Sarcopenia, characterized by a loss of muscle mass and strength with aging, is prevalent in older adults. Although the exact mechanisms underlying sarcopenia are not fully understood, evidence suggests that the loss of mitochondrial integrity in skeletal myocytes has emerged as a pivotal contributor to the complex etiology of sarcopenia. Mitochondria are the primary source of ATP production and are also involved in generating reactive oxygen species (ROS), regulating ion signals, and initiating apoptosis signals in muscle cells. The accumulation of damaged mitochondria due to age-related impairments in any of the mitochondrial quality control (MQC) processes, such as proteostasis, biogenesis, dynamics, and mitophagy, can contribute to the decline in muscle mass and strength associated with aging. Interestingly, a decrease in sex hormones (e.g., 17β-estradiol and testosterone), which occurs with aging, has also been linked to sarcopenia. Indeed, 17β-estradiol and testosterone targeted mitochondria and exhibited activities in regulating mitochondrial functions. Here, we overview the current literature on the key mechanisms by which mitochondrial dysfunction contribute to the development and progression of sarcopenia and the potential modulatory effects of 17β-estradiol and testosterone on mitochondrial function in this context. The advance in its understanding will facilitate the development of potential therapeutic agents to mitigate and manage sarcopenia.

Background Sarcopenia is prevalent and is associated with the occurrence of cardiovascular complications in patients undergoing maintenance hemodialysis (MHD). It is unknown how skeletal muscle may be associated with aspects of myocardial structure and function. This study aimed to evaluate the association between sarcopenia and cardiac structure and function in patients undergoing MHD. We also examined the prognostic role of sarcopenia for mortality and cardiovascular events (CVE) in this population. Methods Participants from a single center underwent bioimpedance body composition analysis to measure skeletal muscle and echocardiography to assess myocardial structure and function. Sarcopenia was diagnosed based on the Asian Working Group for Sarcopenia criteria. The end points were all-cause mortality and CVE. Results Of the 158 participants, 46 (29.1%) had sarcopenia, 102 (64.6%) had left ventricular diastolic dysfunction (LVDD), and 106 (67.0%) had left ventricular hypertrophy (LVH). Participants with sarcopenia had smaller right ventricular sizes (2.54 ± 0.77 vs 2.76 ± 0.28; P < 0.01), inter-ventricular thickness (1.07 ± 0.19 vs 1.14 ± 0.20; P = 0.039), and left ventricular posterior wall thickness (0.96, 0.89–1.10 vs 1.06, 0.95–1.20; P = 0.018). Skeletal muscle mass was strongly correlated with left ventricular mass (LVM) (r = 0.577; P < 0.0001). Furthermore, the risk of LVDD (OR: 4.92, 95% confidence interval (CI) [1.73–13.95]) and LVH (OR: 4.88, 95% CI [1.08–21.96]) was much higher in the sarcopenic group than in the non-sarcopenic group. During a follow-up period of 18 months, 11 (6.9%) patients died, of which seven died (4.4%) of CVE, and 36 (22.8%) experienced CVE. The presence of sarcopenia (adjusted hazard ratio (HR), 6.59; 95% CI [1.08–39.91]; P = 0.041) and low skeletal muscle index (HR, 3.41; 95% CI [1.01–11.57]; P = 0.049) and handgrip strength (HR, 0.88; 95% CI [0.78–0.99]; P = 0.037) independently predicted death. Sarcopenia was a significant predictor of CVE (HR, 10.96; 95% CI [1.14–105.10]; P = 0.038). Conclusion Our findings demonstrated that sarcopenia is associated with LVDD and LVH, and is associated with a higher probability of death and CVE.