An attenuation of markers of free radical damage of lipids and proteins was observed in participants supplemented with Vitamin D. Antioxidant enzyme activities in skeletal muscle differ among patients with different serum vitamin D concentration. Monitoring oxidative stress and VDR protein content might be useful for future studies on the mechanism(s) of vitamin D action in muscle.

Recent studies show that vitamin D deficiency may be responsible for muscle atrophy. The purpose of this study was to investigate markers of muscle atrophy, signalling proteins, and mitochondrial capacity in patients with chronic low back pain with a focus on gender and serum vitamin D level. The study involved patients with chronic low back pain (LBP) qualified for posterior lumbar interbody fusion (PLIF). Patients were divided into three groups: supplemented (SUPL) with vitamin D (3200 IU/day for 5 weeks), placebo with normal levels of vitamin D (SUF), and the placebo group with vitamin D deficiency (DEF). The marker of muscle atrophy including atrogin-1 and protein content for IGF-1, Akt, FOXO3a, PGC-1α, and citrate synthase (CS) activity were determined in collected multifidus muscle. In the paraspinal muscle, IGF-1 levels were higher in the SUF group as compared to both the SUPL and DEF groups (p<0.05). In the SUPL group, we found significantly increased protein content for pAkt (p<0.05) and decreased level of FOXO3a (p<0.05). Atrogin-1 content was significantly different between men and women (p<0.05). The protein content of PGC-1α was significantly higher in the SUF group as compared to the DEF group (p<0.05). CS activity in the paraspinal muscle was higher in the SUPL group than in the DEF group (p<0.05). Our results suggest that vitamin D deficiency is associated with elevated oxidative stress, muscle atrophy, and reduced mitochondrial function in the multifidus muscle. Therefore, vitamin D-deficient LBP patients might have reduced possibilities on early and effective rehabilitation after PLIF surgery.

(1) The study aimed to investigate whether vitamin D3 supplementation would positively affect rats with glucocorticoids-induced muscle atrophy as measured by skeletal muscle mass in two experimental conditions: chronic dexamethasone (DEX) administration and a model of the chronic stress response. (2) The study lasted 28 consecutive days and was performed on 45 male Wistar rats randomly divided into six groups. These included two groups treated by abdominal injection of DEX at a dose of 2 mg/kg/day supplemented with vegetable oil (DEX PL; n = 7) or with vitamin D3 600 IU/kg/day (DEX SUP; n = 8), respectively, and a control group treated with an abdominal injection of saline (CON; n = 6). In addition, there were two groups of rats chronically stressed by cold water immersion (1 hour/day in a glass box with 1-cm-deep ice/water mixture; temperature ~4 °C), which were supplemented with vegetable oil as a placebo (STR PL; n = 9) or vitamin D3 at 600 IU/kg/day (STR SUP; n = 9). The last group was of sham-stressed rats (SHM; n = 6). Blood, soleus, extensor digitorum longus, gastrocnemius, tibialis anterior, and quadriceps femoris muscles were collected and weighed. The heart, liver, spleen, and thymus were removed and weighed immediately after sacrifice. The plasma corticosterone (CORT) and vitamin D3 metabolites were measured. (3) We found elevated CORT levels in both cold water-immersed groups; however, they did not alter body and muscle weight. Body weight and muscle loss occurred in groups with exogenously administered DEX, with the exception of the soleus muscle in rats supplemented with vitamin D3. Decreased serum 25(OH)D3 concentrations in DEX-treated rats were observed, and the cold water immersion did not affect vitamin D3 levels. (4) Our results indicate that DEX-induced muscle loss was abolished in rats supplemented with vitamin D3, especially in the soleus muscle.

Recent studies indicate that activation of hypothalamus-pituitary-adrenocortical axis (HPA) plays the crucial role in stress response, while several lines of evidence mark the bed nucleus of the stria terminalis (BST) as a major mediator of the HPA axis responses to stress. The purpose of this study was to investigate the influence of the corticosterone flux induced by the electrical stimulation of BST on markers of free radical damage of lipids and proteins and antioxidant enzyme activity in skeletal muscle of rats. The male Wistar rats were used and assigned to one of three groups: sham-operated (SHM; n = 6), two-week (ST2; n = 6), and four-week stimulated (ST4; n = 5) groups. Blood, soleus, and extensor digitorum longus muscles were collected. The chronic, 4-week electrical stimulation of the BST evokes increased plasma corticosterone concentration, which resulted in oxidative stress in skeletal muscles. We found higher level of lipid peroxidation markers, lower level of protein oxidation marker, and elevated antioxidant enzyme activity in both muscles. Our findings have also potential implication showing that reaction to the long-term “psychological stress” may lead to free radical damage of muscle.

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