Espen E. Spangenburg, Ph.D.

Espen E. Spangenburg

Associate Professor
East Carolina Diabetes and Obesity Institute

Department of Physiology
The Brody School of Medicine

115 Heart Drive
ECHI - Mail Stop 743
East Carolina University
Greenville, NC 27834

Phone: 252-737-5035
Fax: 252-744-0462

Lab Website


Research Interests

My research program is focused on understanding the endocrine-based regulation of physiological and metabolic function of skeletal muscle.  My lab employs an integrative experimental approach, in which we use cell culture and animal models to define mechanisms that we then work to translate to the human.  Specifically, we have developed skeletal muscle specific-inducible BRCA1 and ER-alpha knock out mice and the ability to ablate BRCA1 or ER-alpha expression in cultured human myotubes through shRNA delivered via AV virus approach. This integrative approach allows us to examine the same loss-of function approach using in vivo animal models and cultured myotubes from humans. My lab has developed a number of techniques that allow us to measure or image metabolic and physiological changes in whole muscle or cultured adult single muscle fibers.  The ability to integrate these approaches gives us a significant experimental advantage because it allows us to make reductionist based measures in a whole muscle or a single muscle cell that retains a true adult functional phenotype.   For example, we have recently developed and/or optimized approaches to measure force, mitochondrial function, deliver cDNA, image lipid droplets or other organelles, and employ co-culture approaches in these single muscle fibers. 


  • 2015-present Associate Professor (with tenure) East Carolina Diabetes and Obesity Institute, Department of Physiology, School of Medicine, East Carolina University, Greenville, NC
  • 2012-2015 Associate Professor School of Public Health University of Maryland, College Park, MD
  • 2006-2012 Assistant Professor School of Public Health University of Maryland, College Park, MD
  • 2003-2006 Assistant Professor, Dual appointments in the Neurobiology, Physiology and Behavior and Department of Physiology and Membrane Biology, University of California-Davis, Davis, CA
  • 2000-2003 Postdoctoral Fellow, Dept. of Biomedical Sciences. University of Missouri, Columbia, MO


(Selected from over 70 peer-reviewed publications; h-index = 24; 1342 times referenced, 4 publications referenced over 100 times.)

For a full list of Pubmed citations, visit

  1. Ryan, T. E., C. A. Schmidt, T. D. Green, E. E. Spangenburg, P. D. Neufer, J. M. McClung.  Targeted expression of Catalase to Mitochondria Protects Against Ischemic Myopathy in High Fat Fed Mice.  Diabetes.  (2016) 65(9) 2553-2568.

  2. Alleman, R.  A. Tsang, T. Ryan, D. Patteson, J. McClung, E. E. Spangenburg, S. R. Shaikh, P. D. Neufer, D. A. Brown Exercise-induced protection against reperfusion arrhythmia involves stabilization of mitochondrial energetics. Am J Physiol (Heart Circ Physiol). (2016) 310: H1360-1370.

  3.  A. P. Valencia, A. E. Schappal, E. M. Morris, J. P. Thyfault, D. A. Lowe, E. E. Spangenburg.  The presence of the ovary prevents hepatic mitochondrial oxidative stress in young and aged female mice through glutathione peroxidase 1. Exp Gerontology.  (2016). 73: 14-22.

  4. Jackson, K. C., E. K. Gidlund, J. Norrbom, A. P. Valencia, D. M. Thomson, R. A. Schuh, D. P. Neufer, E. E. Spangenburg. BRCA1 is a novel regulator of metabolic function in skeletal muscle.  J Lipid Research.  (2014) 55(4): 668-680.
  5. Schuh, R. A., Jackson KC, Schlappal AE, E. E. Spangenburg, Ward CW, Park JH, Dugger N, Shi GL, Fishman PS. Mitochondrial oxygen deficits in skeletal muscle isolated from an Alzheimer’s disease relevant murine model. (2014) BMC Neuroscience. 15: 24-36.
  6. Wohlers, L. M., B. Powell, E. R. Chin, E. E. Spangenburg.  Using a novel co-culture model to dissect the role of intramuscular lipid load on skeletal muscle insulin responsiveness under reduced estrogen conditions.  Am J Physiol (Endo and Meta) (2013) 304 (11): 1199-1212.
  7. Ludlow, A.T., E. E. Spangenburg, E. R. Chin, W. H. Cheng, S. M. Roth. Telomeres shorten in response to oxidative stress in mouse skeletal muscle fibers.  J. Gerontol A Bio Sci Med Sci. (2014) 69 (7): 821-830.
  8. Spangenburg, E. E., K. C. Jackson, R. A. Schuh.  AICAR inhibits oxygen consumption by intact skeletal muscle cells in culture. J Physiol Biochem. (2013) 69(4) 909-917.
  9. Jackson, K. C., L. M. Wohlers, R. M. Lovering, R. A. Schuh, A. C. Maher, A. Bonen, T. R. Koves, O. Ilkayeva, D. M. Thomson, D. M. Muoio, E. E. Spangenburg.  Ectopic lipid deposition and the metabolic profile of skeletal muscle in ovariectomized mice.   Am J Physiol (Reg. Comp. Physiol)  (2013) 304: R206-17.
  10. R. A. Schuh, K. C. Jackson, R. J. Khairallah, C. W. Ward, E. E. Spangenburg.  Measuring mitochondrial respiration in intact single muscle fibers.  Am J Physiol (Reg. Comp. Physiol) (2012) 302: R712-R719.
  11. Spangenburg, E. E., S. J. Pratt, L. M. Wohlers, R. M. Lovering.  Use of BODIPY (493/503) to visually localize intramuscular lipid droplets in skeletal muscle.  Journal of Biomedicine and Biotechnology. (2011) 2011:598358. PMCID: PMC3180081
  12. Wohlers, L. M., S. M. Sweeney, R. M. Lovering, C. W. Ward, E. E. Spangenburg.  Changes in contraction-induced phosphorylation of AMP-activated protein kinase and mitogen activated protein kinases in skeletal muscle after ovariectomy.  J. Cell Biochem.  (2009) 107: 171-178.

Other Experience and Professional Memberships

  • Editorial Board: American Journal of Physiology: Cell Physiology, Journal of Applied Physiology, Frontiers in Skeletal Muscle Physiology, Faculty of 1000 member
  • American Diabetes Study Section Member: 2015-present
  • NIH Grant Review (Ad Hoc): Skeletal Muscle and Exercise Physiology (SMEP) 2011, 2013 (2X), 2014; 2015, 2016 Special Emphasis Panel EMNR-S (2) 2014, MOSS 2013, 2014, 2015; NHBLI-Women’s Health Initiative 2012; SCORE Grants Ad Hoc 2010; RO3 Special Emphasis Study Section, 2005-2010
  • NASA Study Section, Ad Hoc Member, 2004, 2009, 2012; Mail in reviewer 2010, 2011.
  • Medical Research Council (England), Mail-In Reviewer, Fall 2004, 2012
  • Regular Member: American Diabetes Association, American Physiological Society


  • 2014 Leda Amick Wilson UMD Mentor of the Year Award
  • 2011 Best Paper Award UMD School of Public Health Research Interaction Day
  • 2010 Virginia Tech HNFE Outstanding Alumnus Award
  • 2008-2014 NIH Loan Repayment Grant Recipient
  • 2007 New Investigator Award-American Physiological Society-EEP Section
  • 2002 NIH F32 Individual Post-doctoral fellow Award


Research Support


R01 AR0666601-01A1 (PI: Spangenburg)
07/01/2015 – 06/30/2020
BRCA1 is necessary for optimal skeletal muscle function
The major goals of this project are define the role BRCA1 plays in the regulation of skeletal muscle function and mitochondrial function.

#7-14-BS170 (PI: Spangenburg)
American Diabetes Association
Estrogens protect skeletal muscle from metabolic insults.
The major goal of this proposal is mechanistically define how the estrogen receptor alpha protects skeletal muscle from lipid-based insults.

Completed Research Support

5 R21 AR059913 (PI: Spangenburg)
The role of BRCA1 in regulation of lipid metabolism in skeletal muscle.
The major goals of this project are define the role BRCA1 plays in the regulation of lipid metabolism in skeletal muscle.

P-F Maryland Diabetes Research Training Center (DRTC). (PI: Spangenburg)
Estrogens regulate endocrine influences of visceral adipose tissue on skeletal muscle.
The major goal of this project is develop a co-culture system that allows for the ability to mechanistically define the influence of estrogens on visceral adipocytes and skeletal muscle.

5 R21 HL098810 (Co-Investigator)
Potential role of endothelial progenitor cells in cardiovascular risk.
The major goal of this project is define EPC function as it relates to in vivo endothelial function in sedentary and trained older adults.

ARRA R21 HD062868 (Co-Investigator)
Role of maternal exercise environment on transgenerational offspring health.
The major goal of this project was to determine the potential role of "exercise ancestry" on mouse offspring body composition, metabolism, gene expression, and other health outcomes by examining multiple generations of mice with and without exercise training exposures in parental generations.