Voluntary flight has previously been observed to stimulate adrenocortical activity in pigeons and in the present study increased circulating corticosterone levels were observed in adult feral pigeons forced to exercise in a treadwheel. The magnitude of the corticosterone response to treadwheel exercise was related to the speed of the moving drum, and hence to the work rate involved. Rapidly increasing the ambient temperature also stimulated corticosterone secretion in pigeons and masked the stimulatory effect of exercise. Treadwheel locomotion may serve as a laboratory model for the endocrine physiology of exercise and complements studies on flight.

The influence of long-distance flight on corticosterone secretion has been examined in trained racing pigeons. Flights of 315-561 min from release sites 115-557 km from the home loft greatly increased the circulating corticosterone concentration in comparison with the levels in nonexercised controls sampled before release or bled in the loft at the times of release or arrival. The increase in corticosterone concentration was unrelated to the distance flown or duration of flight. Flights of less than 1 min duration (from release sites 100 m from the loft) increased the corticosterone concentration, in comparison with that in the loft controls, but to levels much lower (P less than 0.001) than those following long-distance flights and to concentrations similar to those in birds that were returned to the loft by hand.

Horizontal treadmill exercise induced a marked (P < 0.001) but transitory increase in the level of circulating corticosterone in the plasma of adult male ducks. The decline in corticosterone concentration during exercise is unlikely to be due to a depletion of adrenocortical stores since a marked (P < 0.001) corticosterone response to adrenocorticotrophin (ACTH) administration was observed immediately after exercise, and was of similar magnitude to that induced in nonexercised controls. The corticosterone response to repeated exercise is also transitory, habituating completely within 28 days of the start of daily training. The corticosterone response (P < 0.001) to ACTH challenge is not, however, diminished by training. These results indicate that the habituation of the corticosterone response to either acute or repeated exercise is due to a reduction in endogenous ACTH secretion. A similar mechanism appears to be responsible for the habituation of the corticosterone response to handling and confinement in nonexercised control birds. A marked (P < 0.001) increase in the level of circulating corticosterone was, however, elicited when these birds were exercised, indicating that despite adaptation to handling and confinement the birds remained responsive to the novel stressor of exercise. The corticosterone response of these birds was, however, less than that in untrained birds indicating that the corticosterone response in untrained birds is due to both workload and the stress of handling and confinement.

In immature ducklings injected with hypertonic saline the volume of extrarenal salt gland secretion was unaffected by prior treatment (immediately or 4 hr before salt loading) with long-lasting adrenocorticotrophin (ACTH 100 iu/kg, im) or exogenous corticosterone (1.0 mg/kg, im). Pretreatment with metyrapone, an 11-β-hydroxylase blocker, (80 mg/kg, im) 4 hr before salt loading did not effect the volume of salt gland secretion but delayed the onset of extrarenal excretion. Salt gland function was suppressed in birds pretreated with metyrapone immediately prior to salt loading. The intravenous administration of metyrapone after salt loading immediately reduced salt gland activity, which remained suppressed for at least 40–50 min thereafter. The inhibitory effect of metyrapone on salt gland activity was not counteracted by the subsequent or simultaneous administration of exogenous corticosterone to salt-loaded ducks. These results suggest that acute alterations in adrenocortical activity are not causally responsible for changes in salt gland function.

In 5-6-week-old cockerels the circulating corticosterone concentration was significantly increased in birds i.m. injected 30 and 60 min previously with adrenaline (0.33 mg/kg), noradrenaline (0.33 mg/kg) or a beta-adrenergic agonist (isoprotorenol, 1 mg/kg), but was reduced in birds pretreated with an alpha-adrenergic agonist (phenylephrine, 1 mg/kg). The stimulation of corticosterone secretion induced by a 30 min period of forced exercise (0.04 km/hr; 0 degree incline) was potentiated by noradrenaline, isoprotorenol and phentolamine pretreatment. In response to exogenous adrenocorticotrophin (ACTH, 8 i.u./kg), administered i.v., the increase in the plasma corticosterone concentration was elevated above that in the controls in birds pretreated with adrenaline, noradrenaline, isoprotorenol or phentolamine (an alpha antagonist administered at 1 mg/kg). The corticosterone response to ACTH was suppressed by phenylephrine pretreatment. These results demonstrate that both basal and stimulated levels of adrenocortical activity may be subtly regulated by adrenergic mechanisms acting at a site(s) within the hypothalamo-pituitary-adrenal axis.

The effect of starvation on the corticosterone responses of immature cockerels to acute, novel stress has been determined. The marked corticosterone responses of fed birds to either horizontal treadmill exercise (0.04 km/hr) or intravenous adrenocorticotrophic hormone (ACTH) administration (P < 0.001 in both cases) were reduced by starvation (P < 0.01 and P < 0.001, respectively). This reduction did not appear to be due to either feedback inhibition of corticosterone on the hypothalamus or pituitary, or to reduced adrenal responsiveness to endogenous ACTH. Starvation significantly elevated the basal level of circulating corticosterone (P < 0.001), but the magnitude of this elevation and the level of corticosterone attained were less (P < 0.05) in birds that were accustomed to starvation. This habituation of adrenocortical activity may be due to reduced pituitary ACTH secretion, and was specific in that the corticosterone responses to novel stressors were unaffected.

1.1. Temporal and dose-related effects of adrenocorticotrophin (ACTH) on the concentrations of plasma aldosterone have been determined in immature (5-week-old) and adult (20-week-old) domestic fowl. The influences of handling stress on aldosterone secretion has also been assessed.2.2. ACTH maximally increased plasma aldosterone concentrations 30 min after i.v. administration. In both immature and adult birds the aldosterone response was dose-related. In both cases the minimum response was induced by 1.0 i.u. ACTH/kg; higher doses (up to 20.0 i.u./kg) progressively increasing the aldosterone concentration. The aldosterone responses of adult birds to 5.0, 10.0 and 20.0 i.u. ACTH/kg were greater than those in immature birds.3.3. Plasma aldosterone responses to ACTH were less than plasma corticosterone responses.4.4. The stress of handling and bleeding increased the aldosterone and corticosterone concentrations in immature birds. Both hormones were increased within 3 min of initial handling. The aldosterone and corticosterone levels in birds that were serially bled were higher than those that were held and bled only once.5.5. These results demonstrate that the activation of the hypothalamo-pituitary adrenal axis stimulates in vivo aldosterone release in birds.

The natural environment is composed of various potentially hostile stressors. It is a basic requirement of life that the cells of an organism must be maintained within closely defined physiological limits. The maintenance of a constant interior mileu results from physiological and behavioural homeostatic adaptations. The physiological regulation of homeostatis is achieved by complex endocrine interactions, principally by the hormones secreted from the adrenal glands. In this brief review the responses of the avian adrenal glands to stressful stimuli, the mechanism of adrenal activation, and the function of the adrenal responses will be considered.

Adrenomedullary and adrenocortical responses of 40-day-old cockerels to treadmill exercise (0.4 km/hr, 0° incline) were determined. Plasma concentrations of adrenaline were increased above both resting and control levels (P < 0.001) after 30 min exercise and continued to increase (P < 0.01) until the cessation of exercise. Plasma noradrenaline and dopamine levels were increased after 60 min of exercise (P < 0.01 and 0.05, respectively). The adrenaline component of the plasma catecholamine response increased significantly above that of noradrenaline (P < 0.001). Plasma corticosterone levels were also increased (P < 0.001) during exercise and were closely correlated with plasma adrenaline concentrations. Exercise depleted (P < 0.01) adrenal stores of adrenaline, which were inversely proportional to plasma adrenaline concentrations (P < 0.001). Neither adrenal noradrenaline nor dopamine were significantly correlated with their plasma levels. These results suggest that adrenocortical (corticosterone) and adrenomedullary (adrenaline) responses during exercise may occur in response to similar stimuli or may be interrelated.