Verification of exercise-induced transient postural tachycardia phenotype in Gulf War Illness

Abstract

One third of Gulf War Illness (GWI) subjects in a recent study were found to develop transient postural tachycardia after submaximal exercise stress tests. Post-exercise postural tachycardia is a previously undescribed physiological finding. A new GWI cohort was studied to verify this novel finding and characterize this cardiovascular phenomenon. Subjects followed the same protocol as before. The change in heart rate between recumbent and standing postures (ΔHR) was measured before exercise, and after submaximal bicycle exercise. About one-fourth of the verification cohort (14/57) developed transient postural tachycardia after submaximal exercise. These subjects were the Stress Test Activated Reversible Tachycardia (START) phenotype. The largest change was observed between pre-exercise and time points 2 ± 1 (mean ± SD) hours post exercise (1st Peak Effect). Eleven subjects had Postural Tachycardia Syndrome (POTS) before and after exercise. The remaining subjects had normal ΔHR (12 ± 5 bpm) and no 1st Peak Effect, and were the Stress Test Originated Phantom Perception phenotype (STOPP). These findings indicate that about one-fourth of all Gulf War Illness study participants (24/90) developed transient postural tachycardia after the submaximal exercise stress test. The START phenotype was defined as being distinctly different from POTS. Additional studies are required to examine this phenomenon in other illnesses and to determine pathological mechanisms.

Keywords: Autonomic nervous system; Gulf War Illness; chronic fatigue syndrome; exercise; postural tachycardia.

Conflict of interest statement

None.

Figures

Figure 1

Patient inclusion and categorization: CONSORT (Consolidated Standards of Reporting Trials) flow diagram. Recruitment outcomes for original and verification cohorts.

Figure 2

Individual time courses of average ΔHR before and after exercise. The time courses for average ΔHR changes before and after exercise were drawn for the Original Controls (A), Original STOPP (B), Original START (C), Verification POTS (D), Verification STOPP (E), and Verification START (F) groups. ΔHR was higher at the first time point after exercise (1st peak) in POTS, O-START, and V-START groups. Dotted red lines provide the reference point of ΔHR=30 bpm for POTS and START identification. Black arrows indicate average 1st peak time point. Red arrows indicate start of second exercise stress test. White circles indicate subjects with Florid POTS (n=4). Average pre-exercise ΔHR values were fixed to -5 hours.

Figure 3

First Peak Effect. White bars indicate average pre-exercise ΔHR and grey bars indicate average ΔHR at the first post-exercise time point. O-HC, O-STOPP, and V-STOPP had equivalent ΔHR before and after exercise. Exercise induced 1st peak elevation of ΔHR in O-START and V-START. V-POTS had significantly higher ΔHR before and after exercise. Black lines indicate significance by Tukey’s HSD (P < 0.05). *(P < 0.01 for pre-exercise ΔHR in POTS vs. controls, STOPP, and START, Tukey’s HSD). Mean ± 95% C.I.

Figure 4

Area under the curve for ΔHR after exercise. START and POTS subjects had the largest increases in ΔHR after exercise relative to controls and STOPP subjects. Black lines indicate significance by Tukey’s HSD (P < 0.05). Mean ± 95% C.I.

Figure 5

Time courses for ΔSBP before and after exercise. There were no significant differences in ΔSBP between groups. Red dotted lines provide reference points for postural systolic hypertension and hypotension (± 20 mmHg). Red arrows indicate start of second exercise stress test.

Figure 6

Time courses for ΔDBP before and after exercise. There were no significant differences in ΔDBP between groups. Red dotted lines provide reference points for postural diastolic hypertension (≥ 18 mmHg) and hypotension (≥ 10 mmHg). Red arrows indicate start of second exercise stress test.