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Objective: The purpose of this study was to compare the cardiovascular responses of patients with chronic fatigue syndrome (CFS) to healthy control subjects when performing stressful cognitive tasks before and after strenuous exercise., Method: Beat-by-beat blood pressure and electrocardiogram were recorded on 19 women with CFS and 20 healthy nonexercising (ie, sedentary) women while they performed cognitive tests before, immediately after, and 24 hours after incremental exercise to exhaustion., Results: Diminished heart rate (p <.01) and systolic (p <.01) and diastolic (p <.01) blood pressure responses to stressful cognitive testing were seen in patients with CFS when compared with healthy, sedentary controls. This diminished stress response was seen consistently in patients with CFS across three separate cognitive testing sessions. Also, significant negative correlations between self-ratings of CFS symptom severity and cardiovascular responses were seen (r = -0.62, p <.01)., Conclusions: Women with CFS have a diminished cardiovascular response to cognitive stress; however, exercise did not magnify this effect. Also, the data showed that the patients with the lowest cardiovascular reactivity had the highest ratings of CFS symptom severity, which suggests that the individual response of the patient with CFS to stress plays a role in the common complaint of symptoms worsening after stress.

Objective: The objective of this study was to examine whether inappropriate cardiovascular responses to stressors may underlie symptoms in Gulf War veterans with chronic fatigue., Methods: Psychophysiological stress testing was performed on 51 Gulf War veterans with chronic fatigue (using the 1994 case definition of the Centers for Disease Control and Prevention) and 42 healthy veterans. Hemodynamic responses to cold pressor, speech, and arithmetic stressors were evaluated using impedance cardiography., Results: Veterans with chronic fatigue had diminished blood pressure responses during cognitive (speech and arithmetic) stress tests due to unusually small increases in total peripheral resistance. The cold pressor test, however, evoked similar blood pressure responses in the chronic fatigue and control groups. Low reactivity to cognitive stressors was associated with greater fatigue ratings among ill veterans, whereas an opposite relation was observed among healthy veterans. Self-reported neurocognitive decline was associated with low reactivity to the arithmetic task., Conclusions: These results suggest a physiological basis for some Gulf War veterans' reports of severe chronic fatigue. A greater deficit with responses processed through cerebral centers, as compared with a sensory stimulus (cold pressor), suggests a defect in cortical control of cardiovascular function. More research is needed to determine the specific mechanisms through which the dissociation between behavioral and cardiovascular activities identified in this study may be contributing to symptoms in Gulf War veterans.

Objective: Our previous work showed that stress sensitized the vessels of cardiomyopathic hamsters (CMHs), but only hamsters in the lesion-forming period of their life. We hypothesized that we would find an interaction between stressor intensity and microvascular vulnerability., Method: Male CMHs at ages of 1.5, 2.5, and 3.5 months were stressed with supine immobilization for five consecutive days. Stressor intensity was manipulated by immobilizing groups of CMHs at room temperature for 0 minutes, 15 minutes, 30 minutes, 1 hour, or 2 hours. CMHs were anesthetized and sacrificed 5 days after stress, and their hearts were perfused using a modified Langendorff system. Body weight changes and baseline coronary vascular resistance (CVR) were recorded, and CVR was also measured after coronary artery infusion of arginine vasopressin (AVP)., Results: Stress produced no effect on coronary vasculature in 1.5-month-old CMHs. In 2.5-month-old CMHs, only the two highest-intensity stressors enhanced coronary reactivity to AVP. In 3.5-month-old CMHs, higher-intensity stressors produced a marginal AVP-induced increase in CVR; but this marginal increase was significantly lower than the increases seen with the two highest-stressor intensities in the 2.5-month-old CMHs., Conclusion: The stress-induced coronary hyperreactivity to AVP seen in 2.5-month-old CMHs diminished when microvascular vulnerability was lower in 3.5-month-old CMHs. For 1.5-month-old CMHs, the resting CVR was extremely high, so that the addition of stress produced no further increase. Thus, stressor intensity interacted with microvascular vulnerability to alter the consequences of stress.

This study was conducted to examine the rates of somatization disorder (SD) in the chronic fatigue syndrome (CFS) relative to other fatiguing illness groups. It further addressed the arbitrary nature of the judgments made in assigning psychiatric vs. physical etiology to symptoms in controversial illnesses such as CFS. Patients with CFS (N = 42), multiple sclerosis (MS) (N = 18), and depression (N = 21) were compared with healthy individuals (N = 32) on a structured psychiatric interview. The SD section of the Diagnostic Interview Schedule (DIS) III-R was reanalyzed using different criteria sets to diagnose SD. All subjects received a thorough medical history, physical examination, and DIS interview. CFS patients received diagnostic laboratory testing to rule out other causes of fatigue. This study revealed that changing the attribution of SD symptoms from psychiatric to physical dramatically affected the rates of diagnosing SD in the CFS group. Both the CFS and depressed subjects endorsed a higher percentage of SD symptoms than either the MS or healthy groups, but very few met the strict DSM-III-R criteria for SD. The present study illustrates that the terminology used to interpret the symptoms (ie, psychiatric or physical) will determine which category CFS falls into. The diagnosis of SD is of limited use in populations in which the etiology of the illness has not been established.

Results of earlier experiments suggested that hamsters with inherited heart disease were at a higher risk of succumbing to stress during the vasospastic, lesion-forming period of their lives rather than later when the process of congestive heart failure had begun. To test this hypothesis, we stressed cardiomyopathic hamsters (CMH) whose ages differed by about 3 months; the younger of the two groups of stressed hamsters was in the vasospastic phase of the disease. The stressor was cold immobilization in which stressor intensity was manipulated using two durations of cold exposure. Log rank survival curves revealed no difference in mortality with the more intense stressor. However, significantly fewer of the older hamsters succumbed to the less intense stressor (46% as compared with 85% of the younger CMHs). Examination of the hearts in the experiment where mortality rate was the same for both groups revealed evidence of cardiac dilatation, indicative of heart failure, only in the older hamsters following stress. Since the younger hamsters did not show these changes and since they, but not the older animals, have coronary microvascular spasm and an increased susceptibility to stress, it would appear that the process of coronary vasospasm should be viewed as an independent and additional risk factor in determining the consequences of stress. Because of the effects of stress in the younger cardiomyopathic hamster, we believe that a neural link--which can be activated by stress--may be involved in the pathogenetic process of coronary vasospasm.

Guinea pigs were subjected to Pavlovian fear conditioning (signaled shock) and then infused with a fast acting digitalis preparation on a day when all experimental stimuli except shock were delivered. A significant shortening in latency to the onset of life-threatening digitalis toxicity was found when comparisons were made to control pigs that had never been shocked. This effect was not found in other guinea pigs infused with ouabain after exposure to sessions of unsignaled shock. These experiments indicate that psychological factors, when divorced form physical factors, may produce lethal digitalis toxicity in an organism that would otherwise by asymptomatic. The data from these experiments suggest that the intense arousal associated with a signal that had previously been paired with shock is sufficient to precipitate cardiac arrhythmias in an animal with a predisposition to cardiac automaticity such as is produced by digitalis. Conversely, the less intense arousal associated with unsignaled shock is inadequate to produce this effect. This interpretation indicates that the state of an animal's health will affect its psychosomatic response to signaled or unsignaled shock.

Stress produced heart failure in cardiomyopathic hamsters (CMHs) with subclinical heart disease. CMHs exhibited a variety of peripheral manifestations of heart failure including subcutaneous edema, fluid in the abdominal and thoracic cavities, and increased organ weight. In contrast, stress did not produce heart failure in healthy hamsters. These data indicate that the presence of covert heart disease can dramatically alter the pathogenic consequences of stress.

Restraint stress produced ventricular arrhythmias in seven of seven guinea pigs monitored by a Holter ECG recorder. Couplets and ventricular tachycardia, never seen in unrestrained guinea pigs, were noted in three. The arrhythmias were associated with high heart rates which showed no tendency to decrease during the restraint period.