Advances in exercise to alleviate sarcopenia in older adults by improving mitochondrial dysfunction

Abstract

Sarcopenia is a chronic degenerative disease affecting primarily older adults. A growing aging population is gradually increasing the number of patients suffering from sarcopenia, placing increasing financial pressure on patients’ families and society in general. There is a strong link between mitochondrial dysfunction and sarcopenia pathogenesis. As a result, treating sarcopenia by improving mitochondrial dysfunction is an effective strategy. Numerous studies have demonstrated that exercise has a positive effect on mitochondrial dysfunction when treating sarcopenia. Exercise promotes mitochondrial biogenesis and mitochondrial fusion/division to add new mitochondria or improve dysfunctional mitochondria while maintaining mitochondrial calcium homeostasis, mitochondrial antioxidant defense system, and mitochondrial autophagy to promote normal mitochondrial function. Furthermore, exercise can reduce mitochondrial damage caused by aging by inhibiting mitochondrial oxidative stress, mitochondrial DNA damage, and mitochondrial apoptosis. Exercise effectiveness depends on several factors, including exercise duration, exercise intensity, and exercise form. Therefore, Moderate-intensity exercise over 4 weeks potentially mitigates sarcopenia in older adults by ameliorating mitochondrial dysfunction. HIIT has demonstrated potential as a viable approach to addressing sarcopenia in aged rats. However, further investigation is required to validate its efficacy in treating sarcopenia in older adults.

Combined Nutrition with Exercise: Fueling the Fight Against Sarcopenia Through a Bibliometric Analysis and Review

“…Exercise can help restore mitochondrial function and enhance mitochondrial biogenesis, leading to improved muscle health. 30 …”

“…Exercise can help restore mitochondrial function and enhance mitochondrial biogenesis, leading to improved muscle health. 30 Sex hormones, such as 17β-estradiol and testosterone, play a significant role in the health of skeletal muscle and are implicated in the pathophysiology and mechanisms of sarcopenia. These hormones can impact mitochondrial function through various pathways, including promoting mitochondrial biogenesis, mitophagy (the removal of damaged mitochondria), and ATP production within the mitochondria.…”

Association between the oxidative balance score and low muscle mass in middle-aged US adults

“…Alcohol consumption may disrupt protein metabolism in skeletal muscles and response to anabolic stimuli by reducing overall protein synthesis (58). Additionally, exercise can help reduce mitochondrial damage caused by aging by inhibiting oxidative stress, DNA damage, and apoptosis in mitochondria (59).…”

Mitochondrial involvement in sarcopenia

“…Interestingly, however, exercise‐induced increases in muscle mass and function do not always involve increased oxidative capacity, as the nature of mitochondrial effects appears to depend on the type of exercise 42 . Both endurance and resistance training increase skeletal muscle quality in sarcopenia, but while the benefit of endurance exercise is consistently linked with clear stimulation of mitochondrial biogenesis and increased oxidative capacity, 112–116 mitochondrial effects of resistance exercise are less clear 113,117–120 . Resistance training does not affect mitochondrial biogenesis or mitochondrial content but does indeed alter intrinsic mitochondrial function 121,122 .…”