Affiliation:
1. John Rankin Laboratory of Pulmonary Medicine, University of Wisconsin-Madison Medical School, Madison, Wisconsin;
2. Department of Internal Medicine, University of Utah, Salt Lake City, Utah;
3. Exercise Physiology, ETH Zürich, and Institute of Physiology, University of Zürich, Zürich, Switzerland
4. Department of Medicine, University of Wisconsin-Madison Medical School, Madison, Wisconsin; and
Abstract
We examined the effects of respiratory muscle work [inspiratory (Wr-insp); expiratory (Wr-exp)] and arterial oxygenation (SpO2) on exercise-induced locomotor muscle fatigue in patients with chronic obstructive pulmonary disease (COPD). Eight patients (FEV, 48 ± 4%) performed constant-load cycling to exhaustion (Ctrl; 9.8 ± 1.2 min). In subsequent trials, the identical exercise was repeated with 1) proportional assist ventilation + heliox (PAV); 2) heliox (He:21% O2); 3) 60% O2 inspirate (hyperoxia); or 4) hyperoxic heliox mixture (He:40% O2). Five age-matched healthy control subjects performed Ctrl exercise at the same relative workload but for 14.7 min (≈best COPD performance). Exercise-induced quadriceps fatigue was assessed via changes in quadriceps twitch force (Qtw,pot) from before to 10 min after exercise in response to supramaximal femoral nerve stimulation. During Ctrl, absolute workload (124 ± 6 vs. 62 ± 7 W), Wr-insp (207 ± 18 vs. 301 ± 37 cmH2O·s·min−1), Wr-exp (172 ± 15 vs. 635 ± 58 cmH2O·s·min−1), and SpO2 (96 ± 1% vs. 87 ± 3%) differed between control subjects and patients. Various interventions altered Wr-insp, Wr-exp, and SpO2 from Ctrl (PAV: −55 ± 5%, −21 ± 7%, +6 ± 2%; He:21% O2: −16 ± 2%, −25 ± 5%, +4 ± 1%; hyperoxia: −11 ± 2%, −17 ± 4%, +16 ± 4%; He:40% O2: −22 ± 2%, −27 ± 6%, +15 ± 4%). Ten minutes after Ctrl exercise, Qtw,pot was reduced by 25 ± 2% ( P < 0.01) in all COPD and 2 ± 1% ( P = 0.07) in healthy control subjects. In COPD, ΔQtw,pot was attenuated by one-third after each interventional trial; however, most of the exercise-induced reductions in Qtw,pot remained. Our findings suggest that the high susceptibility to locomotor muscle fatigue in patients with COPD is in part attributable to insufficient O2 transport as a consequence of exaggerated arterial hypoxemia and/or excessive respiratory muscle work but also support a critical role for the well-known altered intrinsic muscle characteristics in these patients.
Publisher
American Physiological Society
Subject
Physiology (medical),Physiology
Cited by
124 articles.
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