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Exercise-induced muscle damage (initial phase)

Prolonged unaccustomed exercise involving muscle lengthening (eccentric) actions can result in ultrastructural muscle disruption, impaired excitation–contraction coupling, inflammation and muscle protein degradation.

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). 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 exercise can produce muscle damage through a series of alterations of two types, some of early onset and mechanical origin while others are consequences of the previous ones and consist on the inflammatory process. The most used models are the eccentric exercise (by isolated contractions, jumps or downhill running) and the post-competition analysis of some test, for example marathon.

This type of exercise called eccentric exercise (rapid stretching of the muscle by contraction) is successfully included in the training of different sport contexts improving strength, muscular power, coordination and performance through the improvement in the recruitment of motor units, a increase in reflex enhancement and changes in the elastic properties of muscle and connective tissue. However, by containing an eccentric exercise phase, it is highly associated with muscle damage and pain.

As older people appear to be more susceptible to exercise-induced muscle damage than younger adults, older people with a genetic predisposition to greater muscle damage, may be at a greater risk of developing muscle–tendon unit injury.

THE INITIAL PHASE OF EXERCISE-INDUCED MUSCLE DAMAGE involves damage to the muscular structures responsible for the contraction of the myofibrils and tends to cause damage to the proteins that form these mechanical structures, such as collagen, actin, myosin, desmin, titin and other proteins that interact with the cellular cytoskeleton.

Gene or region studied

  • ACTN3
  • MYLK2
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