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.

ObjectiveDifferent studies have demonstrated that regular exercise can induce changes in the lipid profile, but results remain inconclusive. Available data suggest that correction of vitamin D deficiency can improve the lipid profile. In this study, we have hypothesized that Nordic Walking training will improve lipid profile in elderly women supplemented with vitamin D.MethodsA total of 109 elderly women (68 ± 5.12 years old) took part in the study. First group [experimental group (EG): 35 women] underwent 12 weeks of Nordic Walking (NW) training combined with vitamin D supplementation (4,000 IU/day), second group [supplementation group (SG): 48 women] was only supplemented with vitamin D (4,000 IU/day), and third group [control group (CG): 31 women] was not subject to any interventions. Blood analysis of total cholesterol (TC), triglycerides (TG), high-density lipoprotein cholesterol (HDL-C), low-density lipoprotein cholesterol (LDL-C), and 25-OH-D3 was performed at baseline and after the 12 weeks of NW training. Additionally, a battery of field tests specifically developed for older adults was used to assess the components of functional fitness. The same blood analysis was repeated for the EG 6 months after the main experiment.ResultsAfter 12 weeks of NW training and vitamin D supplementation, in the EG a decrease in TC, LDL-C, and TG was observed. In the SG, no changes in the lipid profile were observed, whereas in the CG an increase in the HDL-C level was noticed. Positive physical fitness changes were only observed in the EG.ConclusionOur obtained data confirmed baseline assumption that regular exercise induces positive alternations in lipid profile in elderly women supported by supplementation of vitamin D.

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The aim of the study was to verify if coupling 12 weeks of vitamin D supplementation and Nordic walking training favoured lowering the homocysteine (Hcy) level. Ninety-four elderly women were divided into three groups: Nordic walking (NW), supplemented (SG) and control (CG). The NW and SG groups received a weekly dose of 28,000 IU of vitamin D3. A blood analysis was performed at baseline, 1h after the first training session and at the end of the experiment. The amino acid profile (methionine and cysteine) and homocysteine concentration were determined. Additionally, the concentration of myokine was assessed. The first session of NW training reduced serum homocysteine, particularly among women with baseline homocysteine above 10 µmol·L−1: 12.37 ± 2.75 vs. 10.95 ± 3.94 µmol·L−1 (p = 0.05). These changes were accompanied by shifts in the cysteine (p = 0.09) and methionine (p = 0.01) concentration, regardless of the Hcy concentration. Twelve weeks of training significantly decreased the homocysteine (9.91 ± 2.78, vs. 8.90 ± 3.14 µmol·L−1, p = 0.05) and ferritin (94.23 ± 62.49 vs. 73.15 ± 47.04 ng·mL−1, p = 0.05) concentrations in whole NW group. Also, in the NW group, ferritin correlated with the glucose level (r = 0.51, p = 0.00). No changes in the myokine levels were observed after the intervention. Only the brain-derived neurotrophic factor dropped in the NW (42.74 ± 19.92 vs. 31.93 ± 15.91 ng·mL−1, p = 0.01) and SG (37.75 ± 8.08 vs. 16.94 ± 12.78 ng·mL−1, p = 0.00) groups. This study presents a parallel decrease of homocysteine and ferritin in response to regular training supported by vitamin D supplementation.

Because mutation of AMP deaminase 1 gene leading to reduced AMP deaminase activity may result in protection of cardiac function in patients with heart disease, inhibitors of AMP deaminase (AMPD) may have therapeutic applications. This study evaluated the effect of a specific inhibitor of AMP deaminase 3-[2-(3-carboxy-4-bromo-5,6,7,8-tetrahydronaphthyl)ethyl]-3,6,7,8-tetrahydroimidazo [4,5-d][1,3]diazepin-8-ol (AMPDI) on the isolated human enzyme and on nucleotide catabolism in rat cardiomyocytes. AMPDI effectively inhibited isolated human AMPD with an IC(50) = 0.5 micro M. AMPDI was much less effective with isolated cardiomyocytes (IC(50) = 0.5 mM). AMPDI is a very effective inhibitor of AMPD that despite lower efficiency in the cell system examined could be useful for in vivo studies.