Impact of Aging and Exercise on Mitochondrial Quality Control in Skeletal Muscle

Kim, Yuho; Triolo, Matthew; Hood, David A.

doi:10.1155/2017/3165396

Cited by 124 publications

(104 citation statements)

References 200 publications

(251 reference statements)

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“…As mentioned earlier, skeletal muscle oxidative damage increases with age. The autophagy-lysosomal pathway degrades large amounts of skeletal muscle protein, thereby reducing the oxidative damage to the skeletal muscle [58]. Therefore, the decline in skeletal muscle autophagy is not conducive to the prevention of oxidative damage and is closely related to skeletal muscle insulin resistance.…”

Section: Decreased Autophagy Increases the Risk Of Insulin Resistancementioning

confidence: 99%

Mechanism of increased risk of insulin resistance in aging skeletal muscle

Shou

Chen

Xiao

2020

Diabetol Metab Syndr

179

112

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As age increases, the risk of developing type 2 diabetes increases, which is associated with senile skeletal muscle dysfunction. During skeletal muscle aging, mitochondrial dysfunction, intramyocellular lipid accumulation, increased inflammation, oxidative stress, modified activity of insulin sensitivity regulatory enzymes, endoplasmic reticulum stress, decreased autophagy, sarcopenia and over-activated renin-angiotensin system may occur. These changes can impair skeletal muscle insulin sensitivity and increase the risk of insulin resistance and type 2 diabetes during skeletal muscle aging. This review of the mechanism of the increased risk of insulin resistance during skeletal muscle aging will provide a more comprehensive explanation for the increased incidence of type 2 diabetes in elderly individuals, and will also provide a more comprehensive perspective for the prevention and treatment of type 2 diabetes in elderly populations.

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Section: Decreased Autophagy Increases the Risk Of Insulin Resistancementioning

confidence: 99%

Mechanism of increased risk of insulin resistance in aging skeletal muscle

Shou

Chen

Xiao

2020

Diabetol Metab Syndr

179

112

View full text Add to dashboard Cite

show abstract

“…While not tested in PolG mice, exercise training has been shown to prevent the loss of neuromuscular innervation, as master athletes display preserved motor unit number and neuromuscular stability [54]. Therefore, it appears that exercise training in both humans and rodents improves muscle function, muscle mass, and inflammation, which may be associated mitochondrial bioenergetics [21,26,33,36,58]. In the next sections we describe the positive effects of exercise and nutritional lifestyle interventions within the elderly population.…”

Section: Lifestyle Modificationsmentioning

confidence: 99%

Mitochondrial ROS and Aging: Understanding Exercise as a Preventive Tool

Brunetta

Holwerda

Loon

et al. 2019

J. of SCI. IN SPORT AND EXERCISE

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Sarcopenia, which is characterized by reduction in muscle mass and strength, contributes to several age-related conditions, including insulin resistance and frailty. Despite the importance of maintaining muscle mass for healthy aging, the mechanisms contributing to sarcopenia are not fully elucidated. Nevertheless, mitochondria appear to play a key role in the underlying condition, and importantly, respond robustly to exercise interventions. Mitochondria are intracellular organelles largely attributed to maintaining ATP concentrations, however, the importance of this organelle in overall cellular homeostasis has been expanded in the last decades to include redox signaling, calcium homeostasis, inflammation, and apoptosis. Several lines of evidence suggest that mitochondrial bioenergetics are altered in aged skeletal muscle, resulting in an increase in reactive oxygen species (ROS) production, while conversely genetic/pharmacological approaches that attenuate mitochondrial ROS promote healthy aging and maintenance of muscle mass. These observations suggest that increased free radicals are one of the bases of the aging process and related sarcopenia. Here, we reviewed the current knowledge regarding mitochondrial function and redox balance in aged human skeletal muscle, highlighting the implications of redox unbalance on skeletal muscle mass maintenance and muscle health. Additionally, we describe the benefits of exercise and nutrition interventions in the context of improving mitochondrial bioenergetics and functional outcomes regarding skeletal muscle mass and function.

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“…To further clarify the therapeutic mechanisms of CGD on MS, we also measured expression of AMPK and the transcriptional co-activator PGC-1α. AMPK can regulate mitochondrial biogenesis and mitophagy [33][34][35][36]. AMPK activation helps to restore homeostasis of physiologic energy [37].…”

Section: Discussionmentioning

confidence: 99%

Therapeutic Effects of Coccomyxagloeobotrydiformis on the Metabolic Syndrome in Rats

Zheng

Ding

Wei

et al. 2018

Cell Physiol Biochem

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Background/Aims: The metabolic syndrome (MS) is a cluster of metabolic changes that carry a high risk of cardiovascular disease (CVD). A newly discovered microalga, coccomyxagloeobotrydiformis (CGD), has been reported to improve ischemic stroke and metabolism-related indicators. We observed the therapeutic effects of CGD on MS and postulated the underlying mechanism. Methods: A diet-induced MS model in rats was used to observe the therapeutic effects of CGD on MS. Blood-glucose and lipid indices were measured using enzymatic colorimetric kits. A biologic data acquisition and analysis system (BL-420F) was used to evaluate cardiac function. Expression of mitochondrial respiratory chain (MRC) enzymes was measured by immunofluorescence staining. The proteins associated with oxidative stress, apoptosis and inflammation were detected by western blotting. Results: Body weight, abdominal circumference, fasting blood glucose , blood pressure as well as serum levels of total cholesterol, triglycerides and low-density lipoprotein-cholesterol were decreased whereas serum levels of high-density lipoprotein-cholesterol was increased in CGD-treated MS rats. CGD increased left-ventricular systolic pressure, left-ventricular end-diastolic pressure, left-ventricular systolic pressure maximum rate of increase and left-ventricular diastolic pressure maximum rate of decrease in MS rats with cardiovascular complications. CGD up-regulated expression of adenosine monophosphate-activated protein kinase and peroxisome proliferator activated receptor gamma coactivator 1-alpha in the heart, adipose tissue and skeletal muscle. Expression of the MRC subunits of ATPase 6, cytochrome b and succinate dehydrogenase complex, subunit-A was increased whereas that of uncoupling protein-2 decreased in different tissues. CGD showed anti-oxidation effects by increasing expression of superoxide dismutase and decreasing that of malondialdehyde. High expression of Bcl-2 and low expression of Bax and caspase-3 supported the anti-apoptotic effect of CGD on the cardiovascular complications of MS. Conclusion: CGD has a therapeutic effect on MS and associated cardiovascular complications by eliciting mitochondrial protection and having anti-oxidation and anti-apoptosis effects. CGD could be used for MS treatment.

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Impact of Aging and Exercise on Mitochondrial Quality Control in Skeletal Muscle

Cited by 124 publications

References 200 publications

Mechanism of increased risk of insulin resistance in aging skeletal muscle

Mechanism of increased risk of insulin resistance in aging skeletal muscle

Mitochondrial ROS and Aging: Understanding Exercise as a Preventive Tool

Therapeutic Effects of Coccomyxagloeobotrydiformis on the Metabolic Syndrome in Rats

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