Acute high-intensity exercise impairs skeletal muscle respiratory capacity

Purpose The effect of an acute bout of exercise, especially high-intensity exercise, on the function of mitochondrial respiratory complexes is not well understood, with potential implications for both the healthy population and patients undergoing exercise-based rehabilitation. Therefore, this study sought to comprehensively examine respiratory flux through the different complexes of the electron transport chain in skeletal muscle mitochondria before and immediately after high-intensity aerobic exercise. Methods Muscle biopsies of the vastus lateralis were obtained at baseline and immediately after a 5-km time trial performed on a cycle ergometer. Mitochondrial respiratory flux through the complexes of the electron transport chain was measured in permeabilized skeletal muscle fibers by high-resolution respirometry. Results Complex I + II state 3 (state 3_{CI + CII}) respiration, a measure of oxidative phosphorylation capacity, was diminished immediately after the exercise (pre, 27 ± 3 ρm·mg^-1·s^-1; post, 17 ± 2 ρm·mg^-1·s^-1; P < 0.05). This decreased oxidative phosphorylation capacity was predominantly the consequence of attenuated complex II-driven state 3 (state 3_CII) respiration (pre, 17 ± 1 ρm·mg^-1·s^-1; post, 9 ± 2 ρm·mg^-1·s^-1; P < 0.05). Although complex I-driven state 3 (3_CI) respiration was also lower (pre, 20 ± 2 ρm·mg^-1·s^-1; post, 14 ± 4 ρm·mg^-1·s^-1), this did not reach statistical significance (P = 0.27). In contrast, citrate synthase activity, proton leak (state 2 respiration), and complex IV capacity were not significantly altered immediately after the exercise. Conclusions These findings reveal that acute high-intensity aerobic exercise significantly inhibits skeletal muscle state 3_CII and oxidative phosphorylation capacity. This, likely transient, mitochondrial defect might amplify the exercise-induced development of fatigue and play an important role in initiating exercise-induced mitochondrial adaptations.