Exercise training versus propranolol in the treatment of the postural orthostatic tachycardia syndrome

Abstract

We have found recently that exercise training is effective in the treatment of the postural orthostatic tachycardia syndrome (POTS). Whether this nondrug treatment is superior to "standard" drug therapies, such as β-blockade, is unknown. We tested the hypothesis that exercise training but not β-blockade treatment improves symptoms, hemodynamics, and renal-adrenal responses in POTS patients. Nineteen patients (18 women and 1 man) completed a double-blind drug trial (propranolol or placebo) for 4 weeks, followed by 3 months of exercise training. Fifteen age-matched healthy individuals (14 women and 1 man) served as controls. A 2-hour standing test was performed before and after drug treatment and training. Hemodynamics, catecholamines, plasma renin activity, and aldosterone were measured supine and during 2-hour standing. We found that both propranolol and training significantly lowered standing heart rate. Standing cardiac output was lowered after propranolol treatment (P=0.01) but was minimally changed after training. The aldosterone:renin ratio during 2-hour standing remained unchanged after propranolol treatment (4.1±1.7 [SD] before versus 3.9±2.0 after; P=0.46) but modestly increased after training (5.2±2.9 versus 6.5±3.0; P=0.05). Plasma catecholamines were not affected by propranolol or training. Patient quality of life, assessed using the 36-item Short-Form Health Survey, was improved after training (physical functioning score 33±10 before versus 50±9 after; social functioning score 37±9 versus 48±6; both P<0.01) but not after propranolol treatment (34±10 versus 36±11, P=0.63; 39±7 versus 39±5, P=0.73). These results suggest that, for patients with POTS, exercise training is superior to propranolol at restoring upright hemodynamics, normalizing renal-adrenal responsiveness, and improving quality of life.

Figure 1

Systolic blood pressure (SBP) and diastolic blood pressure (DBP) responses during 2-hour standing in healthy controls (filled triangle) and in POTS patients before (open square) and after (filled circle) drug treatment or exercise training. S, supine. Values are expressed as mean±standard error. * P<0.05 compared with pre-treatment or pre-training within the group.

Figure 2

Heart rate (HR) and total peripheral resistance (TPR) responses during 2-hour standing in healthy controls (filled triangle) and in POTS patients before (open square) and after (filled circle) drug treatment or exercise training. S, supine. Values are expressed as mean±standard error. *P<0.05 compared with pre-treatment or pre-training within the group. †P<0.05 compared with healthy controls.

Figure 3

Stroke volume (SV) and cardiac output (CO) responses during 2-hour standing in healthy controls (filled triangle) and in POTS patients before (open square) and after (filled circle) drug treatment or exercise training. S, supine. Values are expressed as mean±standard error. *P<0.05 compared with pre-treatment within the group. †P<0.05 compared with healthy controls.

Figure 4

Plasma renin activity (PRA) and aldosterone (ALDO) increases during 2-hour standing in healthy controls (filled triangle) and in POTS patients before (open square) and after (filled circle) drug treatment or exercise training. S, supine. Values are expressed as mean±standard error. *P<0.05 compared with before treatment within the group. †P<0.05 compared with healthy controls.

Figure 5

Plasma norepinephrine and epinephrine concentration (NE and Epi) responses during 2-hour standing in healthy controls (filled triangle) and in POTS patients before (open square) and after (filled circle) drug treatment or exercise training. S, supine. Values are expressed as mean±standard error.

Figure 6

Effects of exercise training, propranolol and placebo treatment on patient quality of life assessed by the SF-36. Values are expressed as individuals and mean±standard error.