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Biomedical subjects

P Mucci

Publications and source records attributed to P Mucci.

At least 19 recordsLinked to original sources

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.

Adult↗

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.

Adult↗

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.

Adult↗

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.

Adolescent↗

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.

Adult↗

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.

Adult↗

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.

Aged↗

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.

Administration, Oral↗

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.

Adult↗

Effect of ageing on the ventilatory response and lactate kinetics during incremental exercise in man.

We investigated the effects of age on breathing pattern, mouth occlusion pressure, the ratio of mouth occlusion pressure to mean inspiratory flow, and venous blood lactate kinetics during incremental exercise. Mouth occlusion pressure was used as an index of inspiratory neuromuscular activity, and its ratio to mean inspiratory flow was used as an index of the "effective impedance" of the respiratory system. Nine elderly male subjects [mean (SD) age: 68.1 (4.8) years] and nine young male subjects [mean (SD) age: 23.4 (1.3) years] performed an incremental exercise test on a bicycle ergometer. After a warm-up at 30 W, the power was increased by 30 W every 1.5 min until exhaustion. Our results showed that at maximal exercise, power output, breathing pattern, and respiratory exchange values, with the exception of tidal volume and the "effective impedance" of the respiratory system, were significantly higher in the young subjects. The power output and oxygen consumption values at the anaerobic threshold were also significantly higher in the young men. At the same power output, the elderly subjects showed significantly higher values for minute ventilation, respiratory equivalents for oxygen uptake and carbon dioxide output (CO(2)), mean inspiratory flow, occlusion pressure and lactate concentration than the young subjects. At the same CO(2) below the anaerobic threshold (0.5, 0.75, 1.00 and 1.25 l x min(-1)), minute ventilation and lactate concentration were also significantly higher in the elderly subjects. We observed a significantly higher minute ventilation at CO(2) values of 0.5, 0.75, 1.00 (P < 0.001) and 1.25 l x min(-1) (P < 0.05) in the elderly men, and a significantly higher lactate concentration at CO(2) values of 1.00 (P < 0.05) and 1.25 l x min(-1) (P < 0.01). In conclusion, the ventilatory response in elderly subjects is elevated in comparison with that in young subjects, both below and above the anaerobic threshold. This study demonstrates for the first time that this ventilatory increase, both below and above the threshold, is partly due to an increased lactate concentration.

Adult↗

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.

Adult↗

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.

Adult↗

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.

Blood Volume↗

Effects of nitric oxide inhalation on pulmonary gas exchange during exercise in highly trained athletes.

The pathophysiology of exercise-induced hypoxaemia in elite athletes is still unclear but several studies indicate that a diffusion limitation, which could be explained by an interstitial pulmonary oedema, is a major contributing factor. Stress failure would induce a haemodynamical interstitial oedema with inflammatory reaction and release of mediators like histamine. Histamine release was found to be correlated with the hypoxaemia in elite athletes. If stress failure is involved, inhalation of pulmonary vasodilatators such as nitric oxide during exercise in athletes should induce an inhibition of the histamine release and a reversal of the hypoxaemia. Nine male endurance-trained young athletes performed two randomized exercise tests: one without and the other with 15 p.p.m. of inhaled NO. Measurements of histamine release and arterial blood gas analysis were performed at rest and at 50, 75 and 100% VO2max. At rest, inhaled NO induced a decrease in PaO2 and an increase in (Ai-a)DO2 suggesting increased perfusion of units with low V(A)/Q. During exercise, NO inhalation suppressed the histamine release observed without NO and induced a moderation in the decrease in PaO2 and the increase in (Ai-a)DO2 observed between 75 and 100% of VO2max (P < 0.005). In conclusion, this study showed that NO inhalation inhibited exercise-induced histamine release in highly trained athletes, but we were unable to confirm the suppression of exercise-induced hypoxaemia (EIH). An unexpected result was that inhaled NO seemed to have a marked effect on arterial oxygenation in highly trained-athletes, by disturbing gas exchanges.

Administration, Inhalation↗

Basophil releasability in young highly trained and older athletes.

PURPOSE: Exercise-induced hypoxemia in highly trained athletes is associated with an increase in histamine release during exercise. The cells most implicated in blood histamine release are basophils. The aim of this study was to determine whether high-level endurance training induces modifications in histamine releasability from human basophils. METHODS: Seven young highly trained athletes (YA) [aged 26.1+/-1.3 yr (mean +/- SEM)] and seven master athletes (MA) (64.4+/-4.1 yr), all known to develop exercise-induced hypoxemia, were respectively compared with seven young untrained men (YC) (23.0+/-1.5 yr) and seven older untrained men (OC) (61.6+/-1.3 yr). During an incremental exhaustive exercise, blood samples for measurement of anti-IgE-induced histamine release from leukocytes were drawn at rest, VO2max, and recovery. RESULTS: Basophils from "leukocyte-rich" supernatant in YA and MA showed significantly higher histamine release induced by anti-IgE (1 microg x mL(-1) than, respectively, YC (P<0.01) and OC (P<0.05) at rest, VO2ax (P<0.01), and recovery (P<0.01). Basophils in YA and MA also showed a histamine release induced by anti-IgE that was higher at VO2max than at rest (respectively. P<0.01 and P<0.05), but this change was not found in the control groups. CONCLUSION: In conclusion, the basophils in highly trained endurance athletes, both young and older, showed higher anti-IgE-induced histamine release than those of untrained men. This effect of high-level training seemed to be potentiated by exercise.

Adult↗

Ventilation response to CO2 and exercise-induced hypoxaemia in master athletes.

Exercise-induced hypoxaemia (EIH) in master athletes may be related to a diminished exercise hyperpnoea. The aim of this study was to determine whether EIH is associated with a change in the sensitivity of the ventilation response to activation of the central chemoreceptors. The ventilation response to CO2 was measured in nine elderly untrained men (UT) [mean age 66.3 (SEM 3.1) years] and nine master athletes (MA) [mean age 62.7 (SEM 0.8) years] at rest, during moderate exercise (40% maximal oxygen uptake, VO2max), and during strenuous exercise (70% VO2max) using the rebreathing method. Our results showed that the ventilation response to CO2 did not differ with endurance training and/or exercise, that the threshold of the CO2 response (Th) increased with exercise (P < 0.001), that the increase in Th in MA was higher than in UT between rest and moderate exercise [deltaTh(0-40): 8.55 (SEM 1.8) vs 3.06 (SEM 1.72) mmHg, P < 0.05], and that deltaTh(0-40) and Th during moderate exercise were negatively correlated with arterial O2 saturation during maximal exercise (r=0.50, P<O0.05). We concluded therefore that exercise-induced hypoxaemia in master athletes may not be due to a lower ventilation response to CO2, but may be partly related to a greater increase in Th during moderate exercise.

Aged↗