Genetic variation and exercise-induced muscle damage: implications for athletic performance, injury and ageing.

Prolonged unaccustomed exercise involving muscle lengthening (eccentric) actions can result in ultrastructural muscle disruption, impaired excitation-contraction coupling, inflammation and muscle protein degradation. This process is associated with delayed onset muscle soreness and is referred to as exercise-induced muscle damage. Although a certain amount of muscle damage may be necessary for adaptation to occur, excessive damage or inadequate recovery from exercise-induced muscle damage can increase injury risk, particularly in older individuals, who experience more damage and require longer to recover from muscle damaging exercise than younger adults. Furthermore, it is apparent that inter-individual variation exists in the response to exercise-induced muscle damage, and there is evidence that genetic variability may play a key role. Although this area of research is in its infancy, certain gene variations, or polymorphisms have been associated with exercise-induced muscle damage (i.e. individuals with certain genotypes experience greater muscle damage, and require longer recovery, following strenuous exercise). These polymorphisms include ACTN3 (R577X, rs1815739), TNF (-308 G>A, rs1800629), IL6 (-174 G>C, rs1800795), and IGF2 (ApaI, 17200 G>A, rs680). Knowing how someone is likely to respond to a particular type of exercise could help coaches/practitioners individualise the exercise training of their athletes/patients, thus maximising recovery and adaptation, while reducing overload-associated injury risk. The purpose of this review is to provide a critical analysis of the literature concerning gene polymorphisms associated with exercise-induced muscle damage, both in young and older individuals, and to highlight the potential mechanisms underpinning these associations, thus providing a better understanding of exercise-induced muscle damage

Eosinophilic gastroenteritis as the initial manifestation of hypereosinophilic syndrome.

Eosinophilic gastroenteritis, an inflammatory disease of unknown etiology, commonly involves the stomach and small intestine with eosinophilic infiltration. Here, we report an unusual case of eosinophilic gastroenteritis involving the entire digestive tract as a manifestation of hypereosinophilic syndrome (HES). A 22-year-old woman presented to us with diarrhoea, pleural effusion, ascites and marked peripheral oeosinophilia. Stool specimens were negative for parasites, ova, bacteria, and fungi. Endoscopic studies showed pangastritis and duodenitis. Biopsy specimens of the oesophagus, stomach, duodenum, ileum, and colon demonstrated oeosinophilic infiltration. A diagnosis of hypereosinophilic syndrome with eosinophilic gastroenteritis involving the entire digestive tract was made. Hence, she was treated with prednisolone. Symptoms and peripheral oeosinophilia rapidly resolved with treatment, and radiological investigations revealed resolution of effusion. This case illustrates the wide spectrum of clinical manifestation of the disease, whereby it involves the entire digestive tract and it also emphasizes the diagnostic yields of endoscopic biopsies