Muscle fatigue (a reduced power for a given activation) is common following exercise in COPD. Whether muscle fatigue, and reduced maximal voluntary locomotor power, are sufficient to limit whole-body exercise in COPD is unknown. We hypothesized in COPD: 1) exercise is terminated with a locomotor muscle power reserve; 2) reduction in maximal locomotor power is related to ventilatory limitation; and 3) muscle fatigue at intolerance is less than age-matched controls. We used a rapid switch from hyperbolic to isokinetic cycling to measure the decline in peak isokinetic power at the limit of incremental exercise ('performance fatigue') in 13 COPD (FEV1 49±17 %pred) and 12 controls. By establishing the baseline relationship between muscle activity and isokinetic power, we apportioned performance fatigue into the reduction in muscle activation and muscle fatigue. Peak isokinetic power at intolerance was ~130% of peak incremental power in controls (274±73 vs 212±84W, p<0.05), but ~260% in COPD (187±141 vs 72±34W, p<0.05) - greater than controls (p<0.05). Muscle fatigue as a fraction of baseline peak isokinetic power was not different in COPD vs controls (0.11±0.20 vs 0.19±0.11). Baseline to intolerance, the median frequency of maximal isokinetic muscle activity was unchanged in COPD but reduced in controls (+4.3±11.6 vs -5.5±7.6%, p<0.05). Performance fatigue as a fraction of peak incremental power was greater in COPD vs controls and related to resting (FEV1/FVC) and peak exercise (V̇E/MVV) pulmonary function (r2=0.47, r2=0.55, p<0.05). COPD patients are more fatigable than controls, but this fatigue is insufficient to constrain locomotor power and define exercise intolerance.
CORE (COnnecting REpositories)
CORE (COnnecting REpositories)