Effects of indomethacin and polyunsaturated fatty acid diet on exercise-induced hypoxaemia in master athletes

Aguilaniu, B.; Flore, Patrice; Page, E. B.; Maitre, J.; Lacour, J. R.; Perrault, Hélène

doi:10.1007/s004210050304

Cited by 8 publications

(8 citation statements)

References 28 publications

(28 reference statements)

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“…Specific functional characteristics of small and large airway function were not obtained in the present study such that this relationship cannot be verified. On the other hand, in our study, as in other previous reports of submaximal exercise GED (1,2,(15)(16)(17), the maximal exercise challenge consisted of a ramp protocol in which workload is increased every 1-2 min. In such rapid incremental protocols, the time at each exercise stage may be insufficient to allow for stability of ventilatory parameters.…”

Section: Discussionmentioning

confidence: 78%

Early onset of pulmonary gas exchange disturbance during progressive exercise in healthy active men

Aguilaniu¹,

Flore²,

Maitre³

et al. 2002

Journal of Applied Physiology

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Some recent studies of competitive athletes have shown exercise-induced hypoxemia to begin in submaximal exercise. We examined the role of ventilatory factors in the submaximal exercise gas exchange disturbance (GED) of healthy men involved in regular work-related exercise but not in competitive activities. From the 38 national mountain rescue workers evaluated (36 +/- 1 yr), 14 were classified as GED and were compared with 14 subjects matched for age, height, weight, and maximal oxygen uptake (VO2 max; 3.61 +/- 0.12 l/min) and showing a normal response (N). Mean arterial PO2 was already lower than N (P = 0.05) at 40% VO2 max and continued to fall until VO2 max (GED: 80.2 +/- 1.6 vs. N: 91.7 +/- 1.3 Torr). A parallel upward shift in the alveolar-arterial oxygen difference vs. %VO2 max relationship was observed in GED compared with N from the onset throughout the incremental protocol. At submaximal intensities, ideal alveolar PO2, tidal volume, respiratory frequency, and dead space-to-tidal volume ratio were identical between groups. As per the higher arterial PCO2 of GED at VO2 max, subjects with an exaggerated submaximal alveolar-arterial oxygen difference also showed a relative maximal hypoventilation. Results thus suggest the existence of a common denominator that contributes to the GED of submaximal exercise and affects the maximal ventilatory response.

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Section: Discussionmentioning

confidence: 78%

Early onset of pulmonary gas exchange disturbance during progressive exercise in healthy active men

Aguilaniu¹,

Flore²,

Maitre³

et al. 2002

Journal of Applied Physiology

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“…They observed a 27% decrease in filtration pressure, resulting in a 10% decrease in pulmonary arterial pressure. In master athletes, Aguilaniu et al (1,2) observed a decrease in EIH severity after a PUFA diet. Because a PUFA diet is known to improve RBC deformability, a potential contribution of blood parameters to EIH genesis cannot be excluded.…”

Section: Eihmentioning

confidence: 99%

“…Second, high blood viscosity or RBC rigidity causes higher mechanical stress on the blood-gas barrier and may result in membrane disruptions. Aguilaniu et al (1) showed that 6 wk of a polyunsaturated fatty acid (PUFA) diet led to an upward shift in Pa O 2 in master athletes. PUFA regimens are known to improve RBC deformability and to reduce blood viscosity (15); however, hemorheological measurements were not performed in this study (1).…”

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confidence: 99%

Does exercise-induced hypoxemia modify lactate influx into erythrocytes and hemorheological parameters in athletes?

Connes¹,

Bouix²,

Py³

et al. 2004

Journal of Applied Physiology

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. 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...

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“…Several studies have suggested that changes in blood rheology may be involved in both pulmonary capillary damage and gas exchange impairment observed in exercising animals and humans [1,3,20]. RBCs are implicated since adequate blood flow in capillaries for pulmonary gas exchange is primarily dependent on their deformability.…”

Section: Introductionmentioning

confidence: 99%

“…EIH is defined as an inability to maintain an adequate level of oxygenation in arterial blood, leading to low partial pressure of oxygen and low hemoglobin saturation during intense exercise [8]. In master athletes with EIH, Aguilianu et al [1] observed an upward shift in partial pressure of oxygen in arterial blood after six weeks of daily oral supplementation with polyunsaturated fatty acid, a diet known to increase RBC deformability and to decrease hb [15]. Aguilianu et al [1] did not perform hemorheological measurements, and it is still unknown whether hb is higher or RBC deformability is lower in athletes with EIH.…”

Section: Introductionmentioning

confidence: 99%

Is Hemoglobin Desaturation Related to Blood Viscosity in Athletes During Exercise?

Connes¹,

Bouix²,

Durand³

et al. 2004

Int J Sports Med

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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.

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Effects of indomethacin and polyunsaturated fatty acid diet on exercise-induced hypoxaemia in master athletes

Cited by 8 publications

References 28 publications

Early onset of pulmonary gas exchange disturbance during progressive exercise in healthy active men

Early onset of pulmonary gas exchange disturbance during progressive exercise in healthy active men

Does exercise-induced hypoxemia modify lactate influx into erythrocytes and hemorheological parameters in athletes?

Is Hemoglobin Desaturation Related to Blood Viscosity in Athletes During Exercise?

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