The Pleiotropic Effect of Physical Exercise on Mitochondrial Dynamics in Aging Skeletal Muscle

Barbieri, Elena; Agostini, Deborah; Polidori, Emanuela; Potenza, Lucia; Guescini, Michele; Lucertini, Francesco; Annibalini, Giosuè; Stocchi, Laura; Santi, Mauro De; Stocchi, Vilberto

doi:10.1201/b19985-11

Cited by 15 publications

(21 citation statements)

References 144 publications

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“…Mitochondrial dysfunction is usually characterized by the decrease in mitochondrial respiration and the increase in the secretion of l -lactate out of the cell. This effect could be further accompanied by the increased leak of ROS from mitochondrial respiratory chain, diminished mitochondrial membrane potential, or the presence of altered mitochondrial shape and ultrastructure [ 40 , 41 ]. Since l -lactate treatment appeared to trigger mitohormesis and induce PGC1 α activity, we tested whether it could prevent the onset of mitochondrial dysfunction in the skin fibroblasts undergoing replicative aging.…”

Section: Resultsmentioning

confidence: 99%

L-Lactate Protects Skin Fibroblasts against Aging-Associated Mitochondrial DysfunctionviaMitohormesis

Zelenka

Dvořák

Alán

2015

Oxidative Medicine and Cellular Longevity

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A moderate elevation of reactive oxygen species (ROS) production and a mild inhibition of mitochondrial respiratory chain have been associated with a health promotion and a lifespan extension in several animal models of aging. Here, we tested whether this phenomenon called mitohormesis could be mediated by L-lactate. The treatment with 5 mM L-lactate significantly increased H2O2 production and slightly inhibited the respiration in cultured skin fibroblasts and in isolated mitochondria. The L-lactate exposure was associated with oxidation of intracellular glutathione, phosphorylation of 5′AMP-activated protein kinase (AMPK), and induction of peroxisome proliferator-activated receptor gamma coactivator 1α (PGC1α) transcription. A replicative aging of fibroblasts (L0) with a constant (LC), or intermittent 5 mM L-lactate (LI) in media showed that the high-passage LI fibroblasts have higher respiration, lower H2O2 release, and lower secretion of L-lactate compared to L0 and LC. This protection against mitochondrial dysfunction in LI cells was associated with lower activity of mechanistic target of rapamycin complex 1 (mTORC1), less signs of cellular senescence, and increased autophagy compared to L0 and LC. In conclusion, we demonstrated that intermittent but not constant exposure to L-lactate triggers mitohormesis, prevents aging-associated mitochondrial dysfunction, and improves other markers of aging.

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Section: Resultsmentioning

confidence: 99%

L-Lactate Protects Skin Fibroblasts against Aging-Associated Mitochondrial DysfunctionviaMitohormesis

Zelenka

Dvořák

Alán

2015

Oxidative Medicine and Cellular Longevity

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“…Hence, exercise may improve BC outcomes [ 14 ] ( Figure 1 ). Moreover, both long-term training and a single bout of exercise control energy availability and induce a hormetic response that accounts for the physiological cellular stress adaptation [ 83 , 84 ].…”

Section: Evidence Of Mtor Modulation By Exercise In Tnbcmentioning

confidence: 99%

New Insights into the Role of Exercise in Inhibiting mTOR Signaling in Triple‐Negative Breast Cancer

Agostini

Natalucci

Baldelli

et al. 2018

Oxidative Medicine and Cellular Longevity

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Triple-negative breast cancer (TNBC) does not express estrogen receptor, progesterone receptor, and human epidermal growth factor receptor 2 and is characterized by its aggressive nature, lack of targets for targeted therapies, and early peak of recurrence. Due to these specific characteristics, chemotherapy does not usually yield substantial improvements and new target therapies and alternative strategies are needed. The beneficial responses of TNBC survivors to regular exercise, including a reduction in the rate of tumor growth, are becoming increasingly apparent. Physiological adaptations to exercise occur in skeletal muscle but have an impact on the entire body through systemic control of energy homeostasis and metabolism, which in turn influence the TNBC tumor microenvironment. Gaining insights into the causal mechanisms of the therapeutic cancer control properties of regular exercise is important to improve the prescription and implementation of exercise and training in TNBC survivors. Here, we provide new evidence of the effects of exercise on TNBC prevention, control, and outcomes, based on the inhibition of the phosphatidylinositol-3-kinase (PI3K)/protein kinase B (PKB also known as Akt)/mammalian target of rapamycin (mTOR) (PI3K-Akt-mTOR) signaling. These findings have wide-ranging clinical implications for cancer treatment, including recurrence and case management.

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“…It means that insulin alone might amplify the Bcl-2 expression, and the exercise, as an extra boosting factor, promoted the insulin-induced Bcl-2 expression in germ cells. Moreover, it is worth mentioning that exercise training boosts the expression of mitochondrial survival factor in cardiac [18] and skeletal myocytes [49]. In addition, moderate exercise training amplifies the antioxidant status of different tissues [50,51] and enhances the cellular resistance against apoptosis via up-regulating Bcl-2 expression [52].…”

Section: Discussionmentioning

confidence: 99%

Moderate-intensity Exercise Training in Sole and Simultaneous Forms with Insulin Ameliorates the Experimental Type 1 Diabetes-induced Intrinsic Apoptosis in Testicular Tissue

et al. 2019

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The aim of this study was to investigate the ameliorative effect of moderate-intensity exercise training in sole and simultaneous forms with insulin on experimental type 1 diabetes (T1D)-induced apoptosis. A total of 36 mature male Wistar rats were divided into six equally sized groups, including sedentary control (Con), moderate-intensity exercise training (E-sole), sedentary T1D-induced (D-sole), moderate-exercise-trained T1D-induced (DE), insulin-treated sedentary T1D-induced (DI) and exercise-trained, and insulin-treated T1D-induced (DEI) groups. The 6-week exercise training intervention was involved 30 min of moderate-intensity running on a treadmill once daily (5 days/week). Next, tubular differentiation (TDI) and spermiogenesis (SPI) indices were assessed. The Bcl-2, Bax and caspase-3 expressions were determined using RT-PCR, immunohistochemistry and western blot techniques. Finally, the TUNEL staining was used to analyze the apoptosis ratio. The moderate-intensity exercise training in the sole and when simultaneously considered with insulin (DEI) maintained testicular cellularity, up-regulated Bcl-2 expression, reduced Bax expression and ameliorated the diabetes-induced apoptosis. We failed to show remarkable alterations in caspase-3 mRNA and protein levels in the DE group versus D-sole animals. In conclusion, the moderate-intensity exercise training is able to potentially protect testicular cells from T1D-induced intrinsic apoptosis via up-regulating Bcl-2 and downregulating Bax expressions. Moreover, it amplifies the insulin-induced anti-apoptotic impacts.

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The Pleiotropic Effect of Physical Exercise on Mitochondrial Dynamics in Aging Skeletal Muscle

Cited by 15 publications

References 144 publications

L-Lactate Protects Skin Fibroblasts against Aging-Associated Mitochondrial DysfunctionviaMitohormesis

L-Lactate Protects Skin Fibroblasts against Aging-Associated Mitochondrial DysfunctionviaMitohormesis

New Insights into the Role of Exercise in Inhibiting mTOR Signaling in Triple‐Negative Breast Cancer

Moderate-intensity Exercise Training in Sole and Simultaneous Forms with Insulin Ameliorates the Experimental Type 1 Diabetes-induced Intrinsic Apoptosis in Testicular Tissue

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