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.

ERS statement on respiratory muscle testing at rest and during exercise

“…Systemic inflammation is a contributor of muscle dysfunction in COPD [295]. In contrast, local inflammation does not play a role in COPD muscle dysfunction: inflammatory cell counts were very low in the diaphragm and external intercostals of patients with severe COPD with preserved body composition [257].…”

“…Collectively, respiratory muscle dysfunction in patients with COPD is the result of multiple deleterious factors such as lung hyperinflation (mechanical disadvantage), gas exchange abnormalities, impaired bioenergetics (increased cost of breathing) and biological mechanisms (oxidative stress), and structural abnormalities (sarcomere damage and atrophy), while inflammation does not seem to play a major role [295]. This scenario coexists with adaptive features including a switch towards a more oxidative phenotype ( predominance of slow-twitch fibres, increased mitochondrial density and myoglobin content), probably in response to increased mechanical loads.…”

Lifestyle Interventions with a Focus on Nutritional Strategies to Increase Cardiorespiratory Fitness in Chronic Obstructive Pulmonary Disease, Heart Failure, Obesity, Sarcopenia, and Frailty

“…However, some limitations have been described with this test, and its use has not been validated yet. Nutrition interventions aimed at improving exercise tolerance are often combined with PR with the intention of increasing the effects of ET on CRF [34]. A variety of nutritional adjuncts to PR have been studied, including creatine [35][36][37], omega-3 (N-3) polyunsaturated fatty acids (PUFA) [38], dietary nitrates [39][40][41], micronutrient supplementation [42][43][44], and nutrition support supplementation [45][46][47][48][49][50].…”

Will the gains related to pulmonary rehabilitation continue in the first month after rehabilitation?

“…[7] Smoking, nutritional depletion, hypoxia, and hypercapnia, and frequent exacerbation may be some of the physical activity restrictions. [4,19,20] Decreased airflow as a characteristic of COPD becomes more pronounced during maximal effort. An increased respiratory frequency consequently reduces the period of expiration and boosts hyperinflation.…”