Mechanisms underpinning age-related decreases in muscle strength and muscle mass relate to chronic inflammation. Physical activity induces an anti-inflammatory effect, but it is modulated by additional factors. We hypothesized that vitamin D, which has also anti-inflammatory activity will modify adaptation to exercise and reduce inflammation in elderly women. Twenty-seven women aged 67 ± 8 years were included and divided into groups with baseline vitamin D concentration more than 20 ng mL−1 (MVD) and less than 20 ng mL−1 (LVD). Both groups performed 1 h Nordic Walking (NW) training combined with vitamin D supplementation for 12 weeks. Serum concentrations of inflammation markers, branched amino acids, vitamin D, muscle strength and balance were assessed at the baseline and three days after intervention. The training caused the significant decrease in concentration of pro-inflammatory proteins HMGB1 (30 ± 156%; 90% CI) and IL-6 (−10 ± 66%; 90% CI) in MVD group. This effects in group MVD were moderate, indicating vitamin D as one of the modifiers of these exercise-induced changes. Rise of myokine irisin induced by exercise correlated inversely with HMGB1 and the correlation was more pronounced at the baseline as well as after training among MVD participants. Although the intervention caused the leucine level to rise, a comparison of the recorded response between groups and the adjusted effect indicated that the effect was 20% lower in the LVD group. Overall the applied training program was effective in reducing HMGB1 concentration. This drop was accompanied by the rise of myokine irisin and better uptake of leucine among women with higher baseline vitamin D.

BackgroundAt present many young people experience too much body iron accumulation. The reason of this phenomenon is not clear. There is accumulating evidences that not proper diet and lack of exercise could be a main contributing factors. This investigation assessed the effects of a diet rich in simple sugars (glucose or fructose) on exercise-induced hepcidin which is hormone regulating iron metabolism.MethodsA group of physically active young men completed an incremental exercise test before and after a 3-day diet supplemented with fructose (4 g/kg BM) or glucose (4 g/kg BM). After a 1-week break, they crossed over to the alternate mode for the subsequent 3-days period. Venous blood samples were collected before and after 1 h exercise and were analysed for serum hepcidin, IL-6, CRP, iron, and ferritin. The physiological response to exercise was also determined.ResultsThe concentration of hepcidin increased 1 h after exercise for the baseline test (p < 0.05), whereas no changes in hepcidin were observed in men whose diet was supplemented with fructose or glucose. Blood IL-6 increased significantly after exercise only in subjects supplemented with fructose. Changes in hepcidin did not correlate with shifts in serum IL-6.ConclusionsThese data suggest that protective effects of exercise on excess iron accumulation in human body which is mediated by hepcidin can be abrogated by high sugar consumption which is typical for contemporary people.

Purpose: This study aimed to investigate the effects of 12 wk of omega-3 fatty acid supplementation during endurance training on omega-3 index (O3I) and indicators of running performance in amateur long-distance runners. Methods: Twenty-six amateur male long-distance runners ≥29 yr old supplemented omega-3 fatty acid capsules (OMEGA group, n = 14; 2234 mg of eicosapentaenoic acid and 916 mg of docosahexaenoic acid daily) or medium-chain triglycerides capsules as placebo (medium-chain triglyceride [MCT] group, n = 12; 4000 mg of MCT daily) during 12 wk of endurance training. Before and after intervention, blood samples were collected for O3I assessment, and an incremental test to exhaustion and a 1500-m run trial were performed. Results: O3I was significantly increased in the OMEGA group (from 5.8% to 11.6%, P < 0.0001). A significant increase in VO 2peak was observed in the OMEGA group (from 53.6 ± 4.4 to 56.0 ± 3.7 mL•kg −1 ⋅min −1 , P = 0.0219) without such change in MCT group (from 54.7 ± 6.8 to 56.4 ± 5.9 mL•kg −1 ⋅min −1 , P = 0.1308). A positive correlation between the change in O3I and the change in running economy was observed when data of participants from both groups were combined (−0.1808 ± 1.917, P = 0.0020), without such an effect in OMEGA group alone (P = 0.1741). No effect of omega-3 supplementation on 1500-m run results was observed. Conclusions: Twelve weeks of omega-3 fatty acid supplementation at a dose of 2234 mg of eicosapentaenoic acid and 916 mg of docosahexaenoic acid daily during endurance training resulted in the improvement of O3I and running economy and increased VO 2peak without improvement in the 1500-m run trial time in amateur runners.

Background: Vitamin D plays pleiotropic roles in the body and hence, changes in its metabolism and distribution during starvation could play an important role in the adaptive response to famine. We aimed to identify the responses of some vitamin D metabolites to 8 d of fasting and exercise. Methods: A repeated-measures design was implemented, in which 14 male volunteers fasted for 8 d and performed an exercise test before and after fasting. Serum samples were collected on day 1 after night fasting and after 8 d of complete food restriction, before and 1 h and 3 h after exercise. Results: After 8 d of fasting, compared with baseline values, serum 24,25(OH)2D3 and 3-epi-25(OH)D3 levels significantly increased; those of 25(OH)D3 and 1,25(OH)2D3 were unaffected; and those of 25(OH)D2 decreased. Exercise on the first day of fasting induced an increase in serum 3-epi-25(OH)D3 levels, while exercise performed after 8 d of fasting induced an increase in 25(OH)D3, 24,25(OH)2D3, 25(OH)D2, and 3-epi-25(OH)D3 levels. Conclusion: Increases in 24,25(OH)2D3 and 3-epi-25(OH)D3 levels imply that fasting stimulates vitamin D metabolism. The effects of exercise on serum vitamin D metabolites, which are most pronounced after fasting and in subjects with serum 25(OH)D3 above 25 ng/mL, support the notion that fasting and exercise augment vitamin D metabolism.

Alterations in iron metabolism after physical activity are manifested through the rise of blood hepcidin (Hpc) levels. However, in many athletes, no changes in Hpc levels are observed after exercise despite the presence of inflammation. The missing links could be erythropoietin (EPO) and erythroferrone (ERFE), which down-regulate Hpc biosynthesis. EPO, ERFE and Hpc biosynthesis is modified by serum iron through transferrin receptor 2. Consequently, we investigated whether marathon-induced changes in EPO, ERFE and Hpc levels are blood iron-dependent. Twenty-nine healthy male marathon runners were analyzed. Serum iron, ferritin, transferrin, EPO, ERFE and Hpc levels were assessed before, immediately after, and 9 ± 2 days after the marathon. The runners whose serum Hpc decreased after the marathon (n = 15), showed a significant increase in ERFE levels. In athletes whose serum iron levels were below 105 µg/day (n = 15), serum EPO (p = 0.00) and ERFE levels (p = 0.00) increased with no changes in Hpc concentration. However, in athletes with low serum iron, no changes in EPO levels were observed when serum ferritin exceeded 70 ng/mL (n = 7). Conversely, an increase in ERFE levels was observed in marathoners with low serum iron, independently of serum ferritin (n = 7). This indicates modulation of blood iron may affect exercise-induced changes in the EPO/ERFE/Hpc axis. Further study is needed to fully understand the physiological meaning of the interdependence between iron and the EPO/ERFE/Hpc axis.