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Key points

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    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.
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    We determined whether physical ‘reconditioning’ with exercise training improves exercise performance in POTS.
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    A lower SV resulted in a higher HR in POTS at any given oxygen uptake (inline image) during exercise while the cardiac output (inline image)–inline image relationship remained normal. inline image was lower in POTS than healthy sedentary controls.
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    After 3 months of training in POTS, HR became lower at any given inline image due to increased SV without changes in the inline imageinline image relationship. inline image increased due to increased peak SV, and was proportional to total blood volume. HR recovery from exercise was faster after training than before training.
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    Thus, exercise training improves physical fitness and cardiovascular responses during exercise in POTS.

Abstract  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 (inline image) during exercise while the cardiac output (inline image)–inline image relationship was normal. inline image 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 inline image due to increased SV without changes in the inline imageinline image relationship. inline image increased by 11% (P < 0.001) due to increased peak SV (P= 0.021) and was proportional to total blood volume. Peak HR was similar, but HR recovery from exercise was faster after training than before training (P= 0.036 for training and 0.009 for interaction). Resting diastolic function was mostly normal in POTS before training, though diastolic suction was impaired (P= 0.023). There were no changes in any Doppler index after training. These results suggest that short-term exercise training improves physical fitness and cardiovascular responses during exercise in patients with POTS.