Autonomic mechanisms underlying the initial heart rate response to standing were analyzed in nine normal subjects. The normal pattern of response was altered by atropine to a small and gradual R-R interval shortening over 30 beats, with no rebound R-R interval lengthening. With additional propranolol, R-R interval shortening was even less and confined to the first 15-20 beats, whereas propranolol alone did not affect the normal response pattern, showing that this is under vagal control with increased cardiac sympathetic activity occurring only if the vagus is blocked. The response was reproducible in 23 normal subjects. Heart rate variation during quiet standing was almost completely abolished by atropine, but unaffected by propranolol, confirming that it is also under vagal control. In four normal subjects no rebound R-R interval lengthening occurred during either "fast" or "slow" tilt, whereas it was present during both "slow" and "fast" standing. The rebound R-R interval lengthening is determined by the muscular activity involved in standing up, rather than by the speed of the maneuver.

The incidence of painless ischemic heart disease is increased in diabetic patients, and it has been suggested that this may be partly due to diabetic neuropathy involving cardiac afferent nerves. We have performed exercise electrocardiography in middle-aged diabetic men without cardiac symptoms to see if silent myocardial ischemia is more common in patients with neuropathy. Thirty patients had diabetic neuropathy (group 1), and 30 did not (group 2). The groups were matched for age and duration of diabetes. The exercise test was abnormal in 14 patients. A positive test was no more common in patients with diabetic neuropathy. During a mean follow-up period of 50 mo, five patients developed clinical heart disease, four of whom had a positive exercise test. An abnormal exercise ECG is common in diabetic men without cardiac symptoms, but our study does not suggest that the high incidence of silent myocardial ischemia in diabetic patients is related to the presence of diabetic neuropathy. In patients with diabetes a positive exercise test is associated with a high risk of developing clinical heart disease in subsequent years.

1.The heart-rate response during sustained hand grip was studied in four normal subjects before and after intravenous atropine, propranolol and combined cardiac autonomic blockade with both drugs. The results suggest that the increase in heart rate during the first 30 s is due to parasympathetic withdrawal, whereas the further increase between 30 s and 180 s is probably mediated by a combination of parasympathetic withdrawal and sympathetic stimulation.2. The increases in heart rate during each minute of sustained hand grip were compared in 26 normal subjects, 37 diabetic subjects without and 24 diabetic subjects with proven autonomic neuropathy. In the diabetic subjects with autonomic neuropathy the increase in heart rate during the first minute was impaired, whereas the increases during the second and third minutes were similar in all three groups.3. The initial increase in heart rate over the first 30 s of hand grip and the later increase between 30 's and 180 s were compared in nine normal subjects, ten diabetic subjects without and six diabetic subjects with autonomic neuropathy. The increase during thc first 30 s was impaired in the diabetic subjects with autonomic neuropathy, whereas the later phase of the response was similar in all three groups.

The effects of isometric exercise on the maximum amplitude of the praecordial accelerocardiogram (as represented by the DE deflection) have been compared in 6 normal subjects (group i), I2 Animal work has shown that peak acceleration of blood flow in the ascending aorta is highly sensitive to small changes in left ventricular contractility which are insufficient to cause changes in stroke volume or systemic blood pressure (Chung, Chamberlain, and Seed, I974; Noble, Trenchard, and Guz, I966a; Reuben and Littler, I973; Winter et al., I967). It has also been shown in the dog that changes in the maximum amplitude of the praecordial accelerocardiogram correlate closely with changes in peak aortic acceleration in response to a wide range of manoeuvres (Reuben and Littler, I973). Furthermore, it appears that both are relatively independent of heart rate and ventricular loading, at least in the intact organism (Noble et al., 1972; Noble, Trenchard, and Guz, I966a, b; Reuben and Littler, I973).