Mitochondrial adaptations to high‐volume exercise training are rapidly reversed after a reduction in training volume in human skeletal muscle

Increased mitochondrial content and respiration have both been reported after exercise training. However, no study has directly compared how different training volumes influence mitochondrial respiration and markers of mitochondrial biogenesis. Ten healthy men performed high-intensity interval cycling during 3 consecutive training phases; 4 wk of normal-volume training (NVT; 3/wk), followed by 20 d of high-volume training (HVT; 2/d) and 2 wk of reduced-volume training (RVT; 5 sessions). Resting biopsy samples (vastus lateralis) were obtained at baseline and after each phase. No mitochondrial parameter changed after NVT. After HVT, mitochondrial respiration and citrate synthase activity (similar to 40-50%), as well as the protein content of electron transport system (ETS) subunits (similar to 10-40%), and that of peroxisome proliferator-activated receptor gamma coactivator-1 (PGC-1 alpha), NRF1, mitochondrial transcription factor A (TFAM), PHF20, and p53 (similar to 65-170%) all increased compared to baseline; mitochondrial specific respiration remained unchanged. After RVT, all the mitochondrial parameters measured except citrate synthase activity (similar to 36% above initial) were not significantly different compared to baseline (all P > 0.05). Our findings demonstrate that training volume is an important determinant of training-induced mitochondrial adaptations and highlight the rapid reversibility of human skeletal muscle to a reduction in training volume