To assess the relationship between aging and autonomic nervous system function, 
cardiovascular and pupillary autonomic nervous system reflexes were measured in 
subgroups of 103 normal male subjects ranging in age from 19 to 82 years (mean 
age = 39 years). Both the plasma norepinephrine level, a measure of 
cardiovascular sympathetic nervous system activity, and the mean arterial blood 
pressure increased with age (r = 0.68 and 0.67, respectively, both p less than 
0.001). In contrast, the plasma epinephrine level, a measure of adrenomedullary 
sympathetic nervous system activity, was unrelated to age (r = 0.08, p = NS). 
Respiratory variation of heart rate during beta-adrenergic blockade, an index of 
cardiac parasympathetic nervous system activity, was reduced in older subjects 
(r = -0.54, p less than 0.001). Thus, there was evidence of an age-related 
increase of cardiovascular sympathetic nervous system activity and a reduction 
of cardiac parasympathetic nervous system activity. These findings are 
consistent with the hypothesis that there is sympathetic nervous system and 
parasympathetic nervous system compensation of cardiovascular function in 
response to an age-related decrease in baroreceptor sensitivity. However, 
dark-adapted pupil size during parasympathetic nervous system blockade, an index 
of iris sympathetic nervous system activity, declined with age (r = -0.81, p 
less than 0.001). The latency time for the pupillary response to a light 
stimulus, an index of iris parasympathetic nervous system activity, was 
prolonged in older subjects (r = 0.58, p less than 0.001). Thus, both 
sympathetic nervous system and parasympathetic nervous system inputs to the iris 
were diminished in older subjects, findings consistent with the generalized 
decrease of peripheral somatic nerve function that has been reported with aging 
in man. It is concluded that autonomic nervous system function also declines 
with aging, but that other age-related changes such as a decline of baroreceptor 
sensitivity may lead to compensatory autonomic nervous system response, which 
could mask underlying functional defects.