Haemodynamic and ADH responses to central blood volume shifts in cardiac-denervated humans.

Haemodynamic responses and antidiuretic hormone (ADH) were measured during body position changes designed to induce blood volume shifts in 10 cardiac transplant recipients to assess the contribution of cardiac and vascular volume receptors in the control of ADH secretion. Each subject underwent 15 min of a control period in the seated posture, then assumed a lying posture for 30 min at 6 degrees head-down tilt (HDT) followed by 30 min of seated recovery. Venous blood samples and cardiac dimensions (echocardiography) were taken at 0 and 15 min before HDT, 5, 15 and 30 min of HDT, and 5, 15 and 30 min of seated recovery. Blood samples were analysed for haematocrit, plasma osmolality, plasma renin activity (PRA) and ADH. Resting plasma volume (PV) was measured by Evans blue dye and per cent changes in PV during posture changes were calculated from changes in haematocrit. Heart rate (HR) and blood pressure (BP) were recorded every 2 min. In the cardiac transplant subjects, mean HR decreased (BP less than 0.05) from 102 b.p.m. pre-HDT to 94 b.p.m. during HDT and returned to 101 b.p.m. in seated recovery while BP was slightly elevated (P less than 0.05). PV was increased by 6.3% (P less than 0.05) by the end of 30 min of HDT but returned to pre-HDT levels following seated recovery. Plasma osmolality was not altered by posture changes. Mean left ventricular end-diastolic volume increased (P less than 0.05) from 90 +/- 5 ml pre-HDT to 105 +/- 4 ml during HDT and returned to 88 +/- 5 ml in seated recovery. Plasma ADH was reduced by 28% (P less than 0.05) by the end of HDT and returned to pre-HDT levels with seated recovery. PRA was also reduced by 28% (P less than 0.05) with HDT. These responses were similar to those of six normal cardiac-innervated control subjects and one heart-lung recipient. Therefore, cardiac volume receptors are not the only mechanism for the control of ADH release during acute blood volume shifts in man.

Exercise training during long-term beta-blockade treatment in healthy subjects.

Although it is well accepted that treatment with beta-blocking drugs impairs endurance exercise capacity acutely, whether a trained state can be achieved while receiving long-term beta-blocker therapy is controversial. The apparent attenuation of training reported in some studies has given rise to the theory that adrenergic stimulation represents a unifying mechanism by which endurance training effects are produced. This theory is supported by studies of long-term beta-agonist infusions that show apparent training responses. To assess the role of beta-adrenergic stimulation produced by exercise in the development of cardiovascular training effects, 39 healthy men were assigned in a random, double-blind fashion to receive oral propranolol, atenolol or matched placebo. Drug doses were titrated individually to minimize the heart rate response to submaximal exercise (dose ranges: atenolol, 50 to 200 mg/day; propranolol, 160 to 320 mg/day). After beginning chronic drug administration, all subjects participated in an intense, supervised 6-week exercise training program (5 days/week, 45 min/day, at least 75% peak heart rate). Adherence to training was monitored by daily supervision; compliance to the medication regimen was assessed by weekly pill counts, medication diaries and plasma drug assay. Maximal exercise testing was performed before and after training. Peak oxygen consumption increased significantly with training in all 3 groups, whether comparisons were made in the presence or absence of medication. The magnitude of change in oxygen consumption did not differ between groups (F = 0.12, p greater than 0.88). Similarly, peak work rate and duration of work increased in all 3 groups.(ABSTRACT TRUNCATED AT 250 WORDS)

Autonomic contribution to heart rate recovery from exercise in humans.

To assess the contribution of the autonomic nervous system to heart rate recovery following exertion, heart rate was observed after peak treadmill exercise in six men following parasympathetic blockade (PB) with atropine sulfate (0.03 mg/kg), sympathetic blockade (SB) with propranolol hydrochloride (0.20 mg/kg), double blockade (DB) with both drugs, and no drugs (ND). Least-squares analysis of each subject's heart rate (HR) as an exponential function of recovery time (t) was computed for each treatment giving an equation of the form HR = aebt. HRs at rest, peak exercise, and 10 min of recovery, the coefficients a and b, and the least-squares correlation coefficient (r) were compared among treatments by nonparametric analysis of variance and rank-sum multiple comparisons. HR recovered in an exponential manner after dynamic exercise in each subject with each of the treatment modes (P less than 0.01 for each r, mean across all treatments r = 0.94). Coefficients a and b differed the most between PB and SB. At the cessation of exercise the decreases in venous return and the systemic need for cardiac output are accompanied by an exponential HR decline. The exponential character of the cardiodeceleration seen after peak exercise appears to be an intrinsic property of the circulation because it occurred under each experimental condition.

Detection of ozone toxicity during continuous exercise via the effective dose concept.

In evaluating O3 toxicity in humans, the effective dose, expressed as the simple product of concentration, exposure duration and ventilation volume (VE), has been applied only to resting or intermittent exercise (IE) exposures. In the present study, we examined the validity of effective dose in predicting pulmonary function impairment when effective dose was determined both as a simple product and as a weighted function via multiple regression. Eight trained male subjects (ages 22-46) completed 18 protocols, including exposures (via mouthpiece) to filtered air and three levels of O3 concentration (0.20, 0.30, and 0.40 ppm), while exercising continuously for durations ranging from 30 to 80 min. The O3 effective dose was significantly related to pulmonary function impairment and exercise ventilatory pattern alteration. Multiple regression analysis, however, substantiated the predominant importance of O3 concentration, with the threshold for O3 toxicity during exercise at a moderately heavy work load [approximately 65% maximum O2 uptake (VO2 max)] shown to be between 0.20 and 0.30 ppm. Although considerable individual variability in O3 toxicity response was noted, group mean responses in our continuous exercise mouthpiece exposures were similar to those previously observed with IE chamber exposures. Thus while the effective dose concept has notable deficiencies in predicting the individual degree of O3 toxicity, it remains a useful approach and warrants further investigation.

Cardiovascular responses to handgrip isometric exercise in patients following cardiac transplantation.

The effects of cardiac denervation on the hemodynamic responses to isometric handgrip contraction were studied in patients 1--5 years after allograft cardiac transplantation. The objective of these studies was to determine the role of cardioacceleration and myocardial contractility on the increase in systemic arterial pressure during isometric exercise. Initially, noninvasive measurement of brachial artery pressure and heart rate during 60 seconds of isometric exercise at 50% of maximal voluntary contraction (50% MVC) were recorded in 23 cardiac transplant patients, 18 ischemic heart disease patients, and 15 healthy controls. While the increases in arterial pressure were not significantly different among the three groups and the heart rate response for the healthy controls and ischemic heart disease patients were similar, the transplant patient's heart rate remained essentially unchanged. In an attempt to determine the mechanisms for the increase in arterial pressure, despite any increase in heart rate in transplant patients, we recorded left ventricular volumes before and at the end of 50% MVC using fluoroscopy of tantalum midwall myocardial markers in seven cardiac transplant recipients and seven nontransplant cardiac surgery patients. The rise in arterial pressure during isometric exercise in both groups of patients resulted from a significant increase in peripheral vascular resistance but not in stroke volume or cardiac output. These data demonstrate that the rise in arterial pressure observed during isometric exercise can be achieved by increased peripheral vascular resistance alone in patients who lack the capacity to increase heart rate or stroke volume.

Cardiorespiratory responses of cardiac transplant patients to graded, symptom-limited exercise.

The electrocardiographic and ventilatory responses of 15 denervated heart patients who had undergone cardiac transplantation and 14 age-matched, normally innervated men were compared to assess the pattern of response to graded treadmill exercise. A 5-minute postexercise venous lactate sample was also obtained. Respiratory exchange ratio and ventilation (Ve) were higher in denervated patients than in normals during submaximal exercise. Peak values (normals vs denervated) for heart rate (172 vs 159 beats/min), blood pressure (189 vs 167 mm Hg), oxygen uptake (37 vs 25 ml/kg/min), oxygen pulse (0.22 vs 0.16 ml/kg/beat) and work time (26.2 vs 18.0 minutes) were higher in normals than in cardiac transplant recipients. Peak ventilatory equivalent (2.14 vs 3.13 l/ml/kg) and lactate values were higher for transplants than for normal subjects, but there were no significant intergroup differences in peak Ve or in the respiratory exchange ratio. In cardiac transplant recipients, work time correlated inversely with a measure of rejection history (r = -0.59, p less than 0.01). The response of cardiac transplant recipients to treadmill work differs from that of normal men and reflects a diminished ability to meet the oxygen demands of the exercising periphery.

Left ventricular response to isometric exercise in patients with denervated and innervated hearts.

Patients with cardiac denervation resulting from allograft transplantation have been observed to increase their diastolic and systolic blood pressure during isometric exercise without concomitant cardioacceleration. To determine the mechanism for the blood pressure increase, heart rate, blood pressure, and ventricular volumes (measured using fluoroscopy of tantalum midwall myocardial markers) were recorded before and after a 50% maximal voluntary contraction. Seven cardiac transplant recipients (denervated heart) and seven nontransplant patients (innervated heart) were studied. Innervated and denervated heart patients increased systolic blood pressure by 16% and 21% and total peripheral resistance by 20% and 12%, respectively. The percentage responses were not significantly different between groups, except for heart rate, which increased 17% in innervated heart patients and 2% in denervated heart patients (p less than 0.05). Neither group had enhanced contractility or increases in cardiac output, suggesting that the blood pressure increases resulted in both groups from increased peripheral resistance.

Physiological profile of middle-aged male and female tennis players.

Cardiorespiratory characteristics, relative body fat, grip strength and selected skinfolds, circumferences and bone diameters were determined in 25 males and 25 females (31--55 yr) whose exclusive mode of regular exercise was tennis (9.7--11.1 hr/wk). Mean resting heart rates were 54 beats/min for the males and 61 beats/min for the females. Mean resting blood pressures were 117/75 and 107/68 mmHg for the males and females, respectively. Compared to normally active populations of the same age and sex, the tennis players displayed an above average maximal oxygen uptake (mean values equal 50.2 ml/kg.min-1 for the males and 44.2 ml/kg.min-1 for the females), below average relative body fat (mean values equal 19.3% and 20.3% for the males and females, respectively), greater dominant grip strengths, and similar non-dominant grip strengths. The results indicate that either physically superior individuals choose to play tennis, or that regular tennis participation produces above average levels of fitness, or both.

Effects of oxone inhalation on work performance and VO2 max.

Ozone (O3) at near ambient smog alert levels has previously been shown to cause alterations in pulmonary function and exercise response in humans. The present study was designed to investigate the effects of O3 administered during graded bicycle exercise to volitional fatigue on work performance and maximal oxygen uptake (VO2max). Nine subjects performed three tests each while breathing either 0.00, 0.15, or 0.30 ppm O3. Forced vital capacity, residual volume, maximal midexpiratory flow rate, and forced expiratory volume in 1 s were assessed before, immediately after, and 4 h after exercise. O3 exposure resulted in no significant effect on maximal work rate, anaerobic threshold, or any pulmonary function parameter. However, maximal expired minute ventilation was decreased (P less than 0.05) in a dose dependent fashion. Thus, exercise ventilation during maximal work was a more sensitive indicator of the effects of O2 exposure than were standard pulmonary function tests. Although subjective symptoms of discomfort were reported more frequently with increased O2 level, it was concluded that exposure of healthy young men to as much as 0.30 ppm O2 for no more than 30 min of progressively incremented exercise to volitional fatigue, is insufficient to cause a significant decrease in work capacity or V02 max.

Effects of exercise, vitamin E, and ozone on pulmonary function and lipid peroxidation.

Expired pentane, an index of lipid peroxidation, and pulmonary function were measured as a function of exercise for 1 h with and without exposure to 0.3 ppm ozone. In experiment 1, 10 subjects who exercised on a bicycle ergometer at 50% of maximal oxygen consumption while being exposed to 0.3 ppm ozone had increased lung residual volume and decreased vital capacity, maximal midexpiratory flow rate, and forced expiratory volume in 1 s. In experiment 2, breath collected into a spirometer filled with hydrocarbon-scrubbed air showed increased pentane from the stress of exercise but no effect of ozone. During rest and exercise in experiment 3, two of six subjects had higher pentane levels than the other subjects. Following daily supplementation with 1,200 IU dl-alpha-tocopherol for 2 wk, the mean production of pentane during rest and exercise was significantly lowered, and there was no difference in pentane production among the subjects. It was concluded that lipid peroxidation occurs during exercise and that it is attenuated by vitamin E.