Abstract
Persons with chronic fatigue syndrome (CFS) often complain of an inability to maintain activity levels and experience a variety of orthostatic symptoms such as dizziness, trembling, nausea, postural hypotension with bradycardia or tachycardia, sweating, palpitations, paleness, and syncope. Orthostatic intolerance (OI) may be defined as an inability to maintain systolic blood pressure (SBP) within 20 mmHg of resting level upon moving from a supine to upright posture. The primary objective of this study is to determine whether men and women with CFS are more susceptible to OI during a 3-stage head-up tilt (HUT) than non CFS, sedentary subjects matched by age, sex, and ethnicity. The secondary objective is to examine whether possible underlying mechanisms may be predictively associated with OI susceptibility in CFS. Possible causes of OI include autonomic nervous system (ANS) dysfunction and altered hematological profile. Thus, specific aims included within this objective are: 1) to determine whether there are differences in resting cardiovascular function {i.e., blood pressure [BP], heart rate [HR], stroke volume [SV], cardiac output [CO], total peripheral resistance [TPR], and contractility [i.e., ejection fraction (EF), fractional shortening (FS), and the velocity of circumferential shortening corrected by HR (VCFc)]}, ANS function {i.e., beta1-, beta2-, and alpha-receptor sensitivities, baroreceptor sensitivity [BRS], and vagal function [i.e., respiratory sinus arrhythmia (RSA), RSA envelope (RSAE), high frequency (HF) spectral component, and HR range]}, and hematological profile [i.e., red blood cell volume (RBCV), plasma volume (PBV), and total blood volume (TBV)] between CFS and non-CFS groups; and 2) to determine whether cardiovascular, ANS, and hematological measures differentially predicted OI during HUT. The results indicate that OI susceptibility does not occur with greater prevalence in persons with CFS than non-CFS sedentary persons. However, power analyses revealed that with a much larger sample size group differences in OI susceptibility would be found. The CFS group was distinguished from the control group only by differences in blood volume measures. There appears to be no substantive group differences in a range of cardiovascular and ANS measures; moreover, none of these measures, including the blood volume measures, accounted for differences in OI susceptibility. Compensatory mechanisms may be present in CFS for the diminished blood volume that could explain the lack of group differences in OI susceptibility. In addition, future research may find some clues relevant to CFS pathophysiology in the assessment of hemodynamic responses during orthostatic challenge in the present subjects.