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

Abstract

During constant-power output (PO) exercise above lactate threshold (LT), pulmonary O2 uptake (V̇o2p) features a developing slow component (V̇o2pSC). 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 V̇o2pSC. Eleven healthy men were recruited to perform four constant-PO tests at an intensity corresponding to ∼Δ60 (very heavy, VH) where Δ is 60% of the difference between LT and peak V̇o2p. 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 V̇o2p was measured by mass spectrometry and volume turbine. The magnitude of V̇o2pSC 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 V̇o2pSC development. The reduction in 10/50 Hz ratio was correlated ( P < 0.001, r2 = 0.69) with V̇o2pSC amplitude. The temporal and quantitative association of decrements in muscle torque production and V̇o2pSC suggest a common physiological mechanism between skeletal muscle fatigue and loss of muscle efficiency.