Programme Contents

Effects of high-intensity interval exercise, under either induced metabolic acidosis or alkalosis, on the regulation of genes associated with the acid-base regulation in human skeletal muscle

We have previously reported that rats ingesting sodium bicarbonate (NaHCO₃) before training sessions (which reduced the activity-induced decrease in muscle pH) had significantly greater adaptations to exercise training compared to both a control group (no training) and a placebo group (identical training, but ingesting NaCl before each session) (Bishop et al., 2010). This included greater increases in MCT4 protein content (Thomas et al., 2007). The aim of this study was to investigate the effects of work-matched high-intensity interval exercise, under induced metabolic acidosis or alkalosis, on muscle pH changes, Ser³⁰⁰-PDH protein phosphorylation (which reflects pyruvate dehydrogenase complex deactivation) and the mRNA content of genes associated with acid-base regulation in human skeletal muscle. We hypothesized that a higher level of lactate production could regulate the mRNA content of pyruvate dehydrogenase kinase 4 (PDK4) and the monocarboxylate transporters isoforms 1 and 4 (MCT1 and MCT4), and a lower muscle pH could regulate the mRNA content of sodium hydrogen exchanger 1 (NHE1).

Nine active males (Mean ± SD, age 23 ± 5 y, Body mass 78 ± 15 kg, VO_2max 47 ± 7 ml kg^-1 min^-1) performed 9×2-min cycle intervals set at 30% of the difference between the lactate threshold and peak power determined from the lactate threshold test (82±2 % of the peak power), separated by 1 min of passive recovery, on three occasions separated by ∼2 weeks. On each occasion, participants ingested ammonium chloride (0.15 g kg^-1, ACD) or calcium carbonate (0.15 g kg^-1, PLA), which were divided in equal smaller doses and administered 100 and 40 minutes pre-exercise and 10, 70 and 130 minutes post-exercise, or sodium bicarbonate (0.3 g kg^-1, ALK), which was administered in a single dose 100 minutes pre-exercise, in a randomised, counterbalanced order, using a crossover design. Venous blood samples were drawn every 20 minutes from 100 minutes pre-exercise, after the 3^rd, 6^th and 9^th interval, and every 30 min post-exercise until 3 h following exercise. Biopsies were taken from the vastus lateralis muscle pre, post-exercise and 3 h following exercise.

Blood pH and bicarbonate were significantly lower during ACD vs PLA, and higher during ALK vs PLA, from 10 minutes pre-exercise until 3 h following exercise. Blood lactate was lower during ACD vs PLA after the 3^rd exercise interval and significantly higher during ALK vs PLA after the 6^th and 9^thinterval, with no difference between conditions pre and post exercise. Muscle pH was significantly lower post-exercise vs pre-exercise and 3 h following exercise across all conditions with a greater decrease during ACD vs both PLA and ALK, but with no difference between PLA and ALK. Ser³⁰⁰-PDH protein phosphorylation was significantly lower post exercise vs both pre exercise and 3 h following exercise across all conditions, with a greater post-exercise decrease during both ACD and ALK vs PLA. The lower values for ACD vs PLA pre-exercise approached significance (P=0.07). PDK4 mRNA levels were significantly lower during ACD vs PLA pre-exercise, and were increased significantly 3 h following exercise vs pre and post exercise across all conditions. MCT4 mRNA levels significantly increased 3 h following exercise vs post-exercise with no difference vs pre exercise across conditions. No difference was observed for the mRNA levels of MCT1 and NHE1. In contrast to our hypothesis, we did not observe any effect of acid or base ingestion on exercise-induced changes in the mRNA content of genes associated with acid-base regulation in human skeletal muscle. We did however, observe that acid ingestion was associated with a greater exercise-induced decrease in muscle pH, and a greater decrease in Ser³⁰⁰-PDH protein phosphorylation.

Bishop DJ, Thomas C, Moore-Morris T, Tonkonogi M, Sahlin K & Mercier J. (2010). American Journal of Physiology. Endocrinology and Metabolism 299, E225-233.

Thomas C, Bishop D, Moore-Morris T & Mercier J. (2007). American Journal of Physiology. Endocrinology and Metabolism 293, E916-922.