Acute volume loading and exercise capacity in postural tachycardia syndrome

Rocío A. Figueroa, Amy C. Arnold, Victor C. Nwazue, Luis E. Okamoto, Sachin Y. Paranjape, Bonnie K. Black, Andre Diedrich, David Robertson, Italo Biaggioni, Satish R. Raj, Alfredo Gamboa

Research output: Contribution to journalArticle

14 Citations (Scopus)

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 (V? O2peak) in POTS. Nineteen patients with POTS participated in a sequential study. V O2peak was measured on two separate study days, following administration of placebo or 1 liter of iv 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/cm5 vs. placebo 1,184.0 ± 50.8 dyn-s/cm5; P = 0.011), with no effect on HR or blood pressure. During exercise, saline did not produce differences in V O2peak (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 V O2peak or cardiovascular responses to exercise in POTS, despite improvements in resting hemodynamic function.

Original languageEnglish (US)
Pages (from-to)663-668
Number of pages6
JournalJournal of applied physiology
Volume117
Issue number6
DOIs
StatePublished - Sep 15 2014

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Postural Orthostatic Tachycardia Syndrome
Placebos
Exercise
Heart Rate
Hypovolemia
Stroke Volume
Blood Volume
Intravenous Infusions
Cardiac Output
Vascular Resistance
Atrophy
Hemodynamics
Blood Pressure

All Science Journal Classification (ASJC) codes

  • Physiology
  • Physiology (medical)
  • Medicine(all)

Cite this

Figueroa, R. A., Arnold, A. C., Nwazue, V. C., Okamoto, L. E., Paranjape, S. Y., Black, B. K., ... Gamboa, A. (2014). Acute volume loading and exercise capacity in postural tachycardia syndrome. Journal of applied physiology, 117(6), 663-668. https://doi.org/10.1152/japplphysiol.00367.2014
Figueroa, Rocío A. ; Arnold, Amy C. ; Nwazue, Victor C. ; Okamoto, Luis E. ; Paranjape, Sachin Y. ; Black, Bonnie K. ; Diedrich, Andre ; Robertson, David ; Biaggioni, Italo ; Raj, Satish R. ; Gamboa, Alfredo. / Acute volume loading and exercise capacity in postural tachycardia syndrome. In: Journal of applied physiology. 2014 ; Vol. 117, No. 6. pp. 663-668.
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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 (V? O2peak) in POTS. Nineteen patients with POTS participated in a sequential study. V O2peak was measured on two separate study days, following administration of placebo or 1 liter of iv 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/cm5 vs. placebo 1,184.0 ± 50.8 dyn-s/cm5; P = 0.011), with no effect on HR or blood pressure. During exercise, saline did not produce differences in V O2peak (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 V O2peak or cardiovascular responses to exercise in POTS, despite improvements in resting hemodynamic function.",
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Figueroa, RA, Arnold, AC, Nwazue, VC, Okamoto, LE, Paranjape, SY, Black, BK, Diedrich, A, Robertson, D, Biaggioni, I, Raj, SR & Gamboa, A 2014, 'Acute volume loading and exercise capacity in postural tachycardia syndrome', Journal of applied physiology, vol. 117, no. 6, pp. 663-668. https://doi.org/10.1152/japplphysiol.00367.2014

Acute volume loading and exercise capacity in postural tachycardia syndrome. / Figueroa, Rocío A.; Arnold, Amy C.; Nwazue, Victor C.; Okamoto, Luis E.; Paranjape, Sachin Y.; Black, Bonnie K.; Diedrich, Andre; Robertson, David; Biaggioni, Italo; Raj, Satish R.; Gamboa, Alfredo.

In: Journal of applied physiology, Vol. 117, No. 6, 15.09.2014, p. 663-668.

Research output: Contribution to journalArticle

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T1 - Acute volume loading and exercise capacity in postural tachycardia syndrome

AU - Figueroa, Rocío A.

AU - Arnold, Amy C.

AU - Nwazue, Victor C.

AU - Okamoto, Luis E.

AU - Paranjape, Sachin Y.

AU - Black, Bonnie K.

AU - Diedrich, Andre

AU - Robertson, David

AU - Biaggioni, Italo

AU - Raj, Satish R.

AU - Gamboa, Alfredo

PY - 2014/9/15

Y1 - 2014/9/15

N2 - 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 (V? O2peak) in POTS. Nineteen patients with POTS participated in a sequential study. V O2peak was measured on two separate study days, following administration of placebo or 1 liter of iv 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/cm5 vs. placebo 1,184.0 ± 50.8 dyn-s/cm5; P = 0.011), with no effect on HR or blood pressure. During exercise, saline did not produce differences in V O2peak (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 V O2peak or cardiovascular responses to exercise in POTS, despite improvements in resting hemodynamic function.

AB - 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 (V? O2peak) in POTS. Nineteen patients with POTS participated in a sequential study. V O2peak was measured on two separate study days, following administration of placebo or 1 liter of iv 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/cm5 vs. placebo 1,184.0 ± 50.8 dyn-s/cm5; P = 0.011), with no effect on HR or blood pressure. During exercise, saline did not produce differences in V O2peak (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 V O2peak or cardiovascular responses to exercise in POTS, despite improvements in resting hemodynamic function.

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