HUMAN SKELETAL MUSCLE MITOCHONDRIAL RESPONSE TO INTERVAL TRAINING: ROLE OF EXERCISE INTENSITY

Abstract

It has been proposed that intermittent exercise can differentially affect mitochondrial responses to training, with training volume being more important than intensity for increasing skeletal muscle mitochondrial content and with intensity playing a greater role in mitochondrial respiration. To test this hypothesis, we examined markers of skeletal muscle mitochondrial content and respiration in response to two different interval training protocols performed using single-leg cycling, which permitted a within-subjects design. Ten healthy active adults [6 males / 4 females, 22±4 y, peak oxygen uptake (VO2peak) = 42±4 ml/kg/min] were recruited. Each leg was randomized to either a HIIT [4 × (5 min at 65% Wpeak and 2.5 min at 20% Wpeak)] or SIT [4 x (30-s “all-out” sprints and 4 min active recovery)] protocol and completed three exercise sessions/wk over 4 wk for a total of 12 exercise sessions/leg. The mean work performed during each session was 133±32 and 44±8.0 kJ for HIIT and SIT respectively, and the average workload during intervals was 95±25 W and 322±77 W for HIIT and SIT respectively. Citrate synthase (CS) maximal activity increased compared to baseline after training interventions, with the change being greater after SIT vs HIIT (42±25% vs 16±13%, interaction p=0.01). COXIV protein content and succinate-supported state 3 were unchanged. Single-leg VO2peak and time to exhaustion (TTE) increased to a similar extent in both HIIT and SIT (main effect of time, p<0.05). These data suggest that, in contrast to what has been proposed by others, training intensity is more important than volume for increasing mitochondrial content during short-term interval training in human skeletal muscle.