Mechanisms responsible for the acceleration of pulmonary (V)over-circleO2 on-kinetics in humans after prolonged endurance training

The effect of prolonged endurance training on the pulmonary (V) over circleO(2) on-and off-kinetics in humans, in relation to muscle mitochondria biogenesis, is investigated. Eleven untrained physically active men (means +/- SD: age 22.4 +/- 1.5 years, (V) over circleO(2peak) 3,187 +/- 479 ml/min) performed endurance cycling training (4 sessions per week) lasting 20 wk. Training shortened tau(p) of the pulmonary (V) over circleO(2) on-kinetics during moderate-intensity cycling by similar to 19% from 28.3 +/- 5.2 to 23.0 +/- 4.0 s (P = 0.005). tau(p) of the pulmonary (V) over circle off-kinetics decreased by similar to 11% from 33.7 +/- 7.2 to 30.0 +/- 6.6 (P = 0.02). Training increased (in vastus lateralis muscle) mitochondrial DNA copy number in relation to nuclear DNA (mtDNA/nDNA) (+ 53%) (P = 0.014), maximal citrate synthase (CS) activity (+ 38%), and CS protein content (+ 38%) (P = 0.004), whereas maximal cytochrome c oxidase (COX) activity after training tended to be only slightly (+%) elevated (P = 0.08). By applying to the experimental data, our computer model of oxidative phosphorylation (OXPHOS) and using metabolic control analysis, we argue that COX activity is a much better measure of OXPHOS intensity than CS activity. According to the model, in the present study a traininginduced increase in OXPHOS activity accounted for about 0-10% of the decrease in tau(p) of muscle and pulmonary (V) over circleO(2) for the on-transient, whereas the remaining 90-100% is caused by an increase in each-step parallel activation of OXPHOS.