It has been suggested that exercise intensity is of importance in the regulation of increase in pro-inflammatory molecules, but there is still a debate about the effect of duration on these molecules. Therefore, the effect of exercise duration on the serum concentrations of interleukin-6 (IL-6), tumour necrosis factor-α (TNF-α), soluble form of intercellular adhesion molecule-1 (sICAM-1), and matrix metalloproteinase-9 (MMP-9) was studied in 22 half-marathon (HM) and 18 marathon (M) male amateur runners who completed their exercise task in 1.8 ± 0.2 (mean ± standard deviation) and 3.6 ± 0.4 h, respectively (thus, average speed was 11.7 ± 1.5 and 11.9 ± 1.8 km h(-1), respectively). Blood was sampled 2 days before, 15 min after, and 28 h after the race. IL-6, TNF-α, and MMP-9 always increased immediately after exercise, but the increase was larger (P < 0.05) in M versus HM (∆IL-6: 31 ± 24 vs. 5 ± 4 pg ml(-1); ∆TNF-α: 1.7 ± 1.9 vs. 0.5 ± 0.8 pg ml(-1); MMP-9: 288 ± 216 vs. 145 ± 128 ng ml(-1), respectively). sICAM-1 also increased with exercise, but similarly in M and HM (20 ± 40 vs. 23 ± 32 ng ml(-1), respectively). Only sICAM-1 remained elevated 28 h post-exercise in both HM and M, while IL-6, TNF-α, and MMP-9 returned to pre-exercise levels. Competitive HM and M races induce significant increases in IL-6, TNF-α, sICAM-1, and MMP-9 concentrations. As HM and M runners performed the competition with similar absolute intensity, the difference in response between the groups suggests that exercise duration is of importance in the regulation of IL-6, TNF-α, and MMP-9, but not sICAM-1 concentrations in response to prolonged running.

Since hyperglycaemia changes the erythrocyte cell membrane fluidity and impairs cell deformity, our goal was to characterize hemoglobin and red blood cell (RBC) light refractive property changes in diabetic patients. Microscopic investigation was carried out on intact and fixed RBCs. To determine the refractive index (RI): smears of peripheral blood were air dried and fixed for 3 min in methanol. Mixtures of polyvinylpyrolidine and buffer of different pH (1:1) were used as embedding media. Intact RBCs were mixed with a buffered embedding medium, placed on a slide and overlaid with a coverslip. Interference microscopy was used for RI measurements at 18 different pH (pH=2-13). The results showed that curves of the RI of diabetic patients and of a control group were of similar configuration, with one branch in the acidic portion of the pH scale, a maximum and two minima in the neutral (middle) portion, and one branch in the alkaline portion. The curves of the individuals from the control group overlapped each other. To the contrary, the curves of the diabetic patients were not uniform in the neutral portion and the alkaline portion. The curves of the diabetic patients in the neutral zone were shifted towards the alkaline end of the pH scale, and the RBC RI curves were lower in comparison to the control curves. The center maximum of the curves of diabetic patients corresponded to pH=6.6 whereas the central maximum of the control group curves was at pH=6.2-6.8. Contrary to in the diabetic group, intact RBC RI curves in the control group revealed only one significantly different minimum at pH of 7.2 in the neutral zone. Using this method it is possible to show phenotypic differences between uniform type intact and fixed cells, erythrocytes of diabetic patients and of healthy donors.

The aim of this study was to test the hypothesis that exercise would induce inflammatory response characterized by increased pro‐inflammatory cytokines – interleukin‐6 (IL‐6) and tumour necrosis factor‐α (TNF‐α), adhesion molecule, matrix metalloprotease‐9 (MMP‐9) and myeloperoxidase (MPO) levels. Additional aim was to elucidate the possible source of maximal exercise‐induced increase in MMP‐9 concentration. To examine our hypothesis, 26 professional male ice hockey players [age 25 ± 1 (mean ± SEM) years; BMI 25.8 ± 0.4 kg/m2] performed an incremental bicycle test until exhaustion, when maximal oxygen consumption was recorded. Venous blood samples were collected 30 min before and 2 min after exercise. There was an increase in the count of leucocytes (8.7 ± 1.8 versus 5.7 ± 1.3 × 109 cells per l) and IL‐6 (1.24 ± 0.17 versus 0.69 ± 0.13 pg/ml), MPO (72 ± 7 versus 50 ± 4 ng/ml) and MPP‐9 (139 ± 9 versus 110 ± 6 ng/ml) concentrations (P < 0.05) comparing post‐ and pre‐exercise levels. Maximal exercise‐induced increase in MPO correlated with the increases in IL‐6 (P < 0.05, R = 0.54) and MMP‐9 (P < 0.01, R = 0.62) concentrations. Furthermore, increase in IL‐6 correlated with the increase in MMP‐9 concentrations (P < 0.05, R = 0.60). Maximal exercise induces an inflammatory response characterized by leucocytosis and increased IL‐6, MPO and MMP‐9 concentrations. Correlations between increased MPO (marker of neutrophils degranulation) and both increased IL‐6 and MMP‐9 concentrations may suggest that neutrophils could be the main source of these inflammatory biomarkers during maximal exercise. Furthermore, correlation between increases in serum IL‐6 and MMP‐9 concentrations may suggest that IL‐6 could exert modulatory effects on MMP‐9 release during maximal exercise.

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Serum IL-6 with a cut-off value of 4.3pg/mL and WBC with a cut-off value of 10.7×10/μL assessed together will yield more sensitivity for AA.

Aim: To evaluate the levels of nitrite (NO^–₂) and nitrate (NO^–₃) ions and the incorporation of [³H]arachidonic acid (AA) into phospholipids of platelet membranes from coronary artery disease (CAD) patients with and without diabetes (NIDDM). Subjects and Methods: Eighteen CAD patients (group A), 18 CAD patients with NIDDM (group B), and 20 healthy controls (group C) without dyslipidemia, peripheral vascular disease and hypertension were included in the study. The groups were matched for age, sex and body mass index. The diagnosis of CAD was confirmed by coronary angiography. The nitric oxide end products (NOx), NO^–₂ plus NO^–₃ ions in platelet membranes, were determined using a spectrophotometric method based on the Griess reaction. The turnover of phospholipids was evaluated by incorporation of [³H]AA into platelet membrane phospholipids. Results: A significantly smaller amount of NOx ions was in the platelet membrane of groups A (40 ± 8 µmol/l) and B (29 ± 10 µmol/l) than C (57 ± 6 µmol/l), p < 0.001. Conversely a significantly greater amount of [³H]AA was incorporated into platelet phospholipids of group B patients (5,123 ± 1,637 dpm/mg) than groups A (3,159 ± 1,253 dpm/mg; p < 0.002) and C (1,621 ± 417 dpm/mg). An inverse correlation between [³H]AA incorporation and NOx levels was established: r = –0.76 (p < 0.05, n = 36) in CAD patients. Conclusions: Diabetes in CAD patients decreased the ability to produce platelet-derived NO and affects AA metabolism. This may result in higher platelet sensitivity to aggregating stimuli.

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