Date of Award

2000

Degree Type

Thesis

Degree Name

Master of Science

School

School of Biomedical and Sport Science

Faculty

Faculty of Communications, Health and Science

First Advisor

Dr. Paul Sacco

Second Advisor

Dr. Colin James

Abstract

Exercise-induced muscle damage (EIMD) is known to be produced by novel or unaccustomed exercise, especially high force eccentric contractions. Histological myofibre disruption, force loss and muscle soreness are associated with EIMD and have implications for sporting performance. Traditional practices of assessing the extent of disruption to the myofibres is by performing needle biopsies and subsequently analysing the histology of the fibres. Recently there has been interest in investigating whether changes in force production and contractile properties of muscle following damaging exercise correlate strongly with the magnitude of disruption to the myofibres. The main aim of this study was to investigate whether changes in force production and contractile properties of muscle following damaging eccentric exercise correlated with myofibre disruption. In order to test the hypotheses set down in the study 56 mice (C57 BU/10 strain) were randomly assigned to two groups (active and passive). Each main group was then divided into 5 subgroups. Anaesthetised mice performed either 120 active (eccentric contractions) or passive (no muscle contraction) lengthening repetitions after which they were allowed to recover. The right foot was fixed to a foot plate housing a force transducer which was directly attached to the axle of a stepping motor. A stimulating electrode was surgically placed around the peroneal nerve and P. and 1/ 150 Hz ratios were determined. Animals in the active group then performed 5 bouts of 24 stimulated lengthening repetitions at 0.3 amps with a stimulation frequency of IOO Hz. The passive group's protocol was identical with the exception that no stimulation was provided. One repetition for both active and passive groups consisted of a 300 millisecond plantar flexion movement of the foot plate and a 4.7 second dorsi flexion recovery movement to the starting position. Active and passive subgroups were terminated at 3, 6, 10, 15 and 20 days following exercise, prior to which P. and 1/ 150 Hz ratio were determined. Tibialis anterior (TA) muscles were excised at this time from both exercised and contralateral limbs and prepared for later histological examination. Significant differences were evident between the two groups for Po following each bout of 24 lengthening repetitions, 10 minutes following lengthening and on days 3 and 20 of recovery. The only significant differences between the groups in 1/ 150 Hz ratio occurred 10 minutes following lengthening and at day six of recovery (p<0.025). A weak significant correlation was recorded between normalized P. in the days following active lengthening and the magnitude of histological disruption to the TA muscle (r =-0.35; p<0.05). The major findings of this study were that a) there was a weak significant correlation between normalized P. in the days following damaging exercise, and the magnitude of histological disruption to the TA muscle, b) average normalized P. 10 minutes following damaging exercise does not seem to be a good predictor of the magnitude of histological disruption in the days following exercise, and c) The 1/ 150 Hz ratio immediately after, or in the days following damaging exercise does not seem to be a useful predictor of the magnitude of histological myofibre damage. Further investigation into any relationship between changes in P. following eccentric exercise and the magnitude of myofibre disruption at the same time points will help to establish whether the use of force measures are valid to predict the quantity of muscle damage.

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