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

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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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