Induced alkalosis affects mitochondrial but not buffer capacity adaptations to exercise

Life Sciences 2007 (2007) Proc Life Sciences, PC86

Poster Communications: Induced alkalosis affects mitochondrial but not buffer capacity adaptations to exercise

J. Edge1, D. Bishop4, C. Thomas3, J. Mercier2, T. Moore-Morris2

1. Institute of Food Nutrition and Human Health, Massey university, Palmerston North, New Zealand. 2. Institut de biologie, Université Montpellier1, Montpellier, France. 3. LEPHE, Université d’Evry, Colomb, France. 4. Facoltà di Scienze Motorie, Università degli Studi di Verona, Verona, Italy.

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The main purpose of this study was to investigate the role of differing H+ accumulation on changes in muscle buffer capacity (βm). In study 1, 16 human females performed an incremental cycle test to determine maximal oxygen uptake (VO2max) and the lactate threshold before and after training. They were then assigned to placebo (NaCl) or alkalosis groups (NaHCO3). In study 2, 24 male Wistar rats performed an incremental treadmill test to exhaustion and assigned to one of three groups, baseline, placebo or alkalosis. Endurance performance for studies 1 and 2 was determined before and after training. Training for studies 1 and 2 consisted of 12 high-intensity, 2-min intervals performed 3 times a wk for 5-8 wks. The alkalosis groups for studies 1 and 2 ingested NaHCO3 or a placebo prior to each training session. Muscle biopsies from the vastus lateralis (VL) of humans and the soleus (SOL) and extensor digitorum longus (EDL) muscles of the rats were sampled to determine βm. Mitochondrial respiration was determined on the SOL and EDL. Following the training period, there were significant (P0.05) between the groups. Both the human (placebo 1.2-fold v alkalosis 1.6-fold) and rat studies (placebo 8.2-fold v alkalosis 12.5-fold) also resulted in significant (P<0.05) improvements in endurance for both the alkalosis and placebo groups, but with greater improvements for the alkalosis group than the placebo group. In the human study, the lactate threshold improved significantly (P<0.05) more for the alkalosis group than placebo (placebo 15% v alkalosis 26%). Compared to baseline, there was a significant (P<0.05) increase in SOL mitochondrial respiration with training (placebo 30% v alkalosis 67%), with a significantly greater increase for the alkalosis group. As there were similar changes in βm for all groups, our results suggest training intensity may be the key stimulus for increasing βm. Alternatively, the intense nature of our training regimen despite induced alkalosis may have resulted in a sufficient accumulation of H+ and stimulated changes in βm. In both studies, the group ingesting NaHCO3 during training had greater improvements in endurance performance. The greater increase in the lactate threshold and mitochondrial respiration of the alkalosis groups indicates that the improved endurance performance may be related to differences in muscle oxidative capacity.



Where applicable, experiments conform with Society ethical requirements.

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