Mechanisms responsible for the acceleration of pulmonary V̇O2 on-kinetics in humans after prolonged endurance training.

The effect of prolonged endurance training on the pulmonary V̇O2 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, V̇O2peak 3,187±479 ml/min) performed endurance cycling training (4 sessions per week) lasting 20 wk. Training shortened τp of the pulmonary V̇O2 on-kinetics during moderate-intensity cycling by ∼19% from 28.3±5.2 to 23.0±4.0 s (P=0.005). τp of the pulmonary V̇O2 off-kinetics decreased by ∼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 (+5%) 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 training-induced increase in OXPHOS activity accounted for about 0-10% of the decrease in τp of muscle and pulmonary V̇O2 for the on-transient, whereas the remaining 90-100% is caused by an increase in each-step parallel activation of OXPHOS.