a n s l o c a t i o n process. Hence i t would appear t h a t something other than simple d i f f u s i o n l i m i t s the r a t e of l a c a t e e f f l u x . It has been r e p o r t e d t h a t the r a t e of H+ r e l e a s e was dependent upon the e x t e r n a l b i c a r b o n a t e c o n c e n t r a t i o n (Mainwood and Warsley-Brown, 1975). The l i t e r a t u r e i s somewhat i n c o n c l u s i v e as t o whether l a c t a t e passes through the muscle membrane i n i t s d i s s o c i a t e d or u n d i s s o c i a t e d form and whether proton and l a c t a t e r e l e a s e occur at the same r a t e . Whatever the mechanism of l a c t a t e t r a n s f e r , i t does appear t h a t the removal of t h i s i n h i b i t i n g endproduct ( l a c t i c a c i d ) i s a r a t e - l i m i t i n g process (Mainwood and 35 Renaud, 1985). Therefore, i n c r e a s e s i n e x t r a c e l l u l a r pH s h o u l d t h e o r e t i c a l l y augment l a c t a t e e f f l u x from the c e l l , d e l a y i n g the f a l l i n i n t r a c e l l u l a r pH, a l l o w i n g f o r g r e a t e r energy p r o d u c t i o n u l t i m a t e l y enhancing anaerobic performance (Wilkes et a l . , 1983). Decreasing e x t r a c e l l u l a r pH seems to support t h i s concept as a r t i f i c a l l y induced a c i d o s i s (NH4C1 i n g e s t i o n ) has been r e s p o n s i b l e f o r a l i m i t e d muscle g l y c o l y t i c c a p a c i t y , a n d r e d u c t i o n i n l a c t a t e removal from the muscle, r e s u l t i n g i n poor e x e r c i s e performance response (Sutton et a l . , 1981). In t h i s review of l i t e r a t u r e , the mechanisms of energy p r o d u c t i o n d u r i n g maximal e x e r c i s e w i l l be d i s c u s s e d along with the e f f e c t s t h a t proton accumulation has on f a t i q u e process. The c o n s t i t u e n t s which c o n t r i b u t e to s k e l e t a l muscle and blood b u f f e r i n g w i l l be o u t l i n e d to demonstrate how the body maintains a r e l a t i v e l y s t a b l e acid-base balance d e s p i t e the r a p i d p r o d u c t i o n of H+. The blood-muscle l a c a t e r e l a t i o n s h i p i s a l s o d e f i n e d , p a r t i c u l a r l y the l a c t a t e c o n c e n t r a t i o n g r a d i e n t t h a t e x i s t s d u r i n g e x e r c i s e . These mechanisms and f e a t u r e s are i n c l u d e d i n t h i s d i s c u s s i o n i n order to more c l e a r l y understand acid-base r e g u l a t i o n d u r i n g e x e r c i s e . S p e c i f i c emphasis i s p l a c e d on the metabolic response of a r t i f i c a l l y induced acid-base d i s t u r b a n c e s a t the muscle l e v e l i n i s o l a t e d animal muscle p r e p a r a t i o n s and i n whole body homeostatis i n e x e r c i s i n g humans. T h i s w i l l p r ovide i n s i g h t i n t o the f a t i q u e process and the r o l e e x t r a c e l l u l a r f l u i d s p l a y i n d e t e r m i n i n g p h y s i c a l performance c a p a c i t y . 36 L a c t i c A c i d and Muscular Performance During i n t e n s e e x e r c i s e the p r o d u c t i o n of l a c t i c a c i d i s due to the r a p i d a c t i v a t i o n of anaerobic g l y c o l y s i s t o meet the urgent metabolic demands th a t exceed the c a p a c i t y of a e r o b i c metabolism (Stainsby, 1986). The p r o d u c t i o n of ATP d u r i n g anaerobic g l y c o l y s i s i s a s s o c i a t e d with the r e d u c t i o n of pyruvate t o l a c t a t e . Pyruvate a c t s as a temporary e l e c t r o n and proton s t o r e i n the p l a c e of m i t o c h o n d r i a l co-enzymes, o x i d i z i n g n i c o t i n a m i d e adenine d i n u c l e o t i d e (NAD.2H) to NAD so t h i s hydrogen c a r r i e r can continue i t s f u n c t i o n i n the energy m o b i l i z a t i o n r e a c t i o n l e a d i n g t o the form a t i o n of more pyruvate(Keele et al.,1982). Despite being a v a l u a b l e energy source, a continuous h i g h g l y c o l y t i c r a t e , as experienced d u r i n g maximal e x e r c i s e , r e s u l t s i n severe i n t r a m u s c u l a r a c i d o s i s . The accumulation and d i s s o c i a t i o n of the end-product l a c t i c a c i d i s the major c o n t r i b u t o r t o the decrease i n intr a m u s c u l a r pH <pHI) with the remaining 10% c o n t r i b u t e d by ATP h y d r o l y s i s , the formation of glucose 6-phosphate and g l y c e r o l 1-phosphate and the incomplete o x i d a t i o n of f a t t y a c i d s t o B-hydroxybutyrate and a c e t o a c e t a t e (Hultman and S a l h i n , 1980). During i n t e n s e e x e r c i s e i n t r a c e l l u l a r pH i n human s k e l e t a l muscle has been found t o decrease from approximately 7.0 at r e s t t o 6.5 at exhaustion ( S a l h i n et a l . , 1976). T h i s r e d u c t i o n i n i n t r a c e l l u l a r pH a d v e r s e l y e f f e c t s many c e l l u l a r p r o c e s s e s i n h i b i t i n g s e v e r a l g l y c o l y t i c enzymes, r e d u c i n g the supply of ATP, and i n t e r f e r i n g with mechanical f o r c e g e n e r a t i o n by the muscle u l t i m a t e l y r e s u l t i n g i n f a t i q u e . It 37 i s g e n e r a l l y accepted t h a t an e l e v a t e d l a c t a t e c o n c e n t r a t i o n corresponds t o a decrease i n muscle performance ( K a r l s s o n et a l . , 1972; K a r l s s o n et a l . , 1975; F i t t s and H o l l o s z y , 1976). In v i t r o <Danforth, 1965) and i n v i v o s t u d i e s (Sutton et a l . , 1981) have determined t h a t two n o n - e q u i l i b r i u m enzymes phosphqrylase and phosphofructokinase are i n h i b t i e d at low pH and are t h e r e f o r e , p o s s i b l e g l y c o l y t i c r e g u l a t o r s . Apart from d i r e c t l y e f f e c t i n g enzyme a c t i v i t y , an i n c r e a e i n CH+] can a l s o change the i o n i c s t a t e of v a r i o u s g l y c o l y t i c i n t e r m e d i a t e s , i n h i b i t o r s , a c t i v a t o r s and c o - f a c t o r s i n f l u e n c i n g c a t a l y t i c r a t e (Hultman and S a l h i n , 1980). I n t r a c e l l u l a r a c i d o s i s has a l s o been found to have neg a t i v e e f f e c t s on the c o n t r a c t i l e process of the muscle. In s t u d i e s of s k i n n e d s k e l e t a l muscle of f r o g ( F a b i a t o and F a b i a t o , 1978) and r a b b i t muscle (Donaldson and Hermansen, 1978) r e d u c t i o n i n muscle pH lowered maximal t e n s i o n development and decreased the s e n s i t i v i t y of the myofilaments f o r calcium. The i n c r e a s i n g number of protons may compete with c a l c i u m f o r b i n d i n g s i t e s on troponon d i r e c t l y i n t e r f e r i n g with muscle c o n t r a c t i o n by r e d u c i n g the numbers of a v a i l a b l e actomyosin c r o s s - b r i d g e s (Katz, 1970; Brooks and Fahey, 1984). The muscle r e l a x a t i o n phase may be i n h i b i t e d d u r i n g a c i d o s i s due t o a decrease i n ATP/ADP r a t i o s lowing c r o s s - b r i d g e detachment and the r a t e at which c a l c i u m i s pumped i n t o the s a r c o p l a s m i c r e t i c u l i u m (Hultman et a l . , 1981). 38 Another p a s s i b l e mechanism i n which decreases i n pHI may e f f e c t muscle performance i s through i n t e r f e r a n c e of the e l e c t r i c a l a c t i v i t y of muslces. The form of a c t i o n p o t e n i a l s f o l l o w i n g a c t i v i t y i n muscle was r e p o r t e d t o change f o l l o w i n g e x e r c i s e (Hanson, 1974) and the elctromyogram of human s k e l e t a l muscle c e r t a i n l y undergoes changes i n f a t i q u e (Hakkinen and Komi, 1983). However, there i s no c o n c l u s i v e evidence on the i n t e r a c t i o n of f a t i q u e , pHI and n e u r a l muscular impulse (Renaud and Mainwood, 1983). Energy p r o d u c t i o n and muscle f u n c t i o n s are i n h i b i t e d with i n c r e a s e s i n l a c t a t e and the concomitant e l e v a t i o n i n CH+]. Therefore, d u r i n g a c o m p e t i t i v e event i t i s e s s e n t i a l t o n e u t r a l i z e p roton accumulation w i t h i n the c y t o s o l or remove t h i s i n h i b i t i n g end-product from the muscle i n order to s u s t a i n maximal i n t e n s i t y f o r optimal performance. I n t r a c e l l u l a r B u f f e r s It i s e stimated t h a t d u r i n g exhaustive e x e r c i s e the r e l e a s e of H+ t o the u n b u f f e r e d c y t o s o l c o u l d decrease pH t o about 1.5. (Hultman and S a l h i n , 1980). However, the muscle demonstrates a remarkable a b i l i t y t o m a intain r e l a t i v e l y constant pH l e v e l s by the s e q u e s t e r i n g of H+ through d i f f e r e n t b u f f e r i n g processes, B u f f e r c a p a c i t y r e f e r s t o the a b i l i t y of a b u f f e r t o r e s i s t changes i n pH upon a d d i t i o n of H+ or 0H-. S k e l e t a l muscle b u f f e r i n g has been c l a s s i f i e d i n t o t h r e e components each c o n t r i b u t i n g t o the t o t a l c e l l u l a r 39 b u f f e r c a p a c i t y ( S i e s j o and Messeter, 1981). These c o n s t i t u e n t s are: phy s i c o - c h e m i c a l b u f f e r i n g , metabolic b u f f e r i n g p r o c e s s e s and transmembrane f l u x e s of H+ and HC03. Physico-chemical b u f f e r i n g o c c u r s by the simple uptake at Ht by weak bases. During exhaustive e x e r c i s e the major c o n t r i b u t o r s t o t h i s p rocess are c e l l u l a r p r o t e i n s , b i c a r b o n a t e i o n s and i n o r g a n i c phosphates. The amino a c i d h i s t i d i n e and the h i s t i d i n e c o n t a i n i n g d i p e p t i d e s c a r n o s i n e and a n s e r i n e are important b u f f e r s as t h e i r pKa value are w i t h i n the p h y s i o l o g i c a l pH range (Somero, 1981; Woodbury, 1965). As muscle t i s s u e has a h i g h p r o t e i n content i t s b u f f e r f u n c t i o n i s s u b s t a n t i a l a c c o u n t i n g f o r approximately h a l f of the b u f f e r i n g by phy s i c o - c h e m i c a l processes. About 60% OF H+ uptake i n muscle i s due t o phy s i c o - c h e m i c a l b u f f e r i n g (Hultman and S a l h i n , 1980). I n t r a c e l l u l a r HC03 w i l l combine with H+ forming C02 ( v i a H2C03) which can r a p i d l y d i f f u s e through the c e l l membrane. If C02 i s unable t o escape due t o an e l e v a t e d e x t r a c e l l u l a r pC02 t e n s i o n ( c l o s e d system) t h i s p rocess w i l l r e p r e s e n t a r a t h e r i n e f f e c t i v e b u f f e r system. During exhaustive e x e r c i s e t h i s HC03 system c o u l d c o n t r i b u t e as much as 15-18% of t o t a l b u f f e r c a p a c i t y i n v i v o ( S a l h i n , 1978). The second component of i n t r a c e l l u l a r b u f f e r i n g i n v o l v e s the uptake of H+ d u r i n g v a r i o u s metabolic processes. The a b s o r p t i o n of H+ d u r i n g the u t i l i z a t i o n of c r e a t i n e -phosphate (CP) i s the most s i g n i f i c a n t metabolic b u f f e r i n g process. The content of CP i s much high e r i n a predominently g l y c o l y t i c muscle f i b e r compared t o o x i d a t i v e 40 muscle, t h e r e f o r e , the c a p a c i t y f o r t h i s b u f f e r i n g process would be expected to be much high e r i n the h i g h g l y c o l y t i c muscle (Hultman et a l . , 1980). The f o r m a t i o n of inosine-monophosphate (IMP) and the c a t a b o l i s m of amino a c i d d u r i n g exhaustive e x e r c i s e have onl y minor b u f f e r f u n c t i o n s . The t h i r d b u f f e r component of s k e l e t a l muscle i s the transmembrane passage of H+ and HC03. The movement of those ions depend on the p e r m e a b i l i t y of the membrane. S a h l i n et a l . , (1978) i n d i c a t e t h a t d u r i n g s h o r t term e x e r c i s e transmembrane H+/HCD3 f l u x e s are r a t h e r i n s i g n i f i c a n t as the accumulation of l a c t a t e and pyruvate i n the blood i s l i n e a r l y r e l a t e d t o the accumulation of H+ ions. By v i r t u e of i t s h i g h mass, i t s range of metabolic a c t i v i t y and i t s h i g h anaerobic c a p a c i t y , i t has been suggested t h a t s k e l e t a l muscle must be the most important determinant of o v e r a l l b u f f e r i n g c a p a c i t y ( H e i s l e r and P i i p e r , 1972). E x t r a c e l l u l a r B u f f e r s During maximal e x e r c i s e the r a p i d p r o d u c t i o n and accumulation of l a c t i c a c i d w i t h i n the muscle i s r e l e a s e d t o the blood and e x t r a c e l l u l a r f l u i d s . Despite t h i s c o n t i n u a l i n f l u x blood pH remains r e l a t i v e l y s t a b l e by the presence of b u f f e r systems i n the blood. The normal or r e s t i n g pH of blood i s a s l i g h t l y a l k a l i n e 7.40. Only i n extreme c o n d i t i o n s (during severe e x e r c i s e or r e n a l f a i l u r e ) w i l l the blood become t r u l y a c i d i c . The concept a c i d o s i s r e f e r s to a pH l e v e l l e s s than 7.4 while a l k a l o s i s d e s c r i b e s pH higher than 7.4 (Ferguson, 1965). A c i d o s i s and a l k a l o s i s can be 41 c l a s s i f i e d as e i t h e r r e s p i r a t o r y (gaseous) or metabolic (non-gaseous.) M e t a b o l i c a c i d o s i s i s p r i m a r i l y caused by an i n c r e a s e i n plasma [ H+3 while metabolic a l k a l o s i s i s r e l a t e d t o a i n c r e a s e i n plasma [HC03]. R e s p i r a t o r y a c i d o s i s i s caused by an inadequate e l i m i n a t i o n of C02 by the lungs compared to an e x c e s s i v e l o s s of C02 from the lungs d u r i n g r e s p i r a t o r y a l k a l o s i s (Ferguson, 1965; Keele et a l . , 1982). The extreme l i m i t s of b l o o d pH f o r s u r v i v a l are 6.8 t o 7.8. Upon e n t r y i n t o the blood the proton a s s o c i a t e d with l a c t a t e p r o d u c t i o n or other metabolic a c i d s combines with HC03 forming H2C03. H+ + HC03^-H2C03 — ^ C02 + H20 The e f f e c t of i n c r e a s e d C H+3 i s l e s s e n e d by the f o r m a t i o n of a p o t e n i a l l y v o l i t i l e weak a c i d of a (H2G03). T h i s r e a c t i o n r e s u l t s i n the f o r m a t i o n of C02 which can be e x p e l l e d by the lungs through a l v e o l a r v e n t i l a t i o n . R e s p i r a t o r y r e g u l a t i o n i s t h e r e f o r e a very powerful mechanism i n maintaing pH s t a b i l i t y . Any r i s e i n pC02 r e f l e c t s a r i s e i n [H+3 which e x c i t e s the r e s p i r a t o r y c e n t e r to i n c r e a s e v e n t i l a t i o n e l i m i n a t i n g the excess C02 u n t i l homeostasis has been regained. R e s u l t s of a r e c e n t study u s i n g a p r o g r e s s i v e incremental c y c l i n g t e s t shows t h a t decreases i n a r t e r i a l b i carbonate c o n c e n t r a t i o n [HC033 c l o s e l y match i n c r e a s e s i n a r t e r i a l l a c t a t e c o n c e n t r a t i o n (La) (Beaver et a l . , 1986). Bicarbonate and l a c t a t e data was analyzed u s i n g a l o g - l o g t r a n s f o r m a t i o n which i s a s i m i l a r mathematical model used i n 42 determining l a c t a t e t h r e s h o l d (Beaver et a l , , 1955), I n d i v i d u a l a n a l y s i s of t e n s u b j e c t s showed t h a t CHC03] decreases appeared t o l a g s l i g h t l y behind CLa] i n c r e a s e s . The correspondance between these two r e g r e s s i o n models was improved by assuming t h a t the a r t e r i a l CHC03] decrease was delayed u n t i l a r t e r i a l [ L a i had i n c r e a s e d t o 0,4 meg/1. The authors suggest t h a t such a de l a y i s compatible with the presence of i n t r a c e l l u l a r p r o t e i n b u f f e r s and c r e a t i n e phospate u t i l i z a t i o n which would b u f f e r the i n i t i a l i n c r e a s e of l a c t i c a c i d . Beyond t h i s i n i t i a l b u f f e r i n g l a c t i c a c i d i s expected t o be almost e n t i r e l y b u f f e r e d by the bi c a r b o n a t e b u f f e r system. The a d d i t i o n of a s t r o n g a c i d t o the bloo d w i l l not o n l y cause a decrease i n CHC03] but w i l l a l s o decrease the a n i o n i c c o n c e n t r a t i o n of blood p r o t e i n s p a r t i c u l a r l y haemoglobin and t o a l e s s e r extent plasma p r o t e i n s . The r e l e a s e of oxygen from oxyhaemoglobin i n c r e a s e s the a b i l i t y of hemoglobin t o combine with H+. The b u f f e r i n g p r o p e r t i e s of haemoglobin can be a t t r i b u t e d t o i t s h i s t i d i n e component (Keele, et a l . , 1982). During f l u c u a t i o n s i n acid-base balance the kidneys h e l p r e g u l a t e pH by the e x c r e t i o n of v a r i a b l e amounts of a c i d or base. Apart from the kidneys minor r o l e i n l a c t a t e metabolism d u r i n g e x e r c i s e , H+ can be e l i m i n t e d . These protons are a c t i v e l y t r a n s p o r t e d t o the t u b u l a r u r i n e i n exchange f o r Ua+ and e x c r e t e d as ammonium io n s and phosphate io n s (Hultman and S a h l i n , 1980). In the case of a l k a l o s i s 43 whether r e s p i r a t o r y or metabolic, r e n a l compensation i s e f f e c t e d by e x c r e t i o n of a more a l k a l i n e u r i n e c o n t a i n i n g h i g h l e v e l s of HC03 (Keele et a l . , 1982). T h i s compensatory a b i l i t y of the kidneys i s i l l u s t r a t e d by Wilkes et a l . , (1983) where s i x s u b j e c t s o r a l l y i n g e s t e d .3g kg body weight sodium bicarbonate. U r i n i n a r y pH i n c r e a s e d from a mean of 6,71 i n c o n t r o l t o 7,85 with a concurrent i n c r e a s e i n CHC03] from 21.0 m eg/1 t o 182.1 meg/1. The r e s p i r a t o r y compensation (hyperpnoea) a s s o c i a t e d with a c i d o s i s i s never so in t e n s e t o completely o f f s e t the i n f l u x of H+ (Keele et a l . , 1984). Compensation i s completed by the extremely e f f e c t i v e r e n a l e x c r e t i o n of H+. U n l i k e the immediate r e s p i r a t o r y response the kidneys f u n c t i o n over a p e r i o d of perhaps 10-20 hours t o r e s t o r e e q u i l i b r i u m (Mathews and Fox, 1976). It i s t h e r e f o r e the a c t i o n of the bicarbo n a t e b u f f e r system and blood p r o t e i n s t h a t are p r i m a r i l y r e s p o n s i b l e f o r blood pH r e g u l a t i o n d u r i n g strenuous e x e r c i s e . Blood-Muscle L a c t a t e R e l a t i o n s h i p s L a c t a t e i s a dynamic m e t a b o l i t e (Brooks and Fahey, 1984). During r e s t , e x e r c i s e , and re c o v e r y i t i s c o n t i n u a l l y being produced and s t o r e d by the muscle, r e l e a e d t o the venous blo o d and removed from the a r t e r i a l blood. Blood l a c t a t e c o n c e n t r a t i o n r e f l e c t s the i n t e r a c t i o n between the r a t e of l a c t a t e e n t r y i n t o the blood and i t s r a t e of removal. 44 The r e s u l t s of Erooks et al.,(1955? concur with the hy p o t h e s i s of Boyd et a l . , (1981) t h a t the blood l a c t a t e i n f l e c t i o n p o i n t d u r i n g graded e x e r c i s e i s due to a g r e a t e r i n c r e a s e i n l a c t a t e appearance than disappearance. During re c o v e r y and s t e a d y - s t a t e e x e r c i s e when blood l a c t a t e f a l l s toward r e s t i n g l e v e l s the r a t e of removal exceeds r a t e of appearance. L a c t a t e t r a c e r s t u d i e s i n v o l v i n g e x e r c i s i n g humans C J o r f e l d t , 1970; Hubbard, 1973 and Mazzeo et a l . , 1986) and animals (Donavan & Brooks, 1983; Hochachka, et al.,1985) have e s t a b l i s h e d t h a t the primary metabolic f a t e of l a c t a t e i s o x i d a t i o n t o pyruvate and u t i l i z a t i o n i n the Krebs Cycle. H i g h l y o x i d a t i v e a c t i v e and i n a c t i v e s k e l e t a l muscle f i b e r s are l a r g l e y r e s p o n s i b l e f o r the o x i d a t i o n of l a c t a t e (Baldwin et a l . , 1978; Gertz e t a l . , 1981, Brooks et a l . , 1985). The heart, l i v e r and kidney which are e n z y m a t i c a l l y s u i t e d f o r l a c t a t e uptake are i n v o l v e d t o a l e s s e r extent ( B e l c a s t r o and Bonen, 1975). Only a minor p o r t i o n (20%) of l a c t a t e i s re c o n v e r t e d i n an energy consuming process t o glycogen or glucose. F o l l o w i n g maximal e x e r c i s e s e v e r a l i n v e s i t a t i o n s have shown c o n s i d e r a b l y higher l a c t a t e c o n c e n t r a t i o n s i n the muscle than i n the blood. T h i s i m p l i e s t h a t muscle l a c t a t e i s formed more r a p i d l y than i t can be r e l e a s e d (Bergstrom, 1962; Graham, et a l , 1976). S t u d i e s have shown t h a t the c o n e n t r a t i o n of l a c t a t e i n working muscle a f t e r b r i e f maximum e x e r c i s e can be 2-3 times hig h e r than t h a t i n the blood (Karlsson, 1971). Diamant et a l . , (1968) r e p o r t s t h a t a f t e r 3 45 minutes of maximal e x e r c i s e on a b i c y c l e ergomster muscle t i s s u e l a c t a t e c o n c e n t r a t i o n was 19.1 mmol per kg wet muscle compared t o 11.4 mmol/1 i n the blood. The d u r a t i o n and i n t e n s i t y of e x e r c i s e i s an important c o n s i d e r a t i o n i n the r e l a t i o n s h i p between l a c t a t e c o n c e n t r a t i o n i n the muscle and blood. During prolonged e x e r c i s e , a f t e r an 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 values, the g r a d i e n t disappears. Hermansen, <1971) and Ka r l s s o n , (1971) r e p o r t t h a t both muscle and bloo d l a c t a t e c o n c e n t r a t i o n s are s i m i l a r when i n t e n s i t y e x e r c i s e l e a d s t o exhaustion i n 8 minutes or l e s s . A l s o r e l a t e d t o t h i s i s s u e i s an o b s e r v a t i o n by G o l l n i c k et a l . , <1986) t h a t f o l l o w i n g heavy e x e r c i s e the c o n c e n t r a t i o n of l a c t a t e i n the blood c o n t i n u e s t o i n c r e a s e , r e a c h i n g a peak value approximately 5 minutes a f t e r the t e r m i n a t i o n of e x e r c i s e . These p o i n t s i l l u s t r a t e t h a t l a c t a t e i s not f r e e l y d i f f u s a b l e from the muscle as once assumed (Margaria et a l . 1963) and t h a t blood l a c t a t e l e v e l s do not always r e f l e c t the i n t e r n a l s t a t e of the muscle. As notes by Hultman and S a l h i n C1980) i t was proposed by Sachs and Sachs, 1937 t h a t the r e l a t i v e l y slow t r a n s l o c a t i o n of l a c t a t e s e r v e s a p h y s i o l o g i c a l f u n c t i o n p r o t e c t i n g the blood from severe a c i d o s i s . T h i s low d i f f u s i o n r a t e of l a c t i c a c i d from muscle t o blood c o u l d a l s o have a gly c o g e n - s a v i n g purpose, as low e n t r a c e l l u l a r pH i n h i b i t s g l y c o l y s i s . A con t i n u e d glycogen d e g r a d a t i o n t o l a c t a t e c o u l d empty the l o c a l glycogen s t o r e of the muscle 46 w i t h i n 2 minutes. In r e v i e w i n g the i n t e r a c t i o n between pH and g l y c o l y s i s Hockachka and Mommsen <1985) hypothesize t h a t continuous H+ p r o d u c t i o n and accumulation e a r l y i n e x e r c i s e may e s t a b l i s h an optimum pH f o r g l y c o l y s i s . T h i s precedes the e s s e n t i a l l y i n h i b i t o r y e f f e c t s of a s u b s t a n t i a l decrease i n pH. F a c t o r s A f f e c t i n g the Rate of L a c t a t e E f f l u x  Animal S t u d i e s S e v e r a l s t u d i e s have demonstrated t h a t e x t r a c e l l u l a r pH i n f l u e n c e s the e f f l u x of l a c t a t e from the muscle. When supramaximally s t i m u l a t i n g i s o l a t e d blood p e r f u s e d g a s t r o c n e m i i of dogs Hirche et a l . , <1975) found th a t l a c t a t e permeation was n e a r l y three times h i g h e r d u r i n g induced a l k a l o s i s compared t o a c i d o s i s . T h i s s i g n i f i c a n t i n c r e a s e i n l a c t a t e e f f l u x c o u l d not be accounted f o r by minimal changes i n blood flow. Except f o r the f i r s t 5-6 min. of e x e r c i s e , power output and V02 decreased more r a p i d l y i n a c i d o s i s than i n a l k a l o s i s . M e t a b o l i c a c i d o s i s was induced by i n f u s i n g . 5IT HC1 i n t o the a r t e r i a l c i r c u l a t i o n while a l k a l o s i s was induced by NaHC03 or trishydorxymethy1-aminomethane (THAM)infusions; THAM i s a c a t i o n i c b u f f e r . Mainwood and Worsley-Brown <1975) s t u d i e d the r a t e of l a c t a t e e f f l u x from i s o l a t e d f r o g s a r t o r i u s muscle by e q u i l i b r a t i n g the muscle i n d i f f e r e n t b u f f e r s o l u t i o n s a f t e r r a i s i n g i n t e r n a l l a c t a t e by e l e c t r i c a l s t i m u l a t i o n . I n c r e a s i n g the pH of the s o l u t i o n from 7.0 to 8.0 <by i n c r e a s i n g CHC03]) r e s u l t e d i n a two or t h r e e f o l d i n c r e a s e i n peak l a c t a t e e f f l u x . T h i s e f f e c t was independent of the type 47 of b u f f e r system used and changes i n e f f l u x r a t e s occured . q u i t e r a p i d l y when the pH of the s o l u t i o n was changed. C o n d i t i o n s which enhanced the l o s s of H+ and l a c t a t e from the muscle were a l s o a s s o c i a t e d with an improved r e c o v e r y of t w i t c h t e n s i o n . F u r t h e r s t u d i e s showed t h a t the normal steady H+ e f f l u x i s stopped and a c t u a l l y r e v e r s e d when muscles are t r a n s f e r r e d from hi g h t o low b i c a r b o n t e s o l u t i o n s CCechetto and Mainwood, 1978). A more r e c e n t study by Seo (1984) g u a n t i t a t i v e l y analyzed the e f f e c t of e x t r a c e l l u l a r pH on l a c t a t e e f f l u x u s i n g l H - n u c l e a r magnetic resonance (NMR) which n o n d e s t r u c t i v e l y determines s e q u e n t i a l i n t r a 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 . L a c t a t e e f f l u x was shown t o i n c r e a s e i n p r o p o r t i o n t o i t s c o n c e n t r a t i o n d i f f e r e n c e a c r o s s the membrane and the p e r m e a b i l i t y of the membrane t o l a c t a t e i n c r e a s e d with i n c r e a s i n g increments of e x t r a c e l l u l a r pH. By i n f u s i o n of l a c t a t e a f t e r t en minutes of forearm e x e r c i s e J o r f e l d t <1970) found t h a t an i n c r e a s e i n a r t e r i a l l a c t a t e c o n c e n t r a t i o n from 1.1 mmol/1 t o 3.55 mmol/1 decreased the net r e l e a s e of l a c t a t e from 0.48 mmol min t o o. 18 mmol/min. T h i s c l e a r l y shows t h a t the t r a n s l o c a t i o n of l a c t a t e i s i n f l u c e n c e by the e x t r a c e l l u l a r c o n c e n t r a t i o n of l a c t a t e . Human S t u d i e s In 1931 Dennig and c o l l e a g u e s found t h a t a r t i f i c i a l a c i d i f i c a t i o n ' a c h ieved by i n g e s t i o n of 15 grams of NH4C1 on each of 2 days p r i o r t o t e s t i n g r e s u l t e d i n e a r l i e r 48 exhaustion i n endurance running than t h a t encountered d u r i n g normal c o n d i t i o n s . In f u r t h e r t e s t i n g , i n v o l v i n g the same su b j e c t , a s t a t e of a l k a l o s i s was e s t a b l i s h e d by i n g e s t i o n of 10 grams of NaHC03 on each of 2 days before the e x e r c i s e t e s t day. R e s u l t s i n d i c a t e d improvement i n t r e a d m i l l running times and an i n c r e a s e d a b i l i t y t o accumulate an oxygen debt compared t o a s t a t e of a c i d o s i s . Subsequent s t u d i e s conducted at the Harvard F a t i q u e Laboratory r e v e a l e d s i m i l a r r e s u l t s with i n c r e a s e d performance c a p a c i t y and higher maximum blood l a c t a t e c o n c e n t r a t i o n s i n swimmers and runners f o l l o w i n g sodium b i c a r b o n a t e a d m i n i s t r a t i o n ( D i l l e t a l . , 1932; Dennig et a l . , 1937; Dorow et a l . , 1940.). The r e s u l t s of subsequent s t u d i e s based on these i n i t i a l i n v e s t i g a t i o n s are somewhat c o n f l i c t i n g (Johnson and Black, 1953; Margaria e t a l . , 1971; Simmons and Hardt, 1973). As r e p o r t e d i n s e v e r a l more re c e n t papers (Kindermann et a l . , 1977; Wilkes et a l . , 1983; McKenzie et a l . , 1986.) the r e s u l t s of these e a r l i e r s t u d i e s are i n c o n c l u s i v e as i t i s d o u b t f u l t h a t the dose of NaHC03 was adequate enough t o produce a s i g n i f i c a n t a l k a l o s i s . In some cases the e x e r c i s e t a s k was s t r i c t l y a e r o b i c i n nature so the f r a c t i o n of energy d e r i v e d from l a c t a t e p r o d u c t i o n was minimal, not adequately t e s t i n g the e f f e c t of a l k a l o s i s on l a c t i c a c i d accumulation. S t u d i e s t h a t have c o n t r o l l e d these methodological f a u l t s and monitored blood pH, standard b i c a r b o n a t e and l a c t a t e v a l u e s have demonstrated s i g n i f i c a n t ergogenic e f f e c t s and i n c r e a s e d blood l a c t a t e c o n c e n t r a t i o n s d u r i n g 49 induced a l k a l o s i s (Jones et a l . , 1977; Sutton et a l . , 1981; Wilkes et a l . , 1983 and McKenzie et a l . , 1986). However, there are exce p t i o n s . Kindermann et a l . , (1977) i n f u s e d e i t h e r a NaHC03 s o l u t i o n or a T r i s B u f f e r s o l u t i o n t o induce an e l e v a t e d b u f f e r i n g c a p a c t i y i n t e n normal h e a l t h y males u n t i l a s i g n i f i c a n t i n c r e a s e i n pH was detected. These r e s e a r c h e r s found no improvement i n a 400-m run time f o l l o w i n g b u f f e r i n f u s i o n i n r e l a t i o n t o c o n t r o l t r i a l s , c o n c l u d i n g t h a t perhaps the g l y c o l y t i c turnover r a t e i s the performance l i m i t i n g f a c t o r d u r i n g exhaustive s h o r t - t e r m e x e r c i s e . On the c o n t r a r y Inbar e t a l . , (1983) demonstrated t h a t an i n c r e a s e i n p r e - e x e r c i s e blood pH v a l u e s by HaHC03 i n g e s t i o n (10 grams) can l e a d t o a sm a l l but s i g n i f i c a n t improvement i n anaerobic e x e r c i s e c a p a c i t y as determined by the 30 second Wingate Anaerobic Test. An i n v e s t i g a t i o n by Katz et a l . , (1984) showed t h a t an e x e r c i s e bout t h a t produced exhaustion i n 45-100s i s not i n f l u e n c e d by p r e - e x e r c i s e i n g e s t i o n of 0.2 g kg body weight WaHC03. At the c e s s a t i o n of e x e r c i s e and d u r i n g the f i r s t minutes of r e c o v e r y blood pH, base excess, HC03 and l a c t a t e were not a f f e c t e d by the a l k a l i i n g e s t i o n between the c o n t r o l and experimental t r i a l s u n t i l the 9th min. of recovery. T h e r e a f t e r , these v a l u e s where s i g n i f i c a n t l y h i g h e r (p<0.05) d u r i n g a l k a l o s i s i n d i c a t i n g a g r e a t e r l a c t a t e e f f l u x from the muscle and perhaps a more r a p i d r e t u r n t o a r e s t i n g acid-base s t a t u s c o n d i t i o n i n the blood. T h i s s p e c u l a t i o n l e a d t o a follow - u p study by C o s t i l l et a l . , (1984) t o determine the 50 i n f l u e n c e of the enhanced b u f f e r i n g of H"aHC03 on the a b i l i t y t o e x e r c i s e t o exhaustion a f t e r repeated bouts of intense aware? i s a . U n l i k e most other human s t u d i e s muscle sampling was i n c l u d e d f o r muscle pH determination. F o l l o w i n g f i v e 1-min. c y c l i n g bouts at 100% V02 max the f i n a l e xhaustive e x e r c i s e bout i n the a l k a l o t i c c o n t i o n <0.2 g kg body weight) was 42% longer <p<0.01) than the c o n t r o l t r i a l s . A higher muscle pH immediately before the f i f t h c y c l i n g bout and a g r e a t e r drop i n HC03 d u r i n g i n t e r m e d i a t e e x e r c i s e i n the NaHC03 c o n d i t i o n supports the concept of a g r e a t e r e f f l u x of H+ from the muscle as a consequence of the i n c r e a s e d b u f f e r p o t e n i a l of the e x t r a c e l l u l a r f l u i d s . Measurement of r e s t i n g muscle pH before and a f t e r HaHC03 i n g e s t i o n determined t h a t i n t r a c e l l u l a r pH was u n a f f e c t e d by bi c a r b o n a t e i n g e s t i o n . Despite the s i g n i f i c a n t d i f f e r e n c e s observed i n bloo d and muscle pH and blood HC03 values, there was no d i f f e r e n c e between mean bloo d and muscle l a c t a t e v a l u e s between the two treatments. T h i s f e a t u r e i s not c o n s i s t a n t with other acid-base balance s t u d i e s which demonstrate i n c r e a s e d e f f l u x r a t e s of both H+ and l a c t a t e with i n c r e a s e s i n e x t r a c e l l u l a r HC03 (Jones et a l . , 1977, V i l k e s et a l . , 1983). The ergogenic b e n e f i t s of bicarb o n a t e i n g e s t i o n i s a l s o supported by Wilkes e t a l . , (1983) who demonstrated a s i g n i f i c a n t improvement of 2.9 seconds <p<0.05) i n 800m running times of moderately t r a i n e d t r a c k a t h l e t e s f o l l o w i n g i n g e s t i o n of 0.3g NaHCQ3 per kg body weight. It i s s p e c u l a t e d t h a t improved performance, s i g n i f i c a n t l y i n c r e a s e d 51 p o s t - e x e r c i s e blood l a c t a t e and [H+] l e v e l s e v i d e n t d u r i n g a l k a l o s i s i s a consequence of an i n c r e a s e d anaerobic energy c o n t r i b u t i o n due t o a f a c i l i t a t e d H+ and l a c t a t e e f f l u x from the muscle, thereby l e s s e n i n g the f a l l i n i n t r a c e l l u l a r pH and u l t i m a t e l y d e l a y i n g the onset of f a t i q u e . In an e f f o r t t o r e s o l v e some of the c o n t r o v e r s y surrounding the e f f e c t s of pH changes p r i o r t o e x e r c i s e Jones, et al.,(1977) examined the bi o c h e m i c a l and c a r d i o r e s p i r a t o r y responses of induced a l k a l o s i s and a c i d o s i s . F i v e normal h e a l t h y males were a d m i n i s t e r e d 0.3g kg body weight, BTH4C1, NaHC03 or a placebo <CaC03> i n capsule form over a three hour p e r i o d before e x e r c i s e . S u b j e c t s e x e r c i s e d on a b i c y c l e ergometer f o r two 20-minute p e r i o d s at 33% and 66% V02 max and then t o exhaustion a t 95% V02 max. E x e r c i s e times were longest i n the a l k a l o t i c c o n d i t i o n and s h o r t e s t a f t e r NH4C1 i n g e s t i o n . Time t o exhaustion was longest with a l k a l o s i s being compared t o 4.3 min. f o r c o n t r o l and 2.4 min. with a c i d o s i s . Corresponding plasma l a c t a t e c o n c e n t r a t i o n s were s i g n i f i c a n t l y higher <p <0.01) at the 66% work lo a d and exhaustion with a k l a l o s i s compared t o a c i d o s i s . Using an i d e n t i c a l p r o t o c a l a l a t e r study by the same i n v e s t i g a t o r s confirmed these r e s u l t s (Sutton et a l . , 1981). With no appearent d i f f e r e n c e s i n V02, VC02, r e s p i r a t o r y exchange r a t i o or c a r d i a c f u n c t i o n a s s o c i a t e d with the acid-base changes the v a r i a t i o n s i n performance c a p a c i t y were r e p o r t e d t o be mediated through metabolic r a t h e r than oxygen t r a n s p o r t mechanisms. A s u b s t a n t i a l 52 i n c r e a s e i n v e n t i l a t i o n (VE) was found d u r i n g induced a c i d o s i s , however t h i s does not seem to account f o r the reduced endurance times as l o c a l muscle f a t i q u e was s t a t e d by s u b j e c t s t o be the s e n s a t i o n l i m i t i n g f u r t h e r e x e r c i s e . Comparable v e n t i l a t o r y responses were found by Chiesa et a l . , (1969) i n a study of metabolic a c i d o s i s produced by NH4C1. The work by Sutton and c o l l e a g u e s (1981) i s the o n l y human i n v e s t i g a t i o n t h a t examined the i n t r a c e l l u l a r muscle compartment through needle biopsy f o r comparison of v a r i o u s g l y c o l y t i c i n t e r m e d i a t e c o n c e n t r a t i o n s amongst three experimental c o n d i t i o n s . The lower plasma l a c t a t e c o n c e n t r a t i o n d u r i n g e x e r c i s e i n a c i d o s i s , compared with c o n t r o l and a l k a l o s i s , appeared to be due t o an i n h i b i t i o n of muscle g l y c o l y s i s combined with the r e d u c t i o n i n l a c t a t e e f f l u x . I n h i b i t o r s of g l y c o l y s i s which reduces the supply of ATP appeared t o be e l i c t e d by i n h i b i t i o n of PFK a c t i v i t y . L a c t a t e E f f l u x Transport Mechanism S k e l e t a l muscle l a c t a t e d u r i n g strenuous e x e r c i s e i s formed much more r a p i d l y than i t can be r e l e a s e d . Graham et a l . , (1976) examining l a c t a t e e f f l u x i n dog s k e l e t a l muscle suggested t h a t l a c t a t e r e l e a s e i s independant of muscle l a c t a t e c o n c e n t r a t i o n and the muscle/blood l a c t a t e g r a d i e n t . P e r f u s i o n by means of blood flow, s u r f a c e area and d i f f u s i o n d i s t a n c e were determined t o be important r e g u l a t o r s i n l a c t a t e r e l e a s e . Hirche et a l . , (1975) and Crone and G a r l i c k (1970) r e p o r t e d s i m i l a r f i n d i n g s . With experimental data i n c a p i l l a r y p e r m e a b i l i t y u n a v a i l a b l e i t i s assumed 53 c o n s i d e r i n g the molecular weight and r a d i u s of l a c t a t e , t h a t the c a p i l l a r y w a l l does not r e s t r i c t l a c t a t e movement i n t o the venous bloo d (Hirche et a l . , 1975). An i n c r e a s e i n e x e r c i s e i n t e n s i t y i s a s s o c i a t e d with an i n c r e a s e i n l a c t a t e r e l e a s e from the muscle. In order 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 muscle l a c t a t e c o n c e n t r a t i o n and l a c t a t e r e l e a s e from e x e r c i s i n g muscle J o r f e l d t et a l . , (1978) used a constant r a t e dye i n f u s i o n t o c a l c u l a t e the femoral v e n o u s - a r t e r i a l d i f f e r e n c e . R e s u l t s showed t h a t the r e l e a s e of l a c t a t e i n c r e a s e d l i n e a r l y with muscle l a c t a t e c o n e n t r a t i o n up t o about 4-5 mmol/min. A f u r t h e r i n c r e a s e i n muscle l a c t a t e t o about 4 mmol/kg wt. d i d not i n c r e a s e l a c t a t e e f f l u x d e p i t e an i n c r e a s e i n bloo d flow i n d i c a t i n g a s a t u r a t i o n i n the l a c t a t e t r a n s l o c a t i o n process. T h i s f i n d i n g of a s a t u r a t i o n type of k i n e t i c s i s s u b s t a n t i a t e d by v a r i o u s animal s t u d i e s ( K a r l s s o n et a l . , 1972; Hirche et a l . , 1975; Seo, 1984). Such experimental r e s u l t s suggest t h a t perhaps a c a r r i e r mechanism i s i n v o l v e d i n the t r a n s p o r t of l a c t a t e from the working muscle as mediated t r a n s p o r t process u s u a l l y e x h i b i t s a s a t u r a t i o n c h a r a c t e r i s t i c at hig h s u b s t r a t e l e v e l s (Hultman, and S a l h i n 1980; G o l l n i c k et a l , 1986). C a r r i e r mediated l a c t a t e t r a n s f e r has been observed i n a few s p e c i f i c t i s s u e s (Johnson et a l . , 1980; Monson et a l . , 1981). In s t u d y i n g the mouse diaphragm muscle, Koch et a l . , (1981) p r o v i d e d evidence t o suggest t h a t a t l e a s t 75% of l a c t a t e t r a n s f e r was c a r r i e r mediated. 54 As the appearance of l a c t a t e i n the blood i s a s s o c i a t e d with an i n c r e a s e i n CH+] the acid-base s t a t u s of the t i s s u e and b l o o d w i l l depend on whether l a c t a t e and hydrogen i o n s are t r a n s p o r t e d through the c e l l membrance at the same r a t e . Human s t u d i e s ( S a l h i n et a l . , 1976; S a l h i n et a l , . 1978) and i n v i t r o s t u d i e s (Seo, 1984) r e v e a l e d t h a t the f a l l i n plasma CHC03] d u r i n g e x e r c i s e i s approximately equimolar to the r i s e i n plasma l a c t a t e c o n c e n t r a t i o n . S a l h i n * s s t u d i e s a l s o observed an excess accumulation of H+ d u r i n g the e a r l y p a r t of recovery. On the c o n t r a r y e a r l i e r i n v e s t i g a t i o n s i n man r e p o r t e d a s l i g h t l y h i g h e r i n c r e a s e i n base d e f i c i t than c o u l d be accounted f o r by l a c t a t e accumulation (Bouhuys e t a l . , 1966; Osnes and Hermansen, 1972), S i m i l a r f i n d i n g s are r e p o r t e d by Benade and H e i s l e r , (1978) who demonstrated a more r a p i d e f f l u x of H+ than l a c t a t e ions i n the i s o l a t e d r a t diaphragm and f r o g s a r t o r i u s muscle. With the p o s s i b i l i t y of numerous i o n i c s h i f t s o c c u r i n g a c r o s s the m u s c l e - c a p i l l a r y boundary Reybroack et a l . , (1975) c a u t i o n e d t h a t the e n t r y of H+ and l a c t a t e ions i n t o the plasma may not be s t r i c t l y equimolar eventhough the f a l l i n plasma CHC03] i s equimolar t o the r i s e i n plasma l a c t a t e c o n c e n t r a t i o n . S e v e r a l i n v i t r o experiments have attempted to determine i f l a c t a t e passes out of the muscle i n i t s u n d i s s o c i a t e d (nan i o n i c ) form or i n i t s d i s s o c i a t e d ( i o n i c 55 form). E x h i b i t i n g a pKa of 3,9 the e f f l u x of undissociated. l a c t i c a c i d would appear l e s s l i k e l y as about 0.05% e x i s t s i n i t s u n d i s s o c i a t e d form at p h y s i o l o g i c a l pH values. A n a l y s i s of the f r o g s a r t o r i u s muscle p r e p a r a t i o n by Seo (1984) i n d i c a t e s t h a t t r a n s p o r t of l a c t a t e through the membrane occurs i n both i t s i o n i c and n o n i o n i c form and i s estimated to be of s i m i l a r magnitude. Mainwood and Worsley-Brown (1975) found t h a t d e p o l a r i z a t i o n of the c e l l membrance with potassium s u l f a t e reduced the l a c t a t e e f f l u x r a t e when the i s o l a t e d f r o g s a r t o r i u s muscle was bathed i n a low b u f f e r c o n c e n t r a t i o n s o l u t i o n s u g g e s t i n g t h a t the l a c t a t e e f f l u x process i s somewhat dependant on membrane p o t e n i a l . O b s e r v a t i o n s a l s o i n d i c a t e t h a t a l i m i t e d r a t e of l a c t a t e e f f l u x i s i n a u n d i s s o c i a t e d form and the f r a c t i o n i n c r e a s e s with an i n c r e a s e i n e x t e r n a l pH. It i s suggested t h a t d e s p i t e i t s pKa the u n d i s s o c i a t e d molecule ( l a c t i c a c i d ) i s the major permeating s p i e c e s i n v i v o (Reybroack et a l . , 1975; Roos, 1975; Hultman and S a l h i n , 1980). The mechanism f o r H+ and l a c t a t e t r a n s p o r t through the muscle c e l l membrane i s complex and somewhat un c l e a r . However, i t i s w e l l s u b s t a n t i a t e d t h a t H+ and l a c t a t e transmembrane e f f l u x i s a r a t e l i m i t i n g s t e p i n i n t r a c e l l u l a r and e x t r a c e l l u l a r balance and the s t a t u s of the immediate e x t r a c e l l u l a r environment p l a y s a key r o l e i n determing the balance between i n t r a c e l l u l a r and e x t r a c e l l u l a r compartments (Mainwood and Renaud, 1985). 56 L a c t a t e During Recovery With the e x c e p t i o n of the f i r s t few minutes f o l l o w i n g heavy e x e r c i s e t h e r e i s a gradual removal of l a c t a t e from the blood. F o l l o w i n g maximal e x e r c i s e of about approximately 1.5 min, Katz et a l . , (1984) observed t h a t l a c t a t e c o n t i n u e d t o i n c r e a s e and reached a peak at 7-9 minutes p o s t - e x e r c i s e i n both a c o n t r o l and a l k a l i n e c o n d i t i o n . At t h i s time blood l a c t a t e l e v e l s were s i g n i f i c a n t l y h i g h e r i n the a k l a l o t i c group u n t i l 20 minutes p o s t - e x e r c i s e where no d i f f e r e n c e e x i s t e d . A s i m i l a r i n c r e a s e i n blood l a c t a t e v a l u e s was r e p o r t e d by C o s t i l l et a l . , (1984) who observed maximal blood l a c t a t e c o n c e n t r a t i o n s of 13.0 mmol/1 4 to 5 mins. a f t e r repeated bouts of exhauctive e x e r c i s e . Even though the s u b j e c t s were abl e t o e x e r c i s e 47s longer d u r i n g the f i n a l e x haustive bout f o l l o w i n g NaHC03 i n g e s t i o n compared t o c o n t r o l t r i a l s , there was no d i f f e r e n c e between mean va l u e s of bloo d or muscle l a c t a t e . A f t e r 30 minutes of re c o v e r y when blood pH had r e t u r n e d t o p r e - e x e r c i s e l e v e l s blood l a c t i c a c i d c o n c e n t r a t i o n was approximately 6.0 mmol/1 f o r both groups. Other s t u d i e s r e p o r t t h a t depending on the d u r a t i o n and i n t e n s i t y of e x e r c i s e , muscle and blood l a c t a t e c o n c e n t r a t i o n s r e t u r n t o near r e s t i n g v a l u e s w i t h i n 30 t o 60 mins. a f t e r t e r m i n a t i o n of e x e r c i s e (Hermansen and Osnes, 1972; S a l h i n , 1978). During r e c o v e r y the r a t e of l a c t a t e disappearance from the muscle and blood i s i n f l u e n c e d by the l e v e l of 57 a c t i v i t y , Hermansen and S t e n s v o l d <1972) demonstrated that l a c t a t e c l e a r a n c e from blood was slowest with s u b j e c t s who r e s t e d d u r i n g the r e c o v e r y p e r i o d and f a s t e s t when e x e r c i s e was c o n t i n u e d at approximately 60% of the s u b j e c t s V02 max. S e v e r a l other r e s e a r c h e r s have examined the r o l e of e x e r c i s e i n blood l a c t a t e r e d u c t i o n and i t i s g e n e r a l l y accepted t h a t a c t i v e r e c o v e r y i s s u p e r i o r t o complete r e s t ( G i s o l f i et a l . , 1966; Davis et a l . , 1970). The primary mechanism f o r t h i s a c c e l e r a t e d r e d u c t i o n i s l i k e l y due to an i n c r e a s e d b l o o d f l o w which f a c i l i t a t e s the r a t e of o x i d a t i o n w i t h i n the muscle or augments e f f l u x from the muscle t o other t i s s u e s f o r o x i d a t i o n or r e s y n t h e s i s t o glucose C G o l l n i c k et a l . , 1986). Mainwood and Cechetto, (1980) examining the e f f e c t of b i c a r b o n a t e c o n c e n t r a t i o n on f a t i q u e and r e c o v e r y i n r a t diaphragm muscle found i n c r e a s e d e x t e r n a l b i c a r b o n a t e c o n c e n t r a t i o n s enhanced r e c o v e r y of muslce t e n s i o n f o l l o w i n g f a t i q u e . Mainwood and Renaud (1985) p r o v i d e d evidence to suggest t h a t the development of f a t i q u e i s a f f e c t e d r e l a t i v e l y l i t t l e by e x t r a c e l l u l a r pH and i t i s p o s s i b l e t h a t e l e v a t e d e x t e r n a l b i c a r b o n a t e l e v e l s t h a t modulate proton e f f l u x have a more d i r e c t e f f e c t on the r e c o v e r y process. The r a t h e r r a p i d r a t e of r e c o v e r y f a l l o w i n g i n c r e a s e d pH suggest t h a t something f a s t e r than proton e f f l u x may be o c c u r i n g d u r i n g the r e c o v e r y process. Perhaps there are s i t e s on the e x t e r n a l membrane which are pH dependent and 58 r e s p o n s i b l e f o r a l t e r i n g r e c o v e r y r a t e . Whatever the mechanism of the e f f e c t of e x t r a c e l l u l a r pH, the f a c t t h a t i t e x i s t s seems t o be of c o n s i d e r a b l e importance i n the r e g u l a t i o n of muscle performance (Mainwood and Renaud, 1985). The i n f l u e n c e of a r t i f i c a l l y induced acid-base d i s t u r b a n c e s of the blood, on l a c t a t e permeation i s w e l l documented and c o n c l u s i v e . The process i n which these changes can a l t e r performance c a p a c i t y a l s o has t h e o r e t i c a l and p r a c t i c a l support. An i n c r e a s e i n e x t r a c e l l u l a r [HC031 enhances the r a t e of l a c t a t e and H+ e f f l u x , and with some ex c e p t i o n r e s u l t s i n improved performance c a p a b i l i t i e s . C onversely a decrease i n e x t r a c e l l u l a r CHC03] decreases l a c t a t e and H+ e f f l u x which r e p o r t e d l y has adverse e f f e c t s on e x e r c i s e performance c a p a c i t y . M o n i t o r i n g blood pH and CBLa] u s u a l l y r e f l e c t s i n t r a c e l l u l a r changes, however, they do not a l l o w f o r d e t e r m i n a t i o n of i n t r a c e l l u l a r pH. F u r t h e r human r e s e a r c h s h o u l d i n c l u d e more d i r e c t measurements of i n t r a c e l l u l a r ; pH, l a c t a t e c o n c e n t r a t i o n s , a n d b u f f e r c a p a c i t y , at r e s t , f o l l o w i n g a l k a l o t i c and a c i d o t i c treatments and d u r i n g e x e r c i s e and r e c o v e r y to more c l e a r l y e s t a b l i s h the r e l a t i o n s h i p s between the i n t r a c e l l u l a r and e x t r a c e l l u l a r environment. When c o n s i d e r i n g the ergogenic respones of induced acid-base changes, the type and d u r a t i o n of e x e r c i s e performed, and the f i t n e s s l e v e l of the s u b j e c t s c o u l d l e a d to v a r i a t i o n s i n r e s u l t s . 5 9 REFERENCES Baldwin, K. 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The e f f e c t of acute induced metabolic a l k a l o s i s on 800m r a c i n g time. Med.  S c i . S p o r t s Exerc.,15: 277-280, 1983. Woodbury, J.W. R e g u l a t i o n of pH. In: P h y s i o l o g y and B i o p h y s i c s , T.C. Ruch and H.D. Patton (Eds.) P h i l a d e l p h i a : Saunders, 1965, pp. 899-934. 66 APPENDIX B P r e - E x e r c i s e Blood pH and Bicarbonate Values 67 A p p e n d i x B : P r e - E x e r c i s e b l o o d v a l u e s f o r pH and s t a n d a r d b i c a r b o n a t e t o I l ow ing a c i d o s i s , a l k a l o s i s and c o n t r o l t r e a t m e n t s PH btanda rd HUU mtq/L SuBJtl'l Control Acidosis AI kaiosis control Acidosis Alkaiosis 1 7.33 7.21 7.41 24.5 17.4 29.8 2 7.34 7.23 7.37 22.9 21.0 30.8 3 7.34 7.24 7.43 24.9 17.5 31.5 4 7.33 7.20 7.44 25.3 20.0 36.0 5 7.29 7.14 7.37 25.5 16.9 30.6 6 7.38 7.27 7.40 26.1 18.5 30.0 68 APPENDIX C Work Outputs and Power Outputs 69 Appendix C: Work output and power output f o r the s i x minute e x e r c i s e t e s t d u r i n g a c i d o s i s , a l k a l o s i s and c o n t r o l c o n d i t i o n s co en Ol L O CTl L O oo 1— L O o L O CO (  iz <0 oo CO r™ L O 1 — , — CVI CVI L O f— L O o CO L O CVJ CT> LO OJ co o CO "3- "3- CO L O L O L O L O L O L O L O CO L O L O E : CVJ CO CO CO co co CO co CO CO CO CO CO CO CO CO CO CO L O CVJ o CVJ CO LO L O LO 1— O l , — CO O r~ 00 o o L D L O 00 L O L O ro L O CO , CO o CO 00 L O i CVJ CVJ CO o L O L O LO r-. L O CVJ 00 L O CVJ CM CO CO CO CO CO CO CO co CO co CO CO CO CO CO CO ^ CD Ol o <y> oo oo L O , o ^ - CVJ o CVJ CVJ 00 1— CVI ? O =f CVJ L O CVI «a- LO co rsj ^— L O ^ - CTl CO r— i o I — r— co L O L O L O L O L O co L O L O co co CO oo CO CO CO CO CO CO CO CO CO CO CO CO CO CO o 4-> o o L O oo r— CVJ CO o r— «d- CO CO p^ 1— c (O o CVI 1 CO Ol CO CTl CO 00 o CO L D o oo CTl CO , _> O o , I-—• r— CVJ CVI CVI CVJ CVJ CO CVJ CVJ CO CVJ r— CO ro 1 _3 10 T— 1/1 o 7—' ro o r— oo CO CVJ 1—. L O o O L O CO o E : <T\ LO o L O ro CVJ f— CO CO cr> L O £5 CVI ro CO CO -3- CO <t CO o . 1 * 1 Xi O E : p- L O r~ CO o r-~ , — - ro 00 «d- CO CVJ 00 CO oo 1^- IS) O F— 3 3- CM I D o CO CVJ CVJ CVI CO L O CO L O o L O l/l i p— 1— 00 00 oo CO co 00 00 00 00 CO co oo 00 oo oo o TD r-o 1 J J < E : =c J J CO o oo o cC CO <_> CO o CO o CO o a; _> J J -o ao ( — CVJ CO L O L O 70 APPENDIX D E x e r c i s e Blood L a c t a t e C o n c e n t r a t i o n s 71 Appendix D: E x e r c i s e Blood L a c t a t e Concentrations f o r A l k a l o s i s , A c i d o s i s and C o n t r o l Treatments Blood L a c t a t e Concentration (mM) o o L O CO oo CTl oo oo p^ CO LO CTl 20.9 L O O LO' o CM LO LO CM oo CTi <±> CO 20.0 CM CTl ' LO oo o cn o LO o CO LO oo CM L O p~ co oo p^ CM cri LO oo CM CTl CTl CM o LO o p» o CM o LO LO p^ oo p~ LO CM o o o C O o vo 00 LO cn CM LO LO LO cn o LO LO O O C O LO CTl CM P-. C3 CM "51" 1 LO LO CO oo p^ p-. 00 - o & CO oo LO o LO CO cn 06 LO cb LO 00 CTl LO LO CM LO 00 CM 00 LO LO - co p~ LO OO 00 oo CM o o CU CO O o * T r~ CM CM LO r— o o LO cb LO CTl CTl CO LO CM LO LO LO o CO r » C O oo C O •=3-LO cu +-> 3 C o oo C O L O o CM o CM CTl LO CO CTl CM o CTl • C O 00 CTi CM • i— oo o LO cb CM LO o •r-z : cu F o o oo CTl LO o CM CO LO LO CM LO cn LO CM LO 00 1— o LO CM o oo oo <3-cn cn OO LO CM O c n CO f— *i— o C O CM oo o CM co 00 LO o CTl 00 LO LO CM CM LO CTl CO CO LO CTi CTi 00 co r— o r-~ LO P-» o LO 00 o i—-Q . E to LO O o CM oo L O r~ LO CO LO LO CM CTl C O r~- LO CTl LTV LO p~-00 p~. p-» CTi P- . O cn LO LO o LO p^ LO LO oo oo LO 00 £_ (-> £Z o o oo LO c n oo CO LO r~ LO 00 <d-LO CTl C O LO 00 o LO LO LO cn LO CTl LO LO 1— LO cn C O p-. 00 CM p» _> (/) >— o o 00 CO vo i— CO C O co LO * T CTi oo p-* LO p -P-~ CO fc> LO cn CO cn CM oo «3-LO C O LO O o o •-; CM CM LO LO co p-- LO oo CTl c n cn LO LO CO CM C O CM CM CM CM o CM •=!• CM ' CM 1 OO 30 • X UJ LO o O O r-~ CM LO LO CO O oo P - cn LO CO r-» CO }— LO O o T— o 1 CU t_ o_ o 1 o 1 O o 1 O C O 1 o o 1 1— z UJ s : i— <: <: CO C_> <c CO O •=£ CO C_> <£ CO <c CQ o CO o a: 1— H— O 1 1 1 CO CO CM C O LO LO 72 APPENDIX E Recovery Blood L a c t a t e C o n c e n t r a t i o n s 73 Appendix £: Recovery Blood L a c t a t e C o n c e n t r a t i o n s f o r A l k a l o s i s , A c i d o s i s and C o n t r o l Treatments Blood L a c t a t e C o n c e n t r a t i o n (mM) -r— O £_-CD X 10 o O-a> 3 2: ai c : 0. E ro GO ro o • CO LO LO • .—1 co LO CM 00 00 r-. c o LO 00 LO co CTi LO O CTl ' CM 1^-00 C M CVI CO LO C O CTl 00 <— LO CVI LO CO CTv LO c o LO LO r— CTl CTl LO CO cn CO LO CTl 00 LO o LO C M o LO «3-00 CTl <3- I — co 00 LO CO CTl CO 00 00 CTl 00 CTl O •— 00 O r— LO LO cn »*• ,— «3-CTl CVI C O ro CVI o l_ +-> c o o o to o ro I co LO o •f— o CVI 00 CTl LO LO 00 00 CTl LO o LO LO <3-o r— LO CVI r~-LO C O 1 — CTl 00 O 00 CM CO LO LO LO r-» CO CTi ~£5~ LO o LO r-. CTi o LO r— L O 00 LO LO LO o LO 00 o C O o P~- C M CO LO C O LO 00 LO CO CO LO 00 C O L O CM ro 1 — CTi LO CTl LO .— co ro CM LO L O LO C M ro LO LO 00 LO LO CTl LO ro o 1 — o ro LO 00 C O •— c o o CO cvi 1 — r» r— CO 1 — ro CO CTl cn I — 01 C M r— O C M . — o LO CTi O •— o CO L O CO C7> LO •I ro <C <C CO O r-00 o «£ CO O <c 00 o «t CO 0 o I— CO CO LO LO 74 

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