|Stuart Phillips, PhD|
Location: Ivor Wynne Centre, Room E210
The maintenance of a metabolically active skeletal muscle mass is to a great extent underappreciated, particularly where optimal health is concerned. Skeletal muscle, besides its obvious role in locomotion, is a highly important thermogenic (i.e., energy consuming) tissue and the prime determinant of our basal metabolic rate, which for most of us is the largest single contributor to daily energy expenditure. Hence, declines in skeletal muscle mass can lead to increases in body fat mass. Because of its oxidative capacity (i.e., mitochondrial content) skeletal muscle is also a large site of fat oxidation, potentially playing a role in maintaining lipoprotein (cholesterol) and triglyceride homeostasis. Skeletal muscle is also, mostly by virtue of its mass, the primary site of blood glucose disposal; hence, maintaining skeletal muscle mass would also play a role in reducing risk for development of type II diabetes. Finally, the decline in maximal aerobic capacity with age, and with other muscular wasting conditions, including weight loss, has also been found to be due, to a large degree, to a decline in skeletal muscle mass and skeletal muscle quality. My research program has at its centre the following research question, what factors serve to maintain, increase, or decrease skeletal muscle mass? In addition, my research does not only address the absolute mass of skeletal muscle, but also its quality as assessed by the quantity of force it can generate, but also by the metabolic activity of various enzymes and energy consuming pathways.
We use a human model of resistance or aerobic exercise, immobilization, or aging to study the processes that govern: muscle accretion, in the case of resistance exercise; atrophy, in the case of immobilization; and sarcopenia, in the case of aging. In addition, my research group has studied the interaction of feeding different protein composition and varied meal timing on the processes regulating hypertrophy and disuse atrophy. We employ stable isotope tracers of amino acids to metabolically trace the fate of ingested proteins. Muscle biopsies provide us with mechanistic information regarding processes that regulate protein accretion and degradation. We use Western blotting, RT-PCR, histological, and immunohistochemical methods to examine these mechanisms. I am also very interested in conditions in which muscle wasting occurs, particularly in the elderly.
S.M. Phillips. The science of muscle hypertrophy: making dietary protein count. Proc. Nutr. Soc. 70(1): 100-103, 2011.
D.W. West and S.M. Phillips. Anabolic processes in human skeletal muscle: restoring the identities of growth hormone and testosterone. Phys. Sportsmed. 38(3): 97-104, 2010.
E.I. Glover, S.M. Phillips. Resistance exercise and appropriate nutrition to counteract muscle wasting and promote muscle hypertrophy. Curr. Opin. Clin. Nutr. Metab. Care. 13(6): 630-634, 2010.
D.W. West, N.A. Burd, A.W. Staples, and S.M. Phillips. Human exercise-mediated skeletal muscle hypertrophy is an intrinsic process. Int J Biochem Cell Biol. 42(9): 1371-1375, 2010.
S.M. Phillips and R.A. Winett. Uncomplicated resistance training and health-related outcomes: evidence for a public health mandate. Curr. Sports Med. Rep. 9(4):208-13, 2010.
B.R. Oates, E.I. Glover, D.W. West, J.L. Fry, M.A. Tarnopolsky, and S.M. Phillips. Low volume resistance exercise attenuates the decline in strength and muscle mass with immobilization. Muscle Nerve. 42(4): 539-546, 2010.
A.R. Josse, S.S. Sherriffs, A.M. Holwerda, R. Andrews, A.W. Staples, and S.M. Phillips. Effects of capsinoid ingestion of energy expenditure and lipid oxidation at rest and during exercise. Nutr. Metab. (Lond). 7(1):65, 2010.
N.A. Burd, D.W.D. West, A.W. Staples, P.J. Atherton, J.M. Baker, D.R. Moore, A.M. Holwerda, G. Parise, M.J. Rennie, S.K. Baker, and S.M. Phillips. Low-load high volume resistance exercise stimulates muscle protein synthesis more than high-load low volume resistance exercise in young men. PLoS One. 5(8): e12033, 2010.
N.A. Burd, A.M. Holwerda, K.C. Selby, D.W. West, A.W. Staples, N.E. Cain, J.G. Cashaback, J.R. Potvin, S.K. Baker, S.M. Phillips. Resistance exercise volume affects myofibrillar protein synthesis and anabolic signalling molecule phosphorylation in young men. J. Physiol. 588(16): 3119-3130, 2010.
K.R. Howarth, S.M. Phillips, M.J. MacDonald, N.A. Moreau, and M.J. Gibala. Effect of glycogen availability on human skeletal muscle protein turnover during exercise and recovery. J. Appl. Physiol. 109(2): 431-438, 2010.
A.R. Josse, J.E. Tang, M.A. Tarnopolsky, and S.M. Phillips. Body composition and strength changes in women with milk and resistance exercise. Med. Sci. Sports Exerc. 42(6): 122-1130, 2010.
R. Lee, D.W. West, S.M. Phillips, and P. Britz-McKibbin. Differential metabolomics for quantitative assessment of oxidative stress with strenuous exercise and nutritional intervention: thiol-specific regulation of cellular metabolism with N-acetyl-L-cysteine pretreatment. Anal. Chem. 82(7): 2959-2968, 2010.
E.I. Glover, N. Yasuda, M.A. Tarnopolsky, A. Abadi, and S.M. Phillips. No increase in markers for protein breakdown or oxidative stress in humans with short-term limb immobilization. Appl. Physiol. Nutr. Metab. 35(2): 125-133, 2010.
M. Robinson, J. Richards, M. Hickey, D.R. Moore, S.M. Phillips, C. Bell, and B. Miller. Acute b-adrenergic stimulation does not alter mitochondrial protein synthesis or markers of mitochondrial biogenesis in adult men. Am. J. Physiol. Reg. Int. Comp. Physiol. 298(1): R25-R33, 2010.
D.W. West, N.A. Burd, J.E. Tang, D.R. Moore, A.W. Staples, A.M. Holwerda, S.K. Baker, and S.M. Phillips. Elevations in ostensibly anabolic hormones with resistance exercise enhance neither training-induced muscle hypertrophy nor strength of the elbow flexors. J. Appl. Physiol. 108(1): 60-67, 2010.
Kinesiol 3Y03 - Human Nutrition & Metobolism