Five weeks of moderate-intensity endurance training significantly accelerated O2 on-kinetics during moderate-intensity cycling (22.8 vs 30.0 s; P=0.003) without enhanced mitochondrial biogenesis.
Does 5 weeks of moderate-intensity endurance training accelerate O2 on-kinetics without enhancing mitochondrial biogenesis in healthy men?
Short-term moderate-intensity endurance training accelerates O2 on-kinetics prior to the enhancement of muscle mitochondrial biogenesis, possibly related to downregulation of SERCA pumps.
Absolute Event Rate: 22.8% vs 30%
p-value: p=0.003
New Findings 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. 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’ 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 kg −1 min −1 ). Training caused a significant acceleration ( P = 0.003) of 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 the on‐kinetics ( at steady state/Δpower 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 O 2 cost of cycling could be caused by the downregulation of SERCA pumps.
Żołądź et al. (Sat,) conducted a other in Healthy (n=15). Moderate-intensity endurance training vs. Before training (baseline) was evaluated on Time constant of the 'primary' component of O2 on-kinetics during moderate-intensity cycling (s) (p=0.003). Five weeks of moderate-intensity endurance training significantly accelerated O2 on-kinetics during moderate-intensity cycling (22.8 vs 30.0 s; P=0.003) without enhanced mitochondrial biogenesis.