Mechanisms of Attenuation of Pulmonary V'O2 Slow Component in Humans after Prolonged Endurance Training

Abstract

In this study we have examined the effect of prolonged endurance training program on the pulmonary oxygen uptake (V'O2) 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'O2peak 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'O2 during prior low-intensity exercise (20 W) and in shortening of τp of the V'O2 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'O2 on-kinetics by 49% (P = 0.001) and a decrease in the end-exercise V'O2 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'O2peak 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'O2peak 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'O2 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.

Fig 1. Transverse section of human muscle fibers, preserved in epoxy resin.

A representative area of a part of vastus lateralis muscle stained with the mixture of toluidine and methylene blue is showed. The arrows indicate the cross section of capillaries.

Fig 2. Models fitted to subject 3 data collected during baseline-heavy-intensity exercise transition before training and the corresponding residuals.

The arrow represents the size of the slow component, which is defined as the difference between the value reached at the end of the exercise, and the value of the first (fast) exponential component (represented with the broken line).

Fig 3. Plasma lactate concentration [La^-]_pl during an incremental exercise test before (white circles) and after (black circles) 20 weeks of endurance training.

The power output was increased by 30 W every 3 minutes up to 240 W. Note the right-ward shift of the lactate curve after training and especially the difference (P < 0.02 Wilcoxon signed rank test) between [La^-]_pl at 180 W i.e. near to the power output at which the V’O₂ on-kinetics has been determined, before and after the training. Data are given as means ± SD for 11 subjects.

Fig 4. Mean (± SD) values of pulmonary oxygen uptake (V’O₂) for 12 subjects during baseline and during heavy-intensity transition.

Note the training-induced attenuation of the slow component of the V’O₂ on-kinetics during high-intensity cycling.

Fig 5. Experimental V’O₂ and simulated muscle V’O₂, metabolite concentrations and ATP usage/supply fluxes during low-intensity (baseline) and high-intensity cycling exercise in untrained and trained muscle.

(A) Experimental and simulated V’O₂, simulated ADP and pH. (B) Simulated PCr, P_i and ATP. (C) Simulated ATP usage (UT), ATP supply by OXPHOS (OX), ATP supply by anaerobic glycolysis (GL), ATP supply by creatine kinase (CK). Experimental baseline-heavy-intensity exercise transition: after 3 min. Simulated baseline-heavy-intensity exercise transition: after 3.4 min (the delay by 24 s corresponds to the cardio-dynamic phase of the pulmonary V’O₂ on-kinetics). The muscle V’O₂ is calculated based on the assumption that during baseline-intensity exercise (20 W) muscle V’O₂ constitutes ~75% and during heavy-intensity exercise ~85% of the pulmonary V’O₂ (see Ref. [40]).