Muscle disorders are divided into two categories:
Muscle Atrophy is referred to size reduction (but no number reduction) of muscle fibers, And In Degenerative Myopathy, muscle fibers are structurally damaged and degenerated.
Pathogenesis of Muscle Atrophy
Muscle atrophy is mainly characterized by a gradual decrease in muscle mass. Muscle mass reduction is due to loss of sarcoplasm and muscle fibers diameter reduction. In more severe forms, degenerative lesions of the muscle fiber appear. This muscle fiber protein contractor’s reduction in atrophic conditions is accompanied by a parallel increase in connective tissue and especially collagen.
This change in the relationship between contractile and non-contractile elements has been described as "adaptive allomorphism" of the muscle. Type II muscle fibers show the most significant changes in atrophic myopathies.
Clinical manifestations of these morphological changes in muscle atrophies are muscle weakness and easy muscle fatigue, as well as diffuse muscle pain and cramps, especially when trying to perform exercise. These symptoms tend to lower patient’s physical activity level and exacerbate muscle atrophy.
Exercise, especially static exercise, is an effective non-pharmacological treatment of muscle atrophy.
Favorable changes in muscle exercise
Muscle’s morphological and functional changes through systematic strengthening training programs are:
Number and diameter increase of both types of muscle fibers and myofibrils, increase in sarcoplasmic reticulum proteins, increase in blood capillaries, and increase in non-contractile elements. Systematic exercise (isometric, isotonic or all types of exercise in a structured exercise program) improves or completely restores muscle atrophy. In patients with muscle atrophy, static training mainly leads to restoration of their atrophy through a direct mechanical effect on the muscle fibers.
Repeated muscle exercises, as eccentric type exercises, moderate or highly intense, may cause micro-damages in sarcoplasma, which lead to activation of the recovery mechanism of normal morphology or even to compensatory increase in their size.
It is even claimed that with these exercises some Z disks are divided into large myofibers. New myofibers may acquire their normal size and thus eventually increase in number.
Increase in number and volume of mitochondria, as well as biochemical changes, such as increased enzymatic oxidative activity, creatine, ATP, and glycogen concentration. It has been found that exercise increases the number and metabolic functions of mitochondria and lead to increased activity of certain enzymes in the Krebs cycle, increased mitochondrial protein content, and improved fat oxidation and glycolytic activity.
Improving the functional capacity of the muscles, such as increasing the maximum contraction speed, the intensity of the isometric and isotonic contraction, their endurance and strength. The morphological adjustments, as well as the improvement of the metabolic mechanisms with the exercise mentioned above, not only increase the endurance of the skeletal muscles of the limbs in the exercise, but also the general physical adequacy, since they are the main reason for increasing the body's maximum oxygen uptake capacity.
Improving the neuromuscular junction function and the conduction velocity of the nerve stimulation. This is related to the increase in the diameter of the nerve fibers and the thickening of the myelin substance caused by systematic exercise. These improvements in skeletal muscle also lead to an increase in the aerobic capacity of the individual.
An individual exercise program for muscle atrophy requires patient’s functional capacity and performance of skeletal muscles assessments.
The exercise charge must be based on patients’ abilities and characteristics of the current muscular disease.
In patients with myopathy, there are not many randomized studies that implement regular exercise programs.
The results so far show that in patients with myotonic muscular dystrophy (MS) and face-shoulder-arm muscular dystrophy (FSHD), a moderate-intensity exercise program does not cause complications and may contribute to the treatment regimen.
Most studies implement short-term programs lasting 6-12 weeks, with no significant changes. It is obvious that longer interventions are required to achieve favorable morphological and functional adaptations in the skeletal muscles.