Control Exercise Test Research Articles

Cardiovascular adjustments in breath-hold diving: comparison between divers and non-divers in simulated dynamic apnoea

The diving response is the sequence of cardiovascular, respiratory and metabolic adjustments produced by apnoea and further strengthened by cooling of the facial area and/or hypoxia. This study aimed at comparing the cardiovascular response to diving of trained divers with that of a control group. In this order, 14 trained divers were compared with 14 non-divers. By means of impedance cardiography and continuous monitoring of arterial pressure, hemodynamic data were collected during three different experimental sessions. Each session included a cycle-ergometer exercise against a workload of 0.5 W kg(-1) of body mass, pedalling in a steady-state condition. During exercise, each subject randomly accomplished 40 s of breath-hold exercise with face immersion (test A) or in air (test B). A control exercise test with normal breathing (test C) was also performed. Divers showed a faster onset of bradycardic response (ANOVA, P < 0.01) and a faster adjustment in systemic vascular resistance (P < 0.001 for divers vs. controls) than did non-divers. Moreover, cardiac output decreased only in divers during the first phase of test A (P < 0.01 for divers vs. controls). The most striking findings were that divers showed a more rapid cardiovascular adjustment with respect to controls, in particular in heart rate and systemic vascular resistance; moreover, with continued apnoea, a delayed increase in myocardial performance and stroke volume occurred and obscured the cardiovascular effects of the diving response.

Effects of Supplemental O2 Inhalation on Cerebral Oxygenation During Exercise in Patients With Left Ventricular Dysfunction

It has been recently reported that cerebral oxyhemoglobin (O(2)Hb) decreases during exercise in nearly 50% of patients with dilated cardiomyopathy. The present study evaluated whether the inhalation of supplemental O(2) diminishes the decrease in cerebral O(2)Hb during exercise. Ten patients with a left ventricular ejection fraction <50% and a clearly observable decrease in cerebral O(2)Hb during preliminary exercise testing underwent 2 additional symptom-limited incremental exercise tests: 1 while breathing room air (control) and the other while breathing 50% O(2). In the latter test, the switch from room air to 50% O(2) was performed, on average, at 43.0+/-14.2 W. Cerebral O(2)Hb was continuously monitored during exercise using near-infrared spectroscopy. In the control exercise test, cerebral O(2)Hb gradually decreased as the work rate increased in all the subjects. When the subjects breathed 50% O(2), this decrease in cerebral O(2)Hb was diminished. The change in cerebral O(2)Hb from rest to peak exercise during the test under 50% O(2) was significantly higher than that during the control test (-0.23 +/-1.89 vs -2.47+/-1.57 micromol/L, p=0.002). Similarly, the change in the cerebral tissue oxygenation index was significantly higher in the test under 50% O(2) (0.45 +/-4.46 vs -3.33+/-3.06%, p=0.023). Impaired cerebral oxygenation during moderate to heavy intensity exercise in patients with left ventricular dysfunction can be offset by breathing supplemental O(2).

Metabolic responses to oral tryptophan supplementation before exercise in horses

This study was conducted to evaluate the effects of oral tryptophan (Trp) supplementation on exercise capacity and metabolic responses in horses. Three horses had to perform an exercise test: a 15-min warm-up followed by a 60-min walk (1.7 m/s, W1), a 10-min trot (3.1 m/s, T1), a second 60-min walk (1.7 m/s, W2), a second 10-min trot (3.1 m/s, T2) and a final 30-min walk (1.7 m/s, W3) until the horses were unwilling to continue. The horses exercised on a treadmill at a 6% incline and with a constant draught load of 40 kg (0.44 kN). Two hours before exercise horses were given 50 g Trp (9.8-10.7 g Trp/100 kg BW) by nasogastric tube. A control exercise test was conducted without Trp. During the control test, one horse was able to finish the final 30-min walk (W3), whereas two horses finished W3 after Trp administration. Higher plasma Trp levels after Trp administration did not change significantly during exercise (Trp: start exercise, 524 +/- 41 micromol/l; end exercise 547 +/- 20 micromol/l; control: start exercise, 70 +/- 10 micromol/l; end exercise, 58 +/- 21 micromol/l). After Trp supplementation, blood lactate concentrations were significantly lower after the first and second trotting periods. Free fatty acids in plasma increased during exercise without any treatment-related differences. Although experimental plasma Trp levels were seven times higher than the control levels, Trp supplementation had no effect on exercise performance and metabolic responses to draught load exercise.

False-positive Exercise Test Secondary to Wolff-Parkinson-White Syndrome in the Absence of Manifest Preexcitation and Disapperance of ST Depressions After Accessory Pathway Ablation

Wolff-Parkinson-White syndrome with manifest preexcitation is a common cause of false-positive exercise test results. However, false-positive results are extremely rare without manifest preexcitation. We report a case with intermittent Wolff-Parkinson-White syndrome and exercise-induced marked ST depressions in the absence of preexcitation of the QRS complexes. His coronary arteries were normal on angiography and no ST changes were observed in the control exercise test after ablation of the accessory pathway.

The role of supplemental oxygen during submaximal exercise in patients with cystic fibrosis.

Repeated bouts of submaximal exercise are an important part of most pulmonary rehabilitation programmes. Patients with moderate-to-severe cystic fibrosis (CF) often demonstrate oxygen desaturation during submaximal exercise, which may limit their ability to participate in these programmes. This study examines whether arterial desaturation contributes to submaximal exercise limitation by testing whether supplemental O2 improves submaximal exercise capacity. Eight patients with CF (mean forced expiratory volume in one second 41% predicted) each underwent two submaximal exercise tests on a bicycle ergometer at 80% of maximal workload. The two tests were identical except for the addition of supplemental O2 (inspiratory O2 fraction 39%) during one of the tests. Exercise duration was significantly longer in the supplemental O2 study versus control (673+/-63 s versus 835+/-99 s). Arterial O2 saturation was also higher in the supplemental O2 study than the control exercise test (96+/-0.3% versus 86+/-1.5%). There was no statistical difference at end exercise between O2 consumption, minute ventilation and heart rate. There was a significant relationship between improvement in exercise capacity and the amount of desaturation during the control exercise test. Results indicate that supplemental oxygen improves submaximal exercise capacity in patients with moderate-to-severe cystic fibrosis. Oxygen therapy may be an important intervention to improve participation and maximise the benefits of pulmonary exercise rehabilitation programmes.

The effect of volitional breathing on the breathlessness-ventilation relationship during progressive exercise in healthy subjects

The current hypothesis about the generation of breathlessness sensation is that a conscious awareness of reflex activation in the brainstem, rather than sensory feedback from peripheral receptors, is the major factor that gives rise to this sensation. This hypothesis was based on work that showed subjects and patients were less breathless when volitionally copying a hypercapnic breathing pattern [1]. However, later studies have shown no effects of volitional breathing on breathlessness [2]. To investigate the contribution of the cortical drive on modulation of the reflex drive, experiments on volitional breathing per se were conducted during progressive exercise. Sixteen subjects undertook a progressive exercise test on a bicycle ergometer, to a symptom-limited maximum during the course of which breathlessness was estimated each minute using the Visual Analogue Scale (VAS). All subjects had completed control exercise experiments to reach reproducible breathlessness estimations. A control study was followed, 7–10 days later, by a study of volitional breathing. The subjects (all males) had a mean age of 29.6 years (SD ± 9.3). The breathing pattern of a control exercise test (control) was recorded. Following this, an 'appropriate volitional tracking' experiment was conducted in which the subjects attempted to copy the previous control breathing pattern during another control exercise test. The subjects were told to follow the breathing pattern by adjusting a cursor, which was driven by flow through a pneumotachograph (PK Morgan, UK). In control and volitional tracking experiments, ventilation (VE), tidal volume (VT) and respiratory frequency (fR) were plotted against time. Breathlessness estimations were plotted against ventilation, from which slope and intercept values were derived. Mean changes in the saturation of oxygen in arterial blood (SaO2) found at the end of each exercise test were also recorded (Biox IIA, USA). Comparisons were made using a paired t-test. All t-tests were two-tailed and the level of probability taken as significant was 5% (P < 0.05) (Table ​(Table11). Table 1 The mean slope and intercept of VE/time, VT/time and fR/time relationships for both experiments were not significantly different. Mean SaO2 levels also showed no significant changes. Mean slopes of the VAS/VE relationship were also not significantly different. However, the mean intercept of the volitional experiment was significantly increased relative to control. The major finding in this study was that the onset of breathlessness was significantly delayed, though there were no significant changes in any objective physiological data set between control and volitional experiments. We postulate that this delay is due to cortical drive bypassing the medullary rhythm generator, with possible inhibition of the reflex efferent drive projecting to the sensory cortex. This is consistent with the hypothesis that the medullary reflex activity is responsible for the genesis of breathlessness sensation.

Desviación izquierda transitoria del eje eléctrico del QRS durante la prueba de esfuerzo como manifestación de lesión severa proximal de la arteria descendente anterior

The case of a patient in whom transient left axis deviation occurred during a treadmill exercise test is reported. Coronary angiography showed a 90% obstruction of the proximal left anterior descending artery. After a successful coronary angioplasty and stent implantation, a control exercise test was performed without a recurrence of angina or transient intraventricular conduction disturbance, reflecting the ischaemic nature of this abnormality.

Improvement in exercise-induced left ventricular dysfunction by infusion of α-human atrial natriuretic peptide in coronary artery disease

The effects of recombinant α-human atrial natriureric peptide (α-hANP) infusion on acute left ventricular dysfunction provoked by exercise were examined in 14 men with coronary artery disease. Patients performed symptom-limited, graded exercise on a supine bicycle ergometer. Plasma α-hANP and guanosine 3′,5′-monophosphate (cyclic GMP) concentrations as well as hemodynamic variables were measured at rest, during and after exercise. In 14 patients whose pulmonary artery wedge pressure was > 20 mm Hg at peak exercise, the same exercise protocol was repeated at 30 minutes after starting intravenous α-hANP infusion (0.05 μg·kg−1·min−1). In 8 of these patients, a Webster thermodilution catheter was advanced into the coronary sinus for measurement of coronary sinus blood flow. From the control exercise test, plasma α-hANP concentration increased from 86 ± 20 pg/ml at rest to 188 ± 32 pg/ml at peak exercise (p < 0.001), and plasma cyclic GMP concentration increased from 4.8 ± 1.9 pmol/ml at rest to 7.2 ± 2.9 pmol/ml at peak exercise (p < 0.001). Both plasma α-hANP and cyclic GMP concentrations showed a significant positive correlation with pulmonary artery wedge pressure during control exercise. With α-hANP infusion, systolic and diastolic pulmonary artery pressures and pulmonary artery wedge pressure were significantly decreased at all time points during exercise testing. Heart rate was increased and systolic blood pressure was significantly decreased at rest and at 3 minutes of exercise. Diastolic blood pressure, mean blood pressure, systemic vascular resistance, and pulmonary vascular resistance were significantly decreased at rest. Thus, exercise-induced acute left ventricular dysfunction was improved in patients with coronary artery disease by intravenous a-hANP infusion, mainly through preload reduction without an apparent effect on coronary circulation.

Acute effects of nitrates on exercise testing in patients with syndrome X. Clinical and pathophysiological implications.

Sublingual nitrates are much more effective in relieving angina pectoris in patients with coronary artery disease than in patients with syndrome X, but it is not known whether their effect on exercise tolerance is also different in these two groups of patients. Treadmill exercise testing was performed before and after administration of sublingual isosorbide dinitrate (ISDN, 5 mg) in 18 patients with syndrome X (effort angina and normal coronaries, group X) and in 33 patients with documented coronary artery disease (group C). As a selection criterion, all patients had ST-segment depression > or = 1 mm on the control exercise test. Compared with the control test, the main differences in the two groups observed during the exercise test after administration of ISDN were (1) heart rate at 1-mm ST-segment depression was higher (126 +/- 25 versus 104 +/- 15 beats per minute [bpm], P < .01) in group C, whereas it was not different (125 +/- 15 versus 126 +/- 16 beats per minute) in group X; (2) the rate-pressure product at 1-mm ST-segment depression, the time to 1-mm ST-segment depression, and the exercise duration were significantly improved in group C (P < .01 for all) but were worsened in group X (18,047 +/- 4159 versus 20,535 +/- 4507 bpm . mm Hg, P = .014; 268 +/- 312 versus 429 +/- 214 seconds, P < .01; 494 +/- 279 versus 622 +/- 194 seconds, P = .013, respectively); (3) a normalization of the ECG (no ST-segment depression) was obtained in 10 patients (30%) of group C but in only 1 (5%) of group X (P < .01); (4) angina was prevented in 10 of 19 patients of group C but in no patient of group X (P < .01). In patients presenting with anginal chest pain, the effects of sublingual nitrates on exercise testing appear to be clinically useful to distinguish patients with coronary artery stenoses from patients with syndrome X. Indeed, worsening of exercise tolerance is highly predictive of normal coronary arteries. Furthermore, the failure of nitrates to improve exercise tolerance in patients with syndrome X suggests that a deficiency in coronary prearteriolar nitric oxide production is unlikely to play a key role in the pathophysiology of the syndrome.

Effect of alpha 1-adrenergic receptor antagonists on susceptibility to malignant arrhythmias: protection from ventricular fibrillation.

alpha-Adrenergic receptor responsiveness has been reported to increase during myocardial ischemia, correlating with onset of malignant arrhythmias. If alpha-adrenoceptor mechanisms play a significant role in induction of life-threatening arrhythmias, inhibition of these receptors with specific alpha-adrenoceptor antagonists should protect against disturbances in cardiac rhythm. To test this hypothesis, we induced ventricular fibrillation (VF) in 21 mongrel dogs with healed myocardial infarctions (MI) by 2-min coronary artery occlusion during exercise. On a subsequent day, the exercise plus ischemia test was repeated after the alpha 1-adrenoceptor antagonist prazosin HCl (0.5 mg/kg intravenously, i.v.; n = 14) or the alpha 1A-adrenergic receptor subtype antagonist WB4101 (2.0 mg/kg i.v., n = 9). Prazosin elicited a significant reduction in left ventricular systolic pressure (LVSP, control 157.0 +/- 6.5 vs. prazosin 118.5 +/- 2.7 mm Hg) and prevented arrhythmias in 13 of 14 animals (chi square p < 0.001). No other hemodynamic parameters, either before or during the coronary occlusion, were altered by prazosin. WB4101 did not alter any hemodynamic parameters either before or during coronary artery occlusion, yet prevented VF in 7 of 9 animals (chi square p < 0.025), delaying onset of malignant arrhythmias in the remaining animals. A second control exercise plus ischemia test reproducibly induced VF in all animals. Together these data demonstrate that alpha-adrenoceptor antagonists can prevent VF independent of hemodynamic changes. In particular, the data suggest that activation of the alpha 1A-adrenergic receptor subtype may contribute importantly to development of malignant arrhythmias.(ABSTRACT TRUNCATED AT 250 WORDS)

Hemodynamic mechanisms of antianginal action of calcium channel blocker nisoldipine in dynamic exercise-induced angina.

To investigate the mechanism of antianginal action of the calcium channel blocker nisoldipine and to determine the reproducibility of the clinical and hemodynamic events induced by supine leg exercise, 30 patients with stable effort angina pectoris were studied. They were divided into two groups; one group of 19 patients received a single 10-mg dose of nisoldipine orally, and the other group of 11 patients received a single dose of placebo orally. Chest pain was induced in all of 30 patients during the control exercise test. After nisoldipine administration, chest pain was not induced in 13 of 19 patients and was of lessened severity in five patients with the same work load as those performing control exercise. ST segment at peak exercise showed less severe depression after nisoldipine. Systemic vascular resistance was reduced by 38% (p less than 0.001) at rest and 22% (p less than 0.001) at peak exercise, and coronary vascular resistance was reduced by 31% (p less than 0.01) at rest and 18% (p less than 0.01) at peak exercise. Pulmonary artery wedge pressure fell from 6 +/- 1 to 3 +/- 1 mm Hg (p less than 0.001) at rest and from 28 +/- 3 to 11 +/- 2 mm Hg (p less than 0.001) at peak exercise. Coronary sinus flow at rest and myocardial oxygen uptake both at rest and during exercise was not modified by nisoldipine. However, coronary sinus flow at peak exercise increased significantly from 219 +/- 24 to 249 +/- 31 ml/min (p less than 0.01) after nisoldipine, and myocardial oxygen uptake was not significantly changed despite decreased coronary vascular resistance. The clinical and hemodynamic events induced by the exercise during invasive studies (except pulmonary artery wedge pressure at rest) were reproducible after placebo administration. Our data demonstrate that increased coronary blood flow could be the major mechanism of the antianginal action of nisoldipine in supine leg exercise-induced angina.

慢性左室疾患患者の心機能および運動能力に及ぼすＬ‐カルニチンの慢性効果

To assess the clinical efficacy of L-camititine in chronic heart failure, we measured echocardiographic left ventricular dimensions, peak oxygen consumption (peak Vo2), and anaerobic threshold (AT) before and after a long-term administration of L-carnitine (1, 800 mg/day, 12 weeks) in 18 patients with left ventricular dysfunction (I to III in New York Heart Association fuhctional classification). Peak Vo2 and AT were determined by the continuous respiratory gas analysis during a symptom-limited maximal bicycle exercise test. The patiehts were divided into 2 groups according to the presence of exercise-induced ST depression (>0.1 mV) in the control exercise test: 9 patients with ST depression (Group I) and 9 patients without ST depression (Group II). In Group I, exercise-induced ST depression was significantly improved by the chrohic admihistratioh of L-carnitine (0.17±0.03 mV to 0.12±0.03 mV, mean±SE, P<0.05). Coincidentally both peak Vo2 and AT significantly increased after L-carnitine administration when compared to those before administration in Group I (21.3±2.5, 17.2±27 to 24.3±2.3, 20.2±2.3 ml/min·kg, re spectively, mean±SE, P<0.05). In Group II there was no sighificant change in electro cardiographic findings, peak Vo2, or AT by the drug administration. The intemal dimensions and the fractional shortening of the left ventricle were not altered by the L-carnitineadministration in both grotips. Thus, we conclude that L-carhitine can increase exercise capacity in patients with chronic heart failure when they are attended with exercise-induced ST depression, possibly by improving abnormalities in the myocardial fatty acidenergy metabolism during exercise.

Effects of isosorbide dinitrate on exercise capacity in cardiac patients. Relationship between oxygen uptake responses and hemodynamic effects.

Acute effects of oral isosorbide dinitrate on exercise capacity were evaluated in 14 patients with chronic heart disease measuring the anaerobic threshold and left ventricular function during exercise. A symptom-limited exercise test was performed on a bicycle ergometer with work rates increased by 1W every 6 seconds. Left ventricular function was continuously monitored with a computerized cadmium telluride detector following the intravenous injection of technetium-labeled red blood cells. Thirty minutes after the control exercise test, patients were given isosorbide dinitrate, 5 mg orally. The second exercise test was performed 30 min later. Isosorbide dinitrate improved the anaerobic threshold from 715.4 +/- 172.9 to 774.9 +/- 173.5 ml/min (p less than 0.01) and ejection fraction at peak exercise from 36.7 +/- 11.6 to 39.9 +/- 12.3% (p less than 0.05). However, there was no significant change in maximum work rate or peak oxygen uptake. Those patients for whom isosorbide dinitrate resulted in a 10% or greater improvement in the anaerobic threshold had both higher pre-treatment ejection fractions and greater increases in peak exercise ejection fraction following isosorbide dinitrate. Measurements of the anaerobic threshold and left ventricular function during exercise may be useful in the evaluation of the efficacy of vasodilators in cardiac patients.

Cocaine-induced ventricular fibrillation: protection afforded by the calcium antagonist verapamil.

There is increasing evidence that the use of cocaine can trigger lethal cardiac events, including ventricular fibrillation. The mechanism responsible for these lethal cardiac arrhythmias remains to be determined. Therefore, 13 mongrel dogs were instrumented so that heart rate, left ventricular pressure (LVP), and d(LVP)/dt could be measured. After a 3- to 4-wk recovery period, the left circumflex coronary artery was occluded for 2 min, beginning with the last minute of an exercise stress test and continuing for 1 min after the cessation of exercise. None of the dogs developed cardiac arrhythmias during the control exercise plus ischemia test. On a subsequent day, the test was repeated after the injection of cocaine HCl (1.0 mg/kg). Cocaine significantly (P less than 0.01) elevated heart rate, systolic LVP, and d(LVP)/dt, and it elicited cardiac arrhythmias in 12 of the 13 animals during the exercise plus test. In fact, 11 animals developed ventricular fibrillation. Verapamil, a calcium channel antagonist (250 micrograms/kg), attenuated the hemodynamic effects of cocaine and prevented the development of ventricular arrhythmias. These data suggest that cocaine can induce ventricular fibrillation during myocardial ischemia and that these lethal arrhythmias may be prevented by a calcium channel antagonist.

The false positive exercise test: usefulness of sublingual nitroglycerin exercise test and cardiac scintigraphy for differentiating from patients with coronary artery disease.

Exercise tests with sublingual nitroglycerin were performed on 7 patients with true positive and 8 patients with false positive exercise test results. Four of 7 patients with true positive changes and 8 patients with false positive changes underwent exercise cardiac scintigraphy. Scintigrams showed perfusion defects in 4 patients with true positive outcomes, and no perfusion defect in 8 patients with false positive outcomes. Exercise tests with sublingual nitroglycerin were performed with the same load as that without nitroglycerin. In all 7 patients with true positive exercise test results, ST segment depression observed in the control exercise test was not observed in the nitroglycerin exercise test. In the false positive patients, ST segment depression observed in the control exercise test remained unchanged in 7 of 8 patients receiving nitroglycerin. Exercise tests with sublingual nitroglycerin as well as exercise cardiac scintigraphy are valuable tods in differentiating false positive from true positive patients. Furthermore, these data suggest that ST segment depression in the false positive patients may not be related to myocardial ischemia.

運動誘発狭心発作時の心血行動態に及ぼすＩｓｏｓｏｒｂｉｄｅ‐５‐ｍｏｎｏｎｉｔｒａｔｅ（ＴＹ‐１０３６８）の効果

To investigate the hemodynamic effects of isosorbide-5-mononitrate (ISMN), 11 patients with effort angina pectoris were studied.Hemodynamic and echocardiographic measurements were observed at rest and during angina-limited supine multi-stage bicycle ergometer exercise testings before and 120 min after oral administration of 20 mg of ISMN. Compared with the control exercise test, the mean ST-segment at peak exercise showed less depression after ISMN (P<0.001). At rest there were significant decreases in systolic and diastolic blood pressures after ISMN (P<0.001 and P<0.05, respectively). Both at rest and peak exercise there were significant decreases in pulmonary capillary wedge pressure (both P<0.0001), left atrial volume (both P<0.001), and left ventricular end-diastolic volume (both P<0.05), while cardiac index, pressure-rate-product, and systemic vascular resistance remained unchanged. The average peak value for plasma ISMN concentration was 460 ng/ml at 90 min after dosing, and the elimination half-life was 7 hours.These data would indicate that the antianginal effects of ISMN, which is appropriate for its prolonged duration of action, are mainly related to diminishment of myocardial oxygen requirements due to left ventricular preload reduction as a common mechanism.

Effects of S-596, a new beta-adrenoceptor blocking agent on the left ventricular performance of normal subjects during exercise.

The effects of d1-2-(3'-t-butylamino-2'-hydroxypropylthio)-4-(5'-carbamoyl-2'-thi enyl) thiazole hydrochloride (S-596) were evaluated in 9 normal volunteers. Exercise echocardiography was performed in the semi-supine position before and 2, 4 and 24 hours after the oral administration of 15 mg of S-596. Two hours after administration, resting heart rate was unchanged, compared with control, but systolic blood pressure at rest was slightly decreased (114 +/- 6 vs 106 +/- 10 mmHg, p less than 0.05). Left ventricular dimensions were unchanged, but shortening fraction was increased in the resting state (30.3 +/- 4.6 vs 33.1 +/- 4.8%, p less than 0.05). During exercise on oral S-596, heart rate and systolic blood pressure responses were reduced (127 +/- 11 in control vs 108 +/- 6 beats/min on S-596, 198 +/- 25 vs 168 +/- 23 mmHg, p less than 0.001 and 0.05, respectively). Left ventricular end-diastolic dimension was not significantly altered by S-596 compared with the preceding control exercise test; however, end-systolic dimension was significantly larger after beta blockade with S-596 (2.6 +/- 0.4 vs 3.0 +/- 0.4 cm, p less than 0.05). Shortening fraction and cardiac output decreased significantly (43.7 +/- 3.7 vs 40.0 +/- 5.7%, 9.5 +/- 1.4 vs 8.4 +/- 1.3 L/min, p less than 0.05 and 0.01, respectively). These effects of S-596 were maximal at 2 hours after oral administration with reduced response of heart rate to exercise lasting for 24 hours. Compared with the effects of propranolol (30 mg, given orally) in the same subjects, beta-adrenergic blockade during exercise with S-596 was equivalent to or greater than that of propranolol. Thus, S-596 has little, if any, effect on resting left ventricular performance, but demonstrates potent negative chronotropic and inotropic effects during exercise in normal human subjects. Its beta-adrenergic blocking action also has long acting properties, especially its chronotropic effect.

Effects of sleep deprivation on thermoregulation during exercise.

Five fit men completed a practice, control, and sleep deprivation exercise test. Two nights of normal sleep preceded the control test, and 33 h of wakefulness preceded the sleep deprivation test. These tests consisted of 20 min of rest followed by 40 min of cycle-ergometer exercise (50% of peak O2 uptake, VO2) in a temperate (ambient temperature, 28 degrees C; relative humidity, 30%)-environment. Esophageal temperature (Tes), local sweat rate (mds), and chest thermal conductance (kch) were continuously measured. During exercise a 0.7 and 0.5 degrees C rise in Tes was found for the sleep deprivation and control tests, respectively. This increase in Tes values from rest to the end of exercise was greater (P = 0.08) for the sleep deprivation than control test. Total body sweat rate, calculated from Potter balance measurements, was 27% less (P less than 0.01) for the sleep deprivation than the control test. Both mds and kch values were lower (P less than 0.05) during the final 20 min of exercise for the sleep deprivation than control test. Final exercise mds values were 19% lower (P less than 0.05) for the sleep deprivation than control test. An asynchronous rather than a normal synchronous mds pattern was frequently observed during the sleep deprivation test. During the sleep deprivation test, the mds sensitivity (delta mds X delta Tes-1) was 38% lower (P less than 0.01) and kch sensitivity (delta kch X delta Tes-1) was 42% lower (P less than 0.05) than during the control test. These data indicate that sleep deprivation decreases evaporative and dry heat loss during moderate-intensity exercise.

The duration of protection from exercise-induced asthma by inhaled salbutamol, and a comparison with inhaled reproterol

β-Adrenergic bronchodilators can prevent the development of exercise-induced asthma (EIA). To investigate the duration of this effect, we determined the time at which the protective effect of salbutamol diminished significantly in six subjects. All had stable asthma known to be triggered by exercise. Following a control exercise test, identical tests were repeated weekly at various times (1–6 hours) after inhalation of 200 μg of salbutamol. Significant protection (< 75%) was lost in two subjects at 2 hours, in two at 4 hours and in two at 6 hours. A further exercise test was performed after inhalation of 1 mg of reproterol, at the time when salbutamol no longer afforded significant protection. There was a significantly smaller fall in peak expiratory flow rate after exercise (P < 0.01) with reproterol than with salbutamol, at the same time after inhalation. There was no relationship between the degree or duration of protection from EIA and the bronchodilator effect of the drugs, the age and sex of the subjects, the length of asthma history or severity of base-line EIA, except perhaps the requirement for regular treatment with a steroid aerosol or sodium cromoglycate.

The duration of protection from exercise-induced asthma by inhaled salbutamol, and a comparison with inhaled reproterol

β-Adrenergic bronchodilators can prevent the development of exercise-induced asthma (EIA). To investigate the duration of this effect, we determined the time at which the protective effect of salbutamol diminished significantly in six subjects. All had stable asthma known to be triggered by exercise. Following a control exercise test, identical tests were repeated weekly at various times (1–6 hours) after inhalation of 200 μg of salbutamol. Significant protection (< 75%) was lost in two subjects at 2 hours, in two at 4 hours and in two at 6 hours. A further exercise test was performed after inhalation of 1 mg of reproterol, at the time when salbutamol no longer afforded significant protection. There was a significantly smaller fall in peak expiratory flow rate after exercise ( P < 0.01) with reproterol than with salbutamol, at the same time after inhalation. There was no relationship between the degree or duration of protection from EIA and the bronchodilator effect of the drugs, the age and sex of the subjects, the length of asthma history or severity of base-line EIA, except perhaps the requirement for regular treatment with a steroid aerosol or sodium cromoglycate.