Mechanisms responsible for the acceleration of pulmonary V̇o₂on-kinetics in humans after prolonged endurance training

Abstract

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.

Exercise training in chronic heart failure: improving skeletal muscle O2transport and utilization

“…In healthy skeletal muscle, faster V O 2 kinetics after endurance exercise training results primarily from improved oxidative capacity and/or allosteric regulation of mitochondrial respiration (i.e., 1"parallel activation"; Refs. 18,35,36,86,133,207,221,222,242,338,339) (see also Figs. 6 and 7).…”

Slower V˙O2 Kinetics in Older Individuals

“…These considerable improvements in measures of vascularization and endothelium-dependent vasodilation would improve the surface area for O 2 exchange, which might contribute to absence of an ''overshoot'' in the normalized [HHb]/V O 2 ratio in the trained older compared with the untrained older men. Nevertheless, despite the suggestion that improved O 2 provision to the active tissues plays a critical role in controlling the faster V O 2 kinetics observed in trained older individuals, mechanisms of intracellular control discussed in this review (34,35,40,41,68,88,89) are also to be acknowledged as ''limiting'' factors determining the rate of adjustment of oxidative phosphorylation.…”

“…Whereas we have suggested that metabolic control regulates V O 2 kinetics in the range of 20 s and that slower V O 2 kinetics may have a limitation in matching of O 2 delivery to the sites of active muscle utilization, Zoladz and colleagues (88) have proposed that muscle V O 2 on-kinetics is mainly controlled/limited by intramuscular factors of metabolic activation. Based on a computer model of oxidative phosphorylation and metabolic control analysis, the increased ATP usage with exercise is accompanied by simultaneous activation of oxidative phosphorylation complexes (including Complexes I, III, IV, ATP/ADP).…”

Nonparametric modelling of VO<inf>2</inf> response to exercise

“…For most of the previous studies, the Oxygen uptake during exercise (Fig.1) has been considered as an exponential function [1]:…”

“…Several experiments suggest that oxygen consumption is mainly controlled by intramuscular factor related metabolic system [1], [2]. Unlike heart rate, which is affected by mood, stress, etc., the maximum Oxygen uptake is considered as the most accurate measurement of the fitness of cardiorespiratory system.…”