Date of Award

2005

Degree Type

Thesis

Degree Name

Bachelor of Science Honours

Faculty

Faculty of Computing, Health and Science

First Advisor

Dr Melanie Ziman

Abstract

High force eccentric muscle actions, during forcibly lengthening contracting muscle, have been found to produce pronounced muscle damage, especially if exercise is unaccustomed. A cascade of events is initiated in order to repair damaged skeletal muscle tissue including degeneration and regeneration processes. For the duration of muscle regeneration, satellite cells are the primary source of new myoblasts in adult muscle. This process requires activation of quiescent mononucleated satellite cells which proliferate, differentiate and fuse together to form fully functional muscle fibres. The satellite cells are specified by the gene, Pax7, during development. Experimental studies of Pax7 null mice that lack the Pax7 gene revealed that after birth there is little or no skeletal muscle growth or regeneration. Recently polymorphic repeats have been determined within the promoter and intronic regions of the human P AX7 gene. The promoter polymorphism has been shown to alter the transcription efficiency of this promoter in vitro. It is of great interest to note that efficiency of repair of muscle damage varies considerably between individuals. This leads to a conclusion that variation in Pax7 polymorphic sequences between individuals could affect skeletal muscle regeneration by virtue of the crucial role of Pax 7 in satellite cell specification. We have measured allelic variation of Pax7 (promoter and intronic) in population groups and in volunteers undergoing forced exercise induced damage. Preliminary data suggests that there is a significant variation in allele frequencies between the study population groups. With respect to promoter polymorphisms, there is a trend toward high responders being associated with allele 8 (8 CCT repeats) and a trend towards low responders being associated with allele 11 (11CCT repeats). On the other hand, allelic variation with respect to the P AX7 intronic polymorphism cannot explain the observed differences in recovery of force following damage by eccentric exercise.

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