This study measured the adaptive response to exercise training for each of the acid/base transport protein families, including providing isoform-specific evidence for the monocarboxylate transporter (MCT)1/4 chaperone protein basigin and for the electrogenic sodium/bicarbonate cotransporter (NBCe)1. We investigated whether 4 weeks of work-matched, high-intensity interval training (HIIT), performed either just above the lactate threshold (HIITΔ20; n = 8), or close to peak aerobic power (HIITΔ90; n = 8), influenced adaptations in acid/base transport protein abundance, non-bicarbonate muscle buffer capacity (βmin vitro), and exercise capacity in active men. Training intensity did not discriminate between adaptations for most proteins measured, with abundance of MCT1, sodium/hydrogen exchanger (NHE)1, NBCe1, carbonic anhydrase (CA)II, and CAXIV increasing after 4 weeks, while there was little change in CAIII and CAIV abundance. βmin vitro also did not change. However, MCT4 protein content only increased for HIITΔ20 (effect size: 1.06, 90% confidence limits ×/÷0.77), whereas basigin protein content only increased for HIITΔ90 (ES: 1.49, ×/÷1.42). Repeated-sprint ability (5 × 6-s sprints; 24 s passive rest) improved similarly for both groups. Power at the lactate threshold only improved for HIITΔ20 (ES: 0.49; 90% CL ±0.38), while VO2peak did not change for either group. Detraining was characterized by the loss of adaptations for all of the proteins measured and for repeated-sprint ability 6 weeks after removing the stimulus of HIIT. In conclusion, 4 weeks of HIIT induced improvements in each of the acid/base transport protein families, but remarkably, a 40% difference in training intensity did not discriminate between most adaptations.
- pH regulation
- lactate transport
- intracellular buffering
- high-intensity interval training
- Copyright © 2016, Journal of Applied Physiology