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摘要
New Findings center dot What is the central question of this study? A few weeks of endurance training accelerate the oxygen uptake () on-kinetics in humans. The main aim of the present study was to determine whether the acceleration of on-kinetics obtained by a short period of moderate-intensity training can be explained by an intensification of mitochondrial biogenesis. center dot What is the main finding and its importance? We demonstrated that 5 weeks of moderate-intensity training accelerates the 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%26apos; of oxidative phosphorylation could account for the shortening of the on-transient. The effects of 5 weeks of moderate-intensity endurance training on pulmonary oxygen uptake kinetics ( on-kinetics) were studied in 15 healthy men (mean +/- SD: age 22.7 +/- 1.8 years, body weight 76.4 +/- 8.9 kg and maximal 46.0 +/- 3.7 ml kg1 min1). Training caused a significant acceleration (P= 0.003) of on-kinetics during moderate-intensity cycling (time constant of the primary%26apos; 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 min1). No changes in myosin heavy chain distribution, muscle fibre capillarization, level of peroxisome proliferator-activated receptor coactivator 1 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 the on-kinetics ( at steady state/power output). In the early stage of training, the acceleration in on-kinetics during moderate-intensity cycling can occur without enhanced mitochondrial biogenesis or changes in muscle myosin heavy chain distribution and in muscle fibre capillarization. The training-induced decrease of the O2 cost of cycling could be caused by the downregulation of SERCA pumps.
- 出版日期2013-4
