Several studies have suggested that athletes with low hemoglobin saturation during exercise may experience impaired pulmonary blood gas exchange during maximal exercise. Blood viscosity may be implicated in exercise-induced pulmonary hemorrhage in race horses. We hypothesized that blood rheology may contribute to impaired gas exchange and reduced hemoglobin saturation during exercise in humans. A group of 20 highly trained endurance athletes participated in this study, 9 with low hemoglobin saturation during exercise (Low-SpO (2) group) and 11 with normal hemoglobin saturation (High-SpO (2) group). All subjects performed a progressive exercise test conducted to V.O (2max). Venous blood was sampled at rest, 50 % V.O (2max) and maximal exercise. Blood viscosity (etab) was measured at very high shear rate (1000 s (-1)) and 37 degrees C with a falling ball viscometer. The erythrocyte rigidity coefficient, "Tk", was calculated using the Dintenfass equation. At rest, no significant difference in etab was observed between the two groups (3.00 +/- 0.08 mPa . s vs. 3.01 +/- 0.04 mPa . s for the Low-SpO (2) and High-SpO (2) group, respectively). At 50 % V.O (2max) and maximal exercise, etab was higher in Low-SpO (2) (p < 0.01). Tk decreased in High-SpO (2) (p < 0.01) but remained unchanged in the other group during testing. The greater increase in etab in the Low-SpO (2) group during exercise may therefore have been due to the lack of reduction in Tk. As suggested by previous studies, the greater increase in blood viscosity in athletes with low hemoglobin saturation may lead to vascular shear stress. Whether this could impair the blood gas barrier and result in exercise-induced hypoxemia requires further study.

Previous studies showed that erythropoietin not only increases erythrocyte production but is also essential in both the synthesis and the good functioning of several erythrocyte membrane proteins, including band 3. It is still unknown whether anion and/or H(+) fluxes are modified by erythropoietin. This study aimed to evaluate the effect of recombinant human erythropoietin (rHuEPO) injections on lactate transport into erythrocytes via band 3 and H(+)-monocarboxylate transporter MCT-1, two proteins involved in lactate exchange. Nine athletes received subcutaneous rHuEPO (50 U/kg body mass 3 times a week for 4 wk), and seven athletes received a saline solution (placebo group). All subjects were also supplemented with oral iron and vitamins B(9) and B(12). Lactate transport into erythrocytes was studied before and after the rHuEPO treatment at different lactate concentrations (1.6, 8.1, 41, and 81.1 mM). After treatment, MCT-1 lactate uptake was increased at 1.6, 41 (P < 0.01), and 81.1 mM lactate concentration (P < 0.001) although lactate uptake via band 3 and nonionic diffusion were unchanged. MCT-1 maximal velocity increased in the rHuEPO group (P < 0.05), reaching higher values than in the placebo group (P < 0.05) after treatment. Our results show that rHuEPO injections increased MCT-1 lactate influx at low and high lactate concentrations. The increase in MCT-1 maximal velocity suggests that rHuEPO may stimulate MCT-1 synthesis during erythrocyte formation in bone marrow.

. Does exercise-induced hypoxemia modify lactate influx into erythrocytes and hemorheological parameters in athletes? J Appl Physiol 97: 1053-1058. First published April 30, 2004 10.1152/japplphysiol.00993.2003.-This study investigated 1) red blood cells (RBC) rigidity and 2) lactate influxes into RBCs in endurance-trained athletes with and without exercise-induced hypoxemia (EIH). Nine EIH and six non-EIH subjects performed a submaximal steady-state exercise on a cycloergometer at 60% of maximal aerobic power for 10 min, followed by 15 min at 85% of maximal aerobic power. At rest and at the end of exercise, arterialized blood was sampled for analysis of arterialized pressure in oxygen, and venous blood was drawn for analysis of plasma lactate concentrations and hemorheological parameters. Lactate influxes into RBCs were measured at three labeled [U-14 C]lactate concentrations (1.6, 8.1, and 41 mM) on venous blood sampled at rest. The EIH subjects had higher maximal oxygen uptake than non-EIH (P Ͻ 0.05). Total lactate influx was significantly higher in RBCs from EIH compared with non-EIH subjects at 8.1 mM (1,498.1 Ϯ 87.8 vs. 1,035.9 Ϯ 114.8 nmol ⅐ ml Ϫ1 ⅐ min Ϫ1 ; P Ͻ 0.05) and 41 mM (2,562.0 Ϯ 145.0 vs. 1,618.1 Ϯ 149.4 nmol ⅐ ml Ϫ1 ⅐ min Ϫ1 ; P Ͻ 0.01). Monocarboxylate transporter-1-mediated lactate influx was also higher in EIH at 8.1 mM (P Ͻ 0.05) and 41 mM (P Ͻ 0.01). The drop in arterial oxygen partial pressure was negatively correlated with total lactate influx measured at 8.1 mM (r ϭ Ϫ0.82, P Ͻ 0.05) and 41 mM (r ϭ Ϫ0.84, P Ͻ 0.05) in the two groups together. Plasma lactate concentrations and hemorheological data were similar in the two groups at rest and at the end of exercise. The results showed higher monocarboxylate transporter-1-mediated lactate influx in the EIH subjects and suggested that EIH could modify lactate influx into erythrocyte. However, higher lactate influx in EIH subjects was not accompanied by an increase in RBC rigidity. monocarboxylate transporter; endurance; lactate metabolism; hypoxemia; hemorheology TRANSPORT OF LACTATE ACROSS the erythrocyte membrane proceeds by three distinct pathways (9): 1) nonionic diffusion of the undissociated acid; 2) an inorganic anion-exchange system, often referred to as the band 3 system; and 3) a monocarboxylate-specific carrier mechanism (23). Juel et al. (18) recently showed that monocarboxylate transporter-1 (MCT-1) and band 3 expressions were increased with chronic hypoxia exposure, suggesting that these proteins may be upregulated by hypoxia.The functional significance of the hypoxia-induced changes is likely an increase of lactate and H ϩ fluxes from plasma to erythrocyte. During sea-level exercise, some endurance-trained athletes experience arterial hypoxemia [exercise-induced hypoxemia (EIH)] that can be defined as a decrease in both oxygen arterial partial pressure (Pa O 2 ) and arterial hemoglobin saturation during exercise (8). Miyachi and Katayama (21) have reported repeated episodes of EIH during training sessions when endurance athlet...

Design: Growth hormone (GH) has demonstrated water-retaining effects in subjects at rest, whereas other research has indicated that GH may stimulate sweating. Thus, the aim of this study was to investigate the effect of¯uid intake on the exercise-induced GH response. Methods: Seven healthy male volunteers (age: 27X4^1X3 years, weight: 74X5^1X1 kgY height: 179X32X3 cm performed a 40-min submaximal rectangular cycling exercise in two different sessions. The ®rst session (Session 1) was performed without water intake, and the second (Session 2) involved the ingestion of spring water (four intakes) corresponding to the volume of water lost during the ®rst session. Results: In session 1, the water loss was 568^32 mlX In Session 2, the volume of water loss was not signi®cantly different from the volume of¯uid intake 524^16 versus 568^32 ml respectively). The decrease in plasma volume was signi®cantly reduced in Session 2 26X69^1X59% versus 211X31 X89%; P , 0X05X In Session 1, the GH concentration was signi®cantly lower than that during Session 2 after 25 min 3X04^1X05 versus 5X26^1X81; P , 0X05 and after 40 min 13X7^3X55 versus 17X60^4X14 ngaml; P , 0X05 of exercise. The total GH response was signi®cantly lower in Session 1 than in Session 2 136X6^39X2 versus 202X4^58X9 ngamlXmin; P , 0X05X Conclusions: We conclude that the exercise-induced GH response decreases when exercise is performed without¯uid intake.

No abstract