EXERCISE

We tested the hypothesis that ingestion of sodium bicarbonate (NaHCO3) prior to an acute session of high-intensity interval training (HIIT) would augment signalling cascades and gene expression linked to mitochondrial biogenesis in human skeletal muscle. On two occasions separated by ~1 wk, nine men (22±2 y; 78±13 kg, VO2peak = 48±8 mL kg(-1) min(-1); mean ± SD) performed 10x60-s cycling efforts at an intensity eliciting ~90% of maximal heart rate (263±40 W), interspersed with 60 s of recovery. In a double-blind, crossover manner, subjects ingested a total of 0.4 g kg b.w.(-1) NaHCO3 prior toexercise (BICARB) or an equimolar amount of the placebo, sodium chloride (PLAC). Venous blood bicarbonate and pH were elevated at all time points post-ingestion (p<0.05) in BICARB vs. PLAC. During exercise, muscle glycogen utilization (126±47 vs. 53±38 mmol kg d.w.(-1); p<0.05) and blood lactate accumulation (12.8±2.6 vs. 10.5±2.8 mmol L(-1); p<0.05) were greater in BICARB vs. PLAC. The acute exercise-induced increase in the phosphorylation of acetyl-CoA carboxylase, a downstream marker of AMP-activated protein kinase activity, and p38 mitogen-activated protein kinase were similar between treatments (p>0.05). However, the increase in PGC-1α mRNA expression after 3 h of recovery was higher in BICARB vs. PLAC (~7- vs. 5-fold compared to rest, p<0.05). We conclude that NaHCO3 prior to HIIT alters the mRNA expression of this key regulatory protein associated with mitochondrial biogenesis. The elevated PGC-1α mRNA response provides a putative mechanism to explain the enhanced mitochondrial adaptation seen after chronic NaHCO3-supplemented HIIT in rats.