NaHCO3-induced alkalosis reduces the phosphocreatine slow component during heavy-intensity forearm exercise
1 School of Kinesiology, 2 Department of Medical Biophysics, and 3 Lawson Health Research Institute, The University of Western Ontario, London, Ontario, Canada Submitted 25 October 2004 ; accepted in final form 4 July 2005 During heavy-intensity exercise, the mechanisms responsible for the continued...
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Published in | Journal of applied physiology (1985) Vol. 99; no. 5; pp. 1668 - 1675 |
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Main Authors | , , , |
Format | Journal Article |
Language | English |
Published |
Bethesda, MD
Am Physiological Soc
01.11.2005
American Physiological Society |
Subjects | |
Online Access | Get full text |
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Summary: | 1 School of Kinesiology, 2 Department of Medical Biophysics, and 3 Lawson Health Research Institute, The University of Western Ontario, London, Ontario, Canada
Submitted 25 October 2004
; accepted in final form 4 July 2005
During heavy-intensity exercise, the mechanisms responsible for the continued slow decline in phosphocreatine concentration ([PCr]) (PCr slow component) have not been established. In this study, we tested the hypothesis that a reduced intracellular acidosis would result in a greater oxidative flux and, consequently, a reduced magnitude of the PCr slow component. Subjects ( n = 10) performed isotonic wrist flexion in a control trial and in an induced alkalosis (Alk) trial (0.3g/kg oral dose of NaHCO 3 , 90 min before testing). Wrist flexion, at a contraction rate of 0.5 Hz, was performed for 9 min at moderate- (75% of onset of acidosis; intracellular pH threshold) and heavy-intensity (125% intracellular pH threshold) exercise. 31 P-magnetic resonance spectroscopy was used to measure intracellular [H + ], [PCr], [P i ], and [ATP]. The initial recovery data were used to estimate the rate of ATP synthesis and oxidative flux at the end of heavy-intensity exercise. In repeated trials, venous blood sampling was used to measure plasma [H + ], [HCO 3 ], and [Lac ]. Throughout rest and exercise, plasma [H + ] was lower ( P < 0.05) and [HCO 3 ] was elevated ( P < 0.05) in Alk compared with control. During the final 3 min of heavy-intensity exercise, Alk caused a lower ( P < 0.05) intracellular [H + ] [246 (SD 117) vs. 291 nmol/l (SD 129)], a greater ( P < 0.05) [PCr] [12.7 (SD 7.0) vs. 9.9 mmol/l (SD 6.0)], and a reduced accumulation of [ADP] [0.065 (SD 0.031) vs. 0.098 mmol/l (SD 0.059)]. Oxidative flux was similar ( P > 0.05) in the conditions at the end of heavy-intensity exercise. In conclusion, our results are consistent with a reduced intracellular acidosis, causing a decrease in the magnitude of the PCr slow component. The decreased PCr slow component in Alk did not appear to be due to an elevated oxidative flux.
sodium bicarbonate; phosphorus-31 magnetic resonance spectroscopy; acid-base status; muscle energetics
Address for reprint requests and other correspondence: G. D. Marsh, School of Kinesiology, The Univ. of Western Ontario, London, Ontario, Canada N6A-3K7 (e-mail: gdmarsh{at}uwo.ca ) |
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Bibliography: | ObjectType-Article-2 SourceType-Scholarly Journals-1 ObjectType-Feature-1 content type line 23 |
ISSN: | 8750-7587 1522-1601 |
DOI: | 10.1152/japplphysiol.01200.2004 |