Long‐Term Exercise Protects against Cellular Stresses in Aged Mice

Belaya, Irina; Suwa, Masataka; Chen, Tao; Giniatullin, Rashid; Atalay, Mustafa; Kumagai, Shuzo

doi:10.1155/2018/2894247

Cited by 24 publications

(26 citation statements)

References 44 publications

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“…These data indicate an increase in ER stress levels in senile skeletal muscle. Studies on the underlying mechanism have shown that ER function declines during skeletal muscle aging, leading to the accumulation of unfolded or misfolded proteins [11], thereby inducing ER stress. In addition, a high level of mitochondrial ROS can also induce ER stress [66], and the skeletal muscle aging process can produce a large amount of ROS, thereby further promoting ER stress.…”

Section: Er Stress Levels Increases In Aging Skeletal Musclementioning

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: Er Stress Levels Increases In Aging Skeletal Musclementioning

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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“…These studies have helped to characterize the physiological adaptations of healthy human muscle to different types of exercise (Rockl et al, 2007; Trappe et al, 2016). Most of these studies focused on the acute and immediate effects of short bouts of high intensity exercise in either human or mice/rat models (Guelfi et al, 2006; Egan and Zierath, 2013; Petriz et al, 2017), as well as long-term effects of exercise (Crane et al, 2013; Mosole et al, 2014; Belaya et al, 2018). However, very little research has focused on assessing the association of daily physical activity with the muscle proteome in healthy community-dwelling individuals.…”

Section: Introductionmentioning

confidence: 99%

Physical Activity Associated Proteomics of Skeletal Muscle: Being Physically Active in Daily Life May Protect Skeletal Muscle From Aging

et al. 2019

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Muscle strength declines with aging and increasing physical activity is the only intervention known to attenuate this decline. In order to adequately investigate both preventive and therapeutic interventions against sarcopenia, a better understanding of the biological changes that are induced by physical activity in skeletal muscle is required. To determine the effect of physical activity on the skeletal muscle proteome, we utilized liquid-chromatography mass spectrometry to obtain quantitative proteomics data on human skeletal muscle biopsies from 60 well-characterized healthy individuals (20–87 years) who reported heterogeneous levels of physical activity (not active, active, moderately active, and highly active). Over 4,000 proteins were quantified, and higher self-reported physical activity was associated with substantial overrepresentation of proteins associated with mitochondria, TCA cycle, structural and contractile muscle, and genome maintenance. Conversely, proteins related to the spliceosome, transcription regulation, immune function, and apoptosis, DNA damage, and senescence were underrepresented with higher self-reported activity. These differences in observed protein expression were related to different levels of physical activity in daily life and not intense competitive exercise. In most instances, differences in protein levels were directly opposite to those reported in the literature observed with aging. These data suggest that being physically active in daily life has strong and biologically detectable beneficial effects on muscle.

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“…oxidative stress, due to excessive reactive oxygen species (roS) production and impaired antioxidant defense mechanisms, induces a range of pathologies that are believed to be important contributors to the cardiovascular aging process (2,5). recently, Belaya et al (6) reported that long-term wheel running can protect against age-related cellular stress. The endoplasmic reticulum (er) is a specialized organelle where the folding and post-translational maturation of almost all membrane proteins, and most secreted proteins, occur (7).…”

Section: Introductionmentioning

confidence: 99%

Swimming exercise inhibits myocardial ER stress in the hearts of aged mice by enhancing cGMP‑PKG signaling

Pan

Zhang

et al. 2019

Mol Med Report

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The purpose of the present study was to explore aging-associated cardiac dysfunction and the possible mechanism by which swimming exercise modulates cardiac dysfunction in aged mice. aged mice were divided into two groups: i) aged mice; and ii) aged mice subjected to swimming exercises. another cohort of 4-month-old male mice served as the control group. cardiac structure and function in mice were analyzed using hematoxylin and eosin staining, and echocardiography. The levels of oxidative stress were determined by measuring the levels of superoxide dismutase, malondialdehyde and reactive oxygen species (roS). levels of the endoplasmic reticulum (er) stress-related protein PKr-like er kinase, glucose-regulated protein 78 and c/eBP homologous protein were determined to evaluate the level of er stress. The aged group exhibited an abnormal cardiac structure and decreased cardiac function, both of which were ameliorated by swimming exercise. The hearts of the aged mice exhibited pronounced oxidative and er stress, which were ameliorated by exercise, and was accompanied by the reactivation of myocardial cGMP and suppression of cGMP-specific phosphodiesterase type 5 (Pde5). The inhibition of Pde5 attenuated age-induced cardiac dysfunction, blocked roS production and suppressed ER stress. An ER stress inducer abolished the beneficial effects of the swimming exercise on cardiac function and increased roS production. The present study suggested that exercise restored cardiac function in mice with age-induced cardiac dysfunction by inhibiting oxidative stress and er stress, and increasing cGMP-protein kinase G signaling.

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Long‐Term Exercise Protects against Cellular Stresses in Aged Mice

Cited by 24 publications

References 44 publications

Mechanism of increased risk of insulin resistance in aging skeletal muscle

Mechanism of increased risk of insulin resistance in aging skeletal muscle

Physical Activity Associated Proteomics of Skeletal Muscle: Being Physically Active in Daily Life May Protect Skeletal Muscle From Aging

Swimming exercise inhibits myocardial ER stress in the hearts of aged mice by enhancing cGMP‑PKG signaling

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