Exercise and duchenne muscular dystrophy: Toward evidence‐based exercise prescription

Markert, Chad D.; Ambrosio, Fabrisia; Call, Jarrod A.; Grange, Robert W.

doi:10.1002/mus.21987

Cited by 63 publications

(48 citation statements)

References 207 publications

(210 reference statements)

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“…If these acute increases in gene expression associated with each bout of activity are repeated over time, via chronic exercise under the auspices of informed exercise prescription, it may prove beneficial in successfully remodeling the active skeletal muscle to be more resistant to the dystrophic pathology. Clearly, more research, in the form of elegantly designed preclinical and clinical studies, is necessary to address the place of exercise in the lives of DMD patients and their families (12,42).…”

Section: Discussionmentioning

confidence: 99%

Chronic AMPK stimulation attenuates adaptive signaling in dystrophic skeletal muscle

Ljubicic

Khogali

Renaud

et al. 2012

American Journal of Physiology-Cell Physiology

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In the present study, we evaluated how a pharmacologically induced phenotype shift in dystrophic skeletal muscle would affect subsequent intracellular signaling in response to a complementary, adaptive physiological stimulus. mdx mice were treated with the AMP-activated protein kinase (AMPK) activator 5-aminoimidazole-4-carboxamide-1-β-D-ribofuranoside (AICAR; 500 mg·kg(-1)·day(-1)) for 30 days, and then one-half of the animals were subjected to a bout of treadmill running to induce acute AMPK and p38 MAPK signaling. The mRNA levels of phenotypic modifiers, including peroxisome proliferator-activated receptor-δ (PPARδ), PPARγ coactivator-1α (PGC-1α), receptor interacting protein 140 (RIP 140), and silent information regulator two ortholog 1 (SIRT1) were assessed in skeletal muscle, as well as the expression of the protein arginine methyltransferase genes PRMT1 and CARM1. We found unique AMPK and p38 phosphorylation and expression signatures between dystrophic and healthy muscle. In dystrophic skeletal muscle, treadmill running induced PPARδ, PGC-1α, and SIRT1 mRNAs, three molecules that promote the slow, oxidative myogenic program. In the mdx animals that received the chronic AICAR treatment, running-elicited AMPK and p38 phosphorylation was attenuated compared with vehicle-treated mice. Similarly, acute stress-evoked expression of PPARδ, PGC-1α, and SIRT1 was also blunted by chronic pharmacological AMPK stimulation. Skeletal muscle PRMT1 and CARM1 protein contents were higher in mdx mice compared with wild-type littermates. The acute running-evoked induction of PRMT1 and CARM1 mRNAs was also attenuated by the AICAR treatment. Our data demonstrate that prior pharmacological conditioning is a salient determinant in how dystrophic muscle adapts to subsequent complementary, acute physiological stress stimuli. These results provide insight into possible therapeutic applications of synthetic agonists in neuromuscular diseases, such as during chronic administration to Duchenne muscular dystrophy patients.

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Section: Discussionmentioning

confidence: 99%

Chronic AMPK stimulation attenuates adaptive signaling in dystrophic skeletal muscle

Ljubicic

Khogali

Renaud

et al. 2012

American Journal of Physiology-Cell Physiology

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“…], sarcopenia, and cachexia primarily result in atrophy of contractile proteins, especially myosin. Thus, drugs aimed at one group of diseases are unlikely to help the other, and in fact, could make things worse, as has been shown, for example, for exercise in Duchenne muscular dystrophy (DMD) [6].…”

Section: Regulation Of Muscle Homeostasismentioning

confidence: 97%

Prospect for Pharmacological Therapies to Treat Skeletal Muscle Dysfunction

Meriggioli¹,

Roubenoff²

2014

Calcif Tissue Int

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Skeletal muscle weakness is a leading cause of mobility disability in the elderly (sarcopenia), as a complication of acute or chronic illness (cachexia), and due to inherited or acquired muscle diseases (muscular dystrophies, myositides, etc.). As of now, there are no approved drugs that can reliably increase muscle strength and function. However, with our understanding of the regulation of myocyte signaling and homeostasis evolving rapidly, experimental treatments are now entering the clinic. We review the current status of clinical research in pharmacological therapies for muscle disorders.

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“…Although DMD is still incurable, it is not untreatable. Several studies have pointed out the need to study exercise in patients with DMD (34,62,63), with a clear admonition against heavy resistance training and even eccentric exercise (34). Heavy resistance training is possible with neuromuscular diseases that are not severe (71); however, there is a risk of further muscle damage that could have catastrophic consequences in patients with DMD.…”

Section: Muscular Dystrophymentioning

confidence: 99%

“…It is difficult to compare animal studies that use different species of animals, different protocols, and sometimes different outcome measures, but it can be misguided to take the findings from an animal model of a disease (e.g., the mdx mouse) and simply translate them to the human population (86). Thus there is a real need for further studies in patients with DMD and other muscular dystrophies (34,55,62,63).…”

Section: Muscular Dystrophymentioning

confidence: 99%

Eccentric exercise in aging and diseased skeletal muscle: good or bad?

Lovering

Brooks

2014

Journal of Applied Physiology

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Evidence is accumulating regarding the benefits of exercise in people who are more susceptible to injury, such as the elderly, or those with a neuromuscular disease, for example Duchenne muscular dystrophy (DMD). There appears to be a consensus that exercise can be safely performed in aging and diseased muscles, but the role of eccentric exercise is not as clear. Eccentric (lengthening) contractions have risks and benefits. Eccentric contractions are commonly performed on a daily basis, and high-force voluntary eccentric contractions are often employed in strength training paradigms with excellent results; however, high-force eccentric contractions are also linked to muscle damage. This minireview examines the benefits and safety issues of using eccentric exercise in at-risk populations. A common recommendation for all individuals is difficult to achieve, and guidelines are still being established. Some form of exercise is generally recommended with aging and even with diseased muscles, but the prescription (frequency, intensity, and duration) and type (resistance vs. aerobic) of exercise requires personal attention, as there is great diversity in the functional level and comorbidities in the elderly and those with neuromuscular disease.

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Exercise and duchenne muscular dystrophy: Toward evidence‐based exercise prescription

Cited by 63 publications

References 207 publications

Chronic AMPK stimulation attenuates adaptive signaling in dystrophic skeletal muscle

Chronic AMPK stimulation attenuates adaptive signaling in dystrophic skeletal muscle

Prospect for Pharmacological Therapies to Treat Skeletal Muscle Dysfunction

Eccentric exercise in aging and diseased skeletal muscle: good or bad?

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