Skeletal muscle response to inflammation—Lessons for chronic obstructive pulmonary disease

Abstract

To describe how inflammation affects muscle adaptation and performance in people with chronic obstructive pulmonary disease. In chronic obstructive pulmonary disease, an increasingly sedentary lifestyle is a primary contributor to muscle dysfunction that results in a loss of mobility and independence and, ultimately, mortality. Given the systemic chronic inflammation and profound limb muscle atrophy in chronic obstructive pulmonary disease, it is tempting to speculate that the inflammatory process is deleterious to skeletal muscle. In healthy people, however, the inflammatory process initially is dominated by a destructive phase that is tightly regulated and modulates a reparative, regenerative phase. Although the inflammatory process and associated oxidative stress is more closely connected to muscle wasting in animal models of chronic obstructive pulmonary disease, the causative role of inflammation toward muscle atrophy and weakness in people with chronic obstructive pulmonary disease has not been definitively shown. Anti-inflammatory interventions aimed toward tempering muscle wasting and weakness in chronic obstructive pulmonary disease may not prove to be beneficial because of longer-term disruption of the regeneration of muscle tissue. Temporally and spatially targeted interventions aimed toward ameliorating oxidative stress, such as antioxidants, nutritional supplements, and chronic exercise training, may optimize outcomes toward maintaining muscle mass and performance.

Effect of transcutaneous electrical muscle stimulation on muscle volume in patients with septic shock*

“…ICU-acquired weakness is a common complication of critical illness with an incidence ranging from 25% to 58% depending on the patient population and diagnostic approach (30 -32). It is generally accepted that immobilization and inflammatory stimuli are important contributing factors to catabolism of muscle tissue (33) and ICU-acquired weakness (34). Despite the clinical significance of muscle atrophy for loss of function after discharge from intensive care (5), no preventive therapies have been identified as yet.…”

Physical activity, nutritional status and systemic inflammation in COPD

“…Less clear is the ability of exercise training to improve systemic inflammation in COPD patients. We know that exercise can trigger an inflammatory response and oxidative stress in patients with COPD [49][50][51][52]. Noninjurious (moderate intensity and short duration) exercise increases the level of circulating inflammatory cells and cytokines, by stimulating interleukin (IL)-6, IL-10 and IL-1ra but inhibiting tumour necrosis factor (TNF)-a [53][54][55].…”

Association between phthalate exposure and lower handgrip strength in an elderly population: a repeated-measures study

“…The majority of the study participants were women, nonsmokers, non-drinkers, and relatively healthy, which lowers the external generalizability of the current results, especially to populations with lower physical function and more diseases. Considering previous studies that have reported associations between inflammation and decreased muscle strength among severely ill patients, such as those with sepsis or multiple organ failure [42, 43], possibility that phthalate exposure might lead to increased mortality due to weakened diaphragmatic muscle among individuals with lower physical function and more diseases [44] should be investigated in future studies. Second, although handgrip strength is a reliable indicator for whole-body muscle strength, direct measurement in the lower extremities would be more relevant to assess mobility and physical function in the elderly population [45].…”