• Full-Time Faculty and Research Scientists
• Faculty Research in the News
• Recent Faculty Publications
• Open Positions
• Adjunct Faculty
• Part-Time Faculty, Other Researchers, and GSIs
• Staff
• Facilities
• Kin-Help
• Pandemic Continuity Plan

Chris Mendias, Ph.D., A.T.C.

Research Assistant Professor, Athletic Training
Research Assistant Professor, Orthopaedic Surgery

• Areas of Interest
• Research
• Educational Background
• Honors and Awards
• Teaching
• Professional Service
• Selected Publications/Presentations

3732 CCRB
401 Washtenaw Ave.
Ann Arbor, MI 48109-2214
Phone: (734) 764-3250
Fax: (734) 936-1925
cmendias@umich.edu

Office Hours (Fall 2009):
Mon 9:30-11:00am

Full vita>>

Laboratory:

• Orthopaedic Research Laboratories
• Muscle Mechanics Laboratory (leaving Kinesiology site)
• Skeletal Tissue Engineering Laboratory (leaving Kinesiology site)

Areas of Interest

Dr. Mendias is a certified athletic trainer and physiologist interested in skeletal muscle and tendon injury, repair and adaptation to exercise. His studies are aimed at gaining a greater understanding of the genes and signaling pathways that regulate skeletal muscle and tendon structure and function, and in the development of new therapeutic interventions for the treatment of skeletal muscle and tendon injuries and diseases.

Research

Molecular mechanisms of skeletal muscle atrophy and fibrosis

Contraction-induced injuries are the most prevalent injury to skeletal muscle. These injuries occur during active lengthening contractions when muscle fiber stress is of sufficient force to disrupt the ultrastructure of sarcomeres and cause a shearing of the sarcolemma and extracellular matrix. Minimizing inflammation, preventing fibrosis and restoring strength are the basic clinical objectives in the treatment of skeletal muscle injuries. Even with current therapeutic interventions, for moderate and severe muscle injuries strength often does not return to pre-injury levels and the muscle can be more susceptible to subsequent injuries. This decrease in strength and greater susceptibility to injury occurs due to the formation of collagenous scar tissue and a persistent atrophy of muscle fibers in the region surrounding the injury. Current studies are focused on the cytokines myostatin and TGF-beta and their roles in skeletal muscle atrophy and fibrosis. Understanding the molecular mechanisms behind the development of atrophy and fibrosis will allow for the design of novel therapeutic interventions for the treatment of muscle injuries and diseases and prevent the loss of function and decrease in the quality of life that often accompany these conditions.

Tendon biomechanics and molecular mechanotransduction

Tendons transmit force between muscles and bones and are critical components of the musculoskeletal system. In the simplest sense, tendons can be modeled as springs in series with muscle actuators. The spring-like mechanical property of tendons has two important biological functions. First, tendons are extremely efficient in the storage of elastic energy. This elastic energy storage helps to reduce the metabolic demands of muscle during locomotion and delays the onset of muscle fatigue. The second important biological function of tendons is to protect muscles from injury. A strain of muscle fibers by as little as 10% can cause dramatic damage to muscle contractile proteins and decrease the force output of muscle. Tendons protect muscles from damage by limiting the strain placed upon muscles during locomotion. Failure of the tendon to properly adapt to mechanical loading results in a decrease in metabolic efficiency, can lead to the onset of tendonitis and tendonosis, and also makes skeletal muscle more susceptible to contraction-induced injury. Although the changes in tendon mechanical properties in response to mechanical loading has been well studied, the cellular and molecular events behind the adaptation of tendons to mechanical loading is not well understood. Current studies are aimed at determining the signaling pathways and transcription factors that modify the structure and function of tendon extracellular matrix. This research will provide a further understanding of tendon physiology and assist in the development and validation of treatments for tendon injuries and diseases.

Educational Background

University of Michigan, Ann Arbor, MI
Postdoctoral Fellowship, Biomedical Engineering, 2009

University of Michigan, Ann Arbor, MI
Ph.D., Molecular and Integrative Physiology, 2007

University of Arizona, Tucson, AZ
M.S., Physiology, 2003

University of Arizona, Tucson, AZ
B.S., Biology and Athletic Training, 2001

Honors and Awards

Teaching

AT 420. Pharmacology for the Allied Health Professions

MOVESCI 449. Lab Rotation in Exercise Physiology

Professional Service

Manuscript Reviewer

Applied Physiology, Nutrition and Metabolism
IEEE Transactions on Biomedical Engineering
Growth Factors
Journal of Applied Physiology
Journal of Athletic Training
Journal of Gerontology
Journal of Orthopaedic Research
Journal of Sport Rehabilitation

Professional Affiliations

Michigan Athletic Trainers Society
     Communications Committee Chair/Webmaster (2003 – present)

Selected Publications/Presentations

Faulkner JA, Davis CS, Mendias CL and Brooks SV. The aging of elite male athletes: age-related changes in performance and skeletal muscle structure and function. Clinical Journal of Sports Medicine. 2008 Nov;18(6):501-507.

Mendias CL, Bakhurin KI and Faulkner JA. Tendons of myostatin-deficient mice are small, brittle and hypocellular. Proceedings of the National Academy of Sciences. 2008 Jan;105(1):388- 393.

Mendias CL, Marcin JE, Calderon DR and Faulkner JA. Contractile properties of EDL and soleus muscles of myostatin-deficient mice. Journal of Applied Physiology. 2006 Sep;101(3):898- 905.

Mendias CL, Tatsumi R and Allen RE. Role of cyclooxygenase-1 and -2 in satellite cell proliferation, differentiation, and fusion. Muscle and Nerve. 2004 Oct;30(4):497-500.

Mendias CL, Bakhurin KI, Davis CS and Faulkner JA. Increased skeletal muscle mass and improved contractile properties of skeletal muscles of old myostatin-deficient mice. American College of Sports Medicine Annual Meeting, Seattle, WA, May 2009.

Mendias CL, Bakhurin KI, Arruda EM, Brooks SV, Faulkner JA and Larkin LM. Scleraxis is expressed in adult tendons and is upregulated in response to mechanical loading. Experimental Biology/American Physiological Society Annual Meeting, New Orleans, LA, April 2009.

Mendias CL, Bakhurin KI and Faulkner JA. Bigger muscles, smaller tendons -- tendons of myostatin- deficient mice are small, brittle and hypocellular. Experimental Biology/American Physiological Society Annual Meeting, San Diego, CA, April 2008.