Abstract
Myostatin A55T genotype is one of the candidates showing inter-individual variation in skeletal muscle phenotypes. The aim of this study was to investigate the effect of the myostatin A55T genotype on markers of muscle damage after eccentric exercise. Forty-eight young, healthy male college students (age = 24.8 ± 2.2 years, height = 176.7 ± 5.3 cm, weight = 73.7 ± 8.3 kg) were enrolled in this study, and muscle damage was induced through 50 reps of maximal eccentric muscle contraction. As markers of muscle damage, maximal isometric strength (MIS), muscle soreness, creatine kinase (CK), and aspartate transaminase (AST) were measured. Myostatin A55T genotypes were classified into homozygous myostatin A55T allele (AA, n = 34, 72%), heterozygous myostatin A55T allele (AT, n = 13, 26%), and homozygous mutant carriers (TT, n = 1, 2%). After eccentric exercise, the subjects with heterozygous for AT showed markedly quicker MIS recovery compared to the AA group (p = 0.042). However, there were no significant variations in muscle soreness (p = 0.379), CK (p = 0.955), and AST (p = 0.706) among the groups. These results suggest that AT in myostatin A55T genotype may be associated with quicker strength recovery following exercise-induced muscle damage.
Highlights
Repetitive, high-intensity, eccentric muscle contractions cause muscle damage [1]
These results suggest that AT in myostatin A55T genotype may be associated with quicker strength recovery following exercise-induced muscle damage
According to a number of studies, there is an inter-individual variation in the response of muscle damage that appears after eccentric exercise, which has been reported to be affected by age, sex, body composition, training status, and genetic polymorphism, etc. [6,7,8,9,10]
Summary
Repetitive, high-intensity, eccentric muscle contractions cause muscle damage [1]. It produces muscle disruption and excitation–contraction coupling gets impaired, and inflammation and muscle protein degradation occurs [2,3]. According to a number of studies, there is an inter-individual variation in the response of muscle damage that appears after eccentric exercise, which has been reported to be affected by age, sex, body composition, training status, and genetic polymorphism, etc. Myostatin, which is known as growth/differentiation factor-8 (GDF-8), is one of the tumor growth factor (TGF-β) superfamily [14]. Myostatin is known to combine with activin type IIB (ACVR2B)
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