Elsevier

Clinics in Chest Medicine

Volume 21, Issue 4, 1 December 2000, Pages 665-677
Clinics in Chest Medicine

Peripheral Muscle Dysfunction in Chronic Obstructive Pulmonary Disease

https://doi.org/10.1016/S0272-5231(05)70176-3Get rights and content

As their life expectancy has been prolonged with improved medical care, patients with chronic obstructive pulmonary disease (COPD) frequently develop systemic complications of their disease. These complications include osteoporosis, depression, and peripheral muscle dysfunction2 characterized by atrophy, weakness, and low oxidative capacity. These muscle changes have been associated with exercise intolerance,44 poor quality of life115 and reduced survival,108, 127 which occur independently of the impairment in lung function. Physicians dealing with patients with advanced COPD face the challenge of finding innovative ways to improve their patients' level of function despite the irreversible impairment of the primarily diseased organ. In this article, the evidence for peripheral muscle dysfunction in patients with COPD and the possible clinical implications of this problem are discussed. The available therapeutic options for improving peripheral muscle function are also considered.

Section snippets

EVIDENCE OF PERIPHERAL MUSCLE DYSFUNCTION

Peripheral muscle abnormalities described in patients with COPD include:

  • Muscle atrophy109

  • Weakness44, 46

  • Morphologic changes

    • ↓proportion of type I fibers48, 54, 79, 124

    • ↑proportion of type IIb fibers48, 124

    • atrophy of type I and IIa fibers124

    • ↓capillarization124

  • Altered metabolic capacity

    • ↓intramuscular pH36

    • ↓adenosine triphosphate (ATP) concentration36, 41

    • ↑muscle lactate concentration36, 41

    • ↑iononine monophosphate94

    • ↓mitochondrial enzyme activities55, 78

The quadriceps is the most

CAUSES OF SKELETAL MUSCLE DYSFUNCTION IN CHRONIC OBSTRUCTIVE PULMONARY DISEASE

Several factors have been suggested to explain the occurrence of skeletal muscle dysfunction in COPD:

  • Chronic inactivity and disuse atrophy

  • Systemic inflammation

  • Nutritional imbalance

  • Systemic corticosteroids

  • Hypoxemia

  • Electrolyte disturbances

The relative importance of these factors is likely to vary among patients. Peripheral muscle dysfunction is probably multifactorial in origin and is unlikely to be explained by a unique mechanism in all patients. Chronic inactivity,77 systemic inflammation

Exercise Intolerance

Exercise intolerance is a major consequence of COPD. The mechanisms of exercise intolerance are reviewed in the article by Nici later in this issue. Importantly, several observations have made it clear that exercise intolerance in these individuals cannot be explained solely on the basis of limitations in ventilation and gas exchange. The degree of impairment in lung function is a poor predictor of exercise capacity, for instance.58 Perhaps the most striking clinical observation pointing to a

Exercise Training

As reviewed in the article by Bourjeily and Rochester in this issue, several excellent studies have documented that exercise tolerance can be improved with exercise training in patients with COPD.1, 13, 18, 21, 42, 91, 98, 115, 116 Until the 1990s, however, skeletal muscle adaptation to training was not believed to occur in these individuals.6, 7 It was thought that these patients could not achieve a sufficiently high training intensity for the occurrence of a physiologic training effect. This

SUMMARY

Peripheral muscle dysfunction is a common systemic complication of moderate to severe COPD and may contribute to disability, handicap, and premature mortality. In contrast to the lung impairment, which is largely irreversible, peripheral muscle dysfunction is potentially remediable with exercise training, nutritional intervention, oxygen, and anabolic drugs. Therapeutic success is often incomplete, however, and a better understanding of the mechanisms involved in the development of peripheral

ACKNOWLEDGMENTS

Drs Maltais, LeBlanc, and Jobin wish to thank Marthe Bélanger, Sarah Bernard, Marie-Josée Breton, Richard Debigaré, Jean-François Doyon, and François Whittom for their contribution to their research.

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    Address reprint requests to François Maltais, MD, Centre de Pneumologie, Hôpital Laval, Institut Universitaire de Cardiologie, et de Pneumologie de l'Université Laval, 2725 Chemin Ste-Foy, Québec, Québec, Canada, G1V 4G5

    This work was supported in part by the “Fonds de la recherche en santé du Québec,” Québec, and by “la fondation JD Bégin, Université Laval,” Ste-Foy, Québec, Canada.

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