East Carolina University
 
Brody School of Medicine
Department of Physiology


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Dr. Scott E. Gordon, Ph.D.
 

 

\PIRATEDRIVEPhysiologydepartmentalAdministrationYou have mailWebsiteScott,-Gordan-webAssociate Professor

Department of Exercise and Sport Science
Department of Physiology, Brody School of Medicine
Human Performance Laboratory
363 Ward Sports Medicine Building
East Carolina University
Greenville, NC 27858

Email: GordonSc@ecu.edu

Office Phone: (252) 737-2879
Laboratory Phone: (252) 744-1988
Fax: (252) 737-4689
 
Primary Research Interets
Significant skeletal muscle wasting with age can result in lost functional independence, and interventions such as resistance exercise training are not fully effective in restoring muscle mass in elderly individuals. Research in the Gordon lab is attempting to identify hormonal and/or molecular mechanisms of skeletal muscle remodeling with aging, disuse, and overloading/resistance exercise, especially with respect to the muscle protein synthesis. Current projects are specifically examining the mechanisms by which the signaling protein AMP kinase (AMPK, which is elevated in aging muscle and likely acts to suppress protein translation and synthesis) may underlie the atrophy and/or the diminished capacity for growth that both occur predominantly in fast-twitch muscle fibers with age. AMPK is considered to be a primary “metabolic switch” that is activated by intense physical activity (and other forms of energy demand) and shifts metabolism from protein synthesis (muscle building) to protein degradation (muscle breakdown), along with stimulating fat and glucose oxidation to produce energy (ATP). To conserve ATP, AMPK suppresses cellular protein synthesis when cellular energy status is low because protein synthesis is very metabolically expensive. Thus, AMPK activation and protein synthesis are potentially closely related to long-term whole-body metabolism and energy expenditure. This research is also attempting to determine if protein synthesis and growth in aging skeletal muscle can be rescued by exercise interventions or interventions that block AMPK activity.
 
Education
B.A. Bowdoin College, Brunswick, ME
(Major: Biology; Minor: Chemistry)		 1986
M.S. The Pennsylvania State University, University Park, PA
(Major: Exercise Physiology)		 1992
Ph.D. The Pennsylvania State University, University Park, PA
(Major: Physiology; Minor: Gerontology)		 1997
Post-Doctoral University of Texas Medical School, Houston, TX
(NASA Postdoctoral Research Associate in Space Biology)
University of Missouri, Columbia, MO
(National Institutes of Health Postdoctoral Fellow)		 1997-1999
 
1999-2001
 

 
Additional Professional Experience
Biological Science Assistant, United States Army, 1986-1989
Exercise Physiology Division
U. S. Army Research Institute of Environmental Medicine, Natick, MA
 
Selected Professional Memberships and Certifications
American College of Sports Medicine
American Physiological Society
American Society for Gravitational and Space Biology
Gerontological Society of America
National Strength and Conditioning Association
*NSCA Certified Strength and Conditioning Specialist
Researchers against Inactivity-related Diseases
 
Latest Scientific Publications (from 65)
  1. Thomson, D.M., and S.E. Gordon. Diminished overload-induced hypertrophy in aged fast-twitch skeletal muscle is associated with AMPK hyperphosphorylation. J. Appl. Physiol. 98(2):557-564, 2005.

  2. Westerkamp, C.M., and S.E. Gordon. Angiotensin converting enzyme inhibition attenuates myonuclear addition in overloaded slow-twitch skeletal muscle. Am. J. Physiol. Regul. Integr. Comp. Physiol., 289(4):R1223-R1231, 2005.

  3. Thomson, D.M., and S.E. Gordon. Impaired overload-induced muscle growth is associated with diminished translational signaling in aged rat fast-twitch skeletal muscle. J. Physiol. (London), 574(Pt 1):291-305, 2006.

  4. Gordon, S.E., C.M. Westerkamp, K.J. Savage, R.C. Hickner, S.C. George, C.A. Fick, and K.M. McCormick. Basal, but not overload-induced, myonuclear addition is attenuated by L-NAME administration. Can. J. Physiol. Pharmacol., 85:646-651, 2007.

  5. Deschenes, M.R., K. Tenny, M.K. Eason, and S.E. Gordon. Moderate aging does not modulate morphological responsiveness of the neuromuscular system to chronic overload in Fischer 344 rats. Neuroscience 148(4):970-977, 2007.

  6. Thomson, D.M., C.A. Fick, and S.E. Gordon. AMPK activation attenuates S6K1, 4E-BP1, and eEF2 signaling responses to high-frequency electrically stimulated skeletal muscle contractions. J. Appl. Physiol. 104:625-632, 2008.

  7. Gordon, S.E., J.A. Lake, C.M. Westerkamp, and D.M. Thomson. Does AMP-activated protein kinase negatively mediate aged fast-twitch skeletal muscle mass? Exerc. Sport Sci. Rev., 36(4):179-186, 2008.

  8. Thomson, D.M., J.D. Brown, N. Fillmore, S.K. Ellsworth, D.L. Jacobs, W.W. Winder, C.A. Fick, and S.E. Gordon.  AMP-Activated protein kinase response to contractions and AICAR treatment in young adult and old skeletal muscle.  J. Physiol. (London), 587:2077-2086, 2009.
 
Latest Research Funding Support
  1. Principal Investigator, NIH Academic Research Enhancement Award (R15) Grant (PA-03-053): “Aging, AMP Kinase and Skeletal Muscle Overload” (9/05-8/07; $135,000 Direct Costs; $192,375 Total Costs).

  2. Co-Investigator (5%), NIH Traditional Research Project (R01) Grant (PA-03-156): “Age-related Insulin Resistance, Muscle, and Exercise” (10/05-9/10; $1,000,000 Direct Costs; $1,425,000 Total Costs; Joseph A. Houmard, P.I.).

  3. Principal Investigator, American Federation for Aging Research Grant: “Targeted Rescue of Protein Translation and Synthesis in Aged Skeletal Muscle” (7/06-6/08; $53,363 Direct Costs).