AbstractIndices of human skeletal muscle damage and connective tissue breakdown were studied following eccentric and concentric muscle contractions of the knee extensors (KE). Electrically stimulated eccentric contractions of the KE induced delayed onset muscle soreness (DOMS), a delayed increase in serum creatine kinase (CK) activity, and disruption of muscle function. KE maximum isometric contraction force (MVC), MVC with superimposed myostimulation, and muscle force-frequency characteristics (20: 100 Hz stimulated force ratio) were impaired for up to 3 days post exercise. Increased delays in excitationcontraction (E-C) coupling were observed immediately post exercise and on day 3 post exercise. Unaltered contraction and relaxation kinetics suggested that the sarcoplasmic reticulum was not the site of E-C coupling delays. Prior 'conditioning' eccentric exercise bouts of varying duration were used to examine skeletal muscle adaptation to a subsequent bout of 50 eccentric repetitions. All initial bouts (10,30, and 50 repetitions) induced DOMS, a decline in MVC, and reduced 20: 100 Hz stimulated force ratio. Initial bouts of 30 and 50 repetitions elevated serum CK activity (peak activities recorded on day 3 post exercise). The response of these indirect indices of muscle damage appeared to be exercise duration dependent. All initial bouts reduced the soreness associated with the second bout, and no increases in CK were recorded following the second bout. Thus, skeletal muscle adaptation could be induced by a single bout of relatively few eccentric contractions, and increasing prior bout duration did not secure an increased prophylactic effect. Indirect indices of collagen breakdown (serum type 1 collagen concentration and plasma hydroxyproline) following concentric and eccentric exercise protocols indicated that connective tissue breakdown may accompany eccentric exercise-induced muscle damage. Further analysis of collagen breakdown products in urine (pyridinoline, hydroxyproline, and hydroxylysine) indicated that connective tissue may be injured following unaccustomed eccentric exercise. Although mechanisms initiating collagen breakdown could not be determined, it was suggested that a localised accumulation of collagen breakdown products following eccentric exercise may initiate further connective tissue breakdown via the provocation of inflammatory cell margination into the muscle endomysium and perimysium. The susceptibility of untrained human skeletal muscle to eccentric exercise-induced damage has been demonstrated. Also, evidence of collagen breakdown following eccentric muscle contractions has been reported. Further work on the mechanisms of muscle connective injury during and after exercise is required.
PublisherUniversity of Wolverhampton
TypeThesis or dissertation
DescriptionA thesis submitted in partial fulfilment of the requirements of the University of Wolverhampton for the degree of Doctor of Philosophy
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