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

Abstract

When exercising with a small muscle mass, the mass-specific O2 delivery exceeds the muscle oxidative capacity resulting in a lower O2 extraction compared with 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 ((Formula presented.)) and peak power output ((Formula presented.)) during 1L-KE than the control leg (CON; all P <.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 =.010; 40%-83% of (Formula presented.)) with the largest between-leg difference at 83% of (Formula presented.) (O2 extraction: 3.2 ± 2.2% points; arteriovenous O2 difference: 7.1 ± 4.8 mL· L−1; P <.001). At 83% of (Formula presented.), muscle O2 conductance (DMO2; Fick law of diffusion) and the equilibration index Y were higher in TL (P <.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-.73; P =.03), but not with the difference in the capillary-to-fiber ratio (P =.965). In conclusion, endurance training improves O2 extraction during small muscle mass exercise by elevating the muscle oxidative capacity and the recruitment of DMO2, especially evident during high-intensity exercise exploiting a larger fraction of the muscle oxidative capacity.