SARCOPENIA: DEVELOPMENT MECHANISMS IN CHRONIC OBSTRUCTIVE PULMONARY DISEASE AND POSSIBILITY OF PREVENTION

Abstract

The article presents some causes and mechanisms of sarcopenia and osteosarcopenia development in chronic obstructive pulmonary disease (COPD). The focus is on the role of low-grade chronic systemic inflammation and elevated C-reactive protein levels (above 5 mg/L) in the development of anemia, reduction in body mass index, and lean body mass. It is emphasized that systemic manifestations of COPD are often accompanied by malnutrition, skeletal muscle dysfunction, osteoporosis, and anemia — key components of the so-called trophological syndrome, which includes sarcopenia and osteosarcopenia.

The authors note that, apart from inflammation, other contributors to sarcopenia may include increased oxygen consumption by skeletal muscles, hypoxia, prolonged use of medications such as β₂-agonists, long-acting β₂-agonists and muscarinic antagonists, systemic glucocorticoids, and protein malnutrition. Physical deconditioning leads to reduced exercise tolerance, which is directly correlated with patient survival.

Local pathogenic mechanisms of sarcopenia and osteosarcopenia are described in detail, with emphasis on the roles of myostatin, decorin, mitochondrial transformation, hypercapnia, and hypoxia — ultimately leading to degeneration or lysis of skeletal muscle. Limited airflow, muscle fatigue, and dyspnea decrease physical endurance, strength, and contraction speed, especially in the lower limbs. This is attributed to insufficient energy supply, altered chest wall geometry, and diaphragm displacement due to pulmonary hyperinflation. Pathological shortening of sarcolemmal muscle fibers, local protease activation, and uncontrolled oxidative stress in respiratory muscles are also considered contributing factors.

The association between sarcopenia and the stage of COPD is highlighted. In early stages, protein metabolism is altered by increased synthesis and degradation. In later stages, muscle proteolysis predominates, and protein synthesis declines due to progressive hypoxemia, hypercapnia, and reduced anabolic hormone production. During exacerbations, hypoxemia, acidosis, and acute inflammation (primarily due to COPD flare-ups) are the main contributors to muscle dysfunction.

Additionally, mineral metabolism disorders (phosphorus, calcium, copper, etc.) are underscored. These contribute to oxidative damage in cellular membranes and trigger apoptosis or necrosis of myocytes and myofibrils, and, in some cases, necrosis of bone and cartilage tissues. Abnormal protein and vitamin metabolism are also observed. All of these factors contribute to the onset and progression of sarcopenia and osteosarcopenia.

The authors stress the importance of early identification and prevention of these mechanisms and their consequences in COPD patients. They focus on two key preventive strategies: nutritional correction and therapeutic physical activity. Nutritional recommendations include increased intake of high-quality animal protein and essential amino acids, particularly leucine and arginine. Regarding physical rehabilitation, resistance training is emphasized due to its stronger impact on the musculoskeletal system and its ability to prevent both osteoporosis and sarcopenia. Aerobic exercise is noted for its benefits to the respiratory and cardiovascular systems, which is particularly important in COPD management.