Dr. Moore's laboratory is involved in determining
the cellular basis for alterations in intrinsic cardiac contractile
function in response to certain physiological (exercise training)
and pathophysiogical (advanced aging, heart failure) stresses.
A central focus of the laboratory is on myocardial Ca2+ regulation,
and processes that are thought to directly regulate and/or
modulate sarcoreticular and transarcolemmal Ca2+ movement.
Studies are ongoing to determine how aging and exercise training
affect myocardial sodium-calcium exchange, and the protein
expression and function of a variety of voltage-regulated
K+ channels. Another key area of interest is on the potential
roles of cardiac sarcolemmal and mitochondrial ATP-sensitive
K+ channels in exercise training-induced protection of the
heart against ischemia-reperfusion injury. Work in Dr. Moore's
laboratory is supported by grants from the NIH (National Institute
on Aging; National Heart, Lung, Blood Institute) and the American
Dr. Moore is a Professor of Kinesiology and Applied Physiology
and Medicine (Adjunct in Cardiology, UCHSC). He currently
serves an Associate Editor of the Journal of Applied Physiology
and Exercise and Sport Sciences Reviews. Since 1990, he has
served as both a regular and ad hoc grant reviewer for the
National Institutes of Health, American Heart Association,
National Sciences and Engineering Research Council (Canada).
Snyder, SM, BM Palmer, and RL Moore. A mathematical model
of cardiocyte Ca2+ dynamics with a novel representation of
sarcoplasmic reticular Ca2+ control. Biophysical J. 79(1):94-115,
Palmer, BM and RL Moore. Excitation wavelengths for fura
2 provide a linear relationship between [Ca2+] and fluorescence
ratio. Am. J. Physiol. Cell Physiol. 279:C1278-C1284, 2000.
Olsson, M.C. ,B.M. Palmer, L.A. Leinwand, and R.L. Moore.
Gender and aging in a transgenic model of hypertrophic cardiomyopathy.
Am.J.Physiol.:Heart Circ. Physiol., 280:H1136-H1144, 2001.
Jew, K.N., M.C. Olsson, E.A. Mokelke, B.M. Palmer, and R.L.
Moore. Endurance training alters outward K+ current characteristics
in rat cardiocytes. J. Appl. Physiol., 90:1327-1333, 2001.
Jew, K.N. and R.L. Moore. Glibenclamide improves post-ischemic
recovery of myocardial contractile function in trained and
sedentary rats. J. Appl. Physiol. 1545-1554, 2001.
Jew, K.N. and R.L. Moore. Exercise training alters an anoxia-induced,
glibenclamide-sensitive current in rat ventricular cardiocytes.
J. Appl. Physiol.. 92:1473-1479, 2002.