Aging, Training and Exercise

Kretzschmar, M.; Müller, Dieter

doi:10.2165/00007256-199315030-00005

Cited by 72 publications

(8 citation statements)

References 57 publications

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“…running to exhaustion for about 60 min). It is therefore likely that, in relatively longer experiments, the GSH metabolism of muscle cells passes from an initial depletion to subsequent increased levels; this could occur by alteration of the GSH exchange between organs (Kretzschmar and Muller 1993) and/or by increased GSH biosynthesis. In our experiments, depletion in swimming animals was not accompanied by increased GSSG levels in the corresponding organs, as might have been expected from the increasingly oxidized state.…”

Section: Discussionmentioning

confidence: 99%

“…GPX was measured using two substrates, hydrogen peroxide (H 2 O 2 ) and cumene hydroperoxide (CuOOH). Results are expressed as the mean M (SD), n=10 (each sample being derived from the organs of two animals Signi®cance: *P < 0.05 (fasted vs non-fasted); **P < 0.05 (swimming vs non-swimming); ***P < 0.05 (fasted vs swimming) Kretzschmar and Muller 1993) and/or in GSSP formation via sulphydryl/disulphide (SH/SS) exchange reactions with protein SH groups (PSH):…”

Section: Discussionmentioning

confidence: 99%

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Antioxidant status in various tissues of the mouse after fasting and swimming stress

Simplicio

Rossi

Falcinelli

et al. 1997

European Journal of Applied Physiology

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We studied the effect of fasting and swimming stress on a number of non-enzymatic and enzymatic antioxidant factors in various mouse tissues in order to see if their action was synergic. We examined levels of reduced (GSH), oxidized (GSSG) and total glutathione, total SH groups (TSH), sum of GSH and protein sulphydryl groups of cytosolic fractions, and the activities of superoxide dismutase (SOD), catalase, glutathione peroxidase, glutathione reductase in adductor muscle, heart and liver. We also studied blood levels of GSH and glutathione bound to protein by mixed disulphides (GSSP). The case series consisted of four groups of animals (n = 10 for each group), namely no swimming and no fast, no swimming and fast, swimming and no fast, and swimming and fast. Fasting (18 h) resulted in a significant GSH depletion in all of the organs studied (-39% in the liver, -30% in the adductor muscle, -21% in the heart); GSSG increased significantly in the heart (+19%). Swimming to exhaustion, which lasted 3.95 (0.18) min [mean (SD), n = 10] with no significant difference between fast and no fast, resulted in a significant GSH depletion, to a percentage lower than that observed after fasting, in the adductor muscle and heart (-12% and -11%, respectively). In the blood of swimming mice, significant increases in GSH (+10%) and GSSG (+21%) levels were observed, whereas GSSP decreased (-15%). Enzyme activities after swimming were modified in only a few cases, and in a complex way. The findings of GSH depletion and a decrease in SOD activity in the adductor muscle seems to confirm the sensitivity of this organ to an overproduction of reactive oxygen species. At the same time, the GSSP decrease observed in blood was a new and unexpected finding, one that indicates a very prompt adaptation of red cells to increased oxidant states.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Antioxidant status in various tissues of the mouse after fasting and swimming stress

Simplicio

Rossi

Falcinelli

et al. 1997

European Journal of Applied Physiology

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“…Similarly, GSH concentration differs across the skeletal muscle fibres, with the highest concentrations being found in type I fibres [125]. Studies indicate that GSH increases in response to endurance exercise [125–127], which is most likely due to an increase in γ-glutamylcysteine, the rate-limiting enzyme for GSH biosynthesis [127, 128]. Exercise also appears to have a positive effect on other non-enzymatic antioxidants.…”

Section: Exercise: Potential Mechanisms For Preventing Cachexia In Camentioning

confidence: 99%

Cancer cachexia prevention via physical exercise: molecular mechanisms

Gould

Lahart

Carmichael

et al. 2012

J cachexia sarcopenia muscle

168

129

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Cancer cachexia is a debilitating consequence of disease progression, characterised by the significant weight loss through the catabolism of both skeletal muscle and adipose tissue, leading to a reduced mobility and muscle function, fatigue, impaired quality of life and ultimately death occurring with 25–30 % total body weight loss. Degradation of proteins and decreased protein synthesis contributes to catabolism of skeletal muscle, while the loss of adipose tissue results mainly from enhanced lipolysis. These mechanisms appear to be at least, in part, mediated by systemic inflammation. Exercise, by virtue of its anti-inflammatory effect, is shown to be effective at counteracting the muscle catabolism by increasing protein synthesis and reducing protein degradation, thus successfully improving muscle strength, physical function and quality of life in patients with non-cancer-related cachexia. Therefore, by implementing appropriate exercise interventions upon diagnosis and at various stages of treatment, it may be possible to reverse protein degradation, while increasing protein synthesis and lean body mass, thus counteracting the wasting seen in cachexia.

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“…This exercise-induced increase in GSH within muscle fibers is likely due to increased activity of a key enzyme involved in GSH synthesis (190). This enzyme, γ-glutamylcysteine synthase, is the rate limiting enzyme for GSH biosynthesis and is increased in exercise trained muscles following endurance training (227, 252, 364). …”

Section: Introductionmentioning

confidence: 99%

Reactive Oxygen Species: Impact on Skeletal Muscle

Powers

Kavazis

et al. 2011

Comprehensive Physiology

394

384

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It is well established that contracting muscles produce both reactive oxygen and nitrogen species. Although the sources of oxidant production during exercise continue to be debated, growing evidence suggests that mitochondria are not the dominant source. Regardless of the sources of oxidants in contracting muscles, intense and prolonged exercise can result in oxidative damage to both proteins and lipids in the contracting myocytes. Further, oxidants regulate numerous cell signaling pathways and modulate the expression of many genes. This oxidant-mediated change in gene expression involves changes at transcriptional, mRNA stability, and signal transduction levels. Furthermore, numerous products associated with oxidant-modulated genes have been identified and include antioxidant enzymes, stress proteins, and mitochondrial electron transport proteins. Interestingly, low and physiological levels of reactive oxygen species are required for normal force production in skeletal muscle, but high levels of reactive oxygen species result in contractile dysfunction and fatigue. Ongoing research continues to explore the redox-sensitive targets in muscle that are responsible for both redox-regulation of muscle adaptation and oxidant-mediated muscle fatigue.

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Aging, Training and Exercise

Cited by 72 publications

References 57 publications

Antioxidant status in various tissues of the mouse after fasting and swimming stress

Antioxidant status in various tissues of the mouse after fasting and swimming stress

Cancer cachexia prevention via physical exercise: molecular mechanisms

Reactive Oxygen Species: Impact on Skeletal Muscle

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