Objective To study the relationship between single nucleotide polymorphism (A79G) and (T109C) in the second exon of the myoglobin gene and exercise-induced muscle damage. Methods Eighty-five soldiers of CAPF performed a strenuous weight-loading exercise and the time course of serum creatine kinase (CK) activity was measured. Myoglobin gene polymorphism was detected by polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) method. Association between resting CK (CKpre), maximal CK (CKpeak), maxiaml changes in CK (△CK) and gene polymorphism was then analysed. Results The activity of CK [CKpre: (145±33) U/L] gradually increased at 24 h after strenuous exercise and reached peak value at 72 h[CKpeak: (2972±1648) U/L], which then slowly reduced, but still higher than rest level at 120 h. The genotype frequencies (AA=54.1%, AG=40.0%, GG=5.9%) and allele frequencies (A=74.1%, G=25.9%) were coincident with Hardy-Weinberg equilibrium. Compared between groups, CKpre, CKpeak and △CK in (AG+GG)-group were all higher than those in AA genotype group (all P<0.01). Conclusions The single nucleotide polymorphism (A79G) in the second exon of the myoglobin gene might contribute to susceptivity of exercise-induced muscle damage. Subjects with G allele have increased risk for developing muscle damage, whereas AA genotype may have protective effects.
Key words
myoglobin /
gene polymorphism /
exercise-induced muscle damage /
creatine kinase /
subclinical exertcise rhabdomyolysis
{{custom_sec.title}}
{{custom_sec.title}}
{{custom_sec.content}}
References
[1] Kenney K, Landau M E, Gonzalez R S, et al. Serum creatine kinase after exercise: drawing the line between physiological response and exertional rhabdomyolysis[J]. Muscle Nerve, 2012,45(3):356-362.
[2] Heled Y, Bloom M S, Wu T J, et al. CK-MM and ACE genotypes and physiological prediction of the creatine kinase response to exercise[J]. J Appl Physiol, 2007,103(2):504-510.
[3] Alpers J P, Jones L K Jr. Natural history of exertional rhabdomyolysis: a population-based analysis[J]. Muscle Nerve,2010,42(4): 487-91.
[4] Galvez R, Stacy J, Howley A. Exertional rhabdomyolysis in seven division-1 swimming athletes[J]. Clin J Sport Med, 2008,18(4):366-368.
[5] Landau M E, Kenney K, Deuster P, et al. Exertional rhabdomyolysis: a clinical review with a focus on genetic influences[J]. J Clin Neuromuscul Dis, 2012,13(3):122-136.
[6] Johlig L, Valberg S J, Mickelson J R, et al. Epidemiological and genetic study of exertional rhabdomyolysis in a Warmblood horse family in Switzerland[J]. Equine Vet J, 2011,43(2):240-245.
[7] 刘 杰, 骆 媛, 钱远宇, 等. 运动性横纹肌溶解高反应者ACE/CK-MM基因多态性分析[J]. 山东医药, 2009,49(26):21-23.
[8] Devaney J M, Hoffman E P, Gordish-Dressman H, et al. IGF-II gene region polymorphisms related to exertional muscle damage[J]. J Appl Physiol, 2007,102(5):1815-1823.
[9] 杨贤罡, 李燕春, 胡 扬. ACTN3基因R577X多态性与运动能力的关联性研究:Meta分析[J]. 体育科学, 2011,31(3):44-52.
[10] Yamin C, Duarte J A, Oliveira J M, et al. IL6 (-174) and TNFA (-308) promoter polymorphisms are associated with systemic creatine kinase response to eccentric exercise[J]. Eur J Appl Physiol, 2008,104(3):579-586.
[11] Hubal M J, Devaney J M, Hoffman E P, et al. CCL2 and CCR2 polymorphisms are associated with markers of exercise-induced skeletal muscle damage[J]. J Appl Physiol, 2010,108(6):1651-1658.
[12] 吴 剑, 胡 扬, 包大鹏. 中国北方汉族人群肌红蛋白基因第2外显子多态性的研究[J]. 首都体育学院学报, 2009,21(3):346-348.
[13] 吴 剑, 胡 扬, 刘 刚, 等. 肌红蛋白基因多态与有氧训练效果的关联性分析[J]. 中国运动医学杂志, 2005,24(6):650-654.
(2012-09-17