Superior mitochondrial adaptations in human skeletal muscle after interval compared to continuous single-leg cycling matched for total work

Key points A classic unresolved issue in human integrative physiology involves the role of exercise intensity, duration and volume in regulating skeletal muscle adaptations to training. We employed counterweighted single-leg cycling as a unique within-subject model to investigate the role of exercise intensity in promoting training-induced increases in skeletal muscle mitochondrial content. Six sessions of high-intensity interval training performed over 2weeks elicited greater increases in citrate synthase maximal activity and mitochondrial respiration compared to moderate-intensity continuous training matched for total work and session duration. These data suggest that exercise intensity, and/or the pattern of contraction, is an important determinant of exercise-induced skeletal muscle remodelling in humans. We employed counterweighted single-leg cycling as a unique model to investigate the role of exercise intensity in human skeletal muscle remodelling. Ten young active men performed unilateral graded-exercise tests to measure single-leg V.O2, peak and peak power (W-peak). Each leg was randomly assigned to complete six sessions of high-intensity interval training (HIIT) [4x(5min at 65% W-peak and 2.5min at 20% W-peak)] or moderate-intensity continuous training (MICT) (30min at 50% W-peak), which were performed 10min apart on each day, in an alternating order. The work performed per session was matched for MICT (1438.4kJ) and HIIT (1448.5kJ, P>0.05). Post-training, citrate synthase (CS) maximal activity (10.20.8vs. 8.40.9mmolkgprotein(-1)min(-1)) and mass-specific [pmolO(2)center dot(s center dot mgwetweight)(-1)] oxidative phosphorylation capacities (complex I: 23.43.2vs. 17.1 +/- 2.8; complexes I and II: 58.2 +/- 7.5vs. 42.2 +/- 5.3) were greater in HIIT relative to MICT (interaction effects, P<0.05); however, mitochondrial function [i.e. pmolO(2)center dot(s center dot CS maximalactivity)(-1)] measured under various conditions was unaffected by training (P>0.05). In whole muscle, the protein content of COXIV (24%), NDUFA9 (11%) and mitofusin 2 (MFN2) (16%) increased similarly across groups (training effects, P<0.05). Cytochrome c oxidase subunit IV (COXIV) and NADH:ubiquinone oxidoreductase subunit A9 (NDUFA9) were more abundant in type I than type II fibres (P<0.05) but training did not increase the content of COXIV, NDUFA9 or MFN2 in either fibre type (P>0.05). Single-leg V.O2, peak was also unaffected by training (P>0.05). In summary, single-leg cycling performed in an interval compared to a continuous manner elicited superior mitochondrial adaptations in human skeletal muscle despite equal total work. Key points A classic unresolved issue in human integrative physiology involves the role of exercise intensity, duration and volume in regulating skeletal muscle adaptations to training. We employed counterweighted single-leg cycling as a unique within-subject model to investigate the role of exercise intensity in promoting training-induced increases in skeletal muscle mitochondrial content. Six sessions of high-intensity interval training performed over 2weeks elicited greater increases in citrate synthase maximal activity and mitochondrial respiration compared to moderate-intensity continuous training matched for total work and session duration. These data suggest that exercise intensity, and/or the pattern of contraction, is an important determinant of exercise-induced skeletal muscle remodelling in humans.