It is a very common physical response that your muscles become sore after playing sports or doing a strenuous workout. Workouts requiring considerable physical effort often result in muscle damage, but in most cases, muscle damage isn’t a serious health issue. However, excessive muscle damage can cause the release of significant levels of intracellular components into the bloodstream, leading to rhabdomyolysis. Scientists typically look at myoglobin, creatine kinase, lactate dehydrogenase, and aspartate aminotransferase to track muscle proteins and muscle damage. Some investigations have reported increased muscle protein serum levels during ultra-endurance events.
Previous studies have demonstrated that the ACTN3 R577X gene polymorphism, more specifically the TT genotype of rs1815739, influences the extent of muscle damage after eccentric exercise (or slow muscle lengthening exercises). After an eccentric training session, higher muscle protein serum levels and higher pain scores were observed in polymorphism carriers than noncarriers. The ACTN3 gene encodes for the alpha-actinin-3 protein, and the C→T transition at rs1815739 causes a complete protein deficiency. People who have the variant are approximately 20% of the population worldwide. This deficiency does not cause muscle disease but results in differences in skeletal muscle function, including lower muscle strength. ACTN3 is one of the major components muscle fibers (the Z type specifically) and is responsible for key actions Therefore, as Z-disks are the structures most vulnerable to muscle damage, it is plausible that ACTN3 deficiency can interfere with muscle contraction.
Researchers hypothesized that ultrarunners with ACTN3 deficiency (TT genotype of rs1815739) could experience more muscle damage during an ultra-endurance competition based on the findings reported so far. Volunteers for this study included twenty moderately to well-trained ultra-runners who had entered into an official 37.1 km adventure race, more specifically the fourth race of the Hapa Race series consisting of 22.1 km mountain biking, 10.9 km trekking, 4.1 km water trekking, 30 m rope course, and orienteering. Blood samples were collected for genotyping and analysis of muscle protein levels before and after the race. Percentage changes between pre- and post-race for serum myoglobin, creatine kinase, lactate dehydrogenase, and aspartate aminotransferase were significantly greater for those with the TT genotype than those with either the TC or CC genotypes. In addition, further analysis confirmed a larger amount of muscle damage in ultra-runners with the TT genotype. Therefore, athletes with the rs1815739 TT genotype experienced muscle damage after an adventure race.
In conclusion, the initial results of this pilot study strongly suggest pronounced muscle damage in athletes with the TT genotype of rs1815739 who compete in ultra-endurance races. This supports the concept that an important gene variation of the ACTN3 locus contributes to susceptibility to exercise-induced muscle damage. Although further research is required in larger population groups, the findings presented here are novel and clinically relevant. It suggests that ultra-runners with an alpha-actinin-3 deficiency may be more susceptible to rhabdomyolysis and associated health complications during ultra-endurance competitions. Furthermore, polymorphism carriers may also require a longer time for recovery than noncarriers after a race. Read more about the study here:
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