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Michael Friedman, Ph.D. - VCU College of Engineering. Richmond, VA, US

Michael Friedman, Ph.D.

Research Assistant Professor | VCU College of Engineering


Dr. Friedman's research investigates the role of genetic variability in the musculoskeletal response to spaceflight and disuse.






Future Leaders in Mechanobiology Seminar: Michael Friedman




Dr. Michael Friedman is a Research Assistant Professor in Dr. Henry Donahue’s lab in Biomedical Engineering at Virginia Commonwealth University. Michael received a BS in BME from University of Texas at Austin and a MSE and Ph.D. in BME from University of Michigan. Michael received a NASA Translational Research Institute for Space Health Postdoctoral Research Fellow postdoctoral fellowship that studied the effects of genetic variability on the musculoskeletal response to unloading. This groundbreaking work led to young investigator awards from the Orthopaedic Research Society and American Society for Bone and Mineral Research. Additionally, Michael was awarded a NASA TRISH Go for Launch Grant to continue this work as a principal investigator. Michael is interested in establishing a lab studying the effects of mechanical loading and unloading on bone and skeletal muscle, focusing on how aging and disuse negatively affect these tissues.

Areas of Expertise (6)


Exercise Physiology

Skeletal Muscle Physiology




Education (3)

University of Michigan: PhD, Biomedical Engineering 2015

University of Michigan: MSE, Biomedical Engineering 2008

University of Texas at Austin: BS, Biomedical Engineering 2006

Media Appearances (1)

VCU researcher receives NASA funding to study bone, muscle loss in spaceflight

The Commonwealth Times  online


News article announcing the research we are doing for the NASA Go For Launch Award.

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Selected Articles (2)

Genetic variability affects the skeletal response to immobilization in founder strains of the diversity outbred mouse population

Bone Reports

Michael A. Friedman, Abdullah Abood, Bhavya Senwar, Yue Zhang, Camilla Reina Maroni, Virginia L.Ferguson, Charles R.Farber, Henry J.Donahue


Mechanical unloading decreases bone volume and strength. In humans and mice, bone mineral density is highly heritable, and in mice the response to changes in loading varies with genetic background. Thus, genetic variability may affect the response of bone to unloading. As a first step to identify genes involved in bones' response to unloading, we evaluated the effects of unloading in eight inbred mouse strains: C57BL/6J, PWK/PhJ, WSB/EiJ, A/J, 129S1/SvImJ, NOD/ShiLtJ, NZO/HlLtJ, and CAST/EiJ. C57BL/6J and NOD/ShiLtJ mice had the greatest unloading-induced loss of diaphyseal cortical bone volume and strength. NZO/HlLtJ mice had the greatest metaphyseal trabecular bone loss, and C57BL/6J, WSB/EiJ, NOD/ShiLtJ, and CAST/EiJ mice had the greatest epiphyseal trabecular bone loss. Bone loss in the epiphyses displayed the highest heritability. With immobilization, mineral:matrix was reduced, and carbonate:phosphate and crystallinity were increased. A/J mice displayed the greatest unloading-induced loss of mineral:matrix. Changes in gene expression in response to unloading were greatest in NOD/ShiLtJ and CAST/EiJ mice. The most upregulated genes in response to unloading were associated with increased collagen synthesis and extracellular matrix formation. Our results demonstrate a strong differential response to unloading as a function of strain. Diversity outbred (DO) mice are a high-resolution mapping population derived from these eight inbred founder strains. These results suggest DO mice will be highly suited for examining the genetic basis of the skeletal response to unloading.

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Combined mineral-supplemented diet and exercise increases bone mass and strength after eight weeks and maintains increases after eight weeks detraining in adult mice


Michael A. Friedman, Robert P. Szczepankiewicz, David H. Kohn


Exercise has long-lasting benefits to bone mass and structural strength even after cessation. Combining exercise with a calcium- and phosphorus-supplemented diet increases cortical bone mineral content (BMC), area, and yield force more than exercise alone in adult mice. These increases could also be maintained after stopping exercise if the modified diet is maintained. It was hypothesized that combining exercise with a mineral-supplemented diet would lead to greater cortical BMC, area, and yield force immediately after a lengthy exercise program and after an equally long period of non-exercise (detraining) in adult mice. Male, 16-week old C57Bl/6 mice were assigned to 9 weight-matched groups–a baseline group, exercise and non-exercise groups fed a control or mineral-supplemented diet for 8 weeks, exercise + detraining and non-exercise groups fed a control or mineral-supplemented diet for 16 weeks. Exercise + detraining consisted of 8 weeks of exercise followed by 8 weeks without exercise. The daily exercise program consisted of running on a treadmill at 12 m/min, 30 min/day. After 8 weeks, mice fed the supplemented diet had greater tibial cortical BMC and area, trabecular bone volume/tissue volume (BV/TV), bone mineral density (vBMD), yield force, and ultimate force than mice fed the control diet. Exercise increased cortical BMC and area only when coupled with the supplemented diet. After 16 weeks, both exercised and non-exercised mice fed the supplemented diet maintained greater tibial cortical BMC and area, trabecular BV/TV, vBMD, yield force, and ultimate force than mice fed the control diet. Combining exercise with a mineral-supplemented diet leads to greater bone mass and structural strength than exercise alone. These benefits remain after an equally long period of detraining. Long-term use of dietary mineral supplements may help increase and maintain bone mass with aging in adult mice.

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