Exercise as a Therapeutic Strategy for Sarcopenia in Heart Failure: Insights into Underlying Mechanisms

Abstract

Sarcopenia, a syndrome commonly seen in elderly populations, is often characterized by a gradual loss of skeletal muscle, leading to the decline of muscle strength and physical performance. Growing evidence suggests that the prevalence of sarcopenia increases in patients with heart failure (HF), which is a dominant pathogenesis in the aging heart. HF causes diverse metabolic complications that may result in sarcopenia. Therefore, sarcopenia may act as a strong predictor of frailty, disability, and mortality associated with HF. Currently, standard treatments for slowing muscle loss in patients with HF are not available. Therefore, here, we review the pathophysiological mechanisms underlying sarcopenia in HF as well as current knowledge regarding the beneficial effects of exercise on sarcopenia in HF and related mechanisms, including hormonal changes, myostatin, oxidative stress, inflammation, apoptosis, autophagy, the ubiquitin-proteasome system, and insulin resistance.

Effects of different exercise training modes on muscle strength and physical performance in older people with sarcopenia: a systematic review and meta-analysis

“…Second, few studies have investigated the efficacy of different exercise modes to improve health outcomes and fitness levels in older people with sarcopenia . Alternatively, studies have focused on improving health outcomes and fitness in healthy older people [ 34 ], older people with osteoarthritis [ 35 ] or osteoporosis [ 36 ] or heart failure [ 37 ]. The aim of this study is to investigate the efficacy of three exercise training modes (RT, WBVT and MT) on knee extension strength (KES) and physical performance tests (Timed Up and Go [TUG], gait speed [GS] and the Chair Stand [CS]) to provide additional evidence for the treatment and management of sarcopenia in older people.…”

The β3 Adrenergic Receptor Agonist CL316243 Ameliorates the Metabolic Abnormalities of High-Fat Diet-Fed Rats by Activating AMPK/PGC-1α Signaling in Skeletal Muscle

“…The dysfunction or loss of skeletal muscle mass has been shown to contribute to obesity and type 2 diabetes. 5 , 6 Mitochondrial dysfunction and/or a reduction in mitochondrial content has been reported in skeletal muscle and adipose tissue from obese and diabetic subjects. 25 , 26 PGC-1α is a major transcriptional regulator of mitochondrial function in skeletal muscle, 27 , 28 and AMPK acts as a key sensor of energy status in skeletal muscle and regulates glucose and fatty acid metabolism.…”

“… 1 , 2 It is quantitatively the most significant site of peripheral insulin resistance in obesity and diabetes, which are associated with a higher risk of cardiovascular disease. 3 , 4 Furthermore, the loss of skeletal muscle mass and function can contribute to metabolic syndrome, 5 , 6 while the exercise-induced restoration of muscle function is paralleled by an improvement in skeletal muscle insulin sensitivity. 7 , 8 Skeletal muscle insulin resistance is a predictor of the development of type 2 diabetes, and the maintenance of appropriate muscle glucose and lipid disposal helps prevent obesity, diabetes, and metabolic syndrome.…”

Cellular Senescence in Sarcopenia: Possible Mechanisms and Therapeutic Potential

“…One mechanism is that increased concentration of TNF-α induces activation of apoptosis in muscle cells. Also, higher levels of TNF-α and IL-1 are capable of blocking the differentiation of myoblasts ( Cho et al, 2020 ). Additionally, TNF-α, as a major pro-inflammatory cytokine, was demonstrated a concomitant increase in an investigation, which implicated its function as a modifier of up-regulating MuRF1 and atrogin-1 expression, indicating a possible role of UbP-dependent atrophy during advanced age in aged muscle ( Jo et al, 2012 ).…”