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S Zanconato

Publications and source records attributed to S Zanconato.

At least 19 recordsLinked to original sources

Exhaled nitric oxide and exercise-induced bronchoconstriction in asthmatic children.

It is known that exhaled nitric oxide (ENO) is increased in asthmatic individuals, probably as an expression of airway inflammation, but no studies have been reported of ENO and exercise-induced bronchoconstriction (EIB). We assessed the effect of a treadmill exercise challenge on ENO concentration in 24 asthmatic children aged 11.2 +/- 0.4 yr (mean +/- SEM). According to the presence or absence of EIB, the children were divided into an EIB group (n = 10) and a non-EIB group (n = 14). ENO was measured with a single-breath reservoir technique. FEV(1), ENO, and heart rate were measured at baseline and 1, 6, 12, and 18 min after the end of exercise. We also measured ENO in 18 healthy control children aged 10.8 +/- 0.6 yr, of whom nine underwent an exercise challenge identical to that of the asthmatic children. After the exercise test, the mean decrease in FEV(1) was 34% in the EIB group and 5% in the non-EIB group. The EIB group had higher baseline ENO values (12.3 +/- 1.6 ppb) than the healthy children (6.1 +/- 0.2 ppb) (p < 0.01). The time course of ENO was similar in the EIB, non-EIB, and control groups, with no significant changes after exercise (p = NS). In the overall group of asthmatic children there was a significant correlation (r = 0.61, p < 0.01) between baseline (preexercise) ENO and magnitude of the maximal decrease in FEV(1) after exercise. In conclusion, our study shows that ENO levels do not change during acute airway obstruction induced by exercise challenge in asthmatic children. In addition, baseline ENO values correlate with the magnitude of postexercise bronchoconstriction, suggesting that NO may be a predictor of airway hyperresponsiveness to exercise.

Adolescent↗

Corticosteroids decrease exhaled nitric oxide in children with acute asthma.

OBJECTIVES: Nitric oxide (NO) produced in human airways seems to have both homeostatic and proinflammatory actions in the respiratory system. NO production has been shown to be higher in the exhaled air of asthmatic adults than in normal subjects. The aim of this study was to evaluate exhaled NO production during asthma exacerbation in children and the effect of a rescue course of oral steroid therapy. STUDY DESIGN: We measured NO in the exhaled air of 16 children (8 girls and 8 boys, aged 6 to 13 years) with an acute asthmatic episode before and after 5 days of therapy with prednisone, and in 16 healthy children. To measure NO, children inhaled NO-free air and, breathing at tidal volume, exhaled in a circuit from which a chemiluminescence analyzer sampled continuously. To assess the effect of acute changes in bronchial caliber on exhaled NO levels, we measured NO before and after a positive bronchodilation test result with albuterol in seven children with asthma whose disease was stable. RESULTS: In the group with acute asthma (forced expiratory volume in 1 second 62% +/- 4.4% predicted, mean +/- SEM), NO levels were significantly higher (31.3 +/- 4.2 parts per billion [ppb]) than in healthy children (5.4 +/- 0.4 ppb, p < 0.001). Administration of prednisone (1 mg/kg per day orally) for 5 days resulted in a mean decrease of 46% +/- 4% in exhaled NO concentrations (16.5 +/- 2.3 ppb, p < 0.001) compared with baseline, accompanied by a significant improvement in lung function (forced expiratory volume in 1 second 90.7% +/- 4.3% predicted). However, in patients with asthma exhaled NO levels remained significantly higher than in control children (p < 0.001) after steroid treatment. When exhaled NO was measured before and after a positive result after bronchodilator reversibility testing, we found no difference in exhaled NO levels (24 +/- 3.8 ppb vs 23.8 +/- 3 ppb; difference not significant). This demonstrates that inhaled albuterol and acute changes in bronchial caliber do not affect exhaled NO measurement. CONCLUSIONS: These data show that children with asthma exacerbation have high levels of exhaled NO that rapidly decrease with oral steroid therapy. We suggest that measurement of exhaled NO may represent a noninvasive method of monitoring airway inflammation in children with asthma.

Acute Disease↗

Effect of hypoxia on lung, heart, and liver insulin-like growth factor-I gene and receptor expression in the newborn rat.

OBJECTIVES: We examined the effect of 7 days of hypoxia in the newborn rat on: a) body, heart, and lung growth; b) circulating insulin-like growth factor-I (IGF-I); c) lung, heart, and liver IGF-I gene expression; and d) lung IGF-I type 1 receptor gene expression and IGF-I receptor binding. We hypothesize that hypoxic exposure would modify body and organ growth and alter IGF-I gene and receptor expression in an organ specific manner. DESIGN: Randomized, controlled prospective study. SETTING: University research laboratory. SUBJECTS: Eleven newborn rat litters (n = 10 per litter) comprised the hypoxia-exposed group and 11 litters comprised the control group (room air). INTERVENTIONS: Hypoxia-group rats were placed in a chamber with an FIO2 of 0.12 on postnatal day 1. Control group rats breathed room air. Exposure to hypoxia continued for 7 days. MEASUREMENTS AND MAIN RESULTS: Hepatic, lung, and cardiac IGF-I mRNA levels and lung IGF-I type 1 receptor mRNA were analyzed, using the ribonuclease protection assay. Crude membrane extracts were used for competitive binding studies with IGF-I and insulin. Somatic growth in the hypoxic group was reduced by 22% (final weight: hypoxic, 14.8 +/- 1.2 g; control, 17.1 +/- 1.5 g; p < .001). The relative weight (organ weight/body weight [mg/g]) of the heart was increased by 39% (p < .001) in the hypoxic pups compared with the normoxic animals, while the relative weight of the lung was unchanged. With hypoxia, IFG-I mRNA concentrations were significantly increased both in the heart and lung (30% and 33%, respectively, p < .02); but, in contrast, IGF-I mRNA concentrations were not significantly different in the liver. The IGF-I receptor mRNA in the lung was increased by 200% (p < .02) in hypoxia compared with controls. There was no effect of hypoxia on specific or nonspecific binding of IGF-I or insulin in the lung tissue. However, specific binding was 33% greater in the IGF-I compared with the insulin experiments. CONCLUSIONS: a) Hypoxia increased IGF-I mRNA in the heart, and increased both IGF-I mRNA and IGF-I type 1 receptor mRNA in the lung. b) The effects of hypoxia on IFG-I are tissue-specific.

Animals↗

Calf muscle cross-sectional area and peak oxygen uptake and work rate in children and adults.

It is often assumed that the inherent peak muscle metabolic capacity scales in direct proportion to muscle cross-sectional area and is the same in small and large animals (A. V. Hill. Sci. Prog. 38: 208-230, 1950). We wondered whether this relationship between size and function was true during the period of growth and development in humans. Magnetic resonance imaging (MRI) was used to determine calf muscle cross-sectional area (CSA) in 20 children (6-11 yr old, 11 boys) and in 18 adults (23-42 yr old, 10 men). Progressive cycle ergometer exercise was performed to determine peak oxygen uptake (VO2peak) and work rate (WRpeak). The scaling factor (determined by allometric analysis) relating maximal O2 uptake (VO2max) to muscle CSA for the whole sample population was 1.04 +/- 0.12 (SE), but the scaling factor relating WRpeak to muscle CSA was significantly greater (1.37 +/- 0.12). Consistent with this, VO2max/CSA was not affected by body weight, but the WRpeak/CSA increased as a function of weight both in males (P < 0.005) and females (P < 0.05). No differences in VO2max/CSA were found between children and adults. WRpeak/CSA was significantly higher in adults compared with children (P < 0.05). It appears that the inherent peak muscle metabolic capacity is smaller in children than in adults. Moreover, the coupling of muscle capacity with whole body metabolic rate changes during growth in humans.

Adult↗

Effect of training and growth hormone suppression on insulin-like growth factor I mRNA in young rats.

The growth hormone (GH)-insulin-like growth factor I (IGF-I) axis plays a role in the adaptation to exercise training, but IGF-I gene expression in response to exercise training and GH suppression has not been studied. Twenty female rates underwent a 4-wk treadmill training program begun in the prepubertal period (day 14 of life). In 10 of the training rats, GH production was suppressed by anti-GH-releasing hormone antibodies (GH suppressed). IGF-I mRNA and protein levels were measured in liver and hindlimb skeletal muscle. GH suppression reduced IGF-I mRNA expression in the liver to a much greater extent than in the muscle. In the GH control rats, training induced significant increases in hepatic exon 1-derived IGF-I mRNA (mean increase 30%; P < 0.05) and muscle exon 2-derived mRNA (mean increase 35%; P < 0.05). In the GH-suppressed rats, only muscle exon 1-derived transcripts were significantly increased by training (55%; P < 0.05) and this was associated with a significant increase in muscle IGF-I protein levels (P < 0.05). We speculate that the anabolic response to training may involve both GH-dependent increases in IGF-I mRNA in the liver and GH-independent increases in the muscle.

Actins↗

Muscle energetics and pulmonary oxygen uptake kinetics during moderate exercise.

The present study tested whether, during moderate exercise, 1) the dynamic responses of ADP and changes in free energy of ATP hydrolysis (delta GATP) were similar to those of phosphocreatine [PCr; as would be expected for a simple controller of muscle respiration (QO2)] and 2) the rise in pulmonary O2 uptake (VO2) during cycle exercise would reflect the rise in muscle QO2 indicated by the calf PCr kinetics. The responses of PCr, Pi, ADP, and delta GATP were measured from the calf in five subjects during supine treadle exercise using 31P-magnetic resonance spectroscopy and compared with those for VO2, measured breath by breath during upright cycle exercise. The time constants for delta GATP [24.2 +/- 14.2 (SE) s] were not significantly different from those for PCr (26.3 +/- 17.3 s) and Pi (30.7 +/- 22.5 s) (P > 0.05). The time constants for phase 2 VO2 (29.9 +/- 16.8 s) were also similar to those of PCr. In contrast, the dynamics of ADP were distorted from those of PCr due to dynamic changes in pH. These results are consistent with mechanisms of respiratory control that feature substrate control by PCr or thermodynamic control through changes in delta GATP. However, these results are not consistent with substrate control by ADP in a simple fashion. Furthermore, the similarity of time constants for phase 2 VO2 and muscle PCr suggests that phase 2 VO2 kinetics reflect those of muscle QO2 in healthy subjects during moderate exercise.

Adenine Nucleotides↗

Changes in potential controllers of human skeletal muscle respiration during incremental calf exercise.

The purpose of this study was to evaluate the consequences of non-linear changes in phosphocreatine (PCr) and pH during incremental calf exercise on estimates of ADP and cytosolic free energy of ATP hydrolysis (delta GATP). Six subjects performed incremental plantar flexion exercise on a treadle ergometer while muscle P(i) metabolism (PCr, P(i), ATP) and pH were followed using 31P-nuclear magnetic resonance spectroscopy. Changes in ADP and delta GATP were estimated with the assumption that there was equilibrium of the creatine kinase reaction and homogeneous tissue metabolite pools. All six subjects showed a threshold for onset of cellular acidosis that occurred on average at 47.3 +/- 12.7% of peak work rate (PWR). In five of the six subjects, PCr and P(i) showed accelerated rates of change above the threshold for onset of cellular acidosis. In all six subjects, ADP, when correctly calculated considering changes in pH, rose in a curvilinear fashion that was well described by a Michaelis-Menten hyperbola through 60-100% of PWR, with a mean apparent Michaelis-Menten constant of 43.1 +/- 17.1 microM ADP and a predicted maximal oxidative rate at PCr = 0, which was 241 +/- 94% of PWR. delta GATP rose linearly with work rate from -62.9 +/- 1.8 kJ/mol during unloaded treadling to -55.0 +/- 1.8 kJ/mol at PWR. If we assume a linear O2 uptake-to-work rate relationship, these results are most consistent with control of respiration being exerted through delta GATP under these conditions (incremental exercise by human calf muscle).(ABSTRACT TRUNCATED AT 250 WORDS)

Adenosine Diphosphate↗

Effect of growth hormone suppression on exercise training and growth responses in young rats.

Exercise training improves maximal oxygen uptake and endurance times in adult human beings and other animals. The mechanism of this improvement results in part from anabolic effects of exercise and may be mediated by growth hormone (GH). Little is known about the role of GH in the adaptation to exercise in younger, still-developing organisms. To examine this role, we began a 4-wk treadmill exercise training protocol in 14-d-old female rats. GH was suppressed by passive immunization with anti-GH releasing hormone antisera. There were four experimental groups: 1) GH-control (normal GH secretory capacity), untrained (n = 21); 2) GH-suppressed, untrained (n = 13); 3) GH-control, trained (n = 14); and 4) GH-suppressed; trained (n = 11). At the end of the training period, maximal oxygen uptake and treadmill endurance running time were measured. Serum GH and IGF-I were assessed using RIA, and whole hind limb musculature succinate dehydrogenase (an indicator of mitochondrial function) was measured with standard fluorometric technique. Body weight gain was markedly reduced in GH-suppressed rats (mean, 54% of GH-controls in untrained rats and 55% in trained; p < 0.05). No apparent effect of training on linear growth was observed. As expected, serum IGF-I was markedly reduced by GH suppression, but no exercise-induced increase occurred in IGF-I as a result of training in either the GH-control or GH-suppressed rats. In GH-control rats, maximal oxygen uptake and succinate dehydrogenase were 69% and 25% greater, respectively, in trained compared with untrained rats (p < 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Adaptation, Physiological↗

31P-magnetic resonance spectroscopy of leg muscle metabolism during exercise in children and adults.

Gas exchange response to high-intensity exercise differs in children and adults. We hypothesized that these findings are related to a lower anaerobic ATP supply in children. We predicted therefore a maturation of muscle high-energy phosphate metabolism during exercise. To test this hypothesis, we measured calf muscle Pi, phosphocreatine (PCr), and pH with 31P-nuclear magnetic resonance spectroscopy during rest and progressive exercise in 10 children and 8 adults. No differences were found at rest in pH and Pi/PCr between children and adults. Exercise resulted in a greater increase in Pi/PCr (P < 0.001) and decrease in pH (P < 0.0001) in adults than in children. Six adults and five children exhibited a transition from a slow to a faster rate of Pi/PCr increase and pH decrease during exercise. No significant differences were found between the two groups in the initial slow-phase slopes of Pi/PCr and pH as a function of work rate. In contrast, during the fast phase, Pi/PCr increased (slope: adults 23.6 +/- 9.8, children 10.7 +/- 2.5; P < 0.05) and pH decreased (slope: adults -6.0 +/- 1.9, children -3.7 +/- 1.2; P < 0.05) more rapidly in adults than in children. In conclusion, high-intensity exercise results in different kinetics of Pi/PCr and pH between children and adults. These results suggest that children are less able than adults to affect ATP rephosphorylation by anaerobic metabolic pathways during high-intensity exercise.

Adenosine Triphosphate↗

Gas exchange during exercise in diabetic children.

The purpose of this study was to evaluate the cardiorespiratory and metabolic response to exercise in 33 children, aged 9 to 15 years, affected by type I diabetes mellitus, in comparison with 47 age-, sex-, weight-, and height-matched healthy children. All diabetic children were on a mixed split-dose insulin regimen, consisting of both regular and long-acting insulin in the morning and evening. The last insulin injection was administered on average 6 hours before the test. The mean duration of diabetes mellitus was 5.0 +/- 3.1 years. The metabolic control was evaluated on the basis of HbA1 levels (mean, 8.9 +/- 1.8%). Pulmonary function tests and progressive exercise tests on the treadmill were performed. Gas exchange, ventilation, and heart rate (HR) were monitored during the tests. The O2 pulse (VO2/HR) was calculated. There was no difference in the baseline oxygen uptake (VO2) between the diabetic children and the control group. VO2 peak was significantly lower (P less than 0.01) in the diabetic adolescents (41.2 +/- 5.9 mL/min/kg) compared to control subjects (46.3 +/- 9.6 mL/min/kg) and it was achieved at an earlier (P less than 0.01) time of run (7.5 +/- 1.8 vs. 9.1 +/- 2.8 min). Anaerobic threshold and minute ventilation were similar in the two groups. The O2 pulse throughout the test was significantly lower (ANOVA, P less than 0.001) in the diabetic group compared to the controls. No differences were found in resting and post-exercise spirometric values. In conclusion, our study shows that well-controlled diabetic adolescents have a reduced working capacity.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗

Effect of increased metabolic rate on oxygen isotopic fractionation.

16O16O is preferentially used over 18O16O (a stable isotope of oxygen comprising about 0.2% of atmospheric O2) as oxygen is consumed during respiration in humans (Epstein and Zeiri, 1988, Proc. Natl. Acad. Sci. USA 85: 1727-1731). To test the hypothesis that oxygen isotopic fractionation is related to the metabolic rate, 8 healthy adults performed 5 min of constant work rate cycle ergometer exercise below and above their anaerobic threshold. Moreover, 3 subjects performed an incremental exercise to the limit of tolerance. Oxygen uptake (VO2) was measured breath by breath. Samples of the exhaled breath for oxygen isotope measurement were obtained at rest and at various times during exercise and recovery. Oxygen isotopic fractionation was determined by isotope ratio mass spectrometry and calculated as the ratio of the degree of fractionation to the oxygen consumed in the breath sample (Z value). For the constant work rate protocol, both low and high intensity exercise resulted in a significant decrease in Z compared to the rest values (P less than 0.01). However, for the high intensity exercise the reduction in fractionation was greater compared to the low intensity protocol (P less than 0.05). For the incremental test, there was a significant negative correlation between oxygen isotopic fractionation and VO2 expressed as percent of the maximal oxygen uptake (r = -0.91, P less than 0.0001). These data suggest that during exercise low-fractionating processes become more important as limiting steps for O2 transport.

Adult↗

13CO2 washout dynamics during intermittent exercise in children and adults.

To test the hypothesis that children store less CO2 than adults during exercise, we measured breath 13CO2 washout dynamics after oral bolus of [13C]bicarbonate in nine children [8 +/- 1 (SD) yr, 4 boys] and nine (28 +/- 6 yr, 5 males) adults. Gas exchange [O2 uptake and CO2 production (Vco2)] was measured breath by breath during rest and during light (80% of the anaerobic threshold) intermittent exercise. Breath samples were obtained for subsequent analysis of 13CO2 by isotope ratio mass spectrometry. The tracer estimate of Vco2 was highly correlated to Vco2 measured by gas exchange (r = 0.97, P < 0.0001). The mean residence time was shorter in children (50 +/- 5 min) compared with adults (69 +/- 7 min, P < 0.0001) at rest and during exercise (children, 35 +/- 7 min; adults, 50 +/- 11 min, P < 0.001). The estimate of stored CO2 (using mean Vco2 measured by gas exchange and mean residence time derived from tracer washout) was not statistically different at rest between children (254 +/- 36 ml/kg) and adults (232 +/- 37 ml/kg). During exercise, CO2 stores in the adults (304 +/- 46 ml/kg) were significantly increased over rest (P < 0.001), but there was no increase in children (mean exercise value, 254 +/- 38 ml/kg). These data support the hypothesis that CO2 distribution in response to exercise changes during the growth period.

Adult↗

Exercise performance in very low birth weight children at the age of 7-12 years.

Fifteen very low birth weight children, 9 appropriate for gestational age (AGA, mean birth weight 1302 +/- 164 g) and 6 small for gestational age children (SGA, mean birth weight 1263 +/- 117 g), were studied at the age of 7-12 years, and compared to a group of 26 healthy, age-, sex-, and height-matched children born at term. None of the VLBW children had developed chronic bronchopulmonary disease. Pulmonary function tests and progressive exercise tests on a treadmill were performed. Forced vital capacity, forced expiratory volume at 1 s and forced expiratory flow between 25% and 75% of vital capacity were normal for all subjects. No differences were found in maximum oxygen consumption, anaerobic threshold and maximal heart rate between the AGA and SGA children and the respective controls. Both in the AGA and SGA subgroups, the pre-exercise oxygen uptake results were comparable to those of the controls. In the SGA subgroup the energy cost of running was significantly higher with respect to the controls, while no difference was found between the AGA and the control children. In conclusion, children with birth weight less than 1501 g have normal values of aerobic fitness. In SGA children the efficiency of running is slightly reduced.

Anaerobic Threshold↗

Oxygen uptake dynamics during high-intensity exercise in children and adults.

We hypothesized that the O2 uptake (Vo2) response to high-intensity exercise would be different in children than in adults. To test this hypothesis, 22 children (6-12 yr old) and 7 adults (27-40 yr old) performed 6 min of constant-work-rate cycle-ergometer exercise. Sixteen children performed a single test above their anaerobic threshold (AT). In a separate protocol, six children and all adults exercised at low and high intensity. Low-intensity exercise corresponded to the work rate at 80% of each subject's AT. High-intensity exercise (above the AT) was determined first by calculating the difference in work rate between the AT and the maximal Vo2 (delta). Twenty-five, 50, and 75% of this difference were added to the work rate at the subject's AT, and these work rates were referred to as 25% delta, 50% delta, and 75% delta. For exercise at 50% delta and 75% delta, Vo2 increased throughout exercise (O2 drift, linear regression slope of Vo2 as a function of time from 3 to 6 min) in all the adults, and the magnitude of the drift was correlated with increasing work rates in the above-AT range (r = 0.91, P less than 0.0001). In contrast, no O2 drift was observed in over half of the children during above-AT exercise. The O2 drifts were much higher in adults (1.76 +/- 0.63 ml O2.kg-1.min-2 at 75% delta) than in children (0.20 +/- 0.42, P less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

Oxygen cost and oxygen uptake dynamics and recovery with 1 min of exercise in children and adults.

To test the hypothesis that O2 uptake (VO2) dynamics are different in adults and children, we examined the response to and recovery from short bursts of exercise in 10 children (7-11 yr) and 13 adults (26-42 yr). Each subject performed 1 min of cycle ergometer exercise at 50% of the anaerobic threshold (AT), 80% AT, and 50% of the difference between the AT and the maximal O2 uptake (VO2max) and 100 and 125% VO2max. Gas exchange was measured breath by breath. The cumulative O2 cost [the integral of VO2 (over baseline) through exercise and 10 min of recovery (ml O2/J)] was independent of work intensity in both children and adults. In above-AT exercise, O2 cost was significantly higher in children [0.25 +/- 0.05 (SD) ml/J] than in adults (0.18 +/- 0.02 ml/J, P less than 0.01). Recovery dynamics of VO2 in above-AT exercise [measured as the time constant (tau VO2) of the best-fit single exponential] were independent of work intensity in children and adults. Recovery tau VO2 was the same in both groups except at 125% VO2max, where tau VO2 was significantly smaller in children (35.5 +/- 5.9 s) than in adults (46.3 +/- 4 s, P less than 0.001). VO2 responses (i.e., time course, kinetics) to short bursts of exercise are, surprisingly, largely independent of work rate (power output) in both adults and children. In children, certain features of the VO2 response to high-intensity exercise are, to a small but significant degree, different from those in adults, indicating an underlying process of physiological maturation.

Adult↗

Maturation of ventilatory responses to 1-minute exercise.

To test the hypothesis that ventilatory responses to exercise mature during growth in healthy children, we examined CO2 production (VCO2) and minute ventilation (VE) before, during, and for 10 min after 1-min bursts of cycle ergometry exercise. Ten children (range: 7-11 y old) and 13 adults (26-42 y old) exercised at work rates corresponding to 50 and 80% of the anaerobic or lactate threshold, 50% of the difference between anaerobic threshold and maximum O2 consumption, 100% of maximum O2 consumption, and 125% of maximum O2 consumption (125% max). Gas exchange was measured breath by breath. Children recovered faster from high-intensity (above anaerobic threshold) exercise as judged by the time constant of single exponential curve-fits to postexercise VCO2 [55 +/- 10 s (1 SD) at 125%. max in children compared with 92 +/- 17 s at 125% max in adults; p less than 0.001] and VE (58 +/- 10 s at 125% max in children compared with 125 +/- 37 s in adults, p less than 0.001). Although we found no significant difference between VCO2 and VE recovery times in children, VE was significantly slower than VCO2 in adults for high-intensity exercise. Moreover, recovery times in adults increased with work intensity but were independent of them in children. Whereas the CO2 costs [calculated as total CO2 produced above baseline per unit work done (mL.J-1)] increased with work intensity in adults, no similar significant relationship was observed in children.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

Heart rate recovery from 1 minute of exercise in children and adults.

Previous studies demonstrated that the time required for oxygen uptake, CO2 production, and minute ventilation to return to baseline levels after 1-min bursts of exercise is different in children compared with adults. To test the hypothesis that the heart rate (HR) recovery time after exercise is also different in children compared with adults, we examined HR in 10 children (range 7-11 y old) and 12 adults (26-42 y old) for 10 min after 1 min of cycle ergometer exercise. Each subject exercised at work rates corresponding to 80% of the lactate or anaerobic threshold (AT), 50% of the difference between AT and maximal O2 uptake (delta), 100% of maximal uptake, and 125% of maximal uptake. Gas exchange was measured breath by breath. In adults, the HR recovery time increased significantly with work intensity as judged by the time constant of a single exponential curve fit to postburst-exercise HR [23 +/- 8 (SD) s at 80% AT, 55 +/- 16 at 50% delta, 74 +/- 13 at 100% of maximal uptake, and 83 +/- 20 at 125% of maximal uptake]. HR recovery time tended to increase with work intensity in children (16 +/- 7, 20 +/- 4, 23 +/- 7, and 27 +/- 9; for 80% AT, 50% delta, 100% of maximal uptake, and 125% of maximal uptake respectively), but to a much smaller extent, and the HR recovery time was significantly smaller in children in the high-intensity (above AT) range of exercise (p less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

Effect of inhaled disodium cromoglycate and albuterol on energy cost of running in asthmatic children.

The purpose of this study is to evaluate the effect of disodium cromoglycate and albuterol on energy cost of running, gas exchange, and ventilation during maximal exercise in children with exercise-induced asthma (EIA). Twelve children (7.1-15.5 years old) with a history of mild to moderate asthma and EIA performed three maximal exercise tests on a treadmill: 1) test A, without premedication; 2) test B, after premedication with inhaled disodium cromoglycate (DSCG) (40 mg); 3) test C, after premedication with inhaled albuterol (200 micrograms). The energy cost of running was calculated at each minute of exercise. None of the children were limited by dyspnea during the run. The post-exercise fall in FEVi after test A was greater than 20% for each child, the mean fall being 32.8 +/- 11.6%, in comparison with 12.6 +/- 8.9% after test B (P less than 0.001) and 2.5 +/- 5.3% after test C (P less than 0.001). There was no difference in the baseline oxygen uptake for the three tests. Maximum oxygen uptake (VO2 peak) decreased from 43.9 +/- 7.7 mL/min/kg in test A to 37.7 +/- 6.0 mL/min/kg in test B (P less than 0.01) and 39.1 +/- 7.2 mL/min/kg in test C (P less than 0.05). Ventilatory anaerobic threshold in tests B and C was significantly lower than in test A (P less than 0.01). Ventilation (L/min) and energy cost of running (O2 mL/kg/m) were significantly lower in tests B and C than in test A at comparable times. Running time was longer in B and C (P less than 0.05) with respect to A.(ABSTRACT TRUNCATED AT 250 WORDS)

Administration, Inhalation↗