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 ~5%, P = 0.027) in V’O(2) during prior low-intensity exercise (20 W) and in shortening of τ(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 ~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.