title: Vitamin D3 supplementation modulates inflammatory responses from the muscle damage induced by high-intensity exercise in SD rats.
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.
authors.affiliation: Dept. of Food and Nutrition and Research Institute of Obesity Sciences, Sungshin Women's University, Seoul, Republic of Korea.
authors.forename: Munji
authors.initials: M
authors.lastname: Choi
authors.affiliation: Exercise Nutrition & Biochem Lab, Kyung Hee University, Yongin, Republic of Korea.
authors.forename: Hyon
authors.initials: H
authors.lastname: Park
authors.affiliation: Taeneung National Training Center of Korean Olympic Committee, Seoul, Republic of Korea.
authors.forename: Seongsuk
authors.initials: S
authors.lastname: Cho
authors.affiliation: Dept. of Food and Nutrition and Research Institute of Obesity Sciences, Sungshin Women's University, Seoul, Republic of Korea. Electronic address: mlee@sungshin.ac.kr.
authors.forename: Myoungsook
authors.initials: M
authors.lastname: Lee
mesh_terms: D000818:Animals; D015415:Biomarkers / Q000097:blood; D002762:Cholecalciferol / Q000494:pharmacology / Q000627:therapeutic use*; D003402:Creatine Kinase / Q000097:blood; D003593:Cytoplasm / Q000187:drug effects / Q000378:metabolism; D019587:Dietary Supplements; D004797:Enzyme-Linked Immunosorbent Assay; D005786:Gene Expression Regulation / Q000187:drug effects; D007249:Inflammation / Q000188:drug therapy* / Q000235:genetics / Q000473:pathology; D015850:Interleukin-6 / Q000097:blood / Q000235:genetics / Q000378:metabolism; D007770:L-Lactate Dehydrogenase / Q000097:blood; D020935:MAP Kinase Signaling System; D008297:Male; D018482:Muscle, Skeletal / Q000187:drug effects / Q000378:metabolism / Q000473:pathology*; D016328:NF-kappa B / Q000378:metabolism; D010766:Phosphorylation; D010805:Physical Conditioning, Animal / Q000009:adverse effects*; D051381:Rats; D017207:Rats, Sprague-Dawley; D060888:Real-Time Polymerase Chain Reaction; D018167:Receptors, Calcitriol / Q000378:metabolism; D014409:Tumor Necrosis Factor-alpha / Q000097:blood / Q000235:genetics / Q000378:metabolism
chemical_list: D015415:Biomarkers; D015850:Interleukin-6; D016328:NF-kappa B; D018167:Receptors, Calcitriol; D014409:Tumor Necrosis Factor-alpha; D002762:Cholecalciferol; D007770:L-Lactate Dehydrogenase; D003402:Creatine Kinase