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

When exercising with a small muscle mass, the mass‐specific O 2 delivery exceeds the muscle oxidative capacity resulting in a lower O 2 extraction compared with whole‐body exercise. We elevated the muscle oxidative capacity and tested its impact on O 2 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 ˙ O 2 peak ) and peak power output ( W ˙ peak ) during 1L‐KE than the control leg (CON; all P  < .05). Leg O 2 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 O 2 extraction than CON (main effect: 1.7 ± 1.6% points; P  = .010; 40%‐83% ofW ˙ peak ) with the largest between‐leg difference at 83% ofW ˙ peak (O 2 extraction: 3.2 ± 2.2% points; arteriovenous O 2 difference: 7.1 ± 4.8 mL· L −1 ; P  < .001). At 83% ofW ˙ peak , muscle O 2 conductance (D M O 2 ; Fick law of diffusion) and the equilibration index Y were higher in TL ( P  < .01), indicating reduced diffusion limitations. The between‐leg difference in O 2 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 O 2 extraction during small muscle mass exercise by elevating the muscle oxidative capacity and the recruitment of D M O 2, especially evident during high‐intensity exercise exploiting a larger fraction of the muscle oxidative capacity.