Effects of intrinsic aerobic capacity, aging and voluntary running on skeletal muscle sirtuins and heat shock proteins

Karvinen, Sira; Silvennoinen, Mika; Vainio, Petra; Sistonen, Lea; Koch, Lauren G.; Britton, Steven L.; Kainulainen, Heikki

doi:10.1016/j.exger.2016.03.015

Cited by 33 publications

(24 citation statements)

References 186 publications

(277 reference statements)

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“…Our data relative to SIRT1 expression levels in CC did not reveal correlations neither to eNOS levels, nor to treatments. This was not an expected finding, considering previous demonstrations of upregulation of SIRT1 expression and activation by ER, statin and exercise [ 1 , 35 , 36 ]. However, partially explaining our results, a study in the aorta of aged rats failed to demonstrate differences in either eNOS or SIRT1 expression with ER, supporting that in aged animals, differences could be more difficult to detect [ 37 ].…”

Section: Discussioncontrasting

confidence: 49%

“…An in vitro study demonstrated that rosuvastatin does not promote SIRT2 expression in endothelial cells along 24 h [ 35 ]. Also, SIRT2 expression did not increase in the skeletal muscle of female rats subjected to one-year voluntary running intervention [ 36 ]. However, no studies have tested the association of statin and exercise effect on SIRT2 expression.…”

Section: Discussionmentioning

confidence: 99%

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Energy restriction, exercise and atorvastatin treatment improve endothelial dysfunction and inhibit miRNA-155 in the erectile tissue of the aged rat.

et al. 2018

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BackgroundEndothelial dysfunction underlies cardiovascular disease that frequently affects aged individuals. Characterized by local decrease in nitric oxide, it results from down-regulation of endothelial nitric oxide synthase (eNOS) expression/activity. Aiming to elucidate the molecular mechanisms involved in age-related endothelial dysfunction and to unveil potential therapeutic targets, we tested how diet pattern, exercise and atorvastatin modulate the expression of eNOS, inducible NOS (iNOS), endothelin-1, sirtuins (SIRT) and microRNA-155 in the erectile tissue of high-fat fed aged rats.MethodsSprague-Dawley male rats fed with high-fat diet until they completed 12 months were grouped and subjected to energy restriction (ER), ER and atorvastatin, or, ER, atorvastatin and physical exercise. Controls were fed with standard rodent chow. The blood pressure was measured using the tail-cuff method before sacrifice at 18 months. Glucose, total cholesterol, HDL, triglyceride and CRP were assessed in blood and eNOS, endothelin-1, iNOS and sirtuins were detected by immunofluorescence in the penis sections; eNOS, endothelin-1, iNOS, SIRT2–4 and SIRT6–7 were semi-quantified by western blotting in tissue homogenates. MicroRNA-155 was quantified using RT-PCR in formalin-fixed paraffin embedded sections. To compare the studied variables, two-tail student t test was used.ResultsAtorvastatin promotes eNOS expression and is more efficient than ER or exercise in the control of hyperlipidemia and inflammation. Among the studied sirtuins, detected for the first time in the erectile tissue of the aged rat, SIRT2 aligns with eNOS expression. Both proteins exhibit over-expression in animals with combined exercise, atorvastatin and ER. Analysis of microRNA-155 expression also suggests its intervention in the regulation of eNOS expression. ER, particularly when combined with atorvastatin, was able to reverse the increase of iNOS and endothelin-1 in high-fat fed rats.ConclusionsThe present results indicate that the association of ER, atorvastatin and exercise is more efficient than isolated interventions in the prevention of endothelial dysfunction.Electronic supplementary materialThe online version of this article (10.1186/s12986-018-0265-z) contains supplementary material, which is available to authorized users.

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Section: Discussioncontrasting

confidence: 49%

Section: Discussionmentioning

confidence: 99%

Energy restriction, exercise and atorvastatin treatment improve endothelial dysfunction and inhibit miRNA-155 in the erectile tissue of the aged rat.

et al. 2018

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“…Previous studies showed that exercise training increases SIRT3 expression in skeletal muscle [ 18 ]. However, Karvinen et al revealed that high capacity running rats had a higher SIRT3 protein content in skeletal muscle compared to low capacity running rats, contributing to lower mitochondrial protein acetylation [ 51 ]. The discrepancies between our finding and Karvinen et al's finding may attribute to different exercise models.…”

Section: Discussionmentioning

confidence: 99%

Short-Duration Swimming Exercise after Myocardial Infarction Attenuates Cardiac Dysfunction and Regulates Mitochondrial Quality Control in Aged Mice

Zhao

Sun

Tan

et al. 2018

Oxidative Medicine and Cellular Longevity

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Background Exercise benefits to cardiac rehabilitation (CR) following stable myocardial infarction (MI). The suitable exercise duration for aged patients with coronary heart disease (CHD) remains controversial, and the underlying molecular mechanism is still unclear. Methods and Results 18-Month-old mice after stable MI were randomly submitted to different durations of exercise, including 15 and 60 min swimming training (ST) once per day, five times a week for 8 weeks. Compared to sedentary mice, 15 min ST, rather than 60 min ST, significantly augmented left ventricular function, increased survival rate, and suppressed myocardial fibrosis and apoptosis. 15 min ST improved mitochondrial morphology via regulating mitochondrial fission-fusion signaling. 15 min ST regulated mitophagy signaling via inhibiting LC3-II and P62 levels and increasing PINK/Parkin expression. 15 min ST also inhibited ROS production and enhanced antioxidant SOD2 activity. Notably, 15 min ST significantly increased sirtuin (SIRT) 3 level (2.7-fold) in vivo while the inhibition of SIRT3 exacerbated senescent H9c2 cellular LDH release and ROS production under hypoxia. In addition, SIRT3 silencing impairs mitochondrial dynamics and mitophagy in senescent cardiomyocytes against simulated ischemia (SI) injury. Conclusion Collectively, our study demonstrated for the first time that sustained short-duration exercise, rather than long-duration exercise, attenuates cardiac dysfunction after MI in aged mice. It is likely that the positive regulation induced by a short-duration ST regimen on the elevated SIRT3 protein level improved mitochondrial quality control and decreased apoptosis and fibrosis contributed to the observed more resistant phenotype.

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“…As a model of low intrinsic aerobic capacity, LCR rats display symptomology of metabolic syndrome with reduced whole-body and skeletal muscle insulin sensitivity shown here and elsewhere (18–24). Karvinen et al (38) assessed HSPs in aging HCR/LCR muscles; however, this is the first study to fully characterize constitutive expression of HSPs in metabolic tissue of HCR and LCR rats. HSP72 was higher in HCR rats compared with LCR rats, but only in glycolytic skeletal muscles.…”

Section: Discussionmentioning

confidence: 99%

Deficiency in the Heat Stress Response Could Underlie Susceptibility to Metabolic Disease

et al. 2016

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Heat treatment (HT) effectively prevents insulin resistance and glucose intolerance in rats fed a high-fat diet (HFD). The positive metabolic actions of heat shock protein 72 (HSP72), which include increased oxidative capacity and enhanced mitochondrial function, underlie the protective effects of HT. The purpose of this study was to test the ability of HSP72 induction to mitigate the effects of consumption of a short-term 3-day HFD in rats selectively bred to be low-capacity runners (LCRs) and high-capacity runners (HCRs)—selective breeding that results in disparate differences in intrinsic aerobic capacity. HCR and LCR rats were fed a chow or HFD for 3 days and received a single in vivo HT (41°C, for 20 min) or sham treatment (ST). Blood, skeletal muscles, liver, and adipose tissues were harvested 24 h after HT/ST. HT decreased blood glucose levels, adipocyte size, and triglyceride accumulation in liver and muscle and restored insulin sensitivity in glycolytic muscles from LCR rats. As expected, HCR rats were protected from the HFD. Importantly, HSP72 induction was decreased in LCR rats after only 3 days of eating the HFD. Deficiency in the highly conserved stress response mediated by HSPs could underlie susceptibility to metabolic disease with low aerobic capacity.

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Effects of intrinsic aerobic capacity, aging and voluntary running on skeletal muscle sirtuins and heat shock proteins

Cited by 33 publications

References 186 publications

Energy restriction, exercise and atorvastatin treatment improve endothelial dysfunction and inhibit miRNA-155 in the erectile tissue of the aged rat.

Energy restriction, exercise and atorvastatin treatment improve endothelial dysfunction and inhibit miRNA-155 in the erectile tissue of the aged rat.

Short-Duration Swimming Exercise after Myocardial Infarction Attenuates Cardiac Dysfunction and Regulates Mitochondrial Quality Control in Aged Mice

Deficiency in the Heat Stress Response Could Underlie Susceptibility to Metabolic Disease

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