Short‐term exercise training improves the cardiovascular response to exercise in the postural orthostatic tachycardia syndrome

Key points • Recent studies have suggested the presence of cardiac atrophy as a key component of the pathogenesis of the postural orthostatic tachycardia syndrome (POTS), similar to physical deconditioning; exercise intolerance is associated with a reduced stroke volume (SV) in POTS which may be the cause of the high heart rate (HR) at rest and during exercise. • We determined whether physical ‘reconditioning’ with exercise training improves exercise performance in POTS. • A lower SV resulted in a higher HR in POTS at any given oxygen uptake () during exercise while the cardiac output ()– relationship remained normal. was lower in POTS than healthy sedentary controls. • After 3 months of training in POTS, HR became lower at any given due to increased SV without changes in the – relationship. increased due to increased peak SV, and was proportional to total blood volume. HR recovery from exercise was faster after training than before training. • Thus, exercise training improves physical fitness and cardiovascular responses during exercise in POTS. Recent studies have suggested the presence of cardiac atrophy as a key component of the pathogenesis of the postural orthostatic tachycardia syndrome (POTS), similar to physical deconditioning. It has also been shown that exercise intolerance is associated with a reduced stroke volume (SV) in POTS, and that the high heart rate (HR) observed at rest and during exercise in these patients is due to this low SV. We tested the hypotheses that (a) circulatory control during exercise is normal in POTS; and (b) that physical ‘reconditioning’ with exercise training improves exercise performance in patients with POTS. Nineteen (18 women) POTS patients completed a 3 month training programme. Cardiovascular responses during maximal exercise testing were assessed in the upright position before and after training. Resting left ventricular diastolic function was evaluated by Doppler echocardiography. Results were compared with those of 10 well‐matched healthy sedentary controls. A lower SV resulted in a higher HR in POTS at any given oxygen uptake () during exercise while the cardiac output ()– relationship was normal. was lower in POTS than controls (26.1 ± 1.0 (SEM) vs. 36.3 ± 0.9 ml kg−1 min−1; P < 0.001) due to a lower peak SV (65 ± 3 vs. 80 ± 5 ml; P= 0.009). After training in POTS, HR became lower at any given due to increased SV without changes in the – relationship. increased by 11% (P < 0.001) due to increased pe