Human Exercise Endocrinology
The overall research aim is to generate knowledge about the physiological mechanisms by which exercise has a role in the prevention of disease. The particular emphasis is in the modifying role of exercise on the pathophysiological states which are part of the metabolic syndrome cluster, that is hypercholesterolemia, hypertension and obesity. Abnormal endocrinological (hormonal) patterns implicated in the development of the metabolic syndrome are identified and the impact of exercise in the reversal of the endocrine abnormalities is investigated. It is predicted that this information will provide clues to the initial abnormal physiological axis by which the pathophysiology is triggered.
Current Projects
1. The identification of abnormal baseline levels of circulating vasoactive agents in young normotensive offspring with a family history of hypertension
It is thought that vascular and hormonal changes occur well before an increase in high blood pressure. It is well established that endothelial dysfunction (that is the inability to vasodilate normally) already exists in young people who still have a normal blood pressure but also have a family history of hypertension. The aim of the project is to identify any abnormal endocrinology in plasma samples taken from offspring of hypertensives at rest. This information will provide information as to the initial abnormal physiological triggers which may cause/contribute to endothelial dysfunction and the future development of hypertension.
Collaboration: A/Prof Steve Boutcher
Funding support: This project is supported by a $20,000 UNSW Faculty Grant.
2. The identification of abnormal levels of circulating vasoactive agents during stress in young normotensive offspring with a family history of hypertension
 | This project follows from (a) above. It has been shown by Boutcher and colleagues that offspring of hypertensives have a hyper-reactive physiological response to daily stress. A continual state of hyper-responsiveness may contribute to the future pathophysiological state of hypertension. The aim of the project is to identify any abnormal endocrinology in plasma samples taken from offspring of hypertensives during a computerized color-coded word task which is stressful. This information will provide information on abnormal endocrinological pathways which may cause/contribute to endothelial dysfunction and the future development of hypertension. |
Collaboration: A/Prof Steve Boutcher, Dr. Yati Boutcher
Honors student: Mr Kaimin Huang
3. The effect of aerobic exercise on abnormal patterns of vascular endocrinology in offsprings of hypertensives.
This project follows from (a) and (b) above. It has been shown that regular aerobic exercise improves the ability of the arteries and arterioles to stretch (ie. improves endothelial dysfunction). The aim of the project is to show that regular aerobic exercise improves vascular abnormalites as measured by endocrinological disturbances. The study aims to demonstrate that any endrocrinological abnormalities already identified in young people with a family history of hypertension at rest or during stress can be reversed with regular aerobic exercise.
Collaboration: This project is part of a larger project in collaboration with A/Prof Steve Boutcher, A/Prof Abert Avolio and Dr. Yati Boutcher
Funding: This project has been selected for interview for funding with the National Heart Foundation.
4. The effect of lipid-lowering agents on fat metabolism during exercise in dyslipidemic individuals
Previous studies in healthy volunteers have shown that some lipid-lowering agents can interfere with fat metabolism during aerobic exercise. We aim to establish whether a similar impairment in fat metabolism also exists during exercise in a clinical population who have dyslipidemia and are taking lipid-lowering drugs. If so, does this impairment contribute to premature fatigue in these patients during exercise? Which lipid-lowering drugs are more compatible with exercise? How can we modify recommendations of fuel intake pre-, during and post exercise to minimize the effects of premature fatigue in these patients?
Collaboration: Dr Ross Grant (UNSW and The Australiasian Research Institute)
Selected Publications
Matuszek, M.A., Aristoteli, L.P., Bannon, P.G., Hendel, P.N., Hughes, C.F., Jessup, W., Dean, R.T. and Kritharides, L. (2003) Haptoglobin elutes from human atherosclerotic coronary arteries – a potential marker of arterial pathology. Atherosclerosis 168, 389-396.
Matuszek, M.A. and Burcher, E. (2002) Smooth muscle, neurons and interstitial cells of guinea-pig ileum: are there tachykinin NK-1 receptor subtypes? Pharmacology 66, 61-67.
Matuszek, M.A., Comis, A. and Burcher, E. (1999) Binding and functional potency of neurokinin A analogues in the rat fundus: a structure-activity study. Pharmacology 58, 227-235.
Matuszek, M.A., Zeng, X-P., Strigas, J and Burcher, E. (1998) An investigation of tachykinin NK-2 receptor subtypes in the rat. European Journal of Pharmacology 352, 103-109.
Matuszek, M.A., Hodgson, W.C., Sutherland, S.K. & King, R.G. (1994) Pharmacological studies of the venom of an Australian Bulldog ant (Myrmecia pyriformis). Natural Toxins 2, 36-43.
Matuszek, M.A., Hodgson, W.C., King, R.G. and Sutherland, S.K. (1994) Some enzymic activities of two Australian ant venoms: a jumper ant Myrmecia pilosula and a bulldog ant Myrmecia pyriformis. Toxicon 32, 1543-1549.
Matuszek, M.A., Hodgson, W.C., Sutherland, S.K. & King, R.G. (1992) Pharmacological studies of Jumper ant (Myrmecia pilosula) venom: evidence for the presence of histamine, and haemolytic and eicosanoid-releasing factors. Toxicon 30, 1081-1091.