Professor, Chair of Exercise Physiology
Professor, Chair of Exercise Physiology
Human Performance - Exercise Physiology (SOM)
Joint Professor of Physiology and Pharmacology
Physiology & Pharmacology (SOM)
Medical Sciences-Neuroscience, McMaster University. Hamilton, Ontario, Canada L8N 3Z5 Ph.D. ,
Physiology, McMaster University, Hamilton, Ontario, Canada L8S 4K1,
Kinesiology (Honors BS), University of Waterloo, Waterloo, Kinesiology, Ontario,
A Personal Statement
I have a broad background in muscle biology obtained during graduate and postdoctoral training and subsequently as a PI. I was able to establish a role of skeletal fiber proliferation in adult muscle responses to overload. While this finding was initially contrary to the dogma that had been established in muscle biology, our subsequent studies were verified by several other labs, and highlights the plasticity of skeletal muscle to use and to disuse. In our studies we identified clear roles for satellite cell dysfunction as mediating at least in part, the reduced proliferation of muscle fibers in aged animals. As a NIH/NIA funded PI at the Ohio State University and the University of South Florida, I examined aging-induced changes in muscle structure and function and remodeling in skeletal muscle, and satellite cells under loading and wasting conditions (e.g., hindlimb suspension, sarcopenia, and denervation). As an NIH/NIA funded PI at my current institution, I have studied apoptotic signaling and mitochondria function in muscle wasting including the models of hindlimb suspension, denervation and obesity. Our recent investigations have focused on the genetic regulation of Sirt1 activators (resveratrol) and epicatechin containing compounds as a means to reduce muscle wasting in aging. I successfully administered the funded projects (e.g. staffing, research protections, budget), collaborated with other researchers, and produced peer-reviewed publications from each project. Our lab has completed successful and productive research projects in the area of muscle biology and muscle atrophy, which is an area of high relevance for forced bed rest, spinal cord injury, glucocorticoids, cancer cachexia, or aging populations. We have shown an important role for Sirt1 and resveratrol, a Sirt1 activator on skeletal muscle in aging as listed below and the current proposal will examine the mechanisms by which Sirt1 regulates muscle mass and function in old mammals including humans.
- Mohamed JS, Wilson JC, Myers MJ, Sisson KJ and ALWAY, S.E. Dysregulation of SIRT-1 in aging mice increases skeletal muscle fatigue by a PARP-1-dependent mechanism. Aging (Albany NY) 6:1-15, 2014. PMID:25361036
- Bennett, BT, Mohamed, JD and ALWAY SE. Effects of resveratrol on the recovery of muscle mass and function following disuse in the plantaris muscle of aged rats. PLoS One 8(12): e83518, 2013. doi:10.1371/journal.pone.0083518 PMCID: PMC3861503
- Jackson, JR, Ryan MJ, and ALWAY SE. Long-term supplementation with resveratrol alleviates oxidative stress, but does not attenuate sarcopenia in aged Mice. J. Gerontol: Biological Sciences 66 (7):751-764, 2011. PMID: 21454355.
- Jackson, J.R., Ryan MJ, Hao Y, ALWAY SE. Mediation of Antioxidant Capacity and Apoptotic Signaling by Resveratrol Following Muscle Disuse in the Gastrocnemius Muscles of Young and Old Rats. Am J Physiol Regul Integr Comp Physiol. 299 (6): R1572-R1581, 2010. PMCID: PMC20861279
B. Positions and Honors
Positions and Employment
1984-1986 Research Fellow, Medical Research Council Canada and Ontario Gerontology Fellow, Dept. of Kinesiology, University of Waterloo, Ontario, Canada.
10/1986-07/1989 Research Fellow, UT Southwestern Medical Center; Faculty, Human Performance Center, UT Southwestern Medical Center/ST. Paul Hospital, Dallas, TX
07/1989-06/1990 Assistant Professor, Department of Anatomy, Cell Biology and Neuroscience, School of Medicine, Oral Roberts University, Tulsa, OK
07/1990-07/1994 Assistant Professor, Department of Exercise Science, School of Health and Exercise Science, The Ohio State University, Columbus, OH
07/1994-07-1995 Associate Professor (Tenured) Department of Exercise Science, School of Health and Exercise Science, The Ohio State University, Columbus, OH
07/1995-12/1999 Associate Professor, Department of Anatomy, College of Medicine, University of South Florida, Tampa FL
01/2000-06/2005 Associate Professor and Director of Graduate Studies, Division of Exercise Physiology West Virginia University School of Medicine, Morgantown, WV
06/2002-06/2005 Joint Associate Professor, Dept. of Physiology and Pharmacology, West Virginia University School of Medicine, Morgantown, WV
07/2005-present Joint Professor, Dept. of Physiology and Pharmacology, West Virginia University School of Medicine, Morgantown, WV
07/2005-present Professor (Tenured) and Chair, Division of Exercise Physiology West Virginia University School of Medicine
Other Experience and Professional Memberships
1981 - present Fellow, American College of Sports Medicine
1989 - present American Physiological Society
1996 - present American Association for the Advancement of Science
1999 - present Gerontological Society
2012 – present American Kinesiological Society
2014 – present American Diabetes Association
04/2013-present PLOS ONE
05/2005-present Exercise Sports Science Reviews
1992-present Journal of Strength and Conditioning Research
1991-1992 Journal of Applied Sport Science Research
03/2013-present BioMed Research International
01/2013-present International Journal of Applied Exercise Physiology (IJAE)
01/2012-present ISRN Biochemistry
07/2008–present American Journal of Physiology: Regulatory, Integrative and Comparative Physiology
Fellowships and Awards (past 3 years)
2013 Sponsor for Fulbright Scholar Fellowship, Dr. Tigran Petrosyan, University of Armenia. Dr. Petroysan’s award to work with Dr. Alway is from 07/01/2013-06/30/2014
2013 Co-Investigator – salary support for Brain project, a Japanese exchange 01/2013-3/3/2014 (Hideyuki Takahashi, Ph.D., Assistant Professor, Kyushu University, Japan and Yutaka Suzuki, doctoral student, Tohoku University Japan) to work in Dr. Alway’s lab for a research training program in muscle biology.
Review Panels (most recent 3 years)
2012 Scientific Review Committee, Special Emphasis Panel/Scientific Review Group 2012/05 ZRG1 MOSS-T (90) S (02/07-08/2012)
2012 Study section member: SMEP (Skeletal Muscle and Exercise Physiology) 2013/01 (10/04-6, 2012)
2012 Special Emphasis Panel/Scientific Review Group, National Institute on Aging: Skeletal muscle ZAG1 ZIJ-9 JI (10/23/2012)
2012 Special Emphasis Panel/Scientific Review Group, Cellular and Molecular Medicine/CAMM: (11/19/2012)
2013 American Federation for Aging Research, Grant review committee (02/2013)
2013 Special Emphasis Panel/Scientific Review Group, NIAMS2013/08 ZAR1-KM-(M1) (4/15/2013)
2013 Natural Sciences and Engineering Research Council of Canada, Discovery Grant review Committee (4/24/2013)
2013 Member Scientific Review Committee Cellular and Molecular Medicine/2013/08 CAMM 1 (6/3/2013)
2013 Grant Reviewer: NIH, Special Emphasis Panel/Scientific Review Group 2014/01 ASG meeting, 11/25/2013-11/27/2013.
2013 Grant Reviewer: Neurological Foundation of New Zealand 10/08/2013
2014 Grant Reviewer: NIH, Special Emphasis Panel/Scientific Review Group, ZRG1 BDCN-W (02), (07/23/2014)
2014 Grant Reviewer: Wellcome Trust, UK, Senior Research Fellowship in Basic Biomedical Science (07/01/2014)
2014 Grant Reviewer: NIH, Molecular and Integrative Signal Transduction (MIST) Study Section, SEP, ZRG1 CB-G(02), (06/26/2014)
2014 Grant Reviewer: NIH, Special Emphasis Panel/Scientific Review Group, NIAMS 2014/08 ZAR1 XZ (M1) 1 (04/14/2014)
2014 Grant Reviewer, National Strength and Conditioning Association (5/8/2014)
2014 Grant Reviewer: Natural Sciences and Engineering Research Council of Canada RGPIN-2013-01726 - NSERC Biological Systems and Functions (2/6/2014)
2015 Grant Reviewer: PSI (Physician Services Incorporated) Foundation of Ontario (Canada) (01/06/2015)
C. Contribution to Science
- Our work over the past decade and one-half has documented occurrence of increased apoptotic signaling in muscles from old animal models. This apoptotic signaling is elevated in the face of reduced loading and denervation, all leading to muscle wasting. These studies emphasized the role of mitochondrial apoptotic signaling as a likely source for the events triggering apoptotic events, although we did find cross-talk between cytokine and mitochondrial pathways of apoptosis in aging skeletal muscles.
- Siu, P.M., R.W. Bryner, J.K. Martyn and S.E. ALWAY. Apoptotic adaptations from exercise training in skeletal and cardiac muscles. FASEB J.18(10):1150-1152, 2004express article 10.1096/fj.03-1291fje. PMID:15132982
- Siu, P.M., E.E. Pistilli, D.C. Butler and S.E. ALWAY. Aging influences the cellular and molecular responses of apoptosis to skeletal muscle unloading Am. J. Physiol:Cell Physiol. 288:C338-349, 2005. PMID:15483226
- Siu, P.M. and S.E. ALWAY. Mitochondria-associated apoptotic signalling in denervated rat skeletal muscle. J Physiol565: 309-323, 2005. PMID:15774533 PMCID:PMC1464486
- Pistilli, E.E., Jackson, J.J., and S.E. ALWAY. Death receptor associated pro-apoptotic signaling in aged skeletal muscle. Apoptosis. 11: 2115-2126, 2006. PMID:17051337
- Siu, P.M. and S.E. ALWAY. Deficiency of the Bax gene attenuates denervation-induced apoptosis. Apoptosis J. 11: 967-981, 2006. PMID:16763784
- In addition to the contributions described above, with a team of collaborators, I have evaluated the effectiveness of various nutritional intervention models largely with anti-oxidant properties with the goal of determining if muscle function, and muscle mass would be better (e.g., lower sarcopenia, lower muscle wasting in disuse) if the lower oxidant stress leads to reduced apoptotic signaling, improvements in muscle recovery from muscle wasting conditions and to improve satellite cell function in the repair/regeneration process of aged muscles. These studies emphasized contextual factors and the signaling that is associated with nutritional interventions have upon improving muscle function and reducing conditions associated with muscle wasting in aging. This body of work has found some improvements by treatment with resveratrol and catechins containing compounds in muscle function and reductions in muscle loss in aged animals after disuse conditions.
- Ryan MJ, Jackson JR, Hao Y, Leonard SS and ALWAY SE. Inhibition of xanthine oxidase reduces oxidative stress and improves skeletal muscle function in response to electrically stimulated isometric contractions in aged mice. Free Radic Biol Med 51(1):38-52, 2011. PMID: 21530649, PMCID: PMC3430730
- Ryan MJ, Jackson JR, Hao Y, Williamson, C., Hollander JM and ALWAY, S.E. Suppression of oxidative stress by resveratrol after isometric contractions in gastrocnemius muscles of aged mice. J Gerontol A Biol Sci Med Sci 65:815-831, 2010. PMID:20507922, PMCID:PMC2903786
- ALWAY, S.E. N. Edens, S.L. Pereira, JS Mohamed and Bennett, B.T. Epigallocatechin-3-gallate (EGCg) lowers muscle wasting, reduces myonuclear apoptotic signaling, and enhances muscle recovery in fast hindlimb muscles following extended disuse in aged rats. Exp. Gerontol 50:82-94, 2014. PMID:24316035
- Satellite cells are critical to regulate regeneration and repair of muscle and aging reduces satellite cell function. We have tested nutraceuticals to alter satellite cell proliferation and/or differentiation in response to loading and unloading and found that the neutraceuticals independently alter proliferation and differentiation and therefore have the potential to improve muscle repair and regeneration in aging.
- Williamson DL, Butler DC and ALWAY SE. AMPK inhibits myoblast differentiation through a PGC-1α -dependent mechanism. Am J Physiol Endocrinol Metab 297(2):E304-E314,2009. PMID:19491292
- ALWAY SE., Pereira SL, Edens NK, Hao Y and Bennett BT. β-Hydroxy-β-methylbutyrate (HMB) enhances the proliferation of satellite cells in fast muscles of aged rats during recovery from disuse atrophy, Exp. Gerontol. 48(9):973-984, 2013. PMID: 23832076
- ALWAY, S.E., Myers, M.J., Mohamed J.S. Regulation of satellite cell function in sarcopenia. Front in Aging Neurosci 6 (246): 1-15, 2014. PMID: PMC4170136
- ALWAY, S.E, Bennett BT, Wilson JC, Sperringer J, Mohamed JS, Edens NK and Pereira SL. Green tea extract attenuates muscle loss and improves muscle function during disuse, but fails to improve muscle recovery following unloading in aged rats. J Appl Physiol (1985) In Press, 2014. doi: 10.1152/japplphysiol.00674.2014. [Epub ahead of print] PMID: 25414242
- We have also used exercise in human studies in young adult and elderly subjects over several decades, to evaluate the efficacy of increased muscle loading and exercise to reduce the structural and functional consequences of aging, sarcopenia and metabolic diseases. We have found that while aerobic exercise does not reduce the loss of muscle mass with aging, resistance training can slow sarcopenia and reverse the negative functional outcomes of aging and muscle wasting.
- ALWAY, S.E., W.H. Grumbt, J. Stray-Gundersen and W.J. Gonyea, Effects of resistance training on elbow flexors of elite male and female bodybuilders. J. Appl. Physiol. 72:1512-1521, 1992.
- Roman, W.J., J. Fleckenstein, J. Stray-Gundersen, S.E. ALWAY, R. Peshock and W.J. Gonyea Adaptations in the elbow flexors of elderly males following heavy resistance training. J. Appl. Physiol. 72:750-754 1993.
- ALWAY, S.E. A.R. Coggan, M.A Sproul, A.M. Abdugjaijl and P..M. Robataille. Muscle torque in young and older untrained and endurance trained men. J. Gerontol: Biol. Sci. 51A:(3)B195-B201, 1996.
- Ferketich, A.K. T.E. Kirby, and S.E. ALWAY. Cardiovascular and muscular adaptations to combined endurance and strength training in elderly women. Acta Physiol. Scand. 164:259-267, 1998.
- Sharif S, Thomas JM, Donley DA, Gilleland DL, Bonner DE, McCrory JL, Hornsby WG, Zhao H, Lively MW, Hornsby JA and ALWAY SE. Resistance exercise reduces skeletal muscle cachexia and improves muscle function in rheumatoid arthritis. Case Rep Med 2011: 1-7,2011. Article ID 205691, PMID: 3235946
A Complete List of Published Work in PubMed can be found at: http://www.ncbi.nlm.nih.gov/sites/myncbi/stephen.alway.1/bibliography/41160855/public/?sort=date&direction=descending
D. Research Support
Ongoing Research Support
Program to Stimulate Competitive Research (PSCoR) Alway (PI) 01/05/2015-12/30/2015
“Genome-wide Profiling and Functional Analysis of Sirtuin 1-Regulated Transcriptome Networks Associated with Aging Muscles”
The goal of this project is to characterize transcriptome changes and new targets that are candidates for regulation of muscle satellite cell function during muscle repair and regeneration.
West Virginia Clinical and Translational Science Institute Alway (PI) 04/01/2013-4/01/2015
“Phase 1 (T1) Translation of basic to clinical research: Offsetting Sarcopenia with Exercise and Resveratrol”
The goal of this study is to evaluate the efficacy of resveratrol to improve muscle function, fatigue, and mass in aging with and without an exercise intervention.
Healthworks Inc. Alway (PI) 08/01/2013-07/31/2015
Training for graduate students in Exercise Physiology
The goal of this project is to provide research training for graduates interested in rehabilitation opportunities with diabetic and cardiac patients.
Recent Completed Research Support
Abbott Laboratories 100415 Alway (PI) 01/22/2008-05/31/2014
Nutritional reduction of muscle wasting in sarcopenia.
The goal of this study is to evaluate the efficacy of nutritional intervention to improve muscle function, fatigue, and mass during conditions of muscle disuse and reuse.
R01AG021530-01 Alway (PI) 04/01/2004-04/30/2010
Id2 regulation of muscle hypertrophy in aging.
The overall goal of this proposal is to define cellular and molecular mechanisms of actions of Id2 in muscle growth in aging.
K01 NIH/NIAAG026337 Morissette (PI) 12/30/2010-01/30/2011
The role of Myostatin in Cardiac Hypertrophy and Failure
The goal of this proposal provide career development and training opportunities to facilitate the transition of the investigator to an independent researcher in aging. The scientific goal is to utilize a myostatin-deleted mouse model to better understand the potential role of myostatin in vitro and in vivo in controlling cardiac growth during aging. (The project was terminated early due to the death of the PI).
Role: Scientific mentor