Mechanisms Of Attenuation Of Pulmonary V'O-2 Slow Component In Humans After Prolonged Endurance Training

In this study we have examined the effect of prolonged endurance training program on the pulmonary oxygen uptake (V'O-2) kinetics during heavy-intensity cycling-exercise and its impact on maximal cycling and running performance. Twelve healthy, physically active men (mean +/- SD: age 22.33 +/- 1.44 years, V'O-2peak 3198 +/- 458 mL.min(-1)) performed an endurance training composed mainly of moderate-intensity cycling, lasting 20 weeks. Training resulted in a decrease (by similar to 5%, P = 0.027) in V'O-2 during prior low-intensity exercise (20 W) and in shortening of tau(p) of the V'O-2 on-kinetics (30.1 +/- 5.9 s vs. 25.4 +/- 1.5 s, P = 0.007) during subsequent heavy-intensity cycling. This was accompanied by a decrease of the slow component of V'O-2 on-kinetics by 49% (P = 0.001) and a decrease in the end-exercise V'O-2 by similar to 5% (P = 0.005). An increase (P = 0.02) in the vascular endothelial growth factor receptor 2 mRNA level and a tendency (P = 0.06) to higher capillary-to-fiber ratio in the vastus lateralis muscle were found after training (n = 11). No significant effect of training on the V'O-2peak was found (P = 0.12). However, the power output reached at the lactate threshold increased by 19% (P = 0.01). The power output obtained at the V'O-2peak increased by 14% (P = 0.003) and the time of 1,500-m performance decreased by 5% (P = 0.001). Computer modeling of the skeletal muscle bioenergetic system suggests that the training-induced decrease in the slow component of V'O-2 on-kinetics found in the present study is mainly caused by two factors: an intensification of the each-step activation (ESA) of oxidative phosphorylation (OXPHOS) complexes after training and decrease in the "additional" ATP usage rising gradually during heavy-intensity exercise.