The influence of sex, patella tendon properties and the oral contraceptive pill on markers of exercise-induced muscle damage

Introduction: Exercise-induced muscle damage (EIMD) is an accepted consequence of eccentric exercise. Sex differences in EIMD are attributed to tendon properties, fascicle lengthening and direct hormonal influences, however these remain unreported in vivo. Furthermore, the classical definition of ec...

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Bibliographic Details
Main Author: Hicks, Kirsty-Marie
Published: Manchester Metropolitan University 2014
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Online Access:http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.644537
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Summary:Introduction: Exercise-induced muscle damage (EIMD) is an accepted consequence of eccentric exercise. Sex differences in EIMD are attributed to tendon properties, fascicle lengthening and direct hormonal influences, however these remain unreported in vivo. Furthermore, the classical definition of eccentric contractions omits the role of the elastic tendon in determining eccentric fascicle lengthening and subsequent EIMD. Aim: The overall aims of the current thesis were, to investigate the role of the patella tendon during eccentric contractions, to investigate whether muscle and tendon properties are determinants of EIMD and investigate group differences (sex and oral contraceptive (OCP)use) in EIMD. Materials and method: In brief, vastus lateralis (VL) and patella tendon properties were measured in males, females and female OCP users, using a combination of ultrasonography, electromyography and dynamometry. During maximal voluntary eccentric knee extensions ((MVEKE) 12 reps × 6 sets), VL fascicle lengthening and MVEKE torque was recorded every 10 of knee joint angle (20 - 90). Maximal isometric voluntary knee extensor (MVCKE) torque loss, creatine kinase (CK) and muscle soreness were measured pre, post, 48, 96 and 168 hours post damage as markers of EIMD. Main findings: Patella tendon properties appear to act as a mechanical buffer on VL fascicle lengthening during MVEKE in vivo. Furthermore, due to significantly higher patella tendon stiffness, VL fascicle lengthening was significantly greater in males compared to females. Despite evidencing an attenuating role of the patella tendon on VL fascicle lengthening, patella tendon properties did not correlate with any indirect markers of EIMD, nor did they explain group differences in EIMD. Furthermore, MVEKE torque, MVEKE torque made relative to estimated total quadriceps anatomical cross-sectional area and VL fascicle lengthening did not correlate with any functional indirect marker of EIMD, nor did they explain group differences in EIMD. Within the current thesis CK was the only indirect marker of EIMD to be significantly different between the groups (males > females < OCP users). Creatine kinase was consistently lower in the groups with lower circulating oestrogen levels. Therefore, it was concluded that the antioxidant and membrane stabilising role of oestrogen might explain the group differences in CK reported in the current thesis. Conclusion: In agreement with the historical definition, VL fascicles lengthen during MVEKE. Furthermore, it is evident from the current thesis that patella tendon properties determine the magnitude of VL fascicle lengthening during MVEKE, but do not appear to explain the variability or group differences in EIMD.