Faster lactate transport across red blood cell membrane in sickle cell trait carriers.

The physical and physiological behavior of sickle cell trait carriers (AS) is somewhat equivocal under strenuous conditions, although this genetic abnormality is generally considered to be a benign disorder. The occurrence of incidents and severe injuries in AS during exercise might be explained, in part, by the lactic acidosis due to a greater lactate influx into AS red blood cells (RBCs). In the present study, the RBC lactate transport activity via the different pathways was compared between AS and individuals with normal hemoglobin (AA). Sixteen Caribbean students, nine AS and seven AA, performed a progressive and maximal exercise test to determine maximal oxygen consumption. Blood samples were obtained at rest to assess haematological parameters and RBC lactate transport activity. Lactate influxes [total lactate influx and monocarboxylate transporter (MCT-1)-mediated lactate influx] into erythrocytes were measured at four external [14C]-labeled lactate concentrations (1.6, 8.1, 41, and 81.1 mM). The two groups had similar maximal oxygen consumption. Total lactate influx and lactate influx via the MCT-1 pathway were significantly higher in AS compared with AA at 1.6, 41, and 81.1 mM. The maximal lactate transport capacity for MCT-1 was higher in AS than in AA. Although AS and AA had the same maximal aerobic physical fitness, the RBCs from the sickle cell trait carriers took up more lactate at low and high concentrations than the RBCs from AA individuals. The higher MCT-1 maximal lactate transport capacity found in AS suggests greater content or greater activity of MCT-1 in AS RBC membranes.

Does higher red blood cell (RBC) lactate transporter activity explain impaired RBC deformability in sickle cell trait?

Lactate and H(+) are suggested to promote the sickling process in red blood cells (RBCs) containing hemoglobin S. We demonstrated greater activity of the RBC monocarboxylate cotransporter MCT-1, lower RBC deformability and impaired hematological indices in sickle cell trait (SCT) carriers compared to control subjects, suggesting an involvement of MCT-1 in hemorheological disturbances in SCT carriers.

Does repeated and heavy exercise impair blood rheology in carriers of sickle cell trait?

OBJECTIVE: To determine if the time courses of hemorheologic parameters are different between carriers of sickle cell trait (SCT) and subjects with normal hemoglobin in response to exercise. DESIGN: Observational and comparative study. SETTING: Testing was conducted in a laboratory of exercise physiology. PARTICIPANTS: Nine carriers of sickle cell trait (SCT group) and 7 subjects with normal hemoglobin (CONT group) performed an exercise protocol of the repetition of 3 successive maximal ramp exercise tests. INTERVENTIONS: Blood was sampled at rest (TR), at the end of each of the 3 tests (T1, T2, T3), and during the immediate (T2h) and late (T24h, T48h) recovery periods. MAIN OUTCOME MEASUREMENTS: Blood and plasma viscosity (etab and etap, respectively), hematocrit (Hct), and red blood cell (RBC) rigidity (Tk and k indexes) were determined. RESULTS: In both groups, etab significantly increased in response to exercise but the SCT group had significantly higher etab at T3 and T2h. etab then returned to baseline value at T2h in the CONT group and at T24h in the SCT group. Tk and k were not changed by exercise but significantly increased above baseline value in both groups at T24h and T48h. The increase in Tk and k during late recovery was higher in the SCT group than in the CONT group, indicating that SCT carriers had significantly higher RBC rigidity than the CONT group at that time. CONCLUSIONS: The hemorheologic changes induced by exercise in the SCT carriers could trigger microcirculatory disorders during the recovery.

Effects of short supramaximal exercise on hemorheology in sickle cell trait carriers.

This study compared the hemorheological profile at rest and in response to a short supramaximal exercise test between sickle cell trait (SCT) carriers and a control group. Eight SCT carriers and eight control subjects performed a ramp exercise test on a cycle ergometer conducted to maximal oxygen uptake (VO2max). One week later, they performed a supramaximal exercise test consisting of pedaling for 1 min at 110% VO2max. Blood viscosity (eta(b)), plasma viscosity (eta(p)), hematocrit (Hct) and red blood cell (RBC) rigidity were assessed at rest, at the end of exercise and at the 15th, 30th and 60th min of recovery. Exercise increased eta(b), eta(p) and Hct above resting values in both groups and these parameters remained higher until the 15th or 30th min of recovery as compared to resting values. RBC rigidity was unchanged from baseline values in both groups during exercise and recovery. No difference was observed between the two groups for eta(p) and Hct but eta(b) and RBC rigidity were higher in the SCT carriers at every time point compared with the control group. The higher RBC rigidity and eta(b) found in SCT carriers at rest and in response to a brief supramaximal exercise might constitute a risk factor for microcirculatory complications. Indeed, a short supramaximal exercise test may not be completely inoffensive for SCT carriers.

Lactic response in sickle cell trait carriers in comparison with subjects with normal hemoglobin.

OBJECTIVE: The objective of this study was to assess lactic response (mmol/L) during incremental exercise in a specific population of men and women with sickle cell trait. SUBJECTS: Athletic men and women from the French West Indies showing no anemia and/or alpha thalassemia. METHODS: Anemia was ruled out by hemoglobin level, and alpha thalassemia was ruled out by hemoglobin S percentage with concomitant hemoglobin level and mean corpuscular volume. Comparison was made with control subjects with normal hemoglobin, matched for physical fitness, anthropometric data, and sex. All subjects performed an incremental exercise test using a cycle ergometer. Peak oxygen uptake (mL/min) was predicted from an equation at peak exercise. Heart rate (beats/min) was noted continuously, and blood samples were collected for lactic response determination every minute during the incremental exercise test and at 1, 3, and 5 minutes of recovery. RESULTS: Comparison of peak oxygen uptake and heart rate values showed no significant differences in subjects with sickle cell trait versus control subjects during the incremental exercise test. In contrast, analysis of variance revealed significantly lower lactic response time courses during the incremental exercise test and at peak exercise (p < 0.05) in the sickle cell trait group, whereas the heart rate time course was lower during recovery (p < 0.05). CONCLUSION: We conclude that the lower lactic response exhibited by subjects with sickle cell trait during incremental exercise was the result of an adaptive process in red blood cells in relation to either lower lactate production or greater lactate uptake capability than in individuals with normal hemoglobin.