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

Postpartum dyspareunia and sexual functioning : a prospective cohort study

Objectives: Sexual functioning is an important concern for women in the postpartum period. The aim of this research was to investigate the prevalence and determinants of dyspareunia and sexual dysfunction before and after childbirth. Methods: Between November 2013 and April 2014, 109 women in their third trimester of pregnancy were enrolled in a prospective cohort study at Ghent University Hospital. Dyspareunia, sexual functioning and quality of life (QOL) were evaluated at enrolment and again 6 weeks and 6 months postpartum. Sexual functioning and QOL were assessed using validated self-report questionnaires: the Female Sexual Function Index and the Short Form-36 health survey. Dyspareunia was evaluated by a specific self-developed questionnaire. Results: One hundred and nine women were enrolled; respectively, 71 (65.1%), 66 (60.6%) and 64 (58.7%) women returned the questionnaires prepartum, and 6 weeks and 6 months postpartum. Sexual functioning at 6 weeks was predictive of sexual functioning at 6 months postpartum (r(s) = 0.345, p = .015). The prevalence of dyspareunia in the third trimester of pregnancy, and 6 weeks and 6 months postpartum was, respectively, 32.8%, 51.0% and 40.7%. The severity of pain decreased significantly between 6 weeks and 6 months postpartum (p = .003). In the first 6 weeks postpartum, the degree of dyspareunia was significantly associated with breastfeeding (p = .045) and primiparity (p = .020). At 6 months, only the association with primiparity remained significant (p = .022). Conclusions: The impaired postpartum sexual functioning, the high prevalence of dyspareunia postpartum and their impact on QOL indicate the need for further investigation and extensive counselling of pregnant women, especially primiparous women, about sexuality after childbirth