Functional and morphological effects of resistance exercise on disuse-induced skeletal muscle atrophy

Nicastro, Humberto; Zanchi, Nelo Eidy; Luz, Claudia Ribeiro da; Lancha, Antônio Herbert

doi:10.1590/s0100-879x2011007500125

Cited by 13 publications

(9 citation statements)

References 60 publications

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“…The current study also indicates that Ang-(1-7) could have therapeutic potential in combating disuse atrophy. Resistance exercises that promote adaptive functional and structural responses are widely applied in the treatment of disuse atrophy ( Nicastro et al, 2011 ). Notably, exercise training increases Ang-(1-7) levels and Mas receptor expression in the muscles of rats suffering chronic heart failure ( Gomes-Santos et al, 2014 ).…”

Section: Discussionmentioning

confidence: 99%

Angiotensin-(1-7) attenuates disuse skeletal muscle atrophy via the Mas receptor

Morales

Ábrigo

Acuña

et al. 2016

Disease Models &Amp; Mechanisms

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Immobilization is a form of disuse characterized by a loss of strength and muscle mass. Among the main features are decreased IGF-1/Akt signalling and increased ubiquitin-proteasome pathway signalling, which induce greater myosin heavy chain degradation. Activation of the classical renin-angiotensin system (RAS) causes deleterious effects in skeletal muscle, including muscle wasting. In contrast, angiotensin-(1-7) [Ang-(1-7)], a peptide of the non-classical RAS, produces beneficial effects in skeletal muscle. However, the role of Ang-(1-7) in skeletal muscle disuse atrophy and independent of classical RAS activation has not been evaluated. Therefore, we assessed the functions of Ang-(1-7) and the Mas receptor in disuse muscle atrophy in vivo using unilateral cast immobilization of the hind limb in male, 12-week-old wild-type (WT) and Mas-knockout (Mas KO) mice for 1 and 14 days. Additionally, we evaluated the participation of IGF-1/IGFR-1/Akt signalling and ubiquitin-proteasome pathway expression on the effects of Ang-(1-7) immobilization-induced muscle atrophy. Our results found that Ang-(1-7) prevented decreased muscle strength and reduced myofiber diameter, myosin heavy chain levels, and the induction of atrogin-1 and MuRF-1 expressions, all of which normally occur during immobilization. Analyses indicated that Ang-(1-7) increases IGF-1/IGFR-1/Akt pathway signalling through IGFR-1 and Akt phosphorylation, and the concomitant activation of two downstream targets of Akt, p70S6K and FoxO3. These anti-atrophic effects of Ang-(1-7) were not observed in Mas KO mice, indicating crucial participation of the Mas receptor. This report is the first to propose anti-atrophic effects of Ang-(1-7) via the Mas receptor and the participation of the IGF-1/IGFR-1/Akt/p70S6K/FoxO3 mechanism in disuse skeletal muscle atrophy.

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Section: Discussionmentioning

confidence: 99%

Angiotensin-(1-7) attenuates disuse skeletal muscle atrophy via the Mas receptor

Morales

Ábrigo

Acuña

et al. 2016

Disease Models &Amp; Mechanisms

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“…There is evidence showing that RE improves muscle strength among older adults, predominantly with higher intensity training. Great results have also been obtained by using different types of RE, such as flywheel, vascular occlusion, dynamic, isometric, and eccentric [47]. The morphological and functional adaptations to RE include skeletal muscles and nerves, muscle architecture and composition, and myofibrillar proteins accumulation [48].…”

Section: Exercisementioning

confidence: 99%

Sarcopenia and Exercise “The State of the Art”

Musumeci

2017

JFMK

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Skeletal muscle mass reduction might be a consequence of aging (sarcopenia), disease (cachexia) or inactivity (muscle atrophy). Studying the triggering factors leading to muscle loss is important in developing therapies to preserve muscle tissue function. The loss of skeletal muscle proteins is caused by an imbalance between the rate of their synthesis and degradation. Specifically, the conditions characterized by muscle loss involve an adaptation metabolism of increased protein degradation (cachexia), decreased muscle protein synthesis (inactivity), or alteration in both (sarcopenia). Sarcopenia and exercise is the main topic chosen for this review. This is a huge health problem, poorly discussed in the current literature and the aim of this review is to explain and help readers to better understand the differences between "sarcopenia", "cachexia", "muscle atrophy" and the relative beneficial effects of exercise used as a possible therapeutic intervention. Sarcopenia is a component of the fragility syndrome and indicates a significant health issue related to the progressive decline of muscle tissue quality and strength. Exercise is associated with improved life quality, reduced health problems, and prolonged lifespan. The latter suggests that exercise should be considered a fundamental point in the treatment of pathological skeletal muscle mass reduction. The present scientific contribution also seeks to emphasize to the scientific community the positive effects of the adapted physical activity in the elderly as a possible non-pharmacologic treatment to prevent or treat muscle atrophy.

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“…The most common types of exercise used in animal experiments are voluntary wheel running, forced wheel running, treadmill running, swimming, and resistance training [ 8 , 9 ]. Aerobic exercise modalities are suitable for almost every noncommunicable disorder-related research area, while anaerobic training modalities are applicable in a much narrower field of research, including muscle formation studies [ 8 – 11 ]. In this review, we discuss the far-reaching benefits of physical exercise and its interpretation in different animal models.…”

Section: Introductionmentioning

confidence: 99%

Multiple Applications of Different Exercise Modalities with Rodents

Börzsei

Szabó

Hoffmann

et al. 2021

Oxidative Medicine and Cellular Longevity

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A large proportion of chronic diseases can be derived from a sedentary lifestyle. Raising physical activity awareness is indispensable, as lack of exercise is the fourth most common cause of death worldwide. Animal models in different research fields serve as important tools in the study of acute or chronic noncommunicable disorders. With the help of animal-based exercise research, exercise-mediated complex antioxidant and inflammatory pathways can be explored, which knowledge can be transferred to human studies. Whereas sustained physical activity has an enormous number of beneficial effects on many organ systems, these animal models are easily applicable in several research areas. This review is aimed at providing an overall picture of scientific research studies using animal models with a focus on different training modalities. Without wishing to be exhaustive, the most commonly used forms of exercise are presented.

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Functional and morphological effects of resistance exercise on disuse-induced skeletal muscle atrophy

Cited by 13 publications

References 60 publications

Angiotensin-(1-7) attenuates disuse skeletal muscle atrophy via the Mas receptor

Angiotensin-(1-7) attenuates disuse skeletal muscle atrophy via the Mas receptor

Sarcopenia and Exercise “The State of the Art”

Multiple Applications of Different Exercise Modalities with Rodents

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