Habitual exercise program protects murine intestinal, skeletal, and cardiac muscles against aging.
ABSTRACT Aging and aerobic exercise are two conditions known to interfere with health and quality of life, most likely by inducing oxidative stress to the organism. We studied the effects of aging on the morphological and functional properties of skeletal, cardiac, and intestinal muscles and their corresponding oxidative status in C57BL/6 mice and investigated whether a lifelong moderate exercise program would exert a protective effect against some deleterious effects of aging. As expected, aged animals presented a significant reduction of physical performance, accompanied by a decrease of gastrocnemius cross-sectional area and cardiac hypertrophy. However, most interesting was that aging dramatically interfered with the intestinal structure, causing a significant thickening of the ileum muscular layer. Senescent intestinal myocytes displayed many mitochondria with disorganized cristae and the presence of cytosolic lamellar corpuscles. Lipid peroxidation of ileum and gastrocnemius muscle, but not of the heart, increased in aged mice, thus suggesting enhanced oxidative stress. With exception of the intestinal muscle responsiveness, animals submitted to a daily session of 60 min, 5 days/wk, at 13 up to 21 m/min of moderate running in treadmill during animal life span exhibited a reversion of all the observed aging effects on intestinal, skeletal, and heart muscles. The introduction of this lifelong exercise protocol prevented the enhancement of lipid peroxidation and sarcopenia and also preserved cellular and ultracellular structures of the ileum. This is the first time that the protective effect of a lifelong regular aerobic physical activity against the deleterious effects of aging on intestinal muscle was demonstrated.
- SourceAvailable from: Frédéric Derbré[show abstract] [hide abstract]
ABSTRACT: Aging causes a progressive decline in skeletal muscle mass that may lead to decreased strength and functionality. The term sarcopenia is especially used to characterize this geriatric syndrome. Numerous conditions and behaviors are considered to accelerate the progression of sarcopenia such as chronic diseases, malnutrition and physical inactivity. As people in modern countries are more and more sedentary, the impact of physical inactivity on the prevalence of sarcopenia might be more and more important in the future. In this review, we discuss how reactive oxygen species (ROS) could mediate the effects of lifelong inactivity in the onset and progression of age-related sarcopenia. Although the cellular mechanisms responsible for muscle ROS production are not necessarily the same, both inactivity and aging are indeed known to increase basal ROS concentrations in skeletal muscle. New data and literature review are provided showing that chronic ROS overproduction induced by physical inactivity may exacerbate the activation of some redox-sensitive signaling pathways involved in age-related sarcopenia. We also address the scientific evidences implicating the role of ROS overproduction in the precocious failure of aged muscles to activate intracellular signaling responses to contractions.European Journal of Sport Science 03/2012; · 1.15 Impact Factor
- [show abstract] [hide abstract]
ABSTRACT: Acute exercise results in transient change in redox balance. High concentrations of reactive oxygen species (ROS) can lead to oxidative damage to macromolecules. However, moderate periodic increases in ROS, such as experienced with habitual exercise, may activate signal transduction pathways which stimulate increases in endogenous antioxidant systems. This study tested the hypothesis that physically fit older adults would have less oxidative stress than unfit age-matched controls, due to greater circulating concentrations of non-enzymatic antioxidants and greater capacity to upregulate antioxidant enzymes. We compared 37 fit (mean age 65.2 ± 5 years) and 35 unfit (mean age 67.7 ± 4 years) men and women. Fitness status was classified by VO(2 max) and maximal leg power. Basal levels of oxidative stress were assessed by measuring urinary markers of nucleic acid damage and lipid peroxidation. Antioxidant status was assessed by measuring total antioxidant power and ratios of reduced to oxidized glutathione in plasma, at rest. The capacity to counteract an oxidative insult was assessed by measuring changes in plasma F(2)-isoprostanes in response to forearm ischemia-reperfusion. The fit individuals had significantly lower levels of urinary markers of oxidative damage (all P <0.05) and lower F(2)-isoprostane response to the oxidative challenge (P < 0.05), but there were no group differences in antioxidant status. The lower levels of oxidative stress in the fit individuals were not mediated by known effects of exercise training such as adiposity, HDL concentrations, or small molecular weight antioxidants. These data suggest that reduced oxidative stress associated with physical fitness results from differences in activity of antioxidant enzymes.Age 06/2011; 34(4):969-82. · 6.28 Impact Factor
- [show abstract] [hide abstract]
ABSTRACT: This study investigated the influence of lifestyle on aging-related changes in cardiac proteins' oxidative modifications profile. Thirty C57BL/6 strain mice (2 months) were randomly divided into three groups (young Y, old sedentary S, and old active A). The S and A mice were individually placed into standard cages and in cages with running wheels, respectively, for 23 months. Upon killing, heart mitochondrial fractions were obtained for the evaluation of general proteins oxidative modifications profile, the identification of preferential protein targets, and oxidative phosphorylation (OXPHOS) activity. We observed age-related cardiac muscle impairment, evidenced by decreased OXPHOS activity, paralleled by an increased protein susceptibility to carbonylation and nitration. Among the main targets to these posttranslational modifications we found mitochondrial proteins, mainly from OXPHOS complexes, MnSOD and enzymes from lipid metabolism. Lifelong sedentary behavior exacerbated the nitrative damage of mitochondrial proteins, paralleled by a statistically significant decrease of respiratory chain complexes II and III activities. In overall, our results highlight the determinant role of aging in cardiac muscle impairment, which is worsened by a sedentary lifestyle.Arbeitsphysiologie 08/2012; 112(4):1467-74. · 2.66 Impact Factor