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Introduction: Burn trauma damages resting cardiac function; however, it is currently unknown if the cardiovascular response to exercise is likewise impaired. We tested the hypothesis that, in children, burn injury lowers cardiac output (Q˙) and stroke volume (SV) during submaximal exercise., Methods: Five children with 49% ± 4% total body surface area (BSA) burned (two female, 11.7 ± 1 yr, 40.4 ± 18 kg, 141.1 ± 9 cm) and eight similar nonburned controls (five female, 12.5 ± 2 yr, 58.0 ± 17 kg, 147.3 ± 12 cm) with comparable exercise capacity (peak oxygen consumption [peak V˙O2]: 31.9 ± 11 vs 36.8 ± 8 mL O2·kg·min, P = 0.39) participated. The exercise protocol entailed a preexercise (pre-EX) rest period followed by 3-min exercise stages at 20 W and 50 W. V˙O2, HR, Q˙ (via nonrebreathing), SV (Q˙/HR), and arteriovenous O2 difference ([a-v]O2diff, Q˙/ V˙O2) were the primary outcome variables., Results: Using a 2-way factorial ANOVA (group [G] × exercise [EX]), we found that Q˙ was approximately 27% lower in the burned than the nonburned group at 20 W of exercise (burned 5.7 ± 1.0 vs nonburned: 7.9 ± 1.8 L·min) and 50 W of exercise (burned 6.9 ± 1.6 vs nonburned 9.2 ± 3.2 L·min) (G-EX interaction, P = 0.012). SV did not change from rest to exercise in burned children but increased by approximately 24% in the nonburned group (main effect for EX, P = 0.046). Neither [a-v] O2diff nor V˙O2 differed between groups at rest or exercise, but HR response to exercise was reduced in the burn group (G-EX interaction, P = 0.004). When normalized to BSA, SV (index) was similar between groups; however, Q˙ (index) remained attenuated in the burned group (G-EX interaction, P < 0.008)., Conclusions: Burned children have an attenuated cardiovascular response to submaximal exercise. Further investigation of hemodynamic function during exercise will provide insights important for cardiovascular rehabilitation in burned children.

Introduction: Exercise-induced bronchoconstriction (EIB) is thought to result from osmotic and thermal events of air conditioning during exercise at high ventilation rates. The purpose of this study was to evaluate lung function after exercise and eucapnic voluntary hyperventilation (EVH) while breathing both room-temperature and cold-temperature dry bottled air., Methods: Twenty-two subjects were identified as EIB probable by a fall of >or=7% in forced expiratory volume in the first second of exhalation (FEV1) using a 6-min room-temperature EVH challenge (RTEVH; 22.0 degrees C). Subjects then randomly performed three 6-min challenges: cold-temperature EVH (CTEVH; -1 degrees C), room-temperature exercise (RTEX; 22.0 degrees C), and cold-temperature exercise (CTEX; -1 degrees C), with a period of at least 48 h observed between challenges. Spirometry was performed at baseline and at 5, 10, 15, and 20 min postchallenge., Results: Reasonable agreement was found between challenge modes and room-temperature and cold-temperature challenges. Postchallenge percent falls in FEV1 were -15.21, -13.80, -13.12, and -10.69 for RTEVH, CTEVH, RTEX, and CTEX, respectively. RTEVH resulted in a significantly greater percent fall in FEV1 than CTEX (P=0.048); no other differences in FEV1 were observed., Conclusion: Similar postchallenge percent falls in FEV1 for room- and cold-temperature EVH and exercise suggest that dryness is essential to test conditions, as cold temperature did not have an additive effect to the EIB response.

Purpose: In practice, tests of maximal oxygen uptake (.VO2max) are often preceded by a lactate profile, a highly intense but submaximal exercise bout. The .VO2max response to preceding high-intensity submaximal exercise, with or without a rest period, has not been determined. If .VO2max is limited after a lactate profile, exercise-induced hypoxemia (EIH) may explain the deficit. The purposes of this study were to: 1) examine the effects of high-intensity submaximal exercise, with or without rest, on subsequent .VO2max; and 2) evaluate the role of EIH in causing any observed changes., Methods: Ten healthy, well-trained, male cross-country skiers (age = 20.5 +/- 4.7 yr, height = 181.6 +/- 6.0 cm, mass = 72.1 +/- 5.7 kg) completed three exercise trials: an incremental run to fatigue (MAX), MAX preceded by a high-intensity submaximal run (lactate profile) and a 20-min rest period (discontinuous protocol [DC]), and MAX preceded by a high-intensity submaximal exercise run with no rest (continuous protocol [C]). .VO2max, minute ventilation, and arterial oxygen saturation were measured throughout, and diffusion capacity was evaluated 2 min postexercise. RESULTS No significant between trial differences were observed, although the difference between .VO2max determined during the MAX trial (62.7 +/- 6.7 mL.kg-1.min-1) and during the DC trial (58.3 +/- 4.4 mL.kg-1.min-1) approached significance (P = 0.059). DC .VO2max responses could be separated into two groups: five responders whose .VO2max suffered during the DC trial (decreased >7.5% from MAX) and five nonresponders, whose .VO2max was unaffected by preceding submaximal exercise and a rest period. Responders showed greater aerobic capacity during the MAX trial., Conclusion: .VO2max is significantly reduced in approximately 50% of cross-country skiers when a maximal exercise test is preceded by high-intensity submaximal exercise and a 20 min rest period; the role of EIH in causing these reductions is unclear.

Purpose: The aims of this investigation were: 1). to establish the day-to-day reproducibility of open-circuit acetylene breathing for measuring exercise cardiac output (Q(c)) in young and older adults; and 2). to compare estimates of Q(c) from open-circuit acetylene breathing with estimates of Q(c) from previously established closed-circuit acetylene rebreathing., Methods: Twenty men (10 young: 28 +/- 1 yr; 10 older: 61 +/- 1 yr (mean +/- SE)) performed cycle ergometry exercise on 3 separate days. Q(c) was estimated using open-circuit acetylene breathing on 2 d, and closed-circuit acetylene rebreathing on 1 d., Results: Open-circuit acetylene breathing was highly reproducible (young: standard error of measurement (SEM) = 1.52 L.min (-1) limits of agreement (LOA) = 0.2 +/- 4.2 L.min (-1), coefficient of variation 6% < CV < 8%, day 2 = (0.9 x day 1) + 2.4, r = 0.90, P< 0.001, r (2)= 0.82; older: SEM = 0.94 L.min (-1), LOA = 0.1 +/- 2.8 L.min (-1), 4% < CV < 10%, day 2 = (1.0 x day 1) + 0, r = 0.91, < 0.001, r(2) = 0.82). Estimates of Q(c) from open-circuit acetylene breathing demonstrated good agreement with closed-circuit acetylene rebreathing (young: SEM = 1.52 L.min (-1), LOA = 0.9 +/- 4.4 L.min (-1), 5% < CV < 10%, open-circuit = (1.0 x closed-circuit) + 1.5, r = 0.89, < 0.001, r (2) = 0.79; older: SEM = 1.13 L.min (-1), LOA = 0.1 +/- 3.2 L.min (-1), 5% < CV < 9%, open-circuit = (0.9 x closed-circuit) + 1.6, r = 0.88, < 0.001, r(2) = 0.78)., Conclusion: These results demonstrate that open-circuit acetylene breathing provides reproducible measurements of Q(c) during exercise that demonstrate good agreement with values obtained from the acetylene rebreathing procedure in young and older healthy men.

Control of airway function during and after exercise in asthmatics. Med. Sci. Sports Exerc., Vol. 31, No. 1 (Suppl.), pp. S4-S11, 1999. In asthmatics, airway function can be quite variable during exercise depending on the level of exercise intensity, the duration of exercise, and whether the exercise is at constant load or variable in intensity. Airway diameter can be affected by activity of parasympathetic and sympathetic nerves, by systemic mediators such as catecholamines, and by local mediators such as histamine or leukotrienes. Asthmatic airways are populated with more inflammatory cells than normal airways, and bronchoconstrictor mediator release from these cells is probably caused by drying of the mucosa during and after periods of increased ventilation. There are a few bronchodilating mediators present in both asthmatic and normal airways that could protect against this bronchoconstriction, including prostaglandin PGE2 and nitric oxide. Although it is clear that many of the inflammatory mediators play a role in causing bronchoconstriction after exercise, the role of either bronchoconstrictor or bronchodilator mediators in controlling airway function during exercise has yet to be resolved. In addition, the mechanical interaction between lung parenchyma and airways may provide a bronchodilating influence. In conclusion, the variability in airway function during exercise in asthmatics could be caused by balance among various bronchodilator and bronchoconstrictor mediators, but it may also reflect a mechanical effect of varying levels of ventilation.