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.

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.

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).

Factors influencing estimated oxygen uptake during exercise testing soon after myocardial infarction.

To determine the extent to which oxygen uptake (VO2) estimated from exercise testing in healthy adults is applicable to patients tested soon after myocardial infarction, VO2 was measured during symptom-limited treadmill testing 3 and 11 weeks after the acute event. Twenty-two men (Group I) underwent treadmill testing using a "standard" modified Balke protocol (3 miles/h [80 m/min] with 2.5 percent increments in grade every 3 minutes) 3 and 11 weeks after infarction.