Evaluation of muscle-specific and metabolism regulating microRNAs in a chronic swimming rat model

AbstractMaking benefit from the epigenetic effects of environmental factors such as physical activity may result in a considerable improvement in the prevention of chronic civilization diseases. In our chronic swimming rat model, the expression levels of such microRNAs were characterized, that are involved in skeletal muscle differentiation, hypertrophy and fine-tuning of metabolism, which processes are influenced by chronic endurance training, contributing to the metabolic adaptation of skeletal muscle during physical activity. After chronic swimming, the level of miR-128a increased significantly in EDL muscles, which may influence metabolic adaptation and stress response as well. In SOL, the expression level of miR-15b and miR-451 decreased significantly after chronic swimming, which changes are opposite to their previously described increment in insulin resistant skeletal muscle. MiR-451 also targets PGC-1α mRNA, whiches expression level significantly increased in SOL muscles, resulting in enhanced biogenesis and oxidative capacity of mitochondria. In summary, the microRNA expression changes that were observed during our experiments suggest that chronic swim training contributes to a beneficial metabolic profile of skeletal muscle.

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Skeletal muscle oxidative capacity is an independent predictor of physical activity in smokers with and without COPD

10.1183/13993003.congress-2015.oa1985 ◽

2015 ◽

Author(s):

Alessandra Adami ◽

Robert Cao ◽

Janos Porszasz ◽

Richard Casaburi ◽

Harry B. Rossiter

Keyword(s):

Physical Activity ◽

Skeletal Muscle ◽

Independent Predictor ◽

Oxidative Capacity ◽

Muscle Oxidative Capacity

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Differential vulnerability of skeletal muscle feed arteries to dysfunction in insulin resistance: impact of fiber type and daily activity

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.01093.2010 ◽

2011 ◽

Vol 300 (4) ◽

pp. H1434-H1441 ◽

Cited By ~ 24

Author(s):

Shawn B. Bender ◽

Sean C. Newcomer ◽

M. Harold Laughlin

Keyword(s):

Physical Activity ◽

Nitric Oxide ◽

Insulin Resistance ◽

Skeletal Muscle ◽

Sodium Nitroprusside ◽

Fiber Type ◽

Vascular Dysfunction ◽

Insulin Resistant ◽

Long Evans ◽

Feed Arteries

Functional and structural heterogeneity exists among skeletal muscle vascular beds related, in part, to muscle fiber type composition. This study was designed to delineate whether the vulnerability to vascular dysfunction in insulin resistance is uniformly distributed among skeletal muscle vasculatures and whether physical activity modifies this vulnerability. Obese, hyperphagic Otsuka Long-Evans Tokushima fatty rats (20 wk old) were sedentary (OSED) or physically active (OPA; access to running wheels) and compared with age-matched sedentary Long-Evans Tokushima Otsuka (LSED) rats. Vascular responses were determined in isolated, pressurized feed arteries from fast-twitch gastrocnemius (GFAs) and slow-twitch soleus (SFAs) muscles. OSED animals were obese, insulin resistant, and hypertriglyceridemic, traits absent in LSED and OPA rats. GFAs from OSED animals exhibited depressed dilation to ACh, but not sodium nitroprusside, and enhanced vasoconstriction to endothelin-1 (ET-1), but not phenylephrine, compared with those in LSED. Immunoblot analysis suggests reduced endothelial nitric oxide synthase phosphorylation at Ser1177 and endothelin subtype A receptor expression in OSED GFAs. Physical activity prevented reduced nitric oxide-dependent dilation to ACh, but not enhanced ET-1 vasoconstriction, in GFA from OPA animals. Conversely, vasoreactivity of SFAs to ACh and ET-1 were principally similar in all groups, whereas dilation to sodium nitroprusside was enhanced in OSED and OPA rats. These data demonstrate, for the first time, that SFAs from insulin-resistant rats exhibit reduced vulnerability to dysfunction versus GFAs and that physical activity largely prevents GFA dysfunction. We conclude that these results demonstrate that vascular dysfunction associated with insulin resistance is heterogeneously distributed across skeletal muscle vasculatures related, in part, to muscle fiber type and activity level.

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Modulation of Skeletal Muscle Performance and Sarco-and Endoplasmic Reticulum Ca2+ ATPase by Exercise and Adiponectin Gene Therapy in Insulin Resistant Diabetic Rat Model

Science International ◽

10.5567/sciintl.2013.76.84 ◽

2013 ◽

Vol 1 (4) ◽

pp. 76-84

Author(s):

Y. Safwat ◽

N. Yassin ◽

M.M. Gamal El Din ◽

L.A. Kassem

Keyword(s):

Skeletal Muscle ◽

Gene Therapy ◽

Endoplasmic Reticulum ◽

Rat Model ◽

Muscle Performance ◽

Diabetic Rat ◽

Adiponectin Gene ◽

Insulin Resistant ◽

Diabetic Rat Model ◽

Skeletal Muscle Performance

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Effects Of Old Age And Physical Activity On Oxidative Capacity In Human Skeletal Muscle

Medicine & Science in Sports & Exercise ◽

10.1249/01.mss.0000353689.48647.f9 ◽

2009 ◽

Vol 41 ◽

pp. 131 ◽

Cited By ~ 1

Author(s):

Ryan G. Larsen ◽

Damien M. Callahan ◽

Stephen A. Foulis ◽

Jane A. Kent-Braun

Keyword(s):

Physical Activity ◽

Skeletal Muscle ◽

Old Age ◽

Human Skeletal Muscle ◽

Oxidative Capacity

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Racial Differences In Peripheral Insulin Sensitivity and Mitochondrial Capacity in the Absence of Obesity

The Journal of Clinical Endocrinology & Metabolism ◽

10.1210/jc.2014-2512 ◽

2014 ◽

Vol 99 (11) ◽

pp. 4307-4314 ◽

Cited By ~ 35

Author(s):

James P. DeLany ◽

John J. Dubé ◽

Robert A. Standley ◽

Giovanna Distefano ◽

Bret H. Goodpaster ◽

...

Keyword(s):

Physical Activity ◽

Skeletal Muscle ◽

Body Mass Index ◽

Insulin Sensitivity ◽

Body Mass ◽

Oxidative Capacity ◽

Hepatic Insulin Sensitivity ◽

Peripheral Insulin Sensitivity ◽

Mitochondrial Oxidative Capacity ◽

Mitochondrial Capacity

Context: African-American women (AAW) have an increased risk of developing type 2 diabetes compared with Caucasian women (CW). Lower insulin sensitivity has been reported in AAW, but the reasons for this racial difference and the contributions of liver versus skeletal muscle are incompletely understood. Objective: We tested the hypothesis that young, nonobese AAW manifest lower insulin sensitivity specific to skeletal muscle, not liver, and is accompanied by lower skeletal muscle mitochondrial oxidative capacity. Participants and Main Outcome Measures: Twenty-two nonobese (body mass index 22.7 ± 3.1 kg/m2) AAW and 22 matched CW (body mass index 22.7 ± 3.1 kg/m2) underwent characterization of body composition, objectively assessed habitual physical activity, and insulin sensitivity with euglycemic clamps and stable-isotope tracers. Skeletal muscle biopsies were performed for lipid content, fiber typing, and mitochondrial measurements. Results: Peripheral insulin sensitivity was 26% lower in AAW (P < .01), but hepatic insulin sensitivity was similar between groups. Physical activity levels were similar between groups. Lower insulin sensitivity in AAW was not explained by total or central adiposity. Skeletal muscle triglyceride content was similar, but mitochondrial content was lower in AAW. Mitochondrial respiration was 24% lower in AAW and correlated with skeletal muscle insulin sensitivity (r = 0.33, P < .05). Conclusion: When compared with CW, AAW have similar hepatic insulin sensitivity but a muscle phenotype characterized by both lower insulin sensitivity and lower mitochondrial oxidative capacity. These observations occur in the absence of obesity and are not explained by physical activity. The only factor associated with lower insulin sensitivity in AAW was mitochondrial oxidative capacity. Because exercise training improves both mitochondrial capacity and insulin sensitivity, we suggest that it may be of particular benefit as a strategy for diabetes prevention in AAW.

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Skeletal muscle oxidative capacity in young and older women and men

Journal of Applied Physiology ◽

10.1152/jappl.2000.89.3.1072 ◽

2000 ◽

Vol 89 (3) ◽

pp. 1072-1078 ◽

Cited By ~ 122

Author(s):

Jane A. Kent-Braun ◽

Alexander V. Ng

Keyword(s):

Physical Activity ◽

Skeletal Muscle ◽

Recovery Time ◽

Tibialis Anterior Muscle ◽

Oxidative Capacity ◽

Resonance Spectroscopy ◽

Activity Levels ◽

Muscle Oxidative Capacity ◽

Age Related ◽

Postexercise Recovery

It has been suggested that a decline in skeletal muscle oxidative capacity is a general consequence of aging in humans. However, previous studies have not always controlled for the effects of varying levels of physical activity on muscle oxidative capacity. To test the hypothesis that, when matched for comparable habitual physical activity levels, there would be no age-related decline in the oxidative capacity of a locomotor muscle, the postexercise recovery time of phosphocreatine was compared in the tibialis anterior muscle of young [ n = 19; 33.8 ± 4.8 (SD) yr] and older [ n = 18; 75.5 ± 4.5 yr] healthy women and men of similar, relatively low, activity levels. The intramuscular metabolic measurements were accomplished by using phosphorus magnetic resonance spectroscopy. The results indicate that there was no age effect on the postexercise recovery time of phosphocreatine recovery, thus supporting the stated hypothesis. These data suggest that there is no requisite decline in skeletal muscle oxidative capacity with aging in humans, at least through the seventh decade.

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In vivo mitochondrial function in aging skeletal muscle: capacity, flux, and patterns of use

Journal of Applied Physiology ◽

10.1152/japplphysiol.00583.2016 ◽

2016 ◽

Vol 121 (4) ◽

pp. 996-1003 ◽

Cited By ~ 16

Author(s):

Jane A. Kent ◽

Liam F. Fitzgerald

Keyword(s):

Physical Activity ◽

Skeletal Muscle ◽

Mitochondrial Function ◽

Human Skeletal Muscle ◽

Oxidative Capacity ◽

Mitochondrial Content ◽

Atp Production ◽

Age Related ◽

Age Related Changes

Because of the fundamental dependence of mammalian life on adequate mitochondrial function, the question of how and why mitochondria change in old age is the target of intense study. Given the importance of skeletal muscle for the support of mobility and health, this question extends to the need to understand mitochondrial changes in the muscle of older adults, as well. We and others have focused on clarifying the age-related changes in human skeletal muscle mitochondrial function in vivo. These changes include both the maximal capacity for oxidative production of energy (ATP), as well as the relative use of mitochondrial ATP production for powering muscular activity. It has been known for nearly 50 yr that muscle mitochondrial content is highly plastic; exercise training can induce an ∼2-fold increase in mitochondrial content, while disuse has the opposite effect. Here, we suggest that a portion of the age-related changes in mitochondrial function that have been reported are likely the result of behavioral effects, as physical activity influences have not always been accounted for. Further, there is emerging evidence that various muscles may be affected differently by age-related changes in physical activity and movement patterns. In this review, we will focus on age-related changes in oxidative capacity and flux measured in vivo in human skeletal muscle.

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Skeletal muscle metabolic responses to physical activity are muscle type specific in a rat model of chronic kidney disease

Scientific Reports ◽

10.1038/s41598-021-89120-8 ◽

2021 ◽

Vol 11 (1) ◽

Author(s):

Keith G. Avin ◽

Meghan C. Hughes ◽

Neal X. Chen ◽

Shruthi Srinivasan ◽

Kalisha D. O’Neill ◽

...

Keyword(s):

Physical Activity ◽

Skeletal Muscle ◽

Chronic Kidney Disease ◽

Kidney Disease ◽

Rat Model ◽

Mitochondrial Respiration ◽

Wheel Running ◽

Muscle Metabolism ◽

Voluntary Wheel Running ◽

Voluntary Wheel

AbstractChronic kidney disease (CKD) leads to musculoskeletal impairments that are impacted by muscle metabolism. We tested the hypothesis that 10-weeks of voluntary wheel running can improve skeletal muscle mitochondria activity and function in a rat model of CKD. Groups included (n = 12–14/group): (1) normal littermates (NL); (2) CKD, and; (3) CKD-10 weeks of voluntary wheel running (CKD-W). At 35-weeks old the following assays were performed in the soleus and extensor digitorum longus (EDL): targeted metabolomics, mitochondrial respiration, and protein expression. Amino acid-related compounds were reduced in CKD muscle and not restored by physical activity. Mitochondrial respiration in the CKD soleus was increased compared to NL, but not impacted by physical activity. The EDL respiration was not different between NL and CKD, but increased in CKD-wheel rats compared to CKD and NL groups. Our results demonstrate that the soleus may be more susceptible to CKD-induced changes of mitochondrial complex content and respiration, while in the EDL, these alterations were in response the physiological load induced by mild physical activity. Future studies should focus on therapies to improve mitochondrial function in both types of muscle to determine if such treatments can improve the ability to adapt to physical activity in CKD.

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