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Stephen Alway Directory Photo

Stephen E Alway

Senior Assistant Dean for Research and Graduate Studies, Chair Dept. of Human Performance, and Chair of Exercise Physiology
8707D HSS
Morgantown,
WV
26506
Box: 9227
304-293-7105

Credentials

PhD, FACSM - Fellow of the American College of Sports Medicine

Positions

Professor and Chair of Exercise Physiology
Executive Chair, Dept. of Human Performance & Applied Exercise Science
Senior Assistant Dean, Research & Graduate Studies, Professional Programs
Human Performance - Exercise Physiology (SOM)
Admin

Joint Professor of Physiology and Pharmacology
Physiology & Pharmacology (SOM)
Faculty

Faculty
Center for Cardiovascular & Respiratory Sciences (SOM)
Faculty

Education

PhD, Medical Sciences-Neuroscience, McMaster University. Hamilton, Ontario, Canada L8N 3Z5 Ph.D., 1985
MS, Physiology, McMaster University, Hamilton, Ontario, Canada L8S 4K1, 1981
BS, Kinesiology (Honors BS), University of Waterloo, Waterloo, Kinesiology, Ontario, 1978

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.

  1. 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
  2. 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
  3. 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.
  4. 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

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 

08/2015-present

Executive Chairperson, Department of Human Performance and Exercise Science, West Virginia University School of Medicine 

08/2015-present

Senior Assistant Dean for Research and Graduate Studies, Professional Programs, West Virginia University School of Medicine 

Other Experience and Professional Memberships
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
 
Associate Editor

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

Editorial Board

03/2013-present

BioMed Research International

01/2013-present

International Journal of Applied Exercise Physiology

1/2012-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 (past 3 years)       

2016 Grant Reviewer: NIH ZRG1 MOSS-U 82 A, Musculoskeletal, Oral and Skin Sciences AREA  (6/06/2016)
2016 Grant Reviewer: NIH NIAMS: 2016/08 ZAR1-YL-M1 (4/15/2016)
2016 Grant Reviewer: NIH NIAMS 2016/05 ZRG1-MOSS-U-82 (2/10/2016)
2016 Grant Reviewer: NIH NIAMS 2016/05 ZRG1-MOSS-A-02 (3/21/2016)
2015 Chair of Study Section: NIH 2016/01 ZRG1 BDCN-W (04) M Member Conflict: Exercise in Aging (11/12/2015-11/12/2015)
2015 Grant Reviewer: NIH 2016/01 ASG.  Aging Systems and Geriatrics Study Section Study Section member (10/19/2015-10/20/2015).
2015 Grant Reviewer: NIH 2016/01 ZAG1 ZIJ-G (J4) M Physiological Studies on Aging, Study Section member (09/28/2015)
2015 Grant Reviewer: NIH 2015/10 ZRG1 BDCN-J (02) M Neurodegeneration, Study Section member Aging and Aging-Related Processes (07/29/2015)
2015 Grant Reviewer: NIH 10/01/2015 ZAR1 YL M1 Study Section member (6/18/2015 – 6-19/2015)
2015 Grant Reviewer: NIH: 2015/05 ZAR1 XZ (M1) 1 Study Section member (02/18/2015-02/19/2015)
2015 Grant Reviewer: Muscular Dystrophy Campaign, UK (2/5/2015)
2015 Grant Reviewer: NIH: Aging Systems and Geriatrics Study Section Study Section member 2015/05/ASG (3/4/2015-3/5/2015)
2015 Grant Reviewer: PSI (Physician Services Incorporated) Foundation of Ontario (Canada) (01/06/2015)
2014 Grant Reviewer, National Strength and Conditioning Association (5/8/2014)
2014 Member, NIH Special Emphasis Panel/Scientific Review Group Aging, Skeletal and Cardiac Muscle ZRG1 BDCN-W (04) (7/23/2104)
2014 Member, NIH Special Emphasis Panel/Scientific Review Group, NIAMS ZRG1 CB-G (55) (06/26/2014)
2014 Member NIH Special Emphasis Panel/Scientific Review Group, NIAMS 2014/08 ZAR1 XZ (M1) 1 (04/14/2014)
2014 Natural Sciences and Engineering Research Council of Canada (NSERC), RGPIN-2013-01726 - Biological Systems and Functions (01/06/2014) Discovery Grant panel member

C. Contribution to Science

  1. Apoptotic signaling in aged muscles. 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.
    1. 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.  2004;18(10):1150-1152express article 10.1096/fj.03-1291fje.  PMID:15132982
    2. 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. 2005;288:C338-349. PMID:15483226
    3. Siu, P.M. and S.E. ALWAY. Mitochondria-associated apoptotic signalling in denervated rat skeletal muscle. J Physiol 2005;565: 309-323. PMID:15774533 PMCID:PMC1464486
    4. Siu, P.M. and S.E. ALWAY. Deficiency of the Bax gene attenuates denervation-induced apoptosis.   Apoptosis J.  2006;11: 967-981. PMID:16763784

  2. Satellite cells. Satellite cells are critical for regulating muscle regeneration and repair and aging and obesity reduce satellite cell function. More than 15 years ago we found that aging provides adequate proliferation but suppressed differentiation of satellite cell in response to exercise and loading and this was temporally related to reduced muscle fiber formation and hypertrophy in aging. Subsequent to those studies we have investigated satellite cells using various models of aging or obesity.  
    1. ALWAY SE, Martyn JK, Ouyang J, Chaudhrai A and Murlasits ZS. Id2 expression during apoptosis and satellite cell activation in unloaded and loaded quail skeletal muscles. Am J Physiol Regul Integr Comp Physiol   2003;284: R540-R549.
    2. Peterson JM, Bryner R and S.E. ALWAY. Satellite cell proliferation is reduced in muscles of obese Zucker rats, but restored with loading. Am J Physiol Cell Physiol 2008;295:C521-C528. PMCID:PMC2518421
    3. 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.  2013;48(9):973-984. PMID: 23832076 
    4. ALWAY, S.E., Myers, M.J., Mohamed J.S. Regulation of satellite cell function in sarcopenia. Front in Aging Neurosci 2014;6 (246): 1-15. PMID: PMC4170136

  3. Exercise, oxidative stress and mitochondrial function. Our lab has collaborated with other investigators to evaluate the effectiveness of various nutritional intervention models largely with anti-oxidant properties. Our studies showed that reducing oxidative stress improved mitochondrial function and oxidative damage, leading to improved muscle function and muscle mass (e.g., lower sarcopenia, improved muscle function and lower muscle wasting in disuse).  The intervention 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. 
    1. 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  2011;51(1):38-52. PMID: 21530649, PMCID: PMC3430730
    2. Ryan, M.J. H.J. Dudash, M. Docherty, K.B. Geronilla, B.A. Baker, G.G. Haff, R.G. Cutlip, and S.E. ALWAY. Vitamin E and C supplementation reduces oxidative stress and improves antioxidant enzymes and positive muscle work in chronically loaded dorsiflexor muscles of aged rats. Exp Gerontol  2010;45: 882-895. PMID:20705127,  PMCID: PMC3104015
    3. 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 2010;65:815-831. PMID:20507922, PMCID:PMC2903786
    4. Nichols CE, Shepherd DL, Knuckles TL, Thapa D, Stricker JC, Stapleton PA, Minarchick VC, Erdely A, Zeidler-Erdely PC, ALWAY, S.E., Nurkiewicz TR and Hollander JM. Cardiac and mitochondrial dysfunction following acute pulmonary exposure to mountaintop removal mining particulate matter. Am J Physiol Heart Circ Physiol 2015;309: H2017-H2030. PMCID:PMC4698426
  4. Sirtuin 1 in muscle and aging. Sirtuin1 (SIRT1) has been an important regulator of muscle metabolism and potentially longevity. We have studied the SIRT1 and resveratrol (a SIRT1 activator) on muscle in aging and observed that a downregulation of SIRT1 is regulated at least in part by a PARP-1 dependent process. However, dietary interventions to increase SIRT1 activation were not found to improve muscle loss with aging without an additional intervention (e.g., exercise).
    1. 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) 2014;6:1-15. PMID:25361036
    2. 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 2013;8(12): e83518.  doi:10.1371/journal.pone.0083518  PMCID: PMC3861503
    3. 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  2011;66 (7):751-764.  PMID: 21454355. 
    4. 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. 2010;299 (6): R1572-R1581. PMCID: PMC20861279

  5. Catechin and anti-oxidant regulation of muscle wasting in aging. Recently we have evaluated catechins containing compounds that have anti-oxidant properties, with the goal of determining if muscle function, and muscle mass would be improved under disuse and recovery after disuse in aging (e.g., lower sarcopenia, lower muscle wasting in disuse.  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.  We have found some improvements by treatment with catechin containing compounds in muscle function and reductions in muscle loss in aged animals after disuse conditions. This work has provided pilot data for ongoing studies in elderly humans in our lab.
    1. ALWAY, S.E.  N. Edens, S.L. Pereira, JS Mohamed and Bennett, BT. 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 2014;50:82-94.PMID:24316035
    2. ALWAY, SE, 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) 2015;118: 319-330. PMID: 25414242

  6. Obesity. We have studied the suppressive effects of obesity on skeletal muscle apoptotic signaling and muscle satellite cell function in obese Zucker rats, which is a model of metabolic syndrome. We have shown that the obese rats had lower skeletal muscle size, and reduced satellite cell activation as compared to lean Zucker rats of the same age. Our contributions have implicated muscle mitochondrial involvements in both muscle mass and apoptotic signaling in obesity, and this can be modified by exercise.
    1. Peterson JM, Wang Y, Bryner R, Williamson DL and ALWAY, SE. Bax signaling mediates palmitate induced apoptosis in C2C12 myotubes. Am J Physiol Endocrinol Metab: 2008;295:E1307-E1314. PMID:18840766, PMCID:PMC2603553
    2. Peterson JM, Bryner RW, Sindler A, Frisbee JC and ALWAY,  SE. Mitochondria apoptotic signaling is elevated in cardiac but not skeletal muscle in the obese Zucker rat and is reduced with aerobic exercise.  J Appl Physiol  2008;105:1934-1943. PMID:18832755, PMCID:PMC2612474
    3. Peterson JM, Bryner R and S.E. ALWAY. Satellite cell proliferation is reduced in muscles of obese Zucker rats, but restored with loading. Am J Physiol Cell Physiol  2008;295:C521-C528. PMID:18508911, PMCID:PMC2518421
    4. Peterson JM, Bryner R, J.C. Frisbee and S.E. ALWAY. Effects of Exercise and Obesity on UCP3. Content in Rat Hindlimb Muscles. Med. Sci. Sports Exerc. 2008;40 (9) 1616–1622. PMID:18685530

A Complete List of Published Work that is referenced in PubMed (excluding books and Chapters) can be found at:  http://www.ncbi.nlm.nih.gov/myncbi/browse/collection/47358451/?sort=date&direction=descending 

D. Research Support
Ongoing Research Support

Rigel Pharmaceuticals, Inc. Alway (PI) 03/01/2016-02/28/2017
Jax/Stat3 Intervention for Treatment of Disuse Muscle Wasting in Aged Rats. The goal of this project is to determine if inhibition of Jax/Stat3 signaling will reduce muscle wasting during disuse atrophy in aging rats. Role: PI
WV-INBRE Next Generation Sequencing pilot grant. Alway (PI) 08/01/2015-07/31/2016
Genome-wide Profiling of Sirtuin 1-Regulated Transcriptome in Satellite Cell regulated Muscle Repair in Obesity and Aging. The goal of this project is to characterize transcriptome changes and new targets that are candidates for regulation of muscle satellite cell function during repair and regeneration in sarcopenic and obese mice. Role: PI
Program to Stimulate Competitive Research (PSCoR) Alway (PI) 01/05/2015-01/01/2016
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 in aging skeletal muscles. Role: PI
Healthworks Inc. Alway (PI) 08/01/2013-07/31/2017
Training for graduate students in Exercise Physiology. The goal of this project is to provide research training for graduates interested in rehabilitation experiences working with obese, diabetic and cardiac patients. Role: PI

Recent Completed Research Support   (Past 3 years)

U54GM104942 West Virginia Clinical and Translational Science Institute Alway (PI) 04/01/2013-7/01/2015
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. Role: PI
100415 Abbott Laboratories 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. Role: PI

Research Program

West Virginia Clinical & Translational Science Institute