Hakan Fiçicilar

Effect of submaximal and incremental upper extremity exercise on platelet function and the role of blood shear stress

INTRODUCTION Platelets are involved in the pathogenesis of atherosclerosis. Although physical exercise is recommended to prevent atherosclerosis, the effect of exercise on platelet function and the underlying mechanisms of these effects are not completely understood. Accordingly, we aimed to examine the effect of different intensities acute arm exercises on platelet function. In addition, we evaluated the effect of lipid peroxidation and fluid shear rate on platelet response. MATERIALS AND METHODS Twenty four healthy sedentary male volunteers aged 18-24 years performed submaximal and incremental exercises by upper extremity ergometer. The shear rate in the right artery was measured by Power Doppler Ultrasound (US) at rest and immediately after exercise. Pre and postexercise maximum intensities of ADP and collagen-induced platelet aggregation were measured using the impedance technique. Bioluminescent detection of thrombin-induced platelet ATP release and measurement of thromboxane B(2) (TxB(2)) levels (as a marker of thromboxane A(2) (TxA(2)) formation) by enzyme-linked immunoassay were performed before and after exercise. RESULTS AND CONCLUSION Shear rate increased after both submaximal and incremental exercise. Collagen-induced platelet aggregation increased after submaximal exercise, while ADP-induced aggregation and thromboxane B(2) levels did not alter with this protocol. Incremental exercise caused increased collagen and ADP-induced platelet aggregation and thromboxane B(2) levels. Neither of the protocols altered platelet ATP release. It was shown that acute upper extremity exercise increased platelet aggregation, without an increase in platelet release. Collagen-induced signalling pathways were more sensitive than those induced by ADP. The increase in thromboxane B(2) after incremental exercise implied increase in thromboxane A(2) formation and lipid peroxidation. Despite a significant correlation between platelet aggregation and thromboxane B(2) levels at rest, we found no clear-cut relationship between thromboxane A(2) formation, blood shear rate and platelet response to exercise.

The effects of acute and intermittent hypoxia on the expressions of HIF-1α and VEGF in the left and right ventricles of the rabbit heart.

OBJECTIVE Hypoxia-inducible factor-1 alpha (HIF-1α) and vascular endothelial growth factor (VEGF) are involved in signaling mechanisms of cellular responses to hypoxia. These factors have been investigated in tissue samples by simulating different altitudes by changing the percentage of oxygen. We aimed first to evaluate the effect of normobaric, systemic hypoxia (11% O2) on HIF-1α and VEGF mRNA levels in the heart muscle; secondly, to compare the levels of HIF-1α and VEGF mRNA in the left and right ventricle muscles. METHODS In this experimental study, 33 New Zealand male rabbits were assigned to control, acute hypoxia (4 hours) and intermittent hypoxia (4 hours/day for 14 days) groups (n=11/group). Total RNA was isolated from right and left ventricles of the heart. The expressions of HIF-1α and VEGF mRNAs were investigated by using Reverse Transcription Polymerase Chain Reaction (RT-PCR) method. The obtained data were compared by using ANOVA and paired t-test. RESULTS The results indicated that left ventricle VEGF mRNA expressions in both acute and intermittent hypoxia groups (1.08 ± 0.15 and 1.03 ± 0.19, respectively) were higher than that in the control group (0.88 ± 0.15) (p=0.03). Hypoxia treatments did not significantly alter HIF-1α mRNA in both ventricles (p=0.60 and p=0.51 for left and right ventricles, respectively). CONCLUSION Since systemic hypoxia results in induction of VEGF mRNA up-regulation only in left ventricle, it could be related to its higher metabolic activity and oxygen utilization. Hypoxia induced changes in the expression of HIF-1α mRNA may not be the only determining factor for HIF-1/VEGF pathway induction or the observed VEGF induction could be through other hypoxia sensitive pathways.