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LETTER TO THE EDITOR
The letter by Baskurt and Meiselman (2) suggested that a pathological condition, i.e. insufficient vasodilatory reserve, coexistent with SCT was necessary to induce circulatory disorders such as those reported in SCT carriers. Thus an unfavorable internal environment can influence SCT and, unfortunately, may change SCT from an asymptomatic and benign condition into a deleterious one. In line with this observation are the numerous factors well known to worsen SCT, particularly metabolic diseases. If SCT influences diabetic complications (1), in return, none has excluded the influence of diabetes on SCT. In contrast, alpha-thalassemia (AT) has been widely reported to improve SCT. Monchanin et al. (6) examined the effect of exercise on plasma levels of adhesion molecules in SCT athletes. Their findings supported the concept that AT might be considered protective toward microcirculatory disturbances and adhesive phenomena among exercising SCT subjects.
Bergeron et al. (4) studied two subjects with SCT participating in 45 min of brisk walking in a hot environment with or without fluid intake for 3 h prior to and during testing. The authors reported that erythrocyte sickling progressively increased (to 3.5–5.5%) for HbAS carriers during no fluid exercise only. One would point out here that no fluid intake before and during exercise in the heat may be considered as a nonphysiological condition. Thus the main result of this study, in our opinion, was that erythrocyte sickling did not increase in HbAS carriers during exercise with fluid intake, i.e. quite physiological conditions. As concomitantly there was no significant difference in perceived exertion between fluid versus no fluid intake, one would conclude that SCT remained asymptomatic and benign during exercise. Monchanin et al. (5) reported similar observations regarding hemorheological parameters in response to exercise in SCT athletes with or without AT. Although athletes with SCT were found prone to higher RBC rigidity at rest, this alteration was limited by the coexistence of AT, and it was not further impaired in response to exercise in SCT athletes with or without AT.
Finally, the observation of hemorheological alterations at rest and during exercise in SCT does not support the speculative hypothesis of microcirculation disorders, clinical risk, or accidents in these subjects since 1) none of the articles describing hemorheological alterations during exercise in SCT subjects has reported any concomitant accident, 2) the occurrence of an accident in this setting would de facto deny any correlation between hemorheological parameters and clinical status, and 3) so far, it has not been established that hemorheological alterations were the primary cause of accidents in SCT subjects.
FOOTNOTES
Address for reprint requests and other correspondence: D. Le Gallais, Montpellier 1 Univ., Dept. of Sports Sciences, 700 Ave. du Pic St. Loup, F-34090 Montpellier, France (e-mail: daniel.legallais{at}univ-montp1.fr)
REFERENCES
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