Objectives The present study aimed to investigate the anti-inflammatory effects of vitamin D and resistance training in men with type 2 diabetes mellitus and vitamin D deficiency. Design This study was a randomized, placebo-controlled, double-blinded clinical trial. Trial registration code: IRCT20190204042621N1 Participants Forty-eight patients with type 2 diabetes aged 40-65 (from a total of 52 volunteers in Ardabil diabetes clinic) were randomly assigned to either the vitamin D supplementation with resistance training group (VD + RT: n = 12), the resistance training group (RT: n = 12), the vitamin D supplementation group (VD: n = 12), or the control group (CON: n = 12). Intervention The subjects in VD group took vitamin D supplements at 50000 IU per 2 weeks for 3 months; the subjects in RT group exercised 3 times per week for 12 weeks; and the subjects in VD + RT group participated in both treatments. Subjects in CON group were asked to maintain normal daily life pattern for the duration of the study. Measurements Serum Interleukin-6 (IL-6), Tumor Necrosis Factor-alpha (TNF-α) and C-reactive protein (CRP) levels were determined at pre and post-test and the data were compared among the four groups and between two tests (4 × 2) using two-way ANOVA with repeated measures. Results IL-6 decreased significantly (P = 0.001) in all groups (VD + RT = %-71.73, RT = %-65.85, VD = %-61.70). TNF-α decreased significantly (P = 0.001) in VD + RT (%-44.90) and RT (%-40) groups. CRP showed no significant change in any group (P > 0.05). Conclusion Results demonstrated that vitamin D supplementation in addition to resistance training had positive effects on some inflammatory markers in T2D and vitamin D deficient men. Vitamin D supplementation was especially effective when it was complemented with exercise training.

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This study was designed to examine the effect of moderate (MR) and high resistance (HR) training on systemic inflammation and circulating enzymatic antioxidant activity. Thirty males were assigned to HR (n = 10), MR (n = 10), or control (C; n = 10) groups. Resistance training was performed for eight weeks. Activities of superoxide dismutase (SOD), glutathione peroxidase (GPX), creatine kinase (CK), and concentrations of malondialdehyde (MDA), interleukin-6 (IL-6), and tumor necrosis factor-alpha (TNF-α) were measured before and after training in plasma. The results show increased SOD activity in MR (p = 0.026) and HR (p = 0.044) groups. GPX activity in HR (p = 0.012) and MR (p = 0.037) increased significantly more than in C. Whilst a significant reduction in MDA in MR (p = 0.013) and HR (p = 0.023) was observed compared with C, no significant difference in IL-6, TNF-α and CK occurred between groups. We conclude that changes in enzymatic antioxidant defense and inflammatory markers following resistance training are independent of training intensity.

This study was undertaken to investigate the effects of progressive resistance-training (PRT) on plasma oxidative stress and antioxidant enzyme activity in erythrocytes. Twenty male volunteers were randomly assigned to 2 groups: PRT and control. Blood samples were collected before and after 8 wk of PRT and analyzed for enzymatic activities of superoxide dismutase (SOD) and glutathione peroxidase (GPx) in erythrocytes, plasma total antioxidant capacity (TAC), and malondialdehyde concentration (MDA, an index of lipid per oxida- tion in plasma). Resistance training commenced with 8 exercises on nonconsecutive days for 8 wk at 50% of estimated 1-repetition maximum (E1RM) and reached 80% E1RM by Week 8. The results showed that PRT significantly increased erythrocyte SOD activity (1,323 ± 212.52 vs. 1,449.9 ± 173.8 U/g Hb, p = .014). Plasma concentration of MDA also decreased (5.39 ± 1.7 vs. 3.67.4 ± 0.7 nmol/ml, p = .030), although TAC (1.42 ± 0.21 vs. 1.61 ± 0.19 mmol/L, p = .1530) and GPx (39.87 ± 11.5 vs. 48.18 ± 14.48 U/g Hb, p = .883) activity did not undergo any considerable changes. Based on these data, the authors conclude that an 8-wk program of PRT strengthens the defensive system of erythrocytes against free-radical damage and therefore can be applied as a useful approach to alleviate oxidative stress.

Background: It is well known that green tea has antioxidant properties. Accordingly, it is important to investigate the effects of green tea on systemic inflammation and oxidative stress indices in humans during high intensity resistance training, especially in obese men. Objectives: The aim of the present study was to examine the effect of green tea extract supplementation during high intensity resistance exercise training on oxidative stress and systemic inflammation indices in obese men. Methods: Twenty obese men (body mass index ≥ 30) voluntarily participated in the current study and were randomly assigned to groups of green tea and high intensity resistance training (RT) (GR; n = 10) and placebo and high intensity resistance training (PR; n = 10). RT was performed three times a week on non-consecutive days for eight weeks. The training started at 80% of one-repetition maximum (1RM), and training intensity reached to 90-95% of 1RM till the end of the eighth week. The GR group consumed a green tea capsule (500 mg) each day during the eight weeks. Blood samples were collected before and after the intervention and were tested for malondialdehyde (MDA) and total antioxidant capacity (TAC). Concentrations of ofinterleukin-6 (IL-6), tumor necrosis factor-alpha (TNF-alpha), and C-reactive protein (CRP) in plasma were also measured. Results: The results indicated significant (P < 0.05) or near significant improvements in all the measured blood parameters with training, but no further effects (interactions) with ingestion of green tea. Also, we found that there was not any significant relationship between MDA and TAC changes and TNF-alpha and IL-6 in either group after RT intervention and supplementation (P > 0.05). Conclusions: Thus, it can be stated that low-dose green tea supplementation does not influence inflammatory and oxidative stress indices when provided along with exercise training.