Vitamin D3 supplementation modulates inflammatory responses from the muscle damage induced by high-intensity exercise in SD rats

Cytokine. 2013 Jul;63(1):27-35. doi: 10.1016/j.cyto.2013.03.018. Epub 2013 May 10.

Abstract

Vitamin D is an important factor for calcium and phosphorus homeostasis. A negative relationship has been observed between vitamin D status and diseases such as cancer, arthritis, diabetes, and muscle fiber atrophy. However, the relationship between vitamin D and prevention of skeletal muscle damage has not been clearly elucidated. The purpose of this study was to investigate the effects of vitamin D on exercise-induced muscle changes. Rats were divided into 3 groups: (1) sedentary control (C: n=10), (2) high-intensity exercise (HE: n=10), and (3) high-intensity exercise with vitamin D supplementation (HED: n=10; i.p. 1000 IU/kg body weight). Rats were trained for 30 min/day on treadmills (5 days/week for 8 weeks) with the running speed gradually increased up to 30 m/min at a 3° incline. At the end of the training period, the running speed was 38 m/min at a 5° incline. The high-intensity exercise significantly increased plasma creatine kinase (CK) and lactate dehydrogenase (LDH) activity. In addition, IL-6 and TNF-α levels as well as phosphorylation of AMPK, p38, ERK1/2, IKK, and IκB were significantly increased. Vitamin D-treated rats showed a significant decrease in plasma CK level, phosphorylation of AMPK, p38, ERK1/2, IKK, and IκB, and gene expression of IL-6 and TNF-α. Furthermore, the protein expression of vitamin D receptor (VDR) was highly increased in the muscles of HED-treated rats, respectively. Therefore, we concluded that vitamin D may play a pivotal role in exercise-induced muscle damage and inflammation through the modulation of MAPK and NF-κB involved with VDR.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Biomarkers / blood
  • Cholecalciferol / pharmacology
  • Cholecalciferol / therapeutic use*
  • Creatine Kinase / blood
  • Cytoplasm / drug effects
  • Cytoplasm / metabolism
  • Dietary Supplements*
  • Enzyme-Linked Immunosorbent Assay
  • Gene Expression Regulation / drug effects
  • Inflammation / drug therapy*
  • Inflammation / genetics
  • Inflammation / pathology
  • Interleukin-6 / blood
  • Interleukin-6 / genetics
  • Interleukin-6 / metabolism
  • L-Lactate Dehydrogenase / blood
  • MAP Kinase Signaling System
  • Male
  • Muscle, Skeletal / drug effects
  • Muscle, Skeletal / metabolism
  • Muscle, Skeletal / pathology*
  • NF-kappa B / metabolism
  • Phosphorylation
  • Physical Conditioning, Animal / adverse effects*
  • Rats
  • Rats, Sprague-Dawley
  • Real-Time Polymerase Chain Reaction
  • Receptors, Calcitriol / metabolism
  • Tumor Necrosis Factor-alpha / blood
  • Tumor Necrosis Factor-alpha / genetics
  • Tumor Necrosis Factor-alpha / metabolism

Substances

  • Biomarkers
  • Interleukin-6
  • NF-kappa B
  • Receptors, Calcitriol
  • Tumor Necrosis Factor-alpha
  • Cholecalciferol
  • L-Lactate Dehydrogenase
  • Creatine Kinase