Exercise-induced muscle damage (regeneration capacity)

Variants affecting genes involved in the activation of the cells responsible for muscle regeneration are relevant to understanding why some people require more time to recover after a muscle injury.

Muscle damage involves a series of alterations that occur in three main phases: a first phase, in which mechanical damage occurs. The second phase, which is a consequence of the first, in which inflammation occurs and finally the regeneration phase after muscle damage.

The third phase of muscle regeneration involves the active participation of satellite cells. These cells are the stem cells of the muscle and are found around the muscle cells (known as muscle fibers). The satellite cells are activated by substances produced during the previous inflammatory stage and participate in the regeneration of damaged fibers, or replace dead fibers allowing muscle recovery after injury.

As we have indicated, in order for muscle regeneration to occur after exercise, there must be an inflammatory signal through which the satellite cells are activated. There are studies that relate certain genetic variants with this inflammatory signal and, therefore, with a greater or lesser capacity for muscle remodeling. A lower capacity for muscle remodeling implies that a longer recovery is required after an injury. Two genetic polymorphisms have been identified that are related to this inflammatory signal and therefore to a greater or lesser capacity for muscle regeneration. These polymorphisms are found in the SOD2 and SLC30A8 genes.

The SOD2 gene produces the superoxide dismutase 2 protein, which has antioxidant activity, protecting the muscle from free radicals and facilitating muscle regeneration. The lack of functionality of this protein can cause the accumulation of free radicals and cell death of muscle fibers.

On the other hand, the SLC30A8 gene is associated with insulin response, and is indirectly associated with muscle strength and mass, as glycogen synthesis and glucose transport to the muscle are affected.

Number of observed variants

13.5 million variants

Number of variants analyzed in the study

2 variants

Bibliography

Ahmetov II, Naumov VA, Donnikov AE, Maciejewska-Kar?owska A, Kostryukova ES, Larin AK, et al. SOD2 gene polymorphism and muscle damage markers in elite athletes. Free Radic Res, 2014; 48(8):948–55.

Akimoto AK, Miranda-Vilela AL, Alves PCZ, Pereira LC da S, Lordelo GS, Hiragi C de O, et al. Evaluation of gene polymorphisms in exercise-induced oxidative stress and damage. Free Radic Res, 2010; 44(3):322–31.

Baumert P, Lake MJ, Stewart CE, Drust B, Erskine RM. Genetic variation and exercise-induced muscle damage: implications for athletic performance, injury and ageing. Eur J Appl Physiol, 2016; 116(9):1595–625.

Sprouse C, Gordish-Dressman H, Orkunoglu-Suer EF, Lipof JS, Moeckel-Cole S, Patel RR, et al. SLC30A8 Nonsynonymous Variant Is Associated With Recovery Following Exercise and Skeletal Muscle Size and Strength. Diabetes, 2014; 63(1):363–8.

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