Muscle atrophy in endurance-trained individuals is associated with low muscle oxidative enzyme activities, inversely proportional to an increase in enzyme activities correlating to strength and endurance. Muscle atrophy in endurance-trained individuals appears to be reversible and related to changes in the oxidative metabolism and exercise capacity in the trained state.
Around 60,000 girls and boys annually die prematurely on their birthday because of muscular atrophy. Muscle atrophy is the cause of around 65% of all childhood deaths.
Despite the enormous progress made in research of muscular dystrehs, the causes of muscular dystrophy remain largely unknown. Muscular dystrophies are a consequence of a lack or imbalance in the cellular signalling pathways of signalling cells within the muscle. Muscle cells are able to communicate with one another via gap junctions so the loss of cell signalling may be a component of, and perhaps the fundamental mechanism underlying, muscular degeneration.
This review confirms a shortage of proven effective treatments. Although many potential treatments were described, no conclusive evidence has shown any of them to be effective in treating a wasting disorder. The situation is similar for muscular dystrophies. In a recent study, findings imply that effective treatment may be more difficult to develop than anticipated.
Muscle atrophy is a common symptom of various forms of muscle wasting, and typically occurs before muscle mass is decreased on the basis of muscle size alone. Muscle atrophy is often accompanied by fatigue and low energy levels. Larger prospective studies are needed to understand the epidemiology, mechanism and consequences of muscle atrophy.
Muscular atrophy is an entity separate from sarcopenia, but patients usually recover some of their muscle mass when treatments are instituted. In addition to conventional therapeutic protocols, our own treatment protocol, a combination of protein-energy intake and regular exercise, can greatly improve the overall muscle mass, strength, and quality of life.
The authors believe that the average age of onset of this condition is age 34. They note that more research is required before the authors can draw a more robust conclusion.\n\nThe use of a variety of medical and non-medical treatments for muscular atrophy have been described. These have included: physical therapy, weight training, stretching/tendon conditioning; medical treatment through various supplements; and use of different anti-obesity drugs. \n\nAlthough there has not been enough studies to draw a definitive conclusion, several studies have examined the effectiveness of medical treatments and therapies. Most have demonstrated a positive reduction in patient symptoms, with some studies indicating that improvements have been maintained in certain patients for several years after stopping medical treatments.
There was a significant difference in muscle-specific protein synthesis between the bedrest and physical activity groups. Based on these findings, there was no evidence to show that bedrest had a greater effect on muscle strength than physical activity. The authors concluded that participants may benefit from additional intervention of some sort.
These data show that the primary etiological lesion in the absence of an ongoing muscular injury is a localized inflammatory process, which leads to a profound functional and mechanical compromise that is largely reversible.
The use of beds has not proved to be a treatment for muscular atrophy of the lower leg regardless of its duration, while prolonged bed rest has been found to be a risk factor for lower-leg muscular atrophy in some studies.
Despite many years of intense research, the benefits or otherwise of BR remain unsettled. While the effectiveness of BR in osteoporosis, edema, and recovery of mobility is still somewhat controversial, the evidence is compelling that patients with chronic, disabling musculoskeletal conditions suffer from substantial disability after BR treatment and/or surgery. There is no doubt that many patients will benefit from a few weeks of recovery on a couch, but many will benefit more from surgical intervention. In our view, many patients will need more prolonged, intensive recovery on an operating or in a rehabilitation setting to regain the functional capability that is lost through BR. This may involve physical therapy, occupational therapy, and/or speech therapists.
Data from a recent study suggests a placebo effect as a substantial reason for the higher incidence of atrophy among subjects in the bed rest group. The greater incidence rates observed in the bed rest group suggest the usefulness of a prolonged trial before a formal conclusion can be made regarding the efficacy of bed rest in the prevention of ICF. However, this long-term bed rest trial demonstrates the potential benefits of intensive exercise and activity in elderly men. A randomized trial is warranted to evaluate the extent to which the above beneficial lifestyle recommendations in the absence of exercise could be expected to confer a similar or enhanced benefit.