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. 2014 Sep 15;117(6):663-8.
doi: 10.1152/japplphysiol.00367.2014. Epub 2014 Jul 24.

Acute volume loading and exercise capacity in postural tachycardia syndrome

Affiliations

Acute volume loading and exercise capacity in postural tachycardia syndrome

Rocío A Figueroa et al. J Appl Physiol (1985). .

Abstract

Postural tachycardia syndrome (POTS) is associated with exercise intolerance, hypovolemia, and cardiac atrophy, which may contribute to reduced stroke volume and compensatory exaggerated heart rate (HR) increases. Acute volume loading with intravenous (iv) saline reduces HR and improves orthostatic tolerance and symptoms in POTS, but its effect on exercise capacity is unknown. In this study, we determined the effect of iv saline infusion on peak exercise capacity (VO2peak) in POTS. Nineteen patients with POTS participated in a sequential study. VO2peak was measured on two separate study days, following administration of placebo or 1 liter of i.v. saline (NaCl 0.9%). Patients exercised on a semirecumbent bicycle with resistance increased by 25 W every 2 min until maximal effort was achieved. Patients exhibited blood volume deficits (-13.4 ± 1.4% ideal volume), consistent with mild to moderate hypovolemia. At baseline, saline significantly increased stroke volume (saline 80 ± 8 ml vs. placebo 64 ± 4 ml; P = 0.010), increased cardiac output (saline 6.9 ± 0.5 liter/min vs. placebo 5.7 ± 0.2 liter/min; P = 0.021), and reduced systemic vascular resistance (saline 992.6 ± 70.0 dyn-s/cm(5) vs. placebo 1,184.0 ± 50.8 dyn-s/cm(5); P = 0.011), with no effect on HR or blood pressure. During exercise, saline did not produce differences in VO2peak (saline 26.3 ± 1.2 mg·kg(-1)·min(-1) vs. placebo 27.7 ± 1.8 mg·kg(-1)·min(-1); P = 0.615), peak HR [saline 174 ± 4 beats per minute (bpm) vs. placebo 175 ± 3 bpm; P = 0.672] or other cardiovascular parameters. These findings suggest that acute volume loading with saline does not improve VO2peak or cardiovascular responses to exercise in POTS, despite improvements in resting hemodynamic function.

Keywords: POTS; autonomic diseases; deconditioning.

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Figures

Fig. 1.
Fig. 1.
Study participants. Patients with postural tachycardia syndrome (POTS) ages 18–65 yr were enrolled, they were allocated to placebo, and at least 3 days apart they were allocated to intravenous (iv) saline. Nineteen subjects were analyzed.
Fig. 2.
Fig. 2.
Effect of saline on exercise capacity. Exercise capacity was determined following placebo or iv saline infusion in patients with POTS in a semirecumbent position. There were no differences in resting oxygen consumption (V̇o2) (A), resting heart rate (HR) (B), V̇o2 at 75 W (C), HR at 75 W (D), peak V̇o2 (E), or peak HR (F) during exercise testing following placebo vs. saline administration.
Fig. 3.
Fig. 3.
Effect of saline on resting hemodynamic function and cardiovascular responses to exercise. Resting hemodynamic function was assessed in patients with POTS following placebo or iv saline infusion at baseline (0 W) prior to exercise in the semirecumbent position. Baseline stroke volume (SV) (A) and cardiac output (CO) (C) were significantly higher following saline compared with placebo. There was no difference in mean arterial pressure (MAP) (E) between study days, but systemic vascular resistance (SVR) (G) was significantly lower following saline. Hemodynamic function was also assessed during semirecumbent exercise at 75 W (a submaximal resistance reached by all patients with POTS). There were no significant differences in SV (B), CO (D), MAP (F), or SVR (H) following saline vs. placebo administration.

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