Impact of pulmonary system limitations on locomotor muscle fatigue in patients with COPD.
We examined the effects of respiratory muscle work [inspiratory (W(r-insp)); expiratory (W(r-exp))] and arterial oxygenation (Sp(O(2))) 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% O(2)); 3) 60% O(2) inspirate (hyperoxia); or 4) hyperoxic heliox mixture (He:40% O(2)). Five age-matched healthy control subjects performed Ctrl exercise at the same relative workload but for 14.7 min ( approximately best COPD performance). Exercise-induced quadriceps fatigue was assessed via changes in quadriceps twitch force (Q(tw,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), W(r-insp) (207 +/- 18 vs. 301 +/- 37 cmH(2)O x s x min(-1)), W(r-exp) (172 +/- 15 vs. 635 +/- 58 cmH(2)O x s x min(-1)), and Sp(O(2)) (96 +/- 1% vs. 87 +/- 3%) differed between control subjects and patients. Various interventions altered W(r-insp), W(r-exp), and Sp(O(2)) from Ctrl (PAV: -55 +/- 5%, -21 +/- 7%, +6 +/- 2%; He:21% O(2): -16 +/- 2%, -25 +/- 5%, +4 +/- 1%; hyperoxia: -11 +/- 2%, -17 +/- 4%, +16 +/- 4%; He:40% O(2): -22 +/- 2%, -27 +/- 6%, +15 +/- 4%). Ten minutes after Ctrl exercise, Q(tw,pot) was reduced by 25 +/- 2% (P < 0.01) in all COPD and 2 +/- 1% (P = 0.07) in healthy control subjects. In COPD, DeltaQ(tw,pot) was attenuated by one-third after each interventional trial; however, most of the exercise-induced reductions in Q(tw,pot) remained. Our findings suggest that the high susceptibility to locomotor muscle fatigue in patients with COPD is in part attributable to insufficient O(2) 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.
Amann
Markus
M
John Rankin Laboratory of Pulmonary Medicine, University of Wisconsin-Madison Medical School, Madison, Wisconsin, USA. markus.amann@utah.edu
Regan
Mark S
MS
Kobitary
Majd
M
Eldridge
Marlowe W
MW
Boutellier
Urs
U
Pegelow
David F
DF
Dempsey
Jerome A
JA
D000368:Aged; D015444:Exercise / Q000502:physiology*; D006371:Helium; D006801:Humans; D018496:Hyperoxia / Q000503:physiopathology; D000860:Hypoxia / Q000503:physiopathology; D001239:Inhalation; D008168:Lung; D008875:Middle Aged; D018763:Muscle Fatigue / Q000502:physiology*; D010100:Oxygen; D029424:Pulmonary Disease, Chronic Obstructive / Q000503:physiopathology*; D052097:Quadriceps Muscle / Q000502:physiology; D012132:Respiratory Muscles / Q000502:physiology*; D012137:Respiratory System
D006371:Helium; C038949:heliox; D010100:Oxygen
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