Training-induced acceleration of O2 uptake on-kinetics precedes muscle mitochondrial biogenesis in humans

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New FindingsWhat is the central question of this study?A few weeks of endurance training accelerate the oxygen uptake (Symbol) on-kinetics in humans. The main aim of the present study was to determine whether the acceleration ofSymbolon-kinetics obtained by a short period of moderate-intensity training can be explained by an intensification of mitochondrial biogenesis.What is the main finding and its importance?We demonstrated that 5 weeks of moderate-intensity training accelerates theSymbolon-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 theSymbolon-transient.The effects of 5 weeks of moderate-intensity endurance training on pulmonary oxygen uptake kinetics (Symbolon-kinetics) were studied in 15 healthy men (mean ± SD: age 22.7 ± 1.8 years, body weight 76.4 ± 8.9 kg and maximalSymbol46.0 ± 3.7 ml kg−1 min−1). Training caused a significant acceleration (P= 0.003) ofSymbolon-kinetics during moderate-intensity cycling (time constant of the ‘primary’ component 30.0 ± 6.6versus22.8 ± 5.6 s before and after training, respectively) and a significant decrease (P= 0.04) in the amplitude of the primary component (837 ± 351versus801 ± 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, cytochromecand 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 theSymbolon-kinetics (Symbolat steady state/Δpower output). In the early stage of training, the acceleration inSymbolon-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.

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