Abstract

During whole-body physical activity (e.g. cycling) exercise capacity is reduced by an “excess” in oxygen cost (VO2) relative to power output (PO) (i.e. higher VO2/PO ratio) that appears above the lactate threshold (LT). This loss of muscle efficiency, of which type I fibers fatigue and/or increased type II fibers recruitment are putative causes, impairs exercise tolerance. PURPOSE: We tested the hypothesis that a strength training intervention (ST), by increasing maximal force (Fmax) and reducing the recruitment of high-threshold motor units at a given exercise intensity will reduce the “excess” VO2 during a cycling incremental exercise. METHODS: 16 young healthy males were randomly assigned to a control (C) and a strength-training (ST) group (three, one-hour sessions per week). Pre and Post a 5-weeks intervention, VO2/PO relationship during an incremental test to exhaustion was modelled using a double-linear fit: the slopes of the VO2/PO relationship below (S1) and above (S2) the LT were calculated. Peak power deficit ([[Unsupported Character - Symbol Font ]]PO) was calculated as: (maximal aerobic power as estimated based on VO2max and VO2/PO ratio below LT) – (experimentally attained POmax). Parameters were compared using two-way (time, group) MANOVA. RESULTS: Regarding the ST group: Fmax significantly increased (15 ± 5% for squat) while VO2max and POmax did not change (overall mean 3317 ± 405 mlmin−1 and 318 ± 31 watt respectively). A significant “excess” VO2 was present Pre (S2 significantly higher than S1: 9.6 ± 1.4 vs 7.4 ± 1.1 mlmin−1W−1) and disappeared Post training (S2 not different from S1: 7.7 ± 0.7 vs 7.4 ± 0.4 mlmin−1W−1) along with a significant reduction in [INCREMENT]PO (30 ± 20 vs 8 ± 5 W). No changes were detected for the C group. CONCLUSIONS: In agreement with our hypothesis, ST significantly reduced the “excess” VO2 during a cycling incremental exercise. Although further studies are warranted to identify a direct cause-effect relationship, this finding support a role of ST in improving aerobic exercise capacity through an attenuation of muscle inefficiency in the heavy-exercise domain.

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