Mechanisms responsible for the acceleration of pulmonary V O2 on-kinetics in humans after prolonged endurance training. The effect of prolonged endurance training on the pulmonary V O2 on-and off-kinetics in humans, in relation to muscle mitochondria biogenesis, is investigated. Eleven untrained physically active men (means Ϯ SD: age 22.4 Ϯ 1.5 years, V O2peak 3,187 Ϯ 479 ml/min) performed endurance cycling training (4 sessions per week) lasting 20 wk. Training shortened p of the pulmonary V O2

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... on-kinetics during moderate-intensity cycling by ϳ19% from 28.3 Ϯ 5.2 to 23.0 Ϯ 4.0 s (P ϭ 0.005). p of the pulmonary V O2 off-kinetics decreased by ϳ11% from 33.7 Ϯ 7.2 to 30.0 Ϯ 6.6 (P ϭ 0.02). Training increased (in vastus lateralis muscle) mitochondrial DNA copy number in relation to nuclear DNA (mtDNA/nDNA) (ϩ53%) (P ϭ 0.014), maximal citrate synthase (CS) activity (ϩ38%), and CS protein content (ϩ38%) (P ϭ 0.004), whereas maximal cytochrome c oxidase (COX) activity after training tended to be only slightly (ϩ5%) elevated (P ϭ 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 p of muscle and pulmonary V O2 for the on-transient, whereas the remaining 90 -100% is caused by an increase in each-step parallel activation of OXPHOS.