New Findings r What is the central question of this study?A few weeks of endurance training accelerate the oxygen uptake (V O 2 ) on-kinetics in humans. The main aim of the present study was to determine whether the acceleration ofV O 2 onkinetics obtained by a short period of moderate-intensity training can be explained by an intensification of mitochondrial biogenesis. r What is the main finding and its importance?We demonstrated that 5 weeks of moderate-intensity training accelerates theV O 2 on-kinetics during moderate-intensity cycling in the absence of enhanced mitochondrial biogenesis or capillarization in the trained muscles. We postulate that in the early stages of training an intensification of 'parallel activation' of oxidative phosphorylation could account for the shortening of theV O 2 on-transient.The effects of 5 weeks of moderate-intensity endurance training on pulmonary oxygen uptake kinetics (V O 2 on-kinetics) were studied in 15 healthy men (mean ± SD: age 22.7 ± 1.8 years, body weight 76.4 ± 8.9 kg and maximalV O 2 46.0 ± 3.7 ml kg −1 min −1 ). Training caused a significant acceleration (P = 0.003) ofV O 2 on-kinetics during moderate-intensity cycling (time constant of the 'primary' component 30.0 ± 6.6 versus 22.8 ± 5.6 s before and after training, respectively) and a significant decrease (P = 0.04) in the amplitude of the primary component (837 ± 351 versus 801 ± 330 ml min −1 ). No changes in myosin heavy chain distribution, muscle fibre capillarization, level of peroxisome proliferator-activated receptor γ coactivator 1α and other markers of mitochondrial biogenesis (mitochondrial DNA copy number, cytochrome c and cytochrome oxidase subunit I contents) in the vastus lateralis were found after training. A significant downregulation in the content of the sarcoplasmic reticulum ATPase 2 (SERCA2; P = 0.03) and a tendency towards a decrease in SERCA1 (P = 0.055) was found after training. The decrease in SERCA1 was positively correlated (P = 0.05) with the training-induced decrease in the gain of theV O 2 on-kinetics ( V O 2 at steady state/ power output). In the early stage of training, the acceleration inV O 2 on-kinetics during moderate-intensity cycling can occur without enhanced mitochondrial biogenesis or changes in muscle myosin heavy chain distribution and
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.
In this study, we hypothesized that 5 weeks of cycling endurance training can decrease the magnitude of the non-proportional increase in oxygen uptake (˙ V O 2) to power output relationship (˙ V O 2 'excess') at exercise intensities exceeding the lactate threshold (LT). Ten untrained, physically active men performed a bout of incremental cycling exercise until exhaustion before and after training. The mitochondrial DNA copy number, myosin heavy chain composition and content of uncoupling protein 3 and sarcoplasmic reticulum Ca 2+-ATPases (SERCAs) were analysed in muscle biopsies taken from vastus lateralis before and after training. The training resulted in an enhancement of the power-generating capabilities at maximal oxygen uptake (˙ V O 2 max) by ∼7% (P = 0.002) despite there being no changes in ˙ V O 2 max (P = 0.49). This effect was due to a considerable reduction in the magnitude of the ˙ V O 2 'excess' (P < 0.05) above the LT. A decrease in plasma ammonia concentration was found during exercise after training (P < 0.05). A downregulation of SERCA2 in vastus lateralis (P = 0.006) was observed after training. No changes in myosin heavy chain composition, selected electron transport chain proteins, uncoupling protein 3 or the mitochondrial DNA copy number (P > 0.05) were found after training. We conclude that the training-induced increase in power-generating capabilities at ˙ V O 2 max was due to attenuation of the ˙ V O 2 'excess' above the LT. This adaptive response seems to be related to the improvement of muscle metabolic stability, as judged by a lowering of plasma ammonia concentration. The enhancement of muscle metabolic stability after training could be caused by a decrease in ATP usage at a given power output owing to downregulation of SERCA2 pumps. The oxygen cost of cycling above the lactate threshold (LT) can be decreased after a few weeks of endurance training, as expressed by the lowering of the magnitude of the slow component of oxygen uptake (˙ V O 2) kinetics (Casaburi et al. 1987; Womack et al. 1995; Carter et al. 2000). However, the mechanism responsible for this effect remains unclear. There is a growing body of evidence to suggest that the increase in the oxygen cost of work during heavy-intensity exercise is caused by fatigue of the active muscle fibres (Zoladz et al. 2008; Hepple et al. 2010; Cannon et al. 2011) and, in particular, by a disturbance in the concentrations of muscle metabolites, i.e. a decrease in muscle phosphocreatine and a rise in free ADP, free AMP, free inosine monophosphate, creatine, inorganic phosphate and H + , potent to decrease muscle mechanical efficiency (Woledge, 1998; Zoladz et al. 2006). It is well known that endurance training can enhance muscle metabolic stability, i.e. lead to reduced changes in the concentrations of the above-mentioned muscle metabolites for a given ATP turnover (approximately
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
hi@scite.ai
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.