My primary research aim is to understand the mechanisms by which both different intensities and different types of exercise improve mitochondrial function. In addition, I am interested in the impact that these improvements in mitochondrial function have in both health and disease. My research is currently has 3 main goals. First, to quantify the intensities of various different types of exercise across a range of skill and fitness levels. Second, to examine changes in both whole body fitness and mitochondrial function following exercise training of differing types and intensities and how these changes differ between active, sedentary, and overweight/obese young adults. Third, to elucidate the molecular mechanisms underlying exercise induced mitochondrial biogenesis, specifically, to explore post-translational regulation of PGC-1alpha following exercise. It is hoped that this research will help increase our understanding of the mechanisms by which exercise can improve health and the optimal intensities and types of exercise to activate these mechanisms.
Currently seeking master's and doctoral students to commence studies in September 2011.
Gurd B.J., Perry, C.G.R., Heigenhauser, G.J.F., Spriet, L.L. & Bonen, A (2010) High-intensity interval training increases SIRT1 activity in human skeletal muscle. Appl. Physiol. Nut. & Metab. Accepted February 22, 2010.
Holloway G.P.*, Gurd B.J.*, Snook, L.A., Lally, J. and Bonen A (2010) Compensatory increases in nuclear PGC-1a protein are associated with subsarcolemmal mitochondrial adaptations in ZDF rats. Diabetes Epub. Jan 26. *Contributed equally to manuscript
Gurd B.J., Peters S.J., Heigenhauser G.J., LeBlanc P.J., Doherty T.J., Paterson D.H. and Kowalchuk J.M. (2009) Prior heavy exercise elevates pyruvate dehydrogenase activity and muscle oxygenation and speeds O2 uptake kinetics during moderate exercise in older adults. Am. J. Physiol. 297: R877-R884.
Gurd B.J., Yoshida Y., Lally J., Holloway G.P. and Bonen A. (2009) The deacetylase enzyme SIRT1 is not associated with oxidative capacity in rat heart and skeletal muscle and its overexpression reduces mitochondrial biogenesis. J. Physiol. 587: 1817-1828