Increased oxygen extraction and mitochondrial protein expression after small muscle mass endurance training

When exercising with a small muscle mass, the mass-specific O2 delivery exceeds the muscle oxidative capacity resulting in a lower O2 extraction compared to whole-body exercise. We elevated the muscle oxidative capacity and tested its impact on O2 extraction during small muscle mass exercise. Nine individuals conducted six weeks of one-legged knee extension (1L-KE) endurance training. After training, the trained leg (TL) displayed 45% higher citrate synthase and COX-IV protein content in vastus lateralis and 15-22% higher pulmonary oxygen uptake ( V˙ O2peak ) and peak power output ( W˙peak ) during 1L-KE than the control leg (CON; all P<0.05). Leg O2 extraction (catheters) and blood flow (ultrasound Doppler) were measured while both legs exercised simultaneously during 2L-KE at the same submaximal power outputs (real-time feedback-controlled). TL displayed higher O2 extraction than CON (main effect: 1.7±1.6%-points; P=0.010; 40-83% of W˙peak ) with the largest between-leg difference at 83% of W˙peak (O2 extraction: 3.2±2.2%-points; arteriovenous O2 difference: 7.1±4.8 mL·L-1 ; P<0.001). At 83% of W˙peak , muscle O2 conductance (DM O2 ; Fick law of diffusion) and the equilibration index Y were higher in TL (P<0.01), indicating reduced diffusion limitations. The between-leg difference in O2 extraction correlated with the between-leg ratio of citrate synthase and COX-IV (r=72-0.73; P=0.03), but not with the difference in the capillary-to-fibre ratio (P=0.965). In conclusion, endurance training improves O2 extraction during small muscle mass exercise by elevating the muscle oxidative capacity and the recruitment of DM O2 ; especially evident during high-intensity exercise exploiting a larger fraction of the muscle oxidative capacity.