Muscle damage, metabolism, and oxidative stress in <i>mdx</i> mice: Impact of aerobic running

Schill, Kevin E.; Altenberger, Alex. R.; Lowe, Jeovanna; Periasamy, Muthu; Villamena, Frederick A.; Rafael‐Fortney, Jill A.; Devor, Steven T.

doi:10.1002/mus.25015

Cited by 25 publications

(32 citation statements)

References 34 publications

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“…These last researches conducted by Capogrosso et al (2017) and Schill et al (2016) showed that the high intensity exercise caused an adaptation not ideal for the dystrophic muscle, confirming the goal of this intensity already established by The TREAT-NMD recommended protocol “Use of treadmill and wheel exercise for impact on mdx mice phenotype.” So, few researches until now have analyzed treadmill protocols of low intensity that seems to be beneficial to mdx mice muscle.…”

Section: Discussionsupporting

confidence: 60%

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Low-intensity training provokes adaptive extracellular matrix turnover of a muscular dystrophy model

et al. 2017

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Recommendations of therapeutic exercise in Duchenne muscular dystrophy are still controversial. The hypothesis that a low-intensity training (LIT) protocol leads to muscle adaptations on mdx mice model was tested. Dystrophic male mice with 8 weeks old were separated in exercised (mdxE, n= 8) and sedentary (mdxC, n= 8) groups. Wild-type mice were used as control (WT, n= 8) group. Exercised group underwent a LIT protocol (9 m/min, 30 min, 3 days/wk, 60 days) on a horizontal treadmill. At day 60 all animals were analyzed regarding parameters of markers of muscle lesion and extracellular matrix turnover of muscle tissue by collagens fibers on tibial anterior muscle. Histomorphometry attested that centrally located nuclei fibers and the coefficient of variance of minimal Feret’s diameter was similar in mdxE and mdxC groups (P= 1.000) and both groups presented higher mean values than WT group (P< 0.001). Fraction area of collagen fibers of mdxE group was lower than mdxC group (P= 0,027) and similar to WT group (P= 0,751). Intramuscular area of Col3 of the mdxE group was higher than mdxC and WT groups (P<0.001). Intramuscular area of Col1 on the mdxE group was similar to the mdxC group (P= 1.000) and both groups were higher than WT group (P< 0.001). LIT protocol had not influenced muscle injuries resulting from the dystrophin-deficiency membrane fragility. Although, LIT had provoked adaptations on extracellular matrix bringing higher elastic feature to dystrophic muscle tissue.

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Section: Discussionsupporting

confidence: 60%

“…With the same speed of the study of Capogrosso et al (2017) , Schill et al (2016) investigated a 4 weeks of twice-weekly treadmill exercise on mdx mice of 4 weeks old, younger than ours. The exercise regimen consisted of 30 min on a horizontal treadmill running at a speed of 12 m/min.…”

Section: Discussionmentioning

confidence: 99%

Low-intensity training provokes adaptive extracellular matrix turnover of a muscular dystrophy model

et al. 2017

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“…Thus, it seems that running alone, and particularly in combination with sAcvR2B-Fc was not completely tolerable and shifted the redox-balance of the functional dystrophin deficient skeletal muscle to more oxidizing direction. Previously, increased oxidative stress was reported after 4 weeks of running in mdx mice [55]. However, decreased markers of oxidative stress in mdx mice has also been reported after 8 weeks of very low-intensity treadmill running [9] and after 4…”

Section: Discussionmentioning

confidence: 96%

“…However, some studies have even shown that certain markers are negatively altered by exercise in mdx mice, including e.g. calcium homeostasis if the intensity of the exercise is high [55,60]. Clearly, more research is needed on the dose and type of exercise in dystrophic muscle.…”

Section: Discussionmentioning

confidence: 99%

Effects of muscular dystrophy, exercise and blocking activin receptor IIB ligands on the unfolded protein response and oxidative stress

Hulmi

Hentilä

DeRuisseau

et al. 2016

Free Radical Biology and Medicine

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Effects of muscular dystrophy, exercise and blocking activin receptor IIB ligands on the unfolded protein response and oxidative stress, Free Radical Biology and Medicine, http://dx.doi.org/10.1016/j.freeradbiomed.2016.08.017 This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting galley proof before it is published in its final citable form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain.

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“…Muscle dystrophy studies require a specific discussion regarding to the role of physical exercise in the satellite cell niche, since different intensities can be detrimental rather than beneficial . No study, so far, has characterized exercise intensity in the studies with mdx mice although the speed for the treadmill walking training was set at 12 m·min −1 , with a duration of ~ 30 min . This speed is considered low‐intensity exercise training for young C57Bl/6 wild‐type mice based on graded exercise protocols, since the maximal lactate steady state was found at 15 m·min −1 .…”

Section: Potential Role Of Physical Exercise In Restoring the Satellimentioning

confidence: 99%

Chronic inflammation in skeletal muscle impairs satellite cells function during regeneration: can physical exercise restore the satellite cell niche?

et al. 2018

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Chronic inflammation impairs skeletal muscle regeneration. Although many cells are involved in chronic inflammation, macrophages seem to play an important role in impaired muscle regeneration since these cells are associated with skeletal muscle stem cell (namely, satellite cells) activation and fibro-adipogenic progenitor cell (FAP) survival. Specifically, an imbalance of M1 and M2 macrophages seems to lead to impaired satellite cell activation, and these are the main cells that function during skeletal muscle regeneration, after muscle damage. Additionally, this imbalance leads to the accumulation of FAPs in skeletal muscle, with aberrant production of pro-fibrotic factors (e.g., extracellular matrix components), impairing the niche for proper satellite cell activation and differentiation. Treatments aiming to block the inflammatory pro-fibrotic response are partially effective due to their side effects. Therefore, strategies reverting chronic inflammation into a pro-regenerative pattern are required. In this review, we first describe skeletal muscle resident macrophage ontogeny and homeostasis, and explain how macrophages are replenished after muscle injury. We next discuss the potential role of chronic physical activity and exercise in restoring the M1 and M2 macrophage balance and consequently, the satellite cell niche to improve skeletal muscle regeneration after injury.

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Muscle damage, metabolism, and oxidative stress in mdx mice: Impact of aerobic running

Cited by 25 publications

References 34 publications

Low-intensity training provokes adaptive extracellular matrix turnover of a muscular dystrophy model

Low-intensity training provokes adaptive extracellular matrix turnover of a muscular dystrophy model

Effects of muscular dystrophy, exercise and blocking activin receptor IIB ligands on the unfolded protein response and oxidative stress

Chronic inflammation in skeletal muscle impairs satellite cells function during regeneration: can physical exercise restore the satellite cell niche?

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