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Biomedical subjects

H Benoit

Publications and source records attributed to H Benoit.

At least 19 recordsLinked to original sources

Evidence of decrease in peak heart rate in acute hypoxia: effect of exercise-induced arterial hypoxemia.

This study focuses on the influence of the arterial oxygen saturation level at exhaustion on peak heart rate under acute moderate hypoxia, in endurance-trained subjects. Nineteen competing male cyclists performed exhaustive ramp exercise (cycle ergometer) under normoxia and normobaric hypoxia (15 % O (2)). After the normoxic trial, the subjects were divided into those demonstrating exercise-induced arterial hypoxemia during exercise (> 5 % decrease in SaO (2) between rest and the end of exercise, n = 10) and those who did not (n = 9). O (2) uptake, heart rate and arterial O (2) saturation (ear-oximeter) levels were measured. Under hypoxia, peak heart rate decreased for both groups (p < 0.001) and to a greater extent for hypoxemic subjects (p < 0.01). Arterial O (2) saturation under hypoxia was lower for the hypoxemic than for the non-hypoxemic subjects (p < 0.001) and it was correlated to the fall in peak heart rate between normoxia and hypoxia for all subjects (p < 0.01; r = 0.65). Hypoxemic subjects presented greater decrease in maximal O (2) uptake than non-hypoxemic ones (19.6 vs. 15.6 %; p < 0.05). The results confirm the greater decrement in arterial O (2) saturation under hypoxia in hypoxemic subjects and demonstrates a more pronounced reduction in peak heart rate in those subjects compared with non-hypoxemic ones. These data confirm the possible influence of arterial oxygenation on the decrease in peak heart rate in acute hypoxia.

Adult↗

A high blood lactate induced by heavy exercise does not affect the increase in submaximal VO2 with hyperoxia.

Few studies evidenced an enhancement in oxygen uptake (VO2) during submaximal exercise in hyperoxia. This O2 "overconsumption" seems to increase above the lactate threshold. The aim of this study was to determine whether the hyperoxia-induced enhancement in VO2 may be related to a higher metabolism of lactate. Nine healthy males (aged 23.1 years, mean VO2 max= 53.8 ml min-1 kg-1) were randomized to two series of exercise in either normoxia or hyperoxia corresponding to an inspired O2 fraction (FIO2) of 30%. Each series consisted of 6 min cycling at 50% VO2 max (Moderate1), 5 min cycling at 95%VO2 max (Near Max) and then 6 min at 50% VO2 max (Moderate2). In both series Near Max was performed in normoxia. VO2 was significantly greater under hyperoxia than in normoxia during Moderate1 (2192 +/- 189 vs. 2025 +/- 172 ml min-1) and during Moderate2 (2352 +/- 173 vs. 2180+ /- 193 ml min-1). However, the effect of the high FIO2 was not significantly different on VO2Moderate2 (+172+/-137 ml min-1 with [La] approximately 6 mmol l-1) compared to VO2Moderate1 (+166 +/- 133 ml min-1 with [La] approximately 2.4 mmol l-1). [La] at the onset of Moderate2 was not different between normoxia and hyperoxia (10.1 +/- 2.2 vs. 10.9 +/- 1.6 mmol l-1). The results show that VO2 is significantly increased during moderate exercise in hyperoxia. But this O2 overconsumption was not modified by a high [La] induced by a prior heavy exercise. It could be concluded that lactate accumulation is not directly responsible for the increase in O2 overconsumption with intensity during exercise in hyperoxia.

Adaptation, Physiological↗

Effects of moderate hyperoxia on oxygen consumption during submaximal and maximal exercise.

The present study examined the effect of hyperoxia on oxygen uptake (VO(2)) and on maximal oxygen uptake (VO(2max)) during incremental exercise (IE) and constant work rate exercise (CWRE). Ten subjects performed IE on a bicycle ergometer under normoxic and hyperoxic conditions (30% oxygen). They also performed four 12-min bouts of CWRE at 40, 55, 70 and 85% of normoxic VO(2max) (ex1, ex2, ex3 and ex4, respectively) in normoxia and in hyperoxia. VO(2max) was significantly improved by 15.0 (15.2)% under hyperoxia, while performance (maximum workload, W(max)) was improved by only +4.5 (3.0)%. During IE, the slope of the linear regression relating VO(2) to work rate was significantly steeper in hyperoxia than in normoxia [10.80 (0.88) vs 10.06 (0.66) ml x min(-1) x W(-1)]. During CWRE, we found a higher VO(2) at ex1, ex2, ex3 and ex4, and a higher VO(2) slow component at ex4 under hyperoxia. We have shown that breathing hyperoxic gas increases VO(2max), but to an extent that is difficult to explain by an increase in oxygen supply alone. Changes in metabolic response, fibre type recruitment and VO(2) of non-exercising tissue could explain the additional VO(2) for a given submaximal work rate under hyperoxia.

Adult↗

Reference values for peripheral blood B-lymphocyte subpopulations: a basis for multiparametric immunophenotyping of abnormal lymphocytes.

BACKGROUND AND OBJECTIVES: Immunophenotyping has become a useful tool for the differential diagnosis of chronic B-cell lymphoproliferative disorders. The aim of this work was to determine reference values of normal B-cell subpopulations. MATERIAL AND METHODS: Blood samples from 38 healthy volunteers were analyzed by multidimensional flow cytometry, using a panel of directly conjugated antibodies. Results were expressed as percent of positive B cells and as median fluorescence intensity, an indirect assessment of the expression level. RESULTS: CD20, CD22, CD24, CD40, CD79a, CD79b, FMC7, CD11a, CD18, CD44 were positive in the whole B cell population, whereas CD10, CD86, CD103, CD154 and FasL were almost absent from the B-lymphocyte population. 75% were IgD positive. The kappa/lambda ratio was 1.5. CD5, CD23, CD25, CD38, CD43, CD54, CD62L, CD80 and CD95 were positive in different B-cell subpopulations. The utility of all these markers in the differential diagnosis of chronic B-cell lymphoproliferative disorders is discussed. CONCLUSION: In order to interpret a pathological immunophenotype, it is necessary to refer to quantitative and qualitative values of normal B-cell subpopulations.

Adult↗

Diaphragmatic angiogenic growth factor mRNA responses to increased ventilation caused by hypoxia and hypercapnia.

This study investigates the effect of increased ventilation on the expression of messenger ribonucleic acid (mRNA) levels of vascular endothelial growth factor (VEGF), basic fibroblast growth factor (bFGF) and transforming growth factor-beta1 (TGF-beta1) in the diaphragm of intact, awake, spontaneously breathing rats, compared with responses in paralysed, mechanically-ventilated animals at similar blood gas and ventilatory levels. Four groups of intact, rats were studied in a body box, each group breathing one of four gases: room air, 12% oxygen (O2), 5% carbon dioxide (CO2), or 12% O2+5% CO2 for 1 h. Another 4 groups of paralysed, mechanically-ventilated animals were matched for arterial blood gas and ventilatory level. The results showed that VEGF mRNA abundance was increased three-fold and that of bFGF 1.5-fold when 12% O2+5% CO2 were breathed, but TGF-beta1 did not change. A significant linear relationship of VEGF and bFGF mRNA to minute ventilation was observed in awake animals (r=0.98, p<0.02 and r=0.87, p<0.03, respectively). The paralysed, mechanically-ventilated animals showed no mRNA increases for any probe. Systemic hypoxia had no additional effect on VEGF or bFGF levels in the diaphragm. It was concluded that messenger ribonucleic acid for vascular endothelial growth factor and basic fibroblast growth factor in the diaphragm rises significantly as a result of active ventilation and not due to blood gas/pH changes or to passive muscle shortening per se.

Animals↗

Effect of active compression-decompression resuscitation (ACD-CPR) on survival: a combined analysis using individual patient data.

Active compression decompression resuscitation (ACD-CPR) has been developed as an alternative to standard cardiopulmonary resuscitation (S-CPR). To determine the effect of ACD-CPR on survival and neurologic outcome in patients with out-of-hospital cardiac arrest, this combined analysis involved individual patient data from 2866 patients from seven separate randomized prospective prehospital studies who had received ACD-CPR or S-CPR after out-of-hospital cardiac arrest in seven international sites. Significant improvement in 1-h survival (odds ratio (OR) = 0.83; confidence interval (CI): 0.695-0.99; P < 0.05) was found with ACD-CPR (n = 1410) versus S-CPR (n = 1456). The odds ratio for hospital discharge after ACD-CPR was similar (OR = 0.82; CI: 0.609-1.107, P = NS), but this finding was not statistically significant. Using the chi2-test for trend, there was a significant improvement in overall survival with ACD-CPR (P < 0.05) versus S-CPR. This improvement was largely due to the influence of results from one study site. Neurological outcome and complication rates were comparable between groups. Further study is needed to determine which emergency medical services systems may benefit from out-of-hospital use of ACD-CPR.

Aged↗

Effect of NO, vasodilator prostaglandins, and adenosine on skeletal muscle angiogenic growth factor gene expression.

Exercise training results in several muscle adaptations, one of which is angiogenesis. Acutely, exercise leads to release of nitric oxide, prostacyclin (PGI2), and adenosine (A) in the skeletal muscles. In this paper, we asked whether any of these locally released vasodilators, as well as other known dilator prostaglandins (PGE1 and PGE2), have the potential to increase angiogenic growth factor gene expression in resting skeletal muscle. Seven groups of 5-7 female Wistar rats (age 8-12 wk, weight 250 +/- 10 g) were anesthetized and instrumented for carotid artery pressure and electromagnetic femoral artery blood flow measurement. One group acted as control while the other groups each received one of the following six agents by constant arterial infusion (dose in microg/min): A (200), nitroprusside (NP, 4.2), acetylcholine (100), PGE1 (1.9), PGE2 (1.7), and PGI2 (1.7). Each agent reduced peripheral vascular resistance to a similar extent (at least twofold). Densitometric mRNA/18S levels for vascular endothelial growth factor (VEGF) were increased 50% by NP and acetylcholine, were unaffected by PGE1 and PGE2, and were reduced 40% by PGI2. For basic fibroblast growth factor, only PGI2 had any effect, reducing mRNA/18S approximately 25%. For transforming growth factor-beta1, A, NP, and PGE1 led to reduced mRNA/18S, whereas PGE2 slightly increased mRNA/18S. For the principal putative angiogenic growth factor, VEGF, these data suggest that naturally secreted vasodilators in contracting skeletal muscle could be involved in regulation of gene expression, namely, nitric oxide in a positive and PGI2 in a negative direction.

Adenosine↗

A system to simulate gas exchange in humans to control quality of metabolic measurements.

We have developed a gas exchange simulation system (GESS) to assess the quality control in measurements of metabolic gas exchange. The GESS simulates human breathing from rest to maximal exercise. It approximates breath-by-breath waveforms, ventilatory output, gas concentrations, temperature and humidity during inspiration and expiration. A programmable motion control driving two syringes allows the ventilation to be set at any tidal volume (VT), respiratory frequency (f), flow waveform and period of inspiration and expiration. The GESS was tested at various combinations of VT (0.5-2.51) and f(10-60 stroke x min(-1)) and at various fractional concentrations of expired oxygen (0.1294-0.1795); and carbon dioxide (0.0210-0.0690) for a pre-set flow waveform and for expired gases at the same temperature and humidity as room air. Expired gases were collected in a polyethylene bag for measurement of volume and gas concentrations. Accuracy was assessed by calculating the absolute and relative errors on parameters (error=measured-predicted). The overall error in the gas exchange values averaged less than 2% for oxygen uptake and carbon dioxide output, which is within the accuracy of the Douglas bag method.

Carbon Dioxide↗

Validity of oxygen uptake measurements during exercise under moderate hyperoxia.

PURPOSE: The validity of oxygen uptake in hyperoxia (FIO2 = 30%) measured by an automated system (MedGraphics, CPX/D system) was assessed during the simulation of gas exchanges during exercise with a mechanical system and during submaximal exercise by human subjects. METHODS: The simulation system reproduced a stable and accurate VO2 for 30 min (sim-test). This trial was repeated nine times in normoxia and nine times in hyperoxia. Ten subjects also performed two submaximal exercises (55% of normoxic VO2max) on a cycle ergometer at the same absolute power in normoxia and in hyperoxia (ex-test). RESULTS: There was a significant downward drift of the oxygen fraction measurement in hyperoxia (< or = 0.10% for FIO2 and FEO2) during sim-test, but VO2 measurement remained stable in the two conditions. There was also a downward drift of the oxygen fraction measurement in the two conditions (< or = 0.07% for FIO2) during ex-test. VO2 was significantly higher in hyperoxia (+4.6%), and this result was confirmed using a modified Douglas bag method. CONCLUSIONS: These findings show that the CPX/D system is stable and valid for assessing VO2 in moderate hyperoxia.

Adult↗

Angiogenic growth factor mRNA responses to passive and contraction-induced hyperperfusion in skeletal muscle.

It has been proposed that, in skeletal muscle, the angiogenic response to exercise may be signaled by the increase in muscle blood flow, via biomechanical changes in the microcirculation (increased shear stress and/or wall tension). To examine this hypothesis, we compared the change in abundance of vascular endothelial growth factor (VEGF), basic fibroblast growth factor (bFGF), and transforming growth factor-beta1 (TGF-beta1) mRNA in skeletal muscles of the canine leg after 1 h of pump-controlled high blood flow alone (passive hyperperfusion; protocol A) and electrical stimulation of the femoral and sciatic nerves producing muscle contraction (protocol B). The increase in leg blood flow (5.4- and 5. 9-fold change from resting values, respectively) was similar in both groups. Passive hyperperfusion alone did not increase message abundance for VEGF (ratio of mRNA to 18S signals after vs. before hyperperfusion, 0.94 +/- 0.08) or bFGF (1.08 +/- 0.05) but slightly increased that of TGF-beta1 (1.14 +/- 0.07; P < 0.03). In contrast, as previously found in the rat, electrical stimulation provoked more than a threefold increase in VEGF mRNA abundance (3.40 +/- 1.45; P < 0.02). However, electrical stimulation produced no significant changes in either bFGF (1.16 +/- 0.13) or TGF-beta1 (1.31 +/- 0.27). These results suggest that the increased muscle blood flow of exercise does not account for the increased abundance of these angiogenic growth factor mRNA levels in response to acute exercise. We speculate that other factors, such as local hypoxia, metabolite concentration changes, or mechanical effects of contraction per se, may be responsible for the effects of exercise.

Animals↗

Accuracy of pulse oximetry during intense exercise under severe hypoxic conditions.

There is a growing need to measure arterial oxygen saturation with a non-invasive method during heavy exercise under severe hypoxic conditions. Although the accuracy of pulse oximetry has been challenged by several authors, it has not been done under extreme conditions. The purpose of this study was to evaluate the accuracy of a pulse oximeter (Satllite. Datex, Finland) during exercise under hypoxic conditions where arterial oxygen saturation was below 75%, simulating exercise at extreme altitude. Ten healthy non-smoking men performed two exercise studies of 30 min under normoxia and under hypoxia on two consecutive days. The exercise intensity was 80% of maximal O2 consumption of VO2max. Arterial oxygen saturation measured by pulse oximetry was corrected (SpO2[corr]) according to previously published equations and was compared to arterial oxygen saturation (SaO2) in blood samples taken simultaneously from the radial artery. Reference arterial saturation values ranged from 57.2 to 97.6% for the whole data set. This data set was split according to low (SaO2 < or = 75%) and high (SaO2 > 75%) SaO2 values. The error of pulse oximetry (SpO2[corr]-SaO2) was 2.05 (0.87)% [mean (SD)] and 1.80 (1.81)% for high and low SaO2 values, respectively. SpO2[corr] and SaO2 were highly correlated (r = 0.93, SEE = 1.81) for low values. During high-intensity constant workload under severe hypoxic conditions, once corrected, pulse oximetry provides an estimate of SaO2 with a mean error of 2%. Thus, the correction previously described for SpO2 values above 75% saturation applies also to SpO2 values in the range of 57-75% during exercise under hypoxic conditions.

Adult↗

Oxygen uptake during submaximal incremental and constant work load exercises in hypoxia.

The effect of acute hypoxia on oxygen uptake (VO2) was studied during incremental (IE) and constant work load exercises. Twenty-two healthy subjects performed two incremental exercises on a bicycle ergometer under normoxic (21% O2) and hypoxic (10.4% O2) conditions. Fifteen subjects performed a constant work load exercise at the same absolute power (CAP) (116 +/- 33 W), while seven other subjects performed three constant work load exercises at the same relative power (CRP) (50, 60 and 70% of VO2max) in both conditions. VO2 was defined as extraventilatory when the estimation of respiratory muscles O2 consumption was subtracted from the total VO2. During IE, the slope of the linear regression relating VO2 to work rate was higher in normoxia than in hypoxia (11.6 +/- 1.2 ml.l-1.W-1 vs 10.1 +/- 1.1 ml.l-1.W-1, p < 0.01). During CAP, VO2 was lower in normoxia than in hypoxia (1.88 +/- 0.45).min-1 vs 1.96 +/- 0.42 l.min-1, p < 0.01) whereas extraventilatory VO2 was not significantly different (1.80 +/- 0.441.min-1 vs 1.77 +/- 0.36) l.min-1). During CRP, the slope relating VO2 to power output computed from the three work loads was not statistically different between normoxia and hypoxia (delta VO2/delta w = 11.9 +/- 3.1 ml.min-1.W-1 vs 12.3 +/- 1.2 ml.min-1.W-1). These findings showed that during CRP, the metabolic efficiency (delta VO2/delta W) was the same in normoxia and in hypoxia. During CAP, the respiratory muscles O2 consumption might have accounted for the difference in VO2 consumption between hypoxia and normoxia.

Adult↗

Increase in occlusion pressure with ventilation and response to maximal exercise.

Fifteen sedentary or mildly active men (low fit group) and 15 trained male athletes (high fit group) performed an incremental exercise bout on a cycle ergometer until exhaustion. At each submaximal load, minute ventilation (VE) and rate of change of mouth pressure (dP/dt) during a brief airway occlusion were computed. The airway was occluded for 40-200 ms and adjusted according to the level of ventilation. Maximal oxygen uptake (VO2peak) and minute ventilation (VEpeak) were measured during the last increment. dP/dt was related to VE in all subjects as dP/dt = a VECURV. The CURV parameter was 0.99-1.95 with a median of 1.49. The subjects were divided into four groups of seven or eight according to their physical fitness and their CURV value. Low and high CURV subjects had a CURV below and above the median, respectively. VE/VO2peak and VE/VCO2peak were significantly higher in the low CURV than in the high CURV group (P < 0.01 and P < 0.05, respectively). Although factors other than the increase in pulmonary impedance with ventilation may influence CURV, the present results indicate the possible influence of mechanical constraint of breathing on the ventilatory output.

Adolescent↗

Influence of hypoxic ventilatory response on arterial O2 saturation during maximal exercise in acute hypoxia.

The aim of this study was to evaluate the influence of peripheral chemosensitivity estimated by hypoxic ventilatory response (HVR) on arterial oxygen saturation (SaO2) during maximal exercise in acute hypoxia. A group of 16 healthy men performed maximal exercise in two conditions of partial pressure of inspired oxygen (PIO2/149 and 70 mm Hg, 19.8 and 9.3 kPa). Measurements of maximal oxygen uptake (VO2max) and SaO2 using an ear-oximeter were carried out in both conditions of PIO2. The HVR was measured at rest by progressive isocapnic hypoxia and evaluated by the slope of the linear regression between the ventilatory flow (VE) and the SaO2 (delta VE/delta SaO2). The absolute value of HVR (in litres per minute per percentage saturation per kilogram) was correlated to maximal expired VE (r = 0.85, P < 0.001), ventilatory equivalent for CO2 (r = 0.83, P < 0.001) and SaO2 (r = 0.60, P < 0.05) determined during maximal exercise in hypoxia: a significant decrease in VO2max (37%) and SaO2 (32%) for PIO2 of 70 mm Hg (9.3 Pa) was observed (P < 0.001). The correlation between the decline of VO2max and arterial oxygen desaturation failed to reach statistical significance (r = 0.47, P = 0.1). The present findings indicated that the peripheral ventilatory chemosensitivity contributed to the interindividual variability of VE and SaO2 during maximal exercise in acute hypoxia.

Adult↗

Pre-acclimatization to high altitude using exercise with normobaric hypoxic gas mixtures.

Pre-acclimatization was conducted using a new method elaborated in our laboratory, combining high intensity exercise while breathing hypoxia normobaric gas mixtures. The training consisted in a daily training during three weeks, 6 days a week, two hours a day, on bicycle ergometer. Eighteen subjects aging 22.2 +/- 1.4 years (11 males, 7 females) were matched in two similar groups: one group trained in normoxic conditions (NG) while the other group (HG) trained with a progressive decrease of the fraction of inspired oxygen (from 12.2% to 10.0%). Maximal oxygen uptake (VO2max) were measured before and after the protocol period in both hypoxic (VO2max H, FIO2 = 10.4%) and normoxic (VO2max N) conditions, for the 2 groups. Training induced a similar O2max N increase in the two groups. The ratio VO2max H/VO2max N was calculated. As expected, in NG group, this ratio decreased significantly (from 63.9 +/- 4.3 to 57.5 +/- 3.1%, p < 0.01) after the training period compared to the initial value, diminution associated with an elevation of VO2max N (from 48.4 +/- 9.0 to 52.9 +/- 9.0 ml.min-1 x kg-1, p < 0.01). Conversely, in HG group, this ratio was not significantly diminished (from 61.7 +/- 3.8 to 60.5 +/- 5.2%, NS) in spite of a similar increase of VO2max N (from 47.5 +/- 5.5 to 50.7 +/- 4.9 ml.min-1 x kg-1, p < 0.01). This does not follow the diminution of the ratio usually described when VO2max N reach higher values.(ABSTRACT TRUNCATED AT 250 WORDS)

Acclimatization↗

Pharmacokinetics of equilin and equilin sulfate in normal postmenopausal women and men.

The MCRs of equilin sulfate and equilin were determined in normal postmenopausal women and a normal man by single iv injections of either [3H]equilin sulfate or [3H] equilin. After the administration of [3H]equilin sulfate, blood was drawn at various time intervals, and the plasma obtained was fractionated into the unconjugated, sulfate, and glucuronide fractions. The bulk of radioactivity was present in the sulfate fraction, and from this, [3H]equilin sulfate, [3H]17 beta-dihydro-equilin sulfate, [3H]equilenin sulfate, and [3H]17 beta-dihydroequilenin sulfate were isolated and purified, and their concentrations were measured. The disappearance of radioactivity from plasma as equilin sulfate can be described as a function that is the sum of two exponentials. The initial fast component (half-life, 5.2 +/- 1.2 min) represents distribution and transfer from a space, with a mean volume of 12.4 +/- 1.6 liters. The mean value for the rate constant of total removal from the initial volume is 163 +/- 19 U/day, of which 15.8 +/- 2% is irreversible. The mean half-life of the slower component of equilin sulfate is 190 +/- 23 min, and the mean MCR is 176 +/- 44 liters/day . m2. Similarly, after the administration of [3H]equilin to a normal postmenopausal woman and a man, the disappearance of radio-activity from plasma as equilin could be fitted by a single straight line, consistent with a one-compartment system. The half-life of equilin was approximately 19-27 min, and the MCR of equilin was calculated to be 1982 liters/day/m2 in the normal man and 3300 liters/day/m2 in the normal postmenopausal woman. The bulk of [3H]equilin was very rapidly metabolized to mainly equilin sulfate. Small amounts of 17 beta-dihydroequilin sulfate and 17 beta-dihydroequilin were also isolated from the plasma. The in vivo formation of 17 beta-dihydroequilin and its sulfate may be of importance, as this estrogen is approximately 8 times more potent as a uterotropic agent than equilin sulfate.

17-Ketosteroids↗