Journal of applied physiology
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A profound remodeling of the diaphragm and vastus lateralis (VL) occurs in patients with moderate-to-severe chronic obstructive pulmonary disease (COPD). In this mini-review, we discuss the following costal diaphragm remodeling features noted in patients with moderate-to-severe COPD: 1) deletion of serial sarcomeres, 2) increased proportion of slow-twitch fibers, 3) fast-to-slow isoform shift in sarco(endo)plasmic reticulum Ca(2+)-ATPase, 4) increased capacity of oxidative metabolism, 5) oxidative stress, and 6) myofiber atrophy. ⋯ For each of the remodeling features noted in both the VL and costal diaphragm of COPD patients, we present mechanisms that are currently thought to mediate these changes as well as the pathophysiology of each remodeling feature. We hope that our mechanistic presentation stimulates research in this area that focuses on improving the ability of COPD patients to carry out increased activities of daily living.
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Muscle dysfunction often occurs in patients with chronic obstructive pulmonary disease (COPD) and may involve both respiratory and locomotor (peripheral) muscles. The loss of strength and/or endurance in the former can lead to ventilatory insufficiency, whereas in the latter it limits exercise capacity and activities of daily life. Muscle dysfunction is the consequence of complex interactions between local and systemic factors, frequently coexisting in COPD patients. ⋯ Under all these circumstances, protein metabolism imbalance, oxidative stress, inflammatory events, as well as muscle injury may occur, determining the final structure and modulating the function of different muscle groups. Respiratory muscles show signs of injury as well as an increase in several elements involved in aerobic metabolism (proportion of type I fibers, capillary density, and aerobic enzyme activity) whereas limb muscles exhibit a loss of the same elements, injury, and a reduction in fiber size. In the present review we examine the current state of the art of the pathophysiology of muscle dysfunction in COPD.
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Chronic obstructive pulmonary disease (COPD) is a debilitating disease caused by parenchymal damage and irreversible airflow limitation. In addition to lung dysfunction, patients with COPD develop weight loss, malnutrition, poor exercise performance, and skeletal muscle atrophy. The latter has been attributed to an imbalance between muscle protein synthesis and protein degradation. ⋯ Pilot experiments on vastus lateralis muscle samples suggest that the autophagy-lysosome system is induced in COPD patients compared with control subjects. In this review, we summarize recent progress related to molecular structure, regulation, and roles of the autophagy-lysosome pathway in normal and diseased skeletal muscles. We also speculate about regulation and functional importance of this system in skeletal muscle dysfunction in COPD patients.