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Faculty Detail Faculty Entry   
Name MARCAS M BAMMAN  
Campus Address MCLM 966A Zip 0005
Phone 205-996-7937
E-mail mbamman@uab.edu" id="FacultyDetail1EmailAddress"><a href="mailto:mbamman@uab.edu">mbamman@uab.edu</a>
URL www.uab.edu/exercise
 
 

Department Affiliations(s)
Appointment Type Department Division Rank
Center  Arthritis & Musculoskeletal Diseases Center  Arthritis & Musculoskeletal Diseases Center Professor
Center  Center for Aging  Center for Aging Professor
Center  Center for Metabolic Bone Disease  Center for Metabolic Bone Disease Professor
Center  Medicine  Comprehensive Diabetes Ctr Professor
Center  General Clinical Research Center  Ctr for Clinical & Translational Sci Professor
Center  Cell, Developmntl, & Integrative Biology  Ctr for Exercise Medicine Professor
Primary  Cell, Developmntl, & Integrative Biology  Cell, Developmntl, & Integrative Biology Professor
Secondary  Medicine  Med-Gerontology/Geriatrics/Palliative Care Associate Professor

Biographical Sketch 
Dr. Bamman was born in Manhattan, Kansas in 1966 and raised in St. Louis, Missouri. After earning a bachelor of science in exercise science from Kansas State University (1989) and a masters degree in exercise physiology from The University of Alabama at Birmingham (1990), he earned a PhD in the Department of Physiology at the University of Florida College of Medicine (1996). As a PhD candidate, Dr. Bamman traveled to the NASA Johnson Space Center in Houston, Texas where he conducted space flight-related research on skeletal muscle (studying load-mediated physiologic alterations) for nearly three years. He joined the UAB faculty in 1996. Dr. Bamman's research program focuses on skeletal muscle and exercise biology. He is the Director of the UAB Center for Exercise Medicine, and his interdisciplinary, translational research program involves co-investigators from Geriatric Medicine, Cardiology, Surgery, Physical Therapy, and Physiology and Biophysics.

Additional appointments at UAB: Dr. Bamman holds secondary appointments in the Department of Nutrition Sciences and Department of Medicine (Division of Gerontology, Geriatrics, and Palliative Care). He is Associate Director of the Center for Aging, and holds appointments in the Nutrition Obesity Research Center, Comprehensive Diabetes Center, Center for Cardiovascular Biology, Diabetes Research and Training Center, Center for Metabolic Bone Disease, and Center for Biophysical Sciences and Engineering.

Society Memberships
Organization Name Position Held Org Link
American College of Sports Medicine  Fellow  www.acsm.org 
American Physiological Society  Professional Member  www.the-aps.org 
 

Research/Clinical Interest
Title
Skeletal muscle mass regulation
Description
Muscle atrophy and reduced functional capacity are well-established, deleterious consequences of acute (e.g., burn, trauma, disuse) and chronic (e.g., OA/HIV/RA/cancer cachexia, COPD, diabetes mellitus, spinal cord injury) conditions—the most widespread and insidious of which is the degenerative process of normal aging. Because the metabolic and contractile properties of skeletal muscle play essential roles in the overall health and function of the organism, gaining a better understanding of the mechanisms underlying muscle mass and phenotype regulation, as well as key processes to exploit in countermeasure development, is of utmost importance. To this end, mechanisms of adult human skeletal myogenesis and muscle mass regulation remain the overarching areas of study in our laboratory, with a prominent emphasis on the aging muscle. Our primary research objectives span three, inter-related focus areas in human subjects: Objective 1) to determine the cellular and molecular mechanisms driving muscle regeneration following damage or injury, while identifying differences responsible for regeneration impairment in the aging muscle; Objective 2) to better understand the primary etiology of muscle atrophy in acute (burn, trauma) and chronic (sarcopenia, cachexia) conditions; and Objective 3) to determine key processes responsible for myofiber hypertrophy in response to mechanical overload, and to exploit these processes with countermeasures to promote muscle re-growth in atrophied patients. To meet these objectives, we are using genomic, proteomic, and in vitro approaches to study the molecular regulation of muscle protein synthesis, proteolysis, and stem (satellite) cell function in humans experiencing atrophy and resistance training-induced hypertrophy. This translational research program takes full advantage of cellular and molecular studies in our Core Muscle Research Laboratory and in vivo functional assessments during clinical trials in the UAB Center for Exercise Medicine.

Postdoc Positions Available
Date Posted Position Title
No records
 

Selected Publications 
Publication PUBMEDID
Mavalli MD, DiGirolamo DJ, Fan Y, Riddle RC, Campbell KS, van Groen T, Frank SJ, Sperling MA, Esser KA, Bamman MM, and Clemens TL. Distinct growth hormone receptor signaling modes regulate skeletal muscle development and insulin sensitivity in mice. J Clin Invest. 120(11):4007-20, 2010.  20921627 
Bickel CS, JM Cross, and MM Bamman. Exercise dosing to retain resistance training adaptations in young and older adults. Med Sci Sports Exerc. 43(7):1177-87, 2011.  21131862 
Mayhew DL, TA Hornberger, HC Lincoln, and MM Bamman. Eukaryotic initiation factor 2B-epsilon; induces cap-dependent translation and skeletal muscle hypertrophy. J Physiol. 2011, 11 Apr [Epub ahead of print].  21486778 
Kim JS, JK Petrella, JM Cross, and MM Bamman. Load-mediated down-regulation of myostatin mRNA is not sufficient to promote myofiber hypertrophy in humans: a cluster analysis. J Appl Physiol. 103: 1488-95, 2007.  17673556 
Petrella JK, JS Kim, DL Mayhew, and MM Bamman. Potent myofiber hypertrophy during resistance training in humans is associated with satellite cell-mediated myonuclear addition: a cluster analysis. J Appl Physiol. 104(6):1736-42, 2008.  18436694 
Mayhew DL, JS Kim, JM Cross, AA Ferrando, and MM Bamman. Translational signaling responses preceding resistance training-mediated myofiber hypertrophy in young and old humans. J Appl Physiol. 2009 Nov;107(5):1655-62.  19589955 
Thalacker-Mercer A, LJ Dell’Italia, X Cui, JM Cross, and MM Bamman. Differential genomic responses in old vs. young humans despite similar levels of modest muscle damage after resistance loading. Physiological Genomics. 2010 Feb 4;40(3):141-9.  19903761 
Petrella JK, JS Kim, JM Cross, DJ Kosek, and MM Bamman. Efficacy of myonuclear addition may explain differential myofiber growth among resistance trained young and older men and women. Am J Physiol Endocrinol Metab. 291(5):E937-46, 2006.  16772322 
Bamman MM, JK Petrella, JS Kim, DL Mayhew, and JM Cross. Cluster analysis tests the importance of myogenic gene expression during myofiber hypertrophy in humans. J Appl Physiol. 102:2232-9, 2007.  17395765 
Bamman MM, MSF Clarke, DL Feeback, RJ Talmadge, BR Stevens, SA Lieberman, and MC Greenisen. Impact of resistance exercise during bed rest on skeletal muscle sarcopenia and myosin isoform distribution. J Appl Physiol. 84(1):157-163, 1998.  9451630 
 

Keywords
aging, sarcopenia, muscle, disuse, exercise, satellite cell

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