Evaluation of muscle oxygenation by near infrared spectroscopy in patients with facioscapulohumeral muscular dystrophy.

UNLABELLED: The purpose of the study was to determine muscle metabolism adaptation to exercise in facioscapulohumeral muscular dystrophy patients (FSHD) and to study the correlation with clinical functional status (6-min walk test). 8 FSHD patients and 15 age-matched healthy controls (Controls) performed two isokinetic constant-load knee extension exercises: (1) at 20% of their maximal extensors' peak torque (i.e., the same relative workload) and (2) at (20N⋅m) (the same absolute workload) for up to 4 min. All exercises consisted of rhythmic, voluntary, isokinetic, concentric contractions of the quadriceps femoris at 90°/s, whereas the flexion was performed passively at the same speed. Muscle oxygenation in the vastus lateralis was evaluated using near-infrared spectroscopy (NIRS). The FSHD patients displayed a lower maximal peak torque than controls (-41%, p < 0.05). During the two-exercise modalities, deoxygenated haemoglobin (HHb) and total haemoglobin volume (tHb) were lower in the FSHD patients (p < 0.05). The initial muscle deoxygenation time delay was shorter in the control group (FSHD: 15.1 ± 4.1 s vs. CONTROLS: 10.4 ± 2.1 s, p < 0.05). Mean response time and maximal peak torque were both correlated with functional impairment (walking endurance). The results suggest that FSHD patients present an impairment in their capacity to deliver or to use oxygen.

Faster pulmonary oxygen uptake kinetics in children vs adults due to enhancements in oxygen delivery and extraction.

This study aimed to examine if the faster pulmonary oxygen uptake (VO2p) phase 2 in children could be explained by increased O2 availability or extraction at the muscle level. For that purpose, O2 availability and extraction were assessed using deoxyhemoglobin (HHb) estimated by near-infrared spectroscopy during moderate-intensity constant load cycling exercise in children and young adults. Eleven prepubertal boys and 12 men volunteered to participate in the study. They performed one maximal graded exercise to determine the power associated with the gas exchange threshold (GET) and four constant load exercises at 90% of GET. VO2p and HHb were continuously monitored. VO2p , HHb, and estimated capillary blood flow (Qcap) kinetics were modelled after a time delay and characterized by the time to achieve 63% of the amplitude (τ) and by mean response time (MRT: time delay + τ), respectively. Mean values of τ for VO2p (P < 0.001), of MRT for HHb (P < 0.01) and of MRT for Qcap (P < 0.001) were significantly shorter in children. Faster VO2p kinetics have been shown in children; these appear due to both faster O2 extraction and delivery kinetics as indicated by faster HHb and Qcap kinetics, respectively.

Hyperoxia does not accelerate quadriceps muscle deoxygenation kinetics at the onset of heavy exercise cycle.

AIM: The aim of this study was to determine whether an increase in O2 availability induces an alteration of the balance between O2 consumption ((V)O2) and O2 delivery ((Q)O2) at the muscle level. For that, we examined the effect of moderate hyperoxia on muscle deoxygenation kinetics at the onset of heavy-intensity cycling exercise. METHODS: Eight young male adults performed step transitions from 35 W to heavy-intensity exercise corresponding to a power output half-way between the first ventilatory threshold and (V)O2max in normoxia and in hyperoxia (FIO2=0.30). Muscle deoxygenation (HHb) and total hemoglobin (Hbtot) were monitored continuously by near-infrared spectroscopy. HHb data were fit with a mono-exponential model from the onset of exercise up to 90 seconds. RESULTS: Hyperoxia neither altered the delay before the increase in HHb (normoxia: 10.7±1.8 s vs. hyperoxia: 9.5±1.9 s; NS) nor the HHb mean response time (normoxia: 20.6±2.8 s vs. hyperoxia: 19.6±2.3 s; NS). Likewise, Hbtot was not different between normoxia and hyperoxia. CONCLUSION: These results indicate that moderate hyperoxia has no effect on muscle deoxygenation kinetics at the onset of heavy exercise. It suggests that muscle (V)O2 increases at the same rate than O2 delivery when O2 availability is enhanced.

Influence of moderate hypoxia on tolerance to high-intensity exercise.

It remains uncertain as how the reduction in systemic oxygen transport limits high-intensity exercise tolerance. 11 participants (5 males; age 35 ± 10 years; peak [Formula: see text] 3.5 ± 0.4 L min(-1)) performed cycle ergometry to the limit of tolerance: (1) a ramp test to determine ventilatory threshold (VT) and peak [Formula: see text]; (2) three to four constant-load tests in order to model the linear P-t (-1) relationship for estimation of intercept (critical power; CP) and slope (AWC). All tests were performed in a random order under moderate hypoxia (FiO(2) = 0.15) and normoxia. The linearity of the P-t (-1) relationship was retained under hypoxia, with a systematic reduction in CP (220 ± 25 W vs. 190 ± 28 W; P < 0.01) but no significant difference in AWC (11.7 ± 5.5 kJ vs. 12.1 ± 4.4 kJ; P > 0.05). However, large individual variations in the change of the latter were observed (-36 to +66%). A significant relationship was found between the % change in CP (r = 0.80, P < 0.01) and both peak [Formula: see text] (CP: r = -0.65, P < 0.05) and VT values recorded under normoxia (CP: r = -0.65, P < 0.05). The present study demonstrates the aerobic nature of the intercept of the P-t (-1) relationship, i.e. CP. However, the extreme within-individual changes in AWC do not support the original assumption that AWC reflects a finite energy store. Lower hypoxia-induced decrements in CP were observed in aerobically fitter participants. This study also demonstrates the greater ability these participants have to exercise at supra-CP but close to CP workloads under moderate hypoxia.

Difference in breathing strategies during exercise between trained elderly men and women.

This study compared the ventilatory responses and exercise tidal flow-volume (Vt) loops during exercise in order to analyze the influence of gender on breathing strategy in a fit aging population. Sixteen trained elderly men (63.0+/-2.9 years) and eight peer women (62.3 +/- 5.5 years) performed an incremental test on a cycle ergometer. At 90% maximal oxygen consumption (VO2max), the women presented a significantly higher expiratory flow limitation (EFL) than the men (38 +/- 10 vs 17 +/- 8% of Vt, respectively) (P<0.01) and a lower value of expiratory reserve volume relative to forced vital capacity (FVC) compared with the men (16.8 +/- 5.3% vs 23.0 +/- 5.2%, respectively) (P<0.05). Inspiratory reserve volume relative to FVC was significantly higher in women than men at 50% (P<0.05), 70% (P<0.01) and 90%VO2max (25.2 +/- 5.4% vs 12.2 +/- 4.2%, respectively, at 90%VO2max) (P<0.01). Mechanical ventilatory constraints occurred in trained elderly men and women. However, different breathing strategies were observed relative to gender. A significantly higher EFL was measured in women, whereas men rather presented a dynamic hyperinflation. This specific breathing strategy measured in trained elderly women would induce lower ventilatory efficiency than in peer men.

At identical isowork rates, ageing influences cardiorespiratory adaptations in COPD out-patients.

PURPOSE: To determine the extent to which younger COPD patients improve their cardiorespiratory function during exercise in comparison with older COPD patients, as a result of exercise training. METHODS: Thirty-nine COPD patients underwent an exercise program. They were divided into two groups: a younger group (57.2+/-1.0 years, n=18 patients) and an older group (68.8+/-0.6 years, n=21 patients). Forced expiratory volume in 1s was lower than 55% of the predicted value for all patients. RESULTS: After training, VO2 symptom-limited significantly improved by 10.3% and 8.4% for the younger and older COPD patients, respectively (P<0.05). Peak power significantly improved by 25.2% and 17.8% in the younger and older groups, respectively (P<0.05) with a greater improvement for the younger group (P<0.05). At submaximal exercise, ventilation and heart rate significantly decreased after training in the younger COPD patients (P<0.05) with no significant modification in the older COPD patients. CONCLUSIONS: The results suggest that all patients with COPD benefit from exercise rehabilitation at maximal exercise workload, however, according to their age, submaximal cardiorespiratory adaptations were greater in younger patients.

Optimal exercise intensity in trained elderly men and women.

The purpose of our investigation was to suggest a new approach to determine exercise intensities in master elderly athletes. Sixteen trained elderly men (63.0 +/- 2.9 years) and 8 trained elderly women (62.3 +/- 5.5 years), performed an exhaustive exercise test on a cycle ergometer. Rating of perceived exertion (RPE) and heart rate reserve (HRr) were determined at the first and second ventilatory thresholds (VT1 and VT2). There was no significant difference between genders in RPE and HRr, whatever the exercise intensity. RPE scores corresponded to 12.4 +/- 0.9 in men and 12.7 +/- 1.3 in women at VT1. At VT2, RPE was 15.2 +/- 0.8 and 15.3 +/- 1.1 in men and women, respectively. HR at VT1 corresponded to 59.3 +/- 7.0% in men and 59.5 +/- 5.1% in women, whereas at VT2, HR was measured at 80.5 +/- 6.4% and 79.5 +/- 5.9% HRr, in men and women, respectively. Because it is not practical to measure VT1 and VT2 in routine clinical practice, the present study indicated that, in trained older men and women, the RPE value of 12 - 13 and/or 60 % HRr might be used to detect the exercise intensity at VT1. An RPE score of 15 and/or 80 % HRr would appear to be good indexes in the prescription of exercise intensity at VT2.

Effect of prior heavy exercise on muscle deoxygenation kinetics at the onset of subsequent heavy exercise.

This study examines the effect of prior heavy exercise on muscle deoxygenation kinetics at the onset of heavy-intensity cycling exercise. Ten young male adults (20 +/- 2 years) performed two repetitions of step transitions (6 min) from 35 W to heavy-intensity exercise preceded by either no warm-up or by a heavy-intensity exercise. VO2 was measured breath-by-breath, and muscle deoxygenation (HHb) and total hemoglobin (Hb(tot)) were monitored continuously by near-infrared spectroscopy. We used a two-exponential model to describe the VO2 kinetics and a mono-exponential model for the HHb kinetic. The parameters of the phase II VO2 kinetics (TD1 VO2, tau1 VO2 and A1 VO2) were unaffected by prior heavy exercise, while some parameters of local muscle deoxygenation kinetics were significantly faster (TD HHb: 7 +/- 2 vs. 5 +/- 2 s; P < 0.001, MRT HHb: 20 +/- 3 vs. 15+/- 4 s; P < 0.05). Blood lactate, heart rate and Hb(tot) values were significantly higher before the second bout of heavy exercise. These results collectively suggest that the prior heavy exercise probably increased muscle O2 availability and improved O2 utilization at the onset of a subsequent bout of heavy exercise.

Effect of high-intensity interval training and detraining on extra VO2 and on the VO2 slow component.

To examine the effect of 6-week of high-intensity interval training (HIT) and of 6-week of detraining on the VO2/Work Rate (WR) relationship and on the slow component of VO2, nine young male adults performed on cycle ergometer, before, after training and after detraining, an incremental exercise (IE), and a 6-min constant work rate exercise (CWRE) above the first ventilatory threshold (VT1). For each IE, the slope and the intercept of the VO2/WR relationship were calculated with linear regression using data before VT1. The difference between VO2max measured and VO2max expected using the pre-VT1 slope was calculated (extra VO2). The difference between VO2 at 6th min and VO2 at 3rd min during CWRE (DeltaVO2(6'-3')) was also determined. HIT induced significant improvement of most of the aerobic fitness parameters while most of these parameters returned to their pre-training level after detraining. Extra VO2 during IE was reduced after training (130 +/- 100 vs. -29 +/- 175 ml min(-1), P = 0.04) and was not altered after detraining compared to post-training. DeltaVO2(6'-3') during CWRE was unchanged by training and by detraining. We found a significant correlation (r2 = 0.575, P = 0.02) between extra VO2 and DeltaVO2(6'-3') before training. These results show that an alteration of extra VO2 can occur without any change in the VO2 slow component, suggesting a possible dissociation of the two phenomena. Moreover, the fact that extra VO2 did not change after detraining could indicate that this improvement may remain after the loss of other adaptations.

Respiratory muscle oxygenation kinetics: relationships with breathing pattern during exercise.

This work aimed to investigate accessory respiratory muscle oxygenation (RMO(2)) during exercise, using near-infrared spectroscopy, and to study relationships between RMO(2) kinetics and breathing parameters. Nineteen young males (19.3 +/- 1.5 years) performed a maximal incremental test on a cycle ergometer. Changes in breathing pattern were characterized by accelerated rise in the breathing frequency (f (Racc)), plateau of tidal volume (V (Tplateau)) and inflection point in the V. (E)/V (T) relationship (V. (E)/V (T inflection)). First and second ventilatory thresholds (VT1 and VT2) were also determined. RMO (2) kinetics were monitored by NIRS on the serratus anterior. During exercise, all subjects showed reduced RMO (2) (deoxygenation) with a breakdown (B-RMO(2)) at submaximal workload (86 % .VO(2max)). .VO(2) corresponding to B-RMO (2) and to f (Racc), V (Tplateau), .V(E)/V(T inflection), or VT2 were not different. Relationships were found between the .VO(2) at B-RMO(2) and the .VO(2) at f (Racc) (r = 0.88, p < 0.001), V (Tplateau) (r = 0.84, p < 0.001), V. (E)/V (T inflection) (r = 0.58, p < 0.05) or VT2 (r = 0.79, p < 0.001). The amplitude of RMO(2) at maximal workload was weakly related to .VO(2max) (r = 0.58, p < 0.05). B-RMO (2) seems to be due to the change in breathing pattern and especially to the important rise in breathing frequency at the VT2 exercise level. Moreover, subjects who exhibit higher .VO(2max) also exhibit a higher decrease in respiratory muscle oxygenation during exercise.

Effect of prior exercise on the VO2/work rate relationship during incremental exercise and constant work rate exercise.

The disproportionate increase in VO2 ("extra VO2) reported at elevated intensity during incremental exercise (IE) might result from the same physiological mechanisms as the VO2 slow component observed during heavy constant work rate exercise (CWRE). Moreover, it has been demonstrated that prior heavy exercise can diminish the VO2 slow component. The aim of this study was to evaluate whether prior heavy exercise also alters the "extra VO2" during IE. Ten trained sprinters performed three tests on a cycle ergometer: Test 1 was an IE; Test 2 consisted of six minutes of a CWRE (90% of VO2max) followed by six minutes at 35 W and by an IE and Test 3 was composed of two CWRE of six minutes separated by six minutes of exercise at 35 W. For each IE, the slope and the intercept of the VO2/work rate relationship were calculated by linear regression using data before the first Ventilatory Threshold (pre-VT1 slope). The difference between VO2max measured and VO2max expected using the pre-LT slope was calculated (deltaVO2). We also calculated the difference between VO2 at min five and VO2 at min three during CWRE of Test 3 (deltaVO2(5' - 3')). VO2max was significantly higher than VO2exp during IE of Test 1 and Test 2. deltaVO2 during IE did not differ between Test 1 and Test 2 (+ 259 +/- 229 ml x min(-1) vs. + 222 +/- 221 ml x min(-1)). During Test 3, six subjects achieved five minutes of exercise during the second CWRE and deltaVO2(5' - 3') was significantly decreased during the second CWRE (338 +/- 65 ml x min(-1) vs. 68 +/- 98 ml x min(-1), n = 6). These results demonstrate that the amplitude of the "extra VO2"during IE was not affected by prior exercise, whereas the slow component of VO2 evaluated by deltaVO2(5' - 3') during CWRE was lowered. This implies that prior exercise does not have the same effect on the slow component of VO2 and on the "extra VO2". Therefore we were unable to demonstrate a relationship between the VO2 slow component and the extra-VO2 phenomenon during IE.

Attenuated ANF response to exercise in athletes with exercise-induced hypoxemia.

Some highly trained endurance athletes develop an exercise-induced hypoxemia (EIH) at least partially due to a hemodynamic factor with a potential stress failure on pulmonary capillaries. Atrial natriuretic factor (ANF) is a pulmonary vasodilatator and its release during exercise could be reduced with endurance training. We hypothesized that athletes exhibiting EIH, who have a greater training volume than non-EIH athletes, have a reduced ANF release during exercise explaining the pathophysiology of EIH. Ten highly trained EIH-athletes (HT-EIH), ten without EIH (HT-nEIH), and nine untrained (UT) males performed incremental exercise to exhaustion. No between group differences occurred in resting ANF plasma levels. In contrast to HT-nEIH and UT (p < 0.05), HT-EIH showed a smaller increase in ANF concentration between rest and maximal exercise (HT-EIH: 8.12 +/- 0.69 vs. 14.1 +/- 1.86 pmol x l (-1); HT-nEIH: 10.46 +/- 1 vs. 18.7 +/- 1.8 pmol x l (-1); UT: 6.23 +/- 0.95 vs. 20.38 +/- 2.79 pmol x l (-1)). During the recovery, ANF levels decreased significantly in HT-nEIH and UT groups (p < 0.05). Electrolyte values increased in all groups during exercise but were higher in both trained groups. In conclusion, this study suggested that ANF response to exercise may be important for exercise-induced hypoxemia.

Evidence of exercise-induced O2 arterial desaturation in non-elite sportsmen and sportswomen following high-intensity interval-training.

The aim of this study was to investigate the development of exercise-induced hypoxemia (EIH defined as an exercise decrease > 4 % in oxygen arterial saturation, i. e. SaO (2) measured with a portable pulse oximeter) in twelve sportsmen and ten sportswomen (18.5 +/- 0.5 years) who were non-elite and not initially engaged in endurance sport or training. They followed a high-intensity interval-training program to improve V.O (2)max for eight weeks. The training running speeds were set at approximately 140 % V.O (2)max running speed up to 100 % 20-m maximal running speed. Pre- and post-training pulmonary gas exchanges and SaO (2) were measured during an incremental running field-test. After the training period, men and women increased their V.O (2)max (p < 0.001) by 10.0 % and 7.8 %, respectively. Nine subjects (seven men and two women) developed EIH. This phenomenon appeared even in sportsmen with low V.O (2)max from 45 ml x min (-1) x kg (-1) and seemed to be associated with inadequate hyperventilation induced by training: because only this hypoxemic group showed 1) a decrease in maximal ventilatory equivalent in O (2) (V.E/V.O (2), p < 0.01) although maximal ventilation increased (p < 0.01) with training, i. e. in EIH-subjects the ventilatory response increased less than the metabolic demand after the training program; 2) a significant relationship between SaO (2) at maximal workload and the matched V.E/V.O (2) (p < 0.05, r = 0.67) which strengthened a relative hypoventilation implication in EIH. In conclusion, in this field investigation the significant decrease in the minimum SaO (2) inducing the development of EIH after high-intensity interval-training indicates that changes in training conditions could be accompanied in approximately 40 % non-endurance sportive subjects by alterations in the degree of arterial oxyhemoglobin desaturation developing during exercise.

Gender influence on the oxygen consumption of the respiratory muscles in young and older healthy individuals.

To understand the influence of gender on oxygen consumption of respiratory muscles (VO(2)resp), 32 healthy subjects participated in the study (16 males, 16 females). They were divided into four groups: young males, young females, older males and older females. We used a closed circuit device which allowed a continuous increase in external dead space at a constant rate of 300 ml per 90 s and was equipped with a 9-L Gould spirometer filled with 100 % O(2). As log VO(2)tot (total body O(2) consumption) was linearly related to VE, we calculated the slope value (log VO(2)tot/VE) and the Y-intercept (VE = 0) of the semilog regression, representing the increase of VO(2)resp and log VO(2)met (metabolic O(2) consumption). The main results showed that the mean of the individual slope Delta(logVO(2)tot/VE) was steeper in the females than in the males in young and also in older subjects. In addition, VO(2)met in young and older females was lower compared with that in age-matched males. Therefore, we conclude that the oxygen cost of breathing was higher in females versus males subjects.

Effects of salbutamol and caffeine ingestion on exercise metabolism and performance.

This study was designed to assess the effects of acute oral salbutamol and caffeine intake on performance and metabolism during short-term endurance exercise. Eight healthy volunteers participated in the double-blind placebo-controlled randomized cross-over study. Two 10 min cycling trials were performed at a power corresponding to 90 % VO 2 max for the first and a mock test for the second, separated by 10 min of passive recovery after ingestion of placebo (Pla), salbutamol (Sal, 6 mg) and caffeine (Caf, 250 mg). Performance (mean power during the mock test) was not statistically significant between the 3 treatments. Blood lactate was significantly increased after Sal compared to Pla at rest and until the end of the mock test whereas it appeared significantly increased after Caf compared to Pla at the end of the two exercises. Sal increased basal blood glucose and both Sal and Caf induced significant higher plasma insulin concentrations at rest, at the end of the mock test and during the recovery compared to Pla. No significant changes were found in these three variables between the Sal and the Caf treatments. Plasma growth hormone was significantly decreased after Sal after the mock test compared to the two other treatments. In conclusion, under the conditions of this study, neither oral salbutamol nor caffeine intake produce enhancement of short-term performance in non-specific trained subjects despite the substantial shifts in metabolic and hormonal parameters which were found.

Improvement of cognitive function by mental and/or individualized aerobic training in healthy elderly subjects.

The aim of this study was to compare the effects of aerobic and mental training on cognitive function and to determine if the association of the two techniques shows better results. Thirty-two healthy elderly subjects (60 - 76 years) were assigned to one of four groups: aerobic training, mental training, combined aerobic and mental training and a control group. All subjects took two cognitive tests and an incremental exercise test before and after the training period. The intensity of exercise was individualized at the heart rate corresponding to the ventilatory threshold of each subject. After two months, the control group showed no alteration in physiological and cognitive variables. After the training period, the results showed a significant improvement in VO(2)max (F = 4.45, DF = 1, p < 0.05) of 12 % and 11 % in aerobic training and combined aerobic and mental training groups, respectively. Logical memory (F = 4.31, DF = 1, p < 0.05), as well as paired associates learning scores (F = 5.47, DF = 1, p < 0.05) and memory quotient (F = 6.52, DF = 1, p < 0.01) were significantly improved in the three trained groups. The mean difference in memory quotient between pre and post training was significantly higher in the combined aerobic and mental training group compared to aerobic training or mental training groups (F = 11.60, DF = 3, p < 0.001). We conclude that the specific aerobic training and mental training used in this study could induce the same degree of improvement in cognitive function and that combined training seemed to lead to greater effects than either technique alone.

Basophils and exercise-induced hypoxemia in extreme athletes.

This study examined whether the increase in histamine release (%H, i.e., plasma histamine expressed as a percentage of whole blood histamine) associated with exercise-induced hypoxemia (EIH) is related to high training-induced changes in basophil and osmolarity factors in arterial blood. All parameters were measured in 20 endurance athletes, 11 of whom presented an EIH (HT(hyp)) and 9 of whom were nonhypoxemic (HT(nor)), and in 10 untrained control subjects (UT). Measurements were made at rest, at the maximal workload of an incremental exhaustive exercise test, and at the fifth minute of recovery. %H increased during exercise in HT(hyp) (P < 0.01) but did not increase significantly in HT(nor) and UT controls. The results indicated that 1) osmolarity and Na(+) and K(+) concentrations did not differ between the two trained groups and 2) the basophil count and basophil histamine content did not differ among groups. We concluded that the %H increase associated with EIH was not due to a training effect on these parameters. The relatively low increase in histamine content during exercise in HT(hyp) in comparison to HT(nor) (P < 0.05) and UT (P < 0.01) and the low recovery vs. resting basophil count only in HT(hyp) (P < 0.01) suggested an accentuated exercise-induced basophil degranulation in the hypoxemic athletes.

Exercise-induced arterial hypoxaemia in athletes: a review.

During exercise, healthy individuals are able to maintain arterial oxygenation, whereas highly-trained endurance athletes may exhibit an exercise-induced arterial hypoxaemia (EIAH) that seems to reflect a gas exchange abnormality. The effects of EIAH are currently debated, and different hypotheses have been proposed to explain its pathophysiology. For moderate exercise, it appears that a relative hypoventilation induced by endurance training is involved. For high-intensity exercise, ventilation/perfusion (V(A)/Q) mismatching and/or diffusion limitation are thought to occur. The causes of this diffusion limitation are still under debate, with hypotheses being capillary blood volume changes and interstitial pulmonary oedema. Moreover, histamine is released during exercise in individuals exhibiting EIAH, and questions persist as to its relationship with EIAH and its contribution to interstitial pulmonary oedema. Further investigations are needed to better understand the mechanisms involved and to determine the long term consequences of repetitive hypoxaemia in highly trained endurance athletes.

Interleukins 1-beta, -8, and histamine increases in highly trained, exercising athletes.

PURPOSE: Exercise-induced hypoxemia (EIH) in highly trained athletes is associated with an increase in histamine release (%H) during exercise. Certain cytokines, known as histamine-releasing factors, are capable of interacting with basophils and/or mast cells to cause the release of histamine. The aim of this study was to determine whether the increased histamine release in highly trained athletes is related to a high plasma level in interleukin-1 beta (IL-1beta), IL-3, or IL-8 in arterial blood. METHODS: These parameters were measured in 11 endurance athletes (23.2 +/- 1.2 yr (mean +/- SEM)) known to develop exercise-induced hypoxemia and 11 control subjects (25.0 +/- 1.1 yr) at rest, during an incremental exhaustive exercise test, and at the fifth minute of recovery. RESULTS: Histamine release increased between rest and maximal exercise in the athletes (P < 0.01), showing a strong correlation with EIH (r = 0.76, P < 0.01) and was unchanged in the controls. IL-3 plasma concentration was not altered with training and/or with exercise. Circulating IL-8 levels were not different between trained and untrained subjects at any testing level and increased at maximal exercise in both groups (P < 0.01). IL-1beta plasma levels were higher in athletes than in controls (P < 0.05) at each testing level and increased during exercise only in the athletes (P < 0.05). CONCLUSION: An elevated concentration of IL-1beta in plasma and its association with increased IL-8 levels during exercise may partly explain the increase in %H associated with EIH in highly trained athletes. Histamine, IL-8, and IL-1beta releases during exercise reflect an inflammatory reaction, which is probably involved in EIH.

Evidence for an inadequate hyperventilation inducing arterial hypoxemia at submaximal exercise in all highly trained endurance athletes.

PURPOSE: The majority of highly trained endurance athletes with a maximal oxygen uptake greater than 60 mL x min(-1) x kg(-1) develop exercise-induced hypoxemia (EIH). Yet some of them apparently do not. The pathophysiology of EIH seems to be multifactorial, and one explanatory hypothesis is a relative hypoventilation. Nevertheless, conflicting results have been reported concerning its contribution to EIH. The aim of this study was to compare the cardiorespiratory responses to maximal exercise of highly trained endurance athletes demonstrating the same aerobic capacity without EIH (N athletes) and with EIH (H athletes). METHODS: Ten N athletes and twelve H athletes performed an incremental exercise test. Measurements of arterial blood gases and cardiorespiratory parameters were performed at rest and during exercise. RESULTS: All athletes presented a significant decrease in PaO2 (P < 0.05) from rest up to 80% VO2max associated with an increase in PaCO2, both findings consistent with a relative hypoventilation. Then the H athletes, who had a greater training volume per week and a higher second ventilatory threshold than the N athletes (respectively, 17 +/- 1.1 vs 13.1 +/- 0.7 h x wk(-1); 91.8 +/- 1.7 vs 86.1 +/- 1.8% VO2max), presented a continuous PaO2 decrease up to VO2max. This was associated with a widening (Ai-a)DO2. CONCLUSION: This study showed that a relative hypoventilation, probably induced by a high level of endurance training, induced hypoxemia in all athletes. However, a nonventilatory mechanism, perhaps related to the volume of training, seemed to affect gas exchanges beyond the second ventilatory threshold in the H athletes, thereby enhancing EIH.