Muscle wasting and changes in muscle protein metabolism in chronic obstructive pulmonary disease

Abstract

Muscle wasting and changes in muscle protein metabolism in chronic obstructive pulmonary disease. R.T. Jagoe, M.P.K.J. Engelen. #ERS Journals Ltd 2003. ABSTRACT: Loss of skeletal muscle mass is now recognised as an important feature of chronic obstructive pulmonary disease (COPD) which contributes to symptoms and influences prognosis. The changes in skeletal muscle remain poorly understood, largely because only a few studies have been performed to define the adaptations in whole body and muscle protein metabolism in COPD.The first sections of this review summarise background information about skeletal muscle wasting in COPD, and focuses on the studies concerned with amino acid profiles and protein synthesis and degradation rates. To aid interpretation some discussion of the techniques commonly used is included.A variety of different catabolic factors may determine whether chronic obstructive pulmonary disease patients become cachectic. The precise role for each one of these factors as well as the intracellular pathways activated in muscle as a result of chronic obstructive pulmonary disease are unknown and remain to be defined. Details of the actions of a range of different catabolic factors and potential mechanisms will be discussed. A significant proportion of patients with chronic obstructive pulmonary disease (COPD) develop peripheral skeletal muscle wasting and weakness [1,2]. Loss of skeletal muscle mass is reflected by the reduction in fat-free mass (FFM) observed in y20-40% of patients with COPD [3,4], and this has a number of consequences: 1) many studies have now shown that lower FFM is associated with reduced exercise tolerance [3,[5][6][7]. 2) Because muscle power is directly proportional to cross-sectional area, loss of muscle mass is also associated with reduced peripheral muscle strength in COPD [5,8,9]. 3) Many patients with COPD suffer debilitating symptoms and there is now evidence that those with lower FFM also have worse symptom scores in standard COPDrelated quality of life assessment tools, even when compared with COPD patients who have lost fat mass but not FFM [5]. 4) Finally, low body weight has been identified previously as a poor prognostic indicator of survival in COPD [10,11], but a recent retrospective analysis of 142 COPD patients showed that mid-thigh muscle cross-sectional area was a better indicator of prognosis than body mass index [12]. This latter finding reinforces the concept that loss of FFM and in particular muscle mass is a common feature of COPD which has important implications for physical function, health status and survival.Despite increasing interest in skeletal muscle wasting in COPD, the underlying mechanisms remain unclear. Exercisebased pulmonary rehabilitation programmes have been shown to improve muscle function and exercise tolerance for many affected individuals. The success of exercise therapy suggests that deconditioning due to reduced physical activity plays a major role in COPD-related skeletal muscle dysfunction, but it also seems likely that other cata...

Effects of Pulmonary Rehabilitation on Exercise Tolerance in Patients with COPD

“…Similar observation were reported by several investigators 15,[24][25][26][27][28] . In addition, significant improvement in mean Borg score was observed in PR intervened patients but it was not improved in patients without PR after 60 days.…”

“…But literature review suggested that, decreased skeletal muscle mass in the periphery may cause loss of endurance and strength of peripheral muscles to produce decrement in 6MWD in COPD patients 24 . Moreover, restricted working capability for dyspnea may produce disuse atrophy in the peripheral limb muscles which may act as a factor for decrement in peripheral muscle load and muscle wasting in stable COPD patients may cause decrement in overall skeletal muscle mass which may produce exercise intolerance 25 . Again, hyperinflation and overstretching of the alveoli and airway may decrease diffusing membrane surface area for gaseous exchange and diffusing capacity of respiratory membrane in COPD patients may cause decreased oxygenation of blood and ultimately decreased systemic arterial SpO 2 % and increased PCO 2 26 .…”

Detrimental metabolic effects of combining long-term cigarette smoke exposure and high-fat diet in mice

“…Both obesity and cigarette smoking are also important risk factors in many age-related diseases, accelerating the aging process via increasing oxidative stress and inflammation (51). It has been hypothesized (32,52) that weight loss associated with chronic obstructive pulmonary disease commonly observed in long-term smokers is actually due to lean body mass loss. This study, for the first time, examined the combined effects of these two detrimental behaviors, cigarette smoking and consumption of an energy-dense, high-fat diet.…”

Effects of Pulmonary Rehabilitation on Lung Functions in Patients with COPD

“…It has been suggested that, long standing alveolar hypoventilation and dyspnea in the COPD patients may cause increased work of breathing, hypoxia induced decreased ATP production and increased energy expenditure followed by skeletal muscle wasting in these groups of patients. [27][28][29][30] On the other hand, expiratory airflow limitation due to decrease elastic fibres in the alveolar walls and airways have also been suggested as an important contributory factor for lung hyperinflation in this group of patients. As a consequence, there may be increase in inspiratory airflow resistance followed by derangement of ventilatory variables.…”