The slow component of pulmonary O2 uptake accompanies peripheral muscle fatigue during high-intensity exercise

During constant-power output (PO) exercise above lactate threshold (LT), pulmonary O₂ uptake (Vo_2p) features a developing slow component (Vo_2pSC). This progressive increase in O₂ cost of exercise is suggested to be related to the effects of muscle fatigue development. We hypothesized that peripheral muscle fatigue as assessed by contractile impairment would be associated with the Vo_2pSC. Eleven healthy men were recruited to perform four constant-PO tests at an intensity corresponding to ~60 (very heavy, VH) where is 60% of the difference between LT and peak Vo_2p. The VH exercise was completed for each of 3, 8, 13, and 18 min (i.e., VH3, VH8, VH13, VH18) with each preceded by 3 min of cycling at 20 W. Peripheral muscle fatigue was assessed via pre- vs. postexercise measurements of quadriceps torque in response to brief trains of electrical stimulation delivered at low (10 Hz) and high (50 Hz) frequencies. During exercise, breath-by-breath Vo_2p was measured by mass spectrometry and volume turbine. The magnitude of Vo_2pSC increased (P < 0.05) from 224 ± 81 ml/min at VH3 to 520 ± 119, 625 ± 134, and 678 ± 156 ml/min at VH8, VH13, and VH18, respectively. The ratio of the low-to-high frequency (10/50 Hz) response was reduced (P < 0.05) at VH3 (–12 ± 9%) and further reduced (P < 0.05) at VH8 (–25 ± 11%), VH13 (–42 ± 19%), and VH18 (–46 ± 16%), mirroring the temporal pattern of Vo_2pSC development. The reduction in 10/50 Hz ratio was correlated (P < 0.001, r² = 0.69) with Vo_2pSC amplitude. The temporal and quantitative association of decrements in muscle torque production and Vo_2pSC suggest a common physiological mechanism between skeletal muscle fatigue and loss of muscle efficiency.

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