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Please use this identifier to cite or link to this item: http://hdl.handle.net/11375/24767
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dc.contributor.advisorPhillips, Stuart-
dc.contributor.authorMorton, Robert William-
dc.date.accessioned2019-09-04T19:08:28Z-
dc.date.available2019-09-04T19:08:28Z-
dc.date.issued2019-
dc.identifier.urihttp://hdl.handle.net/11375/24767-
dc.description.abstractResistance exercise training (RET) can lead to muscle hypertrophy; however, the relative contribution that exogenous (protein supplementation and specific training variables) versus endogenous (biology inherent to the individual) factors have on RET-induced muscle hypertrophy is controversial. In Study 1, we provided an evidence-based conclusion that protein supplementation during periods of RET results in a small but statistically significant increase in RET-induced muscle hypertrophy. In Study 2, we corroborate previous research and observed that the amount of mass lifted per repetition (load) did not determine RET-induced muscle hypertrophy in resistance-trained men when RET was performed to volitional fatigue. In Study 4, we observed similar muscle fibre activation following resistance exercise with lighter versus heavier loads when both were lifted until volitional fatigue. In Studies 2 and 3, we observed no relationship between circulating anabolic hormones (e.g., testosterone) and RET-induced muscle hypertrophy. Nonetheless, in Study 3, we found significantly greater muscle androgen receptor content in the top versus the bottom quintile of respondents for muscle hypertrophy following 12 weeks of RET indicating that androgen receptor content, and not circulating androgen concentration, may be an important determinant of hypertrophy. Finally, in Study 5, we observed that RET-induced muscle hypertrophy was an consistent within an individual (independent of load and limb) but considerably different between participants. Together, these data suggest that the exogenous factors we studied – protein supplementation and load (when RET was performed to volitional fatigue) – had a relatively small influence on RET-induced muscle hypertrophy. In contrast, we found that endogenous variables, such as intramuscular androgen receptor content and likely other genetic influences, appear to contribute more to the significant heterogeneity seen in RET-induced muscle hypertrophy. Future research in this area should prioritize understanding the biology that underpins the individual variability in RET-induced muscle hypertrophy.en_US
dc.language.isoenen_US
dc.subjectresistance exerciseen_US
dc.subjectskeletal muscleen_US
dc.subjecthypertrophyen_US
dc.subjectstrengthen_US
dc.subjecttestosteroneen_US
dc.titleResistance exercise-induced muscle hypertrophyen_US
dc.title.alternativeEndogenous and exogenous factors and their influence on resistance exercise training-induced muscle hypertrophyen_US
dc.typeThesisen_US
dc.contributor.departmentKinesiologyen_US
dc.description.degreetypeThesisen_US
dc.description.degreeDoctor of Philosophy (PhD)en_US
dc.description.layabstractResistance exercise training (RET) increases muscle size (hypertrophy); however, the relative influence that protein supplementation, specific training variables, and individual (genetic) variation have on the RET-induced hypertrophy is controversial and largely unknown. Broadly, data in this thesis show that protein supplementation slightly augments RET-induced hypertrophy, and that the magnitude of RET-induced hypertrophy may be related to the number of androgen (e.g., testosterone) receptors inside an individual’s muscle. In contrast, we found that neither load nor hormones affect RET-induced hypertrophy. Interestingly, data in this thesis also show that RET-induced hypertrophy is consistent within an individual but varies considerably between people, which illustrates the greater influence that individual variation has on RET-induced hypertrophy. We conclude that when RET is performed with a high degree of effort, protein supplementation and specific training variables confer a relatively small benefit on RET-induced hypertrophy compared to the influence of biological variability between people.en_US
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