Role of exercise in age-related sarcopenia

Yoo, Su-Zi; No, Mi‐Hyun; Heo, Jun‐Won; Park, Dong‐Ho; Kang, Ju‐Hee; Kim, So Hun; Kwak, Hyo‐Bum

doi:10.12965/jer.1836268.134

Cited by 175 publications

(154 citation statements)

References 51 publications

(57 reference statements)

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“…22,38 Furthermore, recent studies have Gait speed as a mediator of the effect of sarcopenia related a decline in gait speed, sarcopenia, pro-inflammatory biomarkers, and functional dependence, 39,40 fostering a vicious cycle that may be broken with physical exercise. 9 There are several plausible explanations for our finding. First, there was a close relationship between sarcopenia, physical performance (gait speed), and dependency.…”

Section: Discussionmentioning

confidence: 87%

“…5,6 It seems that sarcopenia depends on several coadjuvant factors such as inflammatory processes related to aging, nutritional status, intramuscular fat, and genetics, in addition to the reduction of physical activity, which is a crucial precursor of sarcopenia. 2,7 In the context of the aforementioned factors, there is evidence to indicate that both aerobic and resistance training promote a healthy antiinflammatory milieu largely through the release of musclederived myokines, 8 mitigate mitochondria-related dysfunction, 8 and ameliorates age-related loss of muscle mass and strength 9 as well as functional capacity and physical performance. 10 As a locomotor capacity, gait speed is representative of neuromuscular quality (morphological and neuronal) 1 and a critical determining factor for healthy aging.…”

Section: Introductionmentioning

confidence: 99%

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Gait speed as a mediator of the effect of sarcopenia on dependency in activities of daily living

Pérez-Sousa

Venegas-Sanabria

Chavarro-Carvajal

et al. 2019

J cachexia sarcopenia muscle

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Background Sarcopenia in older adults is strongly associated with an increase in dependency in activities of daily living (ADL) and with a decline in gait speed. Interestingly, gait speed has been shown to independently predict mortality. In this context, our study aimed to explore the mediator role of gait speed on the relationship between sarcopenia and dependency in ADL. Methods A cross‐sectional study was conducted in Colombia, 19 705 older adults with a mean age of 70 years, 55.6% women, 16.1% with sarcopenia, and 14.7% mild, moderate, or severe dependency in ADL, according to ‘SABE Survey 2015’. Sarcopenia was assessed by calf circumference and ADL dependence through the Barthel Index. Gait speed was measured over a distance of 3 m. The association between sarcopenia condition and gait speed and dependency level was analysed by linear regression adjusted by covariates. To examine whether gait speed mediated the association between sarcopenia and dependence components of physical function, simple mediation models were generated using ordinary least squares with the macro PROCESS version 3.2, adjusted for age, sex, and body mass index (BMI). Results Significant differences (P < 0.05) were found in gait speed and dependency in ADL between the sarcopenia and non‐sarcopenia groups after adjusting for age, sex, and BMI. BMI was significantly higher in the non‐sarcopenia group whereas dependency was significantly higher in the sarcopenia group (19.6% vs. 13.8%). Results from mediation model regression analysis indicated a significant and direct detrimental effect of sarcopenia on dependency in ADL (β = −0.05; P < 0.001), and a significant indirect effect of gait speed on the direct effect (−0.009 to −0.004). Conclusions The negative effect of sarcopenia on functional dependence was mediated by the gait speed. Therefore, gait speed may positively influence the detrimental effect of sarcopenia for dependency, after adjusting for age, gender, and BMI. Consequently, physical exercise should be promoted and focused to circumvent the gait speed decline associated with age in older people with sarcopenia.

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Section: Discussionmentioning

confidence: 87%

Section: Introductionmentioning

confidence: 99%

Gait speed as a mediator of the effect of sarcopenia on dependency in activities of daily living

Pérez-Sousa

Venegas-Sanabria

Chavarro-Carvajal

et al. 2019

J cachexia sarcopenia muscle

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“…Exercise training increases mitochondrial biogenesis to satisfy elevated energy requirements by increasing oxidative capacity to ensure optimal ATP supply; this has the consequence of favoring lipid metabolism [68][69][70]. Thus, exercise represents a viable therapy, with the potential to reverse the impairment of mitochondrial function associated with diseases such as muscular dystrophy, atrophy, type 2 diabetes, and aging-related sarcopenia [1,2,[71][72][73][74][75][76][77][78][79][80][81].…”

Section: Discussionmentioning

confidence: 99%

Skeletal muscle DNMT3A plays a necessary role in endurance exercise by regulating oxidative capacity of red muscles

et al. 2020

Preprint

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Exercise interventions alter the DNA methylation profile in skeletal muscle, yet little is known about the role of the DNA methylation machinery in exercise capacity. In this study, we found that in oxidative red muscle, DNMT3A expression increases greatly following a bout of endurance exercise. Mice lacking Dnmt3a in skeletal muscle fibers had reduced tolerance to endurance exercise, accompanied by reduced oxidative capacity and reduced mitochondrial counts. Moreover, during exercise, the knockout muscles overproduced reactive oxygen species (ROS), which are major contributors to muscle dysfunction. In mechanistic terms, we demonstrated that Aldh1l1 is a key target of repression by DNMT3A in red muscles.DNMT3A directly regulated the Aldh1l1 transcription by binding to the Aldh1l1 promoter region and altering DNA methylation and histone modification. Enforcing ALDH1L1 expression, leading to elevated NADPH, led to overproduction of ROS by the NADPH oxidase complex (NOX) in myotubes, ultimately resulting in mitochondrial defects. Moreover, both genetic inhibition of ALDH1L1 and pharmacological inhibition of NOX rescued oxidative stress and mitochondrial decline in Dnmt3a-deficient myotubes, confirming the essential role of ALDH1L1-dependent ROS generation as a downstream effector of DNMT3A loss of function. Together, our results reveal that DNMT3A in skeletal muscle plays a pivotal role in endurance exercise by controlling intracellular oxidative stress. 10].Reactive oxygen species (ROS), including oxygen-derived molecules such as hydrogen peroxide (H2O2) and free radicals such as superoxide (•O2 −) and hydroxyl radical (HO•), cause oxidative stress [11,12] . A moderate increase in skeletal muscle ROS production in the acute phase of exercise is thought to activate signaling pathways that lead to cellular adaptation, thereby protecting against future stress [13][14][15][16][17].However, excessive ROS can oxidatively damage macromolecules including DNA, lipids, and proteins, as well as modify cellular redox status and cellular functions; consequently, ROS elevation is also associated with pathophysiological states of muscle and contractile dysfunction [13][14][15][16]. Mitochondria make a large contribution to ROS production at rest, but not during muscle contraction [13,[17][18][19]. The majority of ROS produced during contraction arise from non-mitochondrial sources, such as NADPH oxidase (NOX), located in the microtubules [16,20,21] . The redox-mediated crosstalk between NOX and mitochondria exacerbates ROS production and disrupts redox homeostasis [21][22][23][24]. For example, NOX-derived ROS promote the opening of mitochondrial ATP-sensitive K+ channels [23][24][25]. The resultant potassium influx into the matrix lowers the mitochondrial membrane potential, which causes mitochondrial swelling, opening of permeability transition pores, and elevated ROS production [23][24][25]. In addition, NOX-derived ROS causes leakage of Ca2+ from the sarcoplasmic reticulum or entry of extracellular Ca2+, resulting in mitocho...

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“…There is clear evidence that physical activity or exercise can reduce the risk of physical and mental health problems via multiple direct and indirect mechanisms, including lowering blood pressure, decreasing risk of sarcopenia, improve physical functions and body composition, improving sleep quality, providing opportunities for increased social contacts, and changing levels serotonin and endorphins in the brain (Harris 2018;Stubbs et al 2018;Yoo et al 2018;Warburton & Bredin 2017;Westbury et al 2018). There is also supporting evidence for the beneficial effects of physical exercise on both physical and mental wellbeing (Black et al 2015; PeerJ reviewing PDF | (2019:01:34439:2:0:NEW 21 Mar 2019)…”

Section: Discussionmentioning

confidence: 99%

Peer Review #1 of "Quality of life of older Chinese adults receiving primary care in Wuhan, China: a multi-center study (v0.2)"

2019

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Background. Quality of life (QOL) is an important primary care outcome, but the QOL of older adults treated in primary care is understudied in China. This study examined QOL and its associated factors in older adults treated in Chinese primary care. Methods. A total of 752 older patients (65+ years) were consecutively recruited from 13 primary care centers in Wuhan, China, and interviewed with a standardized questionnaire, concerning socio-demographics, major medical conditions, loneliness, and depression. QOL and depression were measured with the Chinese six-item QOL questionnaire and the shortened Geriatric Depression Scale. Multiple linear regression was used to identify factors associated with poor QOL. Results. The average QOL score of primary care older adults was (20.7±2.5), significantly lower than that of the Chinese general population. Factors significantly associated with poor QOL of Chinese primary care older adults included engaging in manual labor before older adulthood (unstandardized coefficient [β]:

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Role of exercise in age-related sarcopenia

Cited by 175 publications

References 51 publications

Gait speed as a mediator of the effect of sarcopenia on dependency in activities of daily living

Gait speed as a mediator of the effect of sarcopenia on dependency in activities of daily living

Skeletal muscle DNMT3A plays a necessary role in endurance exercise by regulating oxidative capacity of red muscles

Peer Review #1 of "Quality of life of older Chinese adults receiving primary care in Wuhan, China: a multi-center study (v0.2)"

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