A systems-based investigation into vitamin D and skeletal muscle repair, regeneration, and hypertrophy.
Skeletal muscle is a direct target for vitamin D. Observational studies suggest that low 25[OH]D correlates with functional recovery of skeletal muscle following eccentric contractions in humans and crush injury in rats. However, a definitive association is yet to be established. To address this gap in knowledge in relation to damage repair, a randomised, placebo-controlled trial was performed in 20 males with insufficient concentrations of serum 25(OH)D (45 ± 25 nmol/l). Prior to and following 6 wk of supplemental vitamin D3 (4,000 IU/day) or placebo (50 mg of cellulose), participants performed 20 × 10 damaging eccentric contractions of the knee extensors, with peak torque measured over the following 7 days of recovery. Parallel experimentation using isolated human skeletal muscle-derived myoblast cells from biopsies of 14 males with low serum 25(OH)D (37 ± 11 nmol/l) were subjected to mechanical wound injury, which enabled corresponding in vitro studies of muscle repair, regeneration, and hypertrophy in the presence and absence of 10 or 100 nmol 1α,25(OH)2D3. Supplemental vitamin D3 increased serum 25(OH)D and improved recovery of peak torque at 48 h and 7 days postexercise. In vitro, 10 nmol 1α,25(OH)2D3 improved muscle cell migration dynamics and resulted in improved myotube fusion/differentiation at the biochemical, morphological, and molecular level together with increased myotube hypertrophy at 7 and 10 days postdamage. Together, these preliminary data are the first to characterize a role for vitamin D in human skeletal muscle regeneration and suggest that maintaining serum 25(OH)D may be beneficial for enhancing reparative processes and potentially for facilitating subsequent hypertrophy.
Research Institute for Sport and Exercise Science, Liverpool John Moores University, Liverpool, United Kingdom;
Daniel J
DJ
Owens
Research Institute for Sport and Exercise Science, Liverpool John Moores University, Liverpool, United Kingdom;
Adam P
AP
Sharples
Research Institute for Sport and Exercise Science, Liverpool John Moores University, Liverpool, United Kingdom;
Ioanna
I
Polydorou
Research Institute for Sport and Exercise Science, Liverpool John Moores University, Liverpool, United Kingdom;
Nura
N
Alwan
Department of Sport and Exercise Sciences, Glyndwr University, Plas Coch Campus, Wrexham, United Kingdom;
Timothy
T
Donovan
Faculty of Medicine and Health Science, Norwich Medical School, University of East Anglia, Norwich, United Kingdom; and.
Jonathan
J
Tang
Faculty of Medicine and Health Science, Norwich Medical School, University of East Anglia, Norwich, United Kingdom; and.
William D
WD
Fraser
Medical Research Council-Arthritis Research UK Centre for Integrated Research into Musculoskeletal Ageing, University of Liverpool, Liverpool, United Kingdom.
Robert G
RG
Cooper
Research Institute for Sport and Exercise Science, Liverpool John Moores University, Liverpool, United Kingdom;
James P
JP
Morton
Research Institute for Sport and Exercise Science, Liverpool John Moores University, Liverpool, United Kingdom;
Claire
C
Stewart
Research Institute for Sport and Exercise Science, Liverpool John Moores University, Liverpool, United Kingdom; g.l.close@ljmu.ac.uk.
Graeme L
GL
Close
D000284:Administration, Oral; D000293:Adolescent; D000328:Adult; D019587:Dietary Supplements; D006801:Humans; D006984:Hypertrophy / Q000097:blood / Q000188:drug therapy / Q000503:physiopathology; D018482:Muscle, Skeletal / Q000187:drug effects / Q000473:pathology* / Q000503:physiopathology*; D005082:Physical Exertion; D015990:Placebo Effect; D012038:Regeneration / Q000502:physiology*; D049490:Systems Biology / Q000379:methods; D014807:Vitamin D / Q000008:administration & dosage* / Q000097:blood*; D055815:Young Adult
D014807:Vitamin D
muscle damage; regeneration; vitamin D