The relationship between oxygen uptake kinetics and neuromuscular fatigue in high-intensity cycling exercise

Purpose In theory, a slow oxygen uptake (VO2) kinetics leads to a greater accumulation of anaerobic by-products, which can, in turn, induce more neuromuscular fatigue. However, the existence of this relationship has never been tested. Methods After two sessions to measure peak VO2, peak power output (POpeak), and VO2 kinetics responses in the unfatigued state (tau VO2 MOD), 10 healthy young adults performed a 6-min cycling bout at 80% POpeak (INT6-min). VO2 kinetics responses were also measured during INT6-min. Neuromuscular fatigue was measured isometrically pre- and post-INT6-min (immediately post- and 15-s post-INT6-min) with an innovative cycle ergometer. Results Maximal voluntary contraction (MVC) force, high-frequency doublet amplitude, and the ratio of low- to high-frequency doublet amplitudes decreased by 34 +/- 7, 43 +/- 11, and 31 +/- 13%, respectively (all P < 0.01). A significant Spearman's rank correlation was observed between the change in low-frequency doublet force (Delta Db10) immediately after INT6-min and both tau VO2 MOD and tau VO2 INT6-min (rho = -0.68 and rho = -0.67, both P < 0.05). When considering the largest responses from the two neuromuscular evaluations post-INT6-min, significant correlations were also found between tau VO2 MOD and Delta Db10 (rho = -0.74; P < 0.05) and between tau VO2 INT6-min and both Delta Db10 and low-frequency fatigue (rho = -0.70 and rho = -0.66; both P < 0.05). Conclusions The present results suggest that subjects with slow VO2 kinetics experience more peripheral fatigue, in particular more excitation-contraction coupling failure, likely due to a greater accumulation of protons and/or inorganic phosphates.