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Long-term heart damage may result from constant confrontation and defeat

(July 14, 2004) - Bethesda, MD The toughest among us combat soldiers, athletes, or anyone in a high-stress occupation, may claim that they become "hardened" to adversity and defeat. But a new animal study demonstrates that although the body may temporarily adjust to stress, the risk for long-term cardiac problems may be the consequence of daily exposure to confrontation.

Background

Even the most self-controlled individual is susceptible to stress, which is the body's reaction to injurious forces, infections, and various abnormal states that tend to disturb its normal physiological equilibrium. When we exert limited control over environmental stimuli, such physiological and behavioral changes may ultimately produce increased susceptibility to psychosomatic disorders when the brain impacts on bodily functions such as cardiovascular disturbances.

Social stressors have been shown to induce robust short-term activations of the sympathetic-adrenomedullary system and the pituitary-adrenocortical axis. As far as cardiovascular responses to social defeat and subordination are concerned, increases in blood pressure and plasma catecholamine levels (the biochemical response to stress) have been documented in rats, persisting as long as the stimulus was present or shortly thereafter. In addition, experimental stress has produced a considerable increase in heart rate.

Long-term effects of social challenges on a number of physiological and behavioral parameters have also been reported, mainly involving the daily rhythms of heart rate, body temperature, food intake, and exploratory and social activity. Many animal studies indicate that there is a gradual decline in stress when the stress factor, such as changes in habitation, is repeatedly applied. In other words, the body adapts so there is less stress.

However, it was shown recently that rats intermittently exposed to an uncontrollable social stressor (defe
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Contact: Mayer Resnick
mresnick@the-aps.org
301-634-7209
American Physiological Society
19-Jul-2004


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