Blood viscosity is an important determinant of local flow characteristics, which exhibits shear thinning behavior: it decreases exponentially with increasing shear rates. Both hematocrit and plasma viscosity influence blood viscosity. The shear thinning property of blood is mainly attributed to red blood cell (RBC) rheological properties. RBC aggregation occurs at low shear rates, and increases blood viscosity and depends on both cellular (RBC aggregability) and plasma factors. Blood flow in the microcirculation is highly dependent on the ability of RBC to deform, but RBC deformability also affects blood flow in the macrocirculation since a loss of deformability causes a rise in blood viscosity. Indeed, any changes in one or several of these parameters may affect blood viscosity differently. Poiseuille’s Law predicts that any increase in blood viscosity should cause a rise in vascular resistance. However, blood viscosity, through its effects on wall shear stress, is a key modulator of nitric oxide (NO) production by the endothelial NO-synthase. Indeed, any increase in blood viscosity should promote vasodilation. This is the case in healthy individuals when vascular function is intact and able to adapt to blood rheological strains. However, in sickle cell disease (SCD) vascular function is impaired. In this context, any increase in blood viscosity can promote vaso-occlusive like events. We previously showed that sickle cell patients with high blood viscosity usually have more frequent vaso-occlusive crises than those with low blood viscosity. However, while the deformability of RBC decreases during acute vaso-occlusive events in SCD, patients with the highest RBC deformability at steady-state have a higher risk of developing frequent painful vaso-occlusive crises. This paradox seems to be due to the fact that in SCD RBC with the highest deformability are also the most adherent, which would trigger vaso-occlusion. While acute, intense exercise may increase blood viscosity in healthy individuals, recent works conducted in sickle cell patients have shown that light cycling exercise did not cause dramatic changes in blood rheology. Moreover, regular physical exercise has been shown to decrease blood viscosity in sickle cell mice, which could be beneficial for adequate blood flow and tissue perfusion.

The use of nutritional supplements among exercisers in gyms has been never investigated in the Middle East. The aim of the current study was to assess the prevalence intake of nutritional supplements and the potential influencing factors among people exercising in gyms in Beirut city. In this cross-sectional study, 512 exercisers, aged between 20 and 50 years, were randomly selected from gyms. The intake of nutritional supplements was reported among 36.3% (95% confidence interval 32.2–40.5) of participants, with a weak presence of medical supervision. Patterns of supplement use differed by gender and age. Men and younger exercisers were found to focus on supplements associated with performance enhancement and muscle building, while women and older exercisers were more concerned with health-promoting products such as vitamins, minerals, and herbal supplements. An appropriate dissemination of accurate and scientifically sound information regarding the benefits and side effects of nutritional supplements is highly recommended in the sports environment in Beirut city.

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Chronic hemolysis, enhanced oxidative stress, and decreased nitric oxide (NO) bioavailability promote vasculopathy in sickle cell anemia (SCA). Oxidative stress and NO are known to modulate eryptosis in healthy red blood cells (RBCs); however, their role in SCA eryptosis and their impact on the genesis of RBC-derived microparticles (RBC-MPs) remains poorly described. RBC-MPs could play a role in vascular dysfunction in SCA. The aims of this study were to evaluate the roles of oxidative stress and NO in eryptosis and RBC-MPs release, and to determine whether RBC-MPs could be involved in vascular dysfunction in SCA. Markers of eryptosis and oxidative stress, plasma RBC-MPs concentration and arterial stiffness were compared between SCA and healthy (AA) individuals . In-vitro experiments were performed to test: 1) the effects of oxidative stress (antioxidant: n-acetylcysteine (NAC); pro-oxidant: cumene hydroperoxide) and NO (NO donor: sodium nitroprusside (SNP); NO-synthase inhibitor (L-NIO)) on eryptosis, RBC deformability and RBC-MP genesis; 2) the effects of SCA/AA-RBC-MPs on human aortic endothelial cell (HAEC) inflammatory phenotype and TLR4 pathway. Eryptosis, RBC-MPs, oxidative stress and arterial stiffness were increased in SCA. NAC increased RBC deformability and decreased eryptosis and RBC-MPs release, while cumene did the opposite. SNP increased RBC deformability and limited eryptosis, but had no effect on RBC-MPs. L-NIO did not affect these parameters. Arterial stiffness was correlated with RBC-MPs concentration in SCA. RBC-MPs isolated directly from SCA blood increased adhesion molecules expression and the production of cytokines by HAEC compared to those isolated from AA blood. TLR4 inhibition alleviated these effects. Our data show that oxidative stress could promote eryptosis and the release of RBC-MPs that are potentially involved in macrovascular dysfunction in SCA.

The tropical climate imposes a high level of physiological stress during exercise. As a result of this stress, adaptations may be induced and could benefit athletes upon return to a neutral climate. To test this hypothesis, climate effects on swimming performance were assessed in 16 swimmers: 6 trained for 8 days in a tropical climate, 6 trained for 8 days at altitude, and 4 served as a tapering group. The swimming performance was assessed during a 400-m freestyle before the experimental period, and at 10 days and 30 days after. The results demonstrated that only the tropical group increased performance (10.0 +/- 4.2 %, p < 0.03 for the tropical group 30 days after return). No significant change in performance was noted for the two other groups 10 or 30 days post-training. The results of the present study demonstrated that training in a tropical climate significantly enhances performance in swimmers 30 days after return to neutral climate. However, further studies are needed to evaluate the effects of such a climate on performance in other sports.

Aerobic performance is dependent on both cardio-respiratory and peripheral factors with hemodynamic parameters playing a major role. However, whether blood rheology might affect aerobic performance through an effect on hemodynamic factors is not known. The aim of the present study was to assess the relationships between hemodynamic, hemorheological and metabolic parameters in response to a sub-maximal cycling exercise protocol. Ten young sportsmen participated in the present study. Mean arterial pressure (MAP) was measured manually, with thoracic impedance used to monitor cardiac output (Q c): systemic vascular resistance (SVR) was then calculated. Whole blood viscosity (η b) was measured and used to calculate systemic vascular hindrance. Hematocrit (Hct) was determined by microcentrifugation and red blood cell (RBC) deformability (EI) was determined by ecktacytometry. A breath-by-breath gas analyzer was used to measure oxygen uptake (VO 2); the Fick equation was used to calculate arterio-venous oxygen difference [(a-v)O 2 ] from VO 2 and Q c. All measurements were performed at rest, during exercise and during recovery. Compared to baseline, Q c , MAP, Hct, EI, VO 2 , and (a-v)O 2 increased during exercise. η b increased above baseline only at 150W and remained elevated during recovery; the increase in η b during the last level of exercise was associated with a decrease of SVR and systemic vascular hindrance. There was a significant negative correlation between EI and SVR and a significant positive relationship between EI and (a-v)O 2 and between EI and VO 2 across all exercise workloads, thus suggesting a potential role for RBC deformability as a factor affecting aerobic performance via oxygen delivery to tissues. These data lend support to the concept that hemorheological parameters may contribute to hemodynamic and cardio-respiratory adaptations in response to exercise in moderately trained sportsmen.

Exercise induced a short-term energy deficit. However, modifications in the hormonal regulation of food intake in response to short-term heat or heat and exercise exposure seem to be minor and did not induce changes in energy intake. This trial was registered at clinicaltrials.gov as NCT02157233.

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