Cardiovascular and sympathoadrenal responses to stress in swim-trained rats

Abstract
Chronic exposure to swim stress (i.e., training) is associated with functional adaptations of the cardiovascular system. Repeated exposure to tail shock, an emotional stress, often results in deleterious changes in resting blood pressure and myocardial pathology. The pathological adaptation following chronic exposure to tail shock was associated with a larger acute physiological response compared with swim stress. Acute responses to swim and shock stress were compared. The extent to which adaptation to swim training influences responses to predictable tail shock stress was examined. The cardiovascular and sympathoadrenal repsonses to swim stress, using 1% body wt attached to the tail, were compared with predictable tail shock (0.2-0.4 mA intensity, 1-s duration, 1/min) in 2 groups of Long-Evans male rats. In the first, 11 rats were studied following 5-7 wk of swim training, consisting of daily 1-h sessions of swimming with 2% body wt attached to their tails. They were compared with an age-matched nontrained (NT) group (n = 8). During swimming, the trained animals showed significantly lower heart rate (387 .+-. 10 vs. 449 .+-. 18 beats/min) and significantly lower lactate (0.9 .+-. 0.09 vs. 2.0 .+-. 0.24 mmol/l), epinephrine (332 .+-. 57 vs. 739 pg/ml) and corticosterone (32 .+-. 10 vs. 62 .+-. 9 .mu.g/dl) responses. Systolic and diastolic blood pressures were elevated in swim stress by the same degree in trained (167/110 mmHg) and NT (177/116 mmHg) rats. Predictable shock stress elicited elevations in heart rate, plasma catecholamines and corticosterone similar to those produced by swimming, but the elevations in blood pressure were slightly less. There were no differences between trained and NT rats during shock stress. Evidently, swim exercise can be as potent a stressor of the cardiovascular and sympathoadrenal systems as predictable shock stress, and no attenuation of response to tail shock is seen in trained animals upon their 1st exposure to this stressor. [This study has implications for stress-induced hypertension.].