Exercise Training for POTS?

Dear Readers, Postural orthostatic tachycardia syndrome (POTS) is defined as orthostatic intolerance with an increase in heart rate (HR) of at least 30 beats per minute (bpm) or a HR > 120 bpm after standing for 10 minutes, without orthostatic hypotension. Although this is not a primary heart rhythm disorder, electrophysiologists are commonly asked to evaluate these patients because they often present with palpitations and presyncope. The cause is unknown, but there is some evidence that these patients have autonomic dysfunction, and there is data that midodrine can be helpful. A typical patient is a premenopausal woman, and the condition can be very challenging to treat. Patients with POTS have the signs and symptoms similar to patients who have been deconditioned. For example, patients subjected to prolonged periods of bed rest or spaceflight exhibit orthostatic intolerance if deconditioning is allowed to occur. It is possible that, although the underlying problem of POTS is not due to deconditioning, the orthostatic intolerance leads to such inactivity that deconditioning occurs and exacerbates the problem. A logical hypothesis then would be that reconditioning patients with POTS would be helpful. In a recent study published in the Journal of the American College of Cardiology, Fu et al evaluated the effect of exercise training in patients with POTS.1 They were able to enroll 25/54 patients with POTS, who had been referred to their Autonomic Function Clinic in Dallas, Texas, in a specialized exercise training program. Nineteen patients completed the three-month escalating program, which began with exercises 2-4 days per week for 30-45 minutes with a target heart rate of 75%-85% maximum, and progressed to 5-6 days per week. A clever aspect of the regimen was to begin with exercises that did not require upright posture, such as swimming, rowing, and semirecumbent cycling, and progress to upright exercises such as jogging. An interesting observation made in this study was that heart size and mass as measured by MRI in patients with POTS was 16% smaller than those of healthy, sedentary controls matched by age and size. The authors suggest that deconditioning can lead to cardiac atrophy and that exercise training can correct the abnormality. Although this seems difficult to believe, exercise training in this trial did increase cardiac size and mass in patients with POTS. There are several limitations of this trial, including the absence of randomization and the supplemental intervention of volume and salt loading in the exercise training group. However, exercise training decreased upright HR by 9 bpm on average, and 10/19 patients no longer met criteria for POTS. More impressively, there was a marked improvement in quality of life after three months of exercise. Based on this study alone, understanding that patients with POTS tend to be symptomatic despite most current interventions, it seems reasonable to encourage these patients to embark on an exercise program and to consider starting with exercises that can be done in the supine or prone position.