Skeletal Muscle Dysfunction in Chronic Obstructive Pulmonary Disease. What We Know and Can Do for Our Patients

Abstract

Skeletal muscle dysfunction occurs in patients with chronic obstructive pulmonary disease (COPD) and affects both ventilatory and nonventilatory muscle groups. It represents a very important comorbidity that is associated with poor quality of life and reduced survival. It results from a complex combination of functional, metabolic, and anatomical alterations leading to suboptimal muscle work. Muscle atrophy, altered fiber type and metabolism, and chest wall remodeling, in the case of the respiratory muscles, are relevant etiological contributors to this process. Muscle dysfunction worsens during COPD exacerbations, rendering patients progressively less able to perform activities of daily living, and it is also associated with poor outcomes. Muscle recovery measures consisting of a combination of pulmonary rehabilitation, optimized nutrition, and other strategies are associated with better prognosis when administered in stable patients as well as after exacerbations. A deeper understanding of this process' pathophysiology and clinical relevance will facilitate the use of measures to alleviate its effects and potentially improve patients' outcomes. In this review, a general overview of skeletal muscle dysfunction in COPD is offered to highlight its relevance and magnitude to expert practitioners and scientists as well as to the average clinician dealing with patients with chronic respiratory diseases.

Keywords: chronic obstructive pulmonary disease; fiber switch; muscle wasting; skeletal muscle dysfunction; ventilatory muscles.

Figure 1.

Pathophysiology of chronic obstructive pulmonary disease (COPD)-associated muscle dysfunction. Cigarette smoking and other factors, as well as exacerbations, are the main causes of COPD progression, which is associated with peripheral muscle atrophy and fiber switch. Hyperinflation and loss of elastic recoil lead to chest wall geometrical changes that cause diaphragmatic dysfunction. All these events contribute to immobilization and deconditioning, which further cause peripheral muscle dysfunction and deconditioning.

Figure 2.

Holistic approach to prevent and reverse chronic obstructive pulmonary disease (COPD)-associated muscle dysfunction. Combination of optimized diet with resistance and endurance exercise training programs is associated with improved muscle mass and oxidative capacity in locomotor muscles, which in turn decrease fatigue upon exercise. Bronchodilators, cigarette smoking cessation, and occasionally lung volume reduction surgery decrease hyperinflation and lead to better dyspnea control. All these measures contribute to reconditioning and eventually to regaining functional capacity in these patients.