Biomedical subjects

P Connes

Publications and source records attributed to P Connes.

5 recordsLinked to original sources

PubMed2006

Oxygen uptake kinetics during heavy submaximal exercise: Effect of sickle cell trait with or without alpha-thalassemia.

Sickle cell trait (SCT) is a genetic disease affecting the synthesis of normal hemoglobin (Hb) marked by the heterozygous presence of HbA and HbS. It is thought that exercise tolerance and aerobic capacity could be limited in SCT carriers, but that the co-existence of alpha-thalassemia with SCT (SCTAT) could improve exercise response. To examine these issues, we compared the characteristics of VO2 kinetics during a constant heavy exercise among athletes carrying either the SCT (n = 6), the SCTAT (n = 9), or the normal Hb (control group; n = 10). After determination of maximal power output (Ppeak), all subjects underwent a constant heavy cycling exercise lasting 9 min at approximately 70 % Ppeak. Pulmonary VO2 and cardio-respiratory parameters were measured breath-by-breath and the VO2 response was modelled using non-linear regression techniques. The time constant of the VO2 primary component and oxygen deficit were not significantly different among the three groups. The VO2 slow component was 28 % and 33 % higher (p < 0.05) in SCT and SCTAT than in the control groups, respectively. Altogether, athletes with the SCT and the SCTAT had higher heart rate at the beginning (+ 5.2 %) and the end (+ 7.4 %) of the slow component compared to the control group (p < 0.05). These results suggest that SCT and SCTAT subjects are not limited during the first exercise minutes, but are prone to exercise intolerance and to lower aerobic capacity thereafter, due to a higher VO2 slow component, and that alpha-thalassemia does not improve exercise response. The finding of a higher slow component in SCT and SCTAT athletes was possibly due to the loss of O2 availability to muscles, additional fiber recruitment and/or higher cardiac load with time.

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PubMed2006

Lactate distribution in the blood compartments of sickle cell trait carriers during incremental exercise and recovery.

Whether or not whole blood lactate concentration is the same during a ramp exercise test in subjects with sickle cell trait (AS) as in normal subjects remains a point of controversy in the literature. Some studies have shown that the ability to produce or clear circulating lactate might differ between AS and subjects with normal haemoglobin (AA). If this is indeed so, the lactate distribution in the blood compartments should also differ. To test this hypothesis, lactate concentrations in the whole blood, plasma and red blood cells of AS and AA were compared at rest and in response to exercise. Eight AS and 8 AA performed an incremental exercise test. Whole blood, plasma and red blood cell lactate concentrations, the red blood cell : plasma lactate concentration ratio, the plasma-to-red blood cell lactate gradient, haematocrit and cardiorespiratory variables were analysed at rest and during an incremental exercise test and active recovery. Maximal oxygen uptake and ventilatory thresholds were similar in the two groups. No significant difference in whole blood, plasma or red blood cell lactate concentrations was observed between the two groups at rest, during exercise, or during the immediate recovery. Neither the red blood cell : plasma lactate concentration ratio nor the plasma-to-red blood cell lactate gradient differed between groups. Lactate distribution in the blood compartments did not differ between the two groups and this finding suggests that lactate production and/or clearance is quite similar during exercise in AS and AA.

Adult↗

PubMed2006

Does the pattern of repeated sprint ability differ between sickle cell trait carriers and healthy subjects.

Sickle cell trait (SCT) is a genetic abnormality affecting the synthesis of normal haemoglobin [Hb] and is the heterozygous form of sickle cell anaemia. The aim of the present study was to compare the ability to repeat maximal cycling sprints (RSA; repeated sprint ability) between SCT carriers (SCT group, n = 7) and a control group with normal haemoglobin [Hb] (n = 7). The two groups performed a 10-s maximal cycling sprint in order to determine the peak power output (P(peak10)). They then performed an RSA test that consisted of five 6-s maximal cycling sprints interspersed with 24 s of passive recovery. For each sprint, the peak power output (P(peak6)) and the work over the 6-s (W6) were calculated. The sum of each W6 developed during the test was considered to be the total work (W(tot)). The decrements over the repeated sprints for P(peak6) (P(6dec)) and W6 (W(6dec)) were also determined. We found no difference in P(peak10), W(tot) and W(6dec) between the two groups. However, the drop in P(peak6) and W6 during the RSA test appeared earlier in the SCT group and the decrease in P(peak6) over the RSA test was greater in the SCT group than in the control group (p < 0.05). In conclusion, we found that: 1) maximal anaerobic performance determined during a single sprint was not altered by SCT, but 2) repeated sprint ability was different in SCT carriers compared with sportsmen with normal Hb.

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PubMed2005

Effect of endurance training on lung function: a one year study.

OBJECTIVE: To identify in a follow up study airway changes occurring during the course of a sport season in healthy endurance athletes training in a Mediterranean region. METHODS: Respiratory pattern and function were analysed in 13 healthy endurance trained athletes, either during a maximal exercise test, or at rest and during recovery through respiratory manoeuvres (spirometry and closing volume tests). The exercise test was conducted on three different occasions: during basic endurance training and then during the precompetition and competitive periods. RESULTS: During the competitive period, a slight but non-clinically significant decrease was found in forced vital capacity (-3.5%, p = 0.0001) and an increase in slope of phase III (+25%, p = 0.0029), both at rest and after exercise. No concomitant reduction in expiratory flow rates was noticed. During maximal exercise there was a tachypnoeic shift over the course of the year (mean (SEM) breathing frequency and tidal volume were respectively 50 (2) cycles/min and 3.13 (0.09) litres during basic endurance training v 55 (3) cycles/min and 2.98 (0.10) litres during the competitive period; p < 0.05). CONCLUSIONS: This study does not provide significant evidence of lung function impairment in healthy Mediterranean athletes after one year of endurance training.

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PubMed2004

Is hemoglobin desaturation related to blood viscosity in athletes during exercise?

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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