Show simple item record

dc.contributor.authorChild, R. B.
dc.date.accessioned2010-04-15T13:42:30Z
dc.date.available2010-04-15T13:42:30Z
dc.date.issued1997
dc.identifier.urihttp://hdl.handle.net/2436/96616
dc.descriptionA thesis submitted in partial fulfilment of the requirements of the University of Wolverhampton for the degree of Doctor of Philosophy
dc.description.abstractThis thesis reports five novel studies investigating exercise and free radical induced damage to human skeletal muscle, with a review of related literature. It has been proposed muscle adapts to eccentric exercise by increasing its resting length. The first study investigated the effects of manipulating knee extensor (KE) length during eccentric actions, on indices of muscle damage and knee angle specific force production. This study provided evidence that exercise performed at a long muscle length increased the damage susceptibility of the KE muscles, and produced a transient increase in muscle length. Investigations using animals suggest the generation of high muscle forces contributes to initial injury. Surprisingly this effect has not been studied using a well controlled methodology in humans. The second investigation manipulated peak force during eccentric actions, using electrical myostimulation, and provided evidence that peak force was an important mechanical factor in initial muscle injury. In rodents, exercise myopathy can compromise muscle antioxidant status, possibly resulting in free radical mediated injury. The third study investigated if these events occurred in human muscle, following eccentric exercise. Muscle myopathy did not compromise muscle antioxidant status or elevate lipid peroxidation indices 4 days and 7 days after exercise, suggesting free radicals did not contribute to muscle damage at these times. In the previous study functional measures were not collected in the days following exercise and biochemical data were not collected in the 2 days following exercise. Therefore the fourth study evaluated indices of muscle damage and lipid peroxidation indices in blood, to determine if free radicals might contribute to delayed indices of muscle damage. Evidence of increased lipid peroxidation in the first 2 days after exercise, suggest free radicals might contribute to delayed muscle damage. The effects of high intensity aerobic exercise on serum antioxidant capacity have not been reported previously. The final study showed running a half marathon increased serum antioxidant capacity, although this did not prevent lipid peroxidation or myocellular and lysosomal enzyme release.
dc.formatapplication/pdf
dc.language.isoen
dc.publisherUniversity of Wolverhampton
dc.titleExercise and free radical induced damage to human skeletal muscle
dc.typeThesis or dissertation
dc.type.qualificationnamePhD
dc.type.qualificationlevelDoctoral
rioxxterms.licenseref.urihttps://creativecommons.org/licenses/by-nc-nd/4.0/
refterms.dateFOA2020-05-04T08:45:13Z
html.description.abstractThis thesis reports five novel studies investigating exercise and free radical induced damage to human skeletal muscle, with a review of related literature. It has been proposed muscle adapts to eccentric exercise by increasing its resting length. The first study investigated the effects of manipulating knee extensor (KE) length during eccentric actions, on indices of muscle damage and knee angle specific force production. This study provided evidence that exercise performed at a long muscle length increased the damage susceptibility of the KE muscles, and produced a transient increase in muscle length. Investigations using animals suggest the generation of high muscle forces contributes to initial injury. Surprisingly this effect has not been studied using a well controlled methodology in humans. The second investigation manipulated peak force during eccentric actions, using electrical myostimulation, and provided evidence that peak force was an important mechanical factor in initial muscle injury. In rodents, exercise myopathy can compromise muscle antioxidant status, possibly resulting in free radical mediated injury. The third study investigated if these events occurred in human muscle, following eccentric exercise. Muscle myopathy did not compromise muscle antioxidant status or elevate lipid peroxidation indices 4 days and 7 days after exercise, suggesting free radicals did not contribute to muscle damage at these times. In the previous study functional measures were not collected in the days following exercise and biochemical data were not collected in the 2 days following exercise. Therefore the fourth study evaluated indices of muscle damage and lipid peroxidation indices in blood, to determine if free radicals might contribute to delayed indices of muscle damage. Evidence of increased lipid peroxidation in the first 2 days after exercise, suggest free radicals might contribute to delayed muscle damage. The effects of high intensity aerobic exercise on serum antioxidant capacity have not been reported previously. The final study showed running a half marathon increased serum antioxidant capacity, although this did not prevent lipid peroxidation or myocellular and lysosomal enzyme release.


Files in this item

Thumbnail
Name:
Child_PhDthesis.pdf
Size:
14.48Mb
Format:
PDF

This item appears in the following Collection(s)

Show simple item record

https://creativecommons.org/licenses/by-nc-nd/4.0/
Except where otherwise noted, this item's license is described as https://creativecommons.org/licenses/by-nc-nd/4.0/