Haemoreological Responses

Hemoreological Responses To Exercising In Warm Environment

Philippe Connes1,2, Julien Tripette1,2, Marie-Dominique Hardy-Dessources2 and Olivier Hue1 1Laboratoire ACTES (EA 3596), Département de Physiologie, Faculté des Sciences du Sport, Université des Antilles et de la Guyane, 97159 Pointe à Pitre, Guadeloupe, French West Indies. 2UMR Inserm 763, CHU de Pointe à Pitre, Université des Antilles et de la Guyane, 97159 Pointe à Pitre, Guadeloupe, French West Indies.

In healthy subjects and in patients, the performance of the cardiovascular system is of primary concern because it determines adequate tissue perfusion and oxygenation.

The rate of delivery of oxygen and nutrients to tissues depends on their concentrations and on the rate of blood flow. The latter is determined by the cardiac output and by the resistance to blood flow in the peripheral circulation.

The resistance to blood flow is mainly determined by two factors: 1) vascular hindrance (i.e. geometry of vessels) and 2) blood viscosity. According to the Poiseuille’ equation (Poiseuille, 1835), vascular geometry is considered to be the most important factor of blood flow resistance.

However, it has been demonstrated that normovolemic hemodilution inducing changes in blood viscosity (ηb) affected the pressure-flow relationship in animals (Replogle et al, 1970) and human beings (Laks et al, 1973), characterized by a decrease in blood flow resistance. These results prove that ηb plays a major role in determining blood flow resistance and adequate tissue perfusion and oxygenation. Moreover, impairment in RBC deformability may adversely affect capillary recruitment and physiological mechanisms that ensure adequate delivery of oxygen to tissue (Parthasarathi et al, 1999).

At least, Kim et al (2006) demonstrated that elevated RBC aggregation is associated with decreased functional capillary density (i.e. the number of capillaries with blood flow). Among the factors that potentially limit aerobic fitness, hemorheological factors such as blood and plasma viscosities, hematocrit (Hct), RBC deformability and aggregation are often neglected by exercise physiologist (Connes et al, 2006). However, correlation between VO2max and blood viscosity factors have been reported (Brun et al, 1998) and involvement of blood rheology in the cascade of oxygen from lungs to muscles has been suspected (Parthasarathi et al, 1999; Hisa et al, 1999).

Moreover, blood rheological changes induced by exercise might participate to some medical complications observed in animals (Boucher et al, in press) and humans (Caillaud et al, 2002; Senturk et al, 2005; Tripette et al, 2007), particularly when exercise stops and blood flow recovers resting values which limit the rhefluidifying effect of blood flow to compensate for the increase in ηb.

Of potential interest is the additional strain of warm and humid environment on hemorheological responses during exercise that could major the effects of blood rheological properties on exercise performance and physiological responses. Although many studies investigated the changes in blood rheology during exercise in temperate conditions, very few studies investigated blood rheological responses in tropical environment.

In temperate conditions, cycling exercise usually increases ηb. This increase is due to the increase in plasma viscosity (ηp) and Hct (Brun et al, 1998). In addition, cycling exercise changes the deformability of RBCs, with the direction of changes (impairment or improvement) depending on the kind of exercise performed (maximal or submaximal) and on the population studied (hypoxemic athletes, sickle cell trait carriers, trained or untrained subjects, etc.) (Hardeman et al, 1995; Brun et al, 1998; 2007; Connes et al, 2004; Tripette et al, 2007). Decreased RBC deformability participates in the increase in ηb, whereas improvement in RBC deformability attenuates the effects of increased ηp and Hct on ηb.

At least, RBC aggregation seems to be not influenced by cycling exercise (Connes et al, 2007). When aerobic running exercise is considered, the results are different. For example, Neuhaus et al (1992; 1994) reported no change in ηb, ηp, Hct, RBC deformability and aggregation after a marathon as compared to before.

The lack of change during the marathon might be attributed to the ad libitum fluid intake by runners (Neuhaus et al, 1992). In contrast, Reinhart et al (1983; 1989) observed decreased RBC deformability (filtrability) and increased proportion of stomatocyte in blood after a 100-km running race. Wood et al (1991) also investigated the changes in blood rheology induced by a 48 km running race in mountainous terrain.

They reported an increase in ηb increased at low shear rate. The authors proposed this increase was due to changes in RBC aggregation but the shear rate used in that study was not low enough to make adequate conclusion.

Despite the increase in ηp at high shear rate and the lack of change in Hct, the authors also observed no change in ηb at high shear rate: this was surely explained by an improvement in RBC deformability (Wood et al, 1991).

In summary, the results obtained in running protocol on blood rheology are very confusing and probably dependent on the population tested, the environmental conditions and on the hemorheological methodology used.

Therefore, we recently studied the hemorheological response in recreational sportsmen during a 10 km race conducted in warm and humid environment (tropical climate) (Tripette et al, unpublished observations).

Although all the subjects were authorized to drink ad libitum during the race, they lose weight. Indeed, one may suggest that all subjects were dehydrated after the race. However, we observed no change in Hct and ηb. Indeed, it is possible that fluid re-distribution occurs during running exercise that limits the effects of dehydration on hemoconcentration. In contrast with results obtained by Reinhart et al (1983; 1989) or by Wood et al (1991), we reported no significant change in RBC deformability.

In addition, the cumulative effects of running race and tropical climate did not affect RBC aggregation. However, although RBC deformability was not decreased after the race as compared to before the race, we observed a decrease in RBC elasticity; that means that RBCs were able to deform normally but their ability to recover resting shape after being deformed was impaired. Alterations of this rheological property could make the blood less elastic with potential consequences on the propagation of the pulse throughout the arterial system (Thurston, 1976).

The mechanisms of such a phenomenon are unknown but studies investigating the integrity of RBC membrane and alterations of structural proteins such as spectrin, actin, band 3 or ankyrin are clearly warranted.

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