Towards Personalized Management of Sarcopenia in COPD

Abstract

The awareness of the presence and consequences of sarcopenia has significantly increased over the past decade. Sarcopenia is defined as gradual loss of muscle mass and strength and ultimately loss of physical performance associated with aging and chronic disease. The prevalence of sarcopenia is higher in chronic obstructive pulmonary disease (COPD) compared to age-matched controls. Current literature suggests that next to physical inactivity, COPD-specific alterations in physiological processes contribute to accelerated development of sarcopenia. Sarcopenia in COPD can be assessed according to current guidelines, but during physical performance testing, ventilatory limitation should be considered. Treatment of muscle impairment can halt or even reverse sarcopenia, despite respiratory impairment. Exercise training and protein supplementation are currently at the basis of sarcopenia treatment. Furthermore, effective current and new interventions targeting the pulmonary system (eg, smoking cessation, bronchodilators and lung volume reduction surgery) may also facilitate muscle maintenance. Better understanding of disease-specific pathophysiological mechanisms involved in the accelerated development of sarcopenia in COPD will provide new leads to refine nutritional, exercise and physical activity interventions and develop pharmacological co-interventions.

Keywords: anabolics; chronic obstructive pulmonary disease; exercise; nutrition; nutritional assessment; skeletal muscle.

Figure 1

Pathophysiology of sarcopenia in COPD: Age and COPD can be considered as initial determinants of disease specific and shared triggers (in blue) that initiate independent and interrelated pathophysiological mechanisms through alterations of multiple muscle cell signaling pathways (which have been discussed extensively by other authors such as Langen et al and Abdulai et al37). Eventually these converge on and deregulate three key processes (in orange) responsible for muscle homeostasis, leading to sarcopenia.