Although dystrophic muscles are more vulnerable to injuries caused by eccentric contractions than healthy muscles 27, 28, many physiological tasks such as walking or sitting involve eccentric contractions. There are no studies in the literature that address low-intensity eccentric exercise in dystrophic muscles for a long period of time. These studies include muscles that were immobilized and used low-intensity exercise, because it is known that a high-intensity eccentric training can lead to irreversible muscle damage. The most common types of training used in studies with dystrophic mice include running on a flat treadmill 18, running on wheels, or swimming for long periods of time (10–16 weeks) 15– 17, 19.Įccentric exercise, which can lead to muscle injury 19– 22, has also been shown to partially re-establish some of the cytoarchitectural features in disused muscles, especially when incorporated in a training protocol conducted for long periods of time 23– 26.
There are also significant improvements in strength, resistance to fatigue and muscle morphology after 10–16 weeks of treadmill training 15– 17. Low-intensity training (LIT) in treadmill running improves the overall function of mdx muscles, reduces oxidative stress and inflammation, while increasing their mitochondrial capacity 10– 12 and oxidative capacity 13, 14. Studies conducted with mdx mice, an animal model for DMD, have shown that physical training can improve muscle function without aggravating the disease. Currently, there is no consensus on the best type, frequency and intensity of exercise to be used with DMD 7– 9. Although the effects of exercise for DMD are still controversial 6, 7, there is an increasing interest in the potential benefits of physical training, since it is cost-effective and non-invasive. There is no cure for DMD, but there are rehabilitation exercise programs aimed to slow the progression of the disease 5. Lack of dystrophin in muscle fibers leads to mechanical damage, impaired Ca 2+ homeostasis, increased proteolysis and widespread cellular dysfunction 2– 4, resulting in weakness and loss of muscle function. Dystrophin and the dystrophin-glycoprotein complex have an important role in the sarcolemma membrane integrity during muscle contraction. DMD affects one in every 5000 boys 1 and causes many deficiencies including an impaired mobility, wheel chair confinement, respiratory and cardiac failure. The results show that LIET can improve the functionality of dystrophic soleus muscle in mice.ĭuchenne muscular dystrophy (DMD) is a lethal pediatric muscle disorder caused by a mutation in the region Xp 21.2 (dystrophin gene) that leads to an absence of dystrophin protein. Muscles of the mdx training group-21 days showed an improvement in morphological characteristics and an increase of active force when compared to the sedentary mdx group. After the training sessions, animals were euthanized, and fragments of soleus muscles were removed for immunofluorescence and histological analyses, and measurements of active force and Ca 2+ sensitivity of the contractile apparatus. Thirty-six male mdx mice were randomized into six groups (n = 6/each): mdx sedentary group mdx training group-3 days mdx training group-21 days wild-type sedentary group wild-type training group-3 days and wild-type training group-21 days. The purpose of this study was to investigate the effects of 21 days of LIET in dystrophic soleus muscle.
Recently, LIET has also been used for rehabilitating dystrophic muscles, but its effects are still unclear. Low-intensity eccentric training (LIET) has been used as a rehabilitation method in skeletal muscles after disuse. Duchene muscular dystrophy (DMD) is caused by the absence of the protein dystrophin, which leads to muscle weakness, progressive degeneration, and eventually death due to respiratory failure.
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