Galloway S D, Maughan R J
Department of Environmental and Occupational Medicine, University Medical School, Aberdeen, Scotland, UK.
Eur J Appl Physiol Occup Physiol. 1996;74(4):384-9. doi: 10.1007/BF02226936.
To examine the effects of alkalosis on the metabolic response to prolonged exercise, seven healthy males cycled for 1 h at approximately 70% of maximum oxygen uptake on two occasions, 1-week apart. Starting 3 h prior to exercise, subjects consumed either CaCO3 (placebo) or NaHCO3 (0.3 g.kg-1 body mass) over a 2-h period. Arterialised-venous blood samples were drawn before and during exercise for the determination of acid-base status and blood metabolites (lactate, glucose, glycerol and plasma free fatty acids). Expired gas was collected during exercise for determination of oxygen uptake (VO2) and respiratory exchange ratio to estimate fuel oxidation rates. Ratings of perceived exertion (RPE) and heart rates were also recorded. A significant (P < 0.01) alkalosis was observed at all times following bicarbonate ingestion. Blood lactate was significantly (P < 0.05) higher at all sample times throughout exercise following bicarbonate ingestion. Blood lactate concentration [mean (SEM)] reached peak values of 2.90 (0.16) and 4.24 (0.45) mmol.l-1 following 20 min of exercise following placebo and bicarbonate, respectively. No differences between treatments were noted at any time for the other metabolites. VO2 and RPE were significantly higher (P < 0.01) with the bicarbonate trial. At a constant power output increases in VO2 are generally associated with increases in fat oxidation, however, no evidence for an altered fuel oxidation was obtained in the present study. The differences in blood lactate indicate that induced alkalosis increased lactate efflux from muscle, but it cannot be confirmed whether this represents an increased rate of glycolysis within the muscle.
