B-49 Free Communication/Slide - Muscle 2: MAY 28, 2008 3:15 PM - 5:15 PM ROOM: Sagamore 6
PURPOSE: Recent research has shown that sodium bicarbonate (NaHCO3) supplementation during interval training results in greater improvements in mitochondrial respiration and endurance performance. It was hypothesised that this may have been due to a negative effect of metabolic acidosis on the up-regulation of genes responsible for aerobic adaptations. A key regulator of mitochondrial biogenesis is peroxisome proliferator activated receptor gamma co-activator (PGC-1)alpha. The purpose of this study was to determine the effects of metabolically-induced acidosis on the exercise-mediated mRNA response of PGC-1alpha mRNA expression.
METHODS: Eight active males (Mean±SD, age, 25 +/− 6 y, body mass 83.7 +/− 9.0 kg, VO2max 47.6 +/− 7.6 mL/kg/min) performed 10x2 min cycle intervals at 80% VO2max intensity on two separate occasions (separated by ~2 weeks). Participants ingested either ammonium chloride (ACIDOSIS) or calcium carbonate (PLACEBO) the day before and on the day of the exercise trial in a randomized, counterbalanced order, using a crossover design. Biopsies were taken from the vastus lateralis muscle before, immediately after exercise, and also after 2 and 6 h of recovery. The RNA content of PGC-1alpha was determined by RT-PCR and normalized to total cDNA content determined by OliGreen.
RESULTS: Exercise markedly increased PGC-1alpha mRNA content at 2 and 6 h of recovery in both conditions. However, ACIDOSIS was associated with a suppressed response relative to the PLACEBO condition at 2 and 6 h of recovery (~2-3 fold decrease, respectively; P<0.05). A similar response was also observed for citrate synthase mRNA at 2 h of recovery.
CONCLUSION: The present data demonstrate that metabolic acidosis reduces exercise-induced up-regulation of PGC-1alpha mRNA suggesting that metabolic acidosis may interfere with training-induced mitochondrial biogenesis.