Abstract
This study investigated whether the variability observed in the
markers of exercise-induced muscle damage (EIMD) has a genetic etiology.
Sixteen pairs of identical twins performed 24 maximal eccentric contractions
(24MAX) using the elbow flexors. EIMD indicators were measured pre-24MAX and
three days post-24MAX and included: post-exercise force deficit, maximal
isometric force (ISO), plasma creatine kinase (CK), myoglobin (Mb), and joint
range of motion. Force-time curves were recorded throughout the 24MAX. Twin
siblings were alike for pre-exercise ISO (intraclass
R = 0.89) and CK (R = 0.76)
(p < 0.001), but were discordant for post-exercise force
deficit (R = 0.29), CK (R = 0.15),
and Mb (R = 0.17) (p > 0.05). In
comparison with individuals minimally affected by the 24MAX, those who
experienced the greatest force deficit 3 days post-exercise
(> 50 %) were characterised by the greater application
of eccentric force at longer muscle lengths (23.1 % vs
17.3 %) (p < 0.05). This study demonstrates that
twins do not experience the same level of EIMD following identical exercise
bouts. This suggests that the individual variability following high-force
eccentric exercise cannot be attributed to genetic differences, refuting the
idea that an inherited subclinical predisposition is responsible. From these
results, a potential mechanism for the repeated bout effect is discussed.
Key words
Genetics - monozygous - muscle injury - force deficit - creatine kinase - repeated
bout effect
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Dr. J. Gulbin
Division of Sports Sciences/Sports Medicine · Australian
Institute of Sport
PO Box 176 · Belconnen ACT 2616 · Australia
·
Phone: (+61) 2 6214 1619
Fax: (+61) 2 6214 1603
Email: gulbinj@ausport.gov.au
