21 July 2004
Confrontation, Defeat Can Cause Serious Heart Problems
by Kate Melville
Soldiers, athletes, or anyone in a high-stress occupation, often say that they become "hardened" to adversity and defeat. But a new animal study suggests 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.
Most available animal studies focus on cardiac impact after the injection of drugs that mimic the nervous system. This new study took a different approach, analyzing whether acute and long-term sympathovagal responsivity to intermittent defeat episodes are affected by a chronic psychosocial challenge. The study appeared in the American Journal of Physiology - Heart and Circulatory Physiology.
The study analyzed the short- and long-term pathophysiological effects of chronic psychosocial stress in male mice, consisting of 15-day continuous sensory contact and daily intermittent agonistic interaction with a dominant animal. The researchers evaluated changes in heart rate and sympathovagal balance during the 1st, 4th, and 15th agonistic episodes. The assessment of long-term effects took into account the changes in the circadian rhythms of HR and the consequences on myocardial structure.
The study found that each social defeat episode produced a certain level of acute sympathetic-adrenomedullary responsiveness that was present throughout the whole chronic stress protocol. However, the researchers also found a gradual reduction in acute cardiac autonomic responsiveness across repeated challenge episodes. In other words, the shift of sympathovagal balance toward a sympathetic dominance was gradually reduced from the first to the last acute defeat experience.
As for long-term consequences on chronobiological parameters, average night and day values of heart rate rose significantly in the first days of chronic stress and were associated with a reduction in the amplitude of day-night oscillation. In addition, physical activity was significantly depressed in both circadian phases and throughout the stress treatment.
During chronic psychosocial stress, animals exhibited heart rate rhythmicity disturbance that was substantially over after a few days of chronic adverse cohabitation. This evidence was in line with the observation of a clear habituation-like effect in terms of acute cardiac autonomic responsiveness. This link between habituation of acute cardiovascular responses and relatively rapid (yet gradual) normalization of heart rate rhythmicity suggests that mice adapt to adverse social conditions.
Despite this coping capacity, the researchers provided evidence that chronic psychosocial stress induces permanent cardiac structural changes with the appearance of numerous scattered microscopic foci of fibrosis. This offers a hypothesize that a psychosocial challenge of longer duration might be able to produce a more severe structural damage, which in turn represents a substrate predisposing to higher susceptibility to arrhythmias. The body may seem to adapt - but long-term damage to the heart may already be occurring.