Heat stress alters hemodynamic responses during the Valsalva maneuver

Scott L. Davis, Craig G. Crandall

Research output: Contribution to journalArticle

6 Citations (Scopus)

Abstract

The Valsalva maneuver can be used as a noninvasive index of autonomic control of blood pressure and heart rate. The purpose of this investigation was to test the hypothesis that sympathetic mediated vasoconstriction, as referenced by hemodynamic responses during late phase II (phase IIb) of the Valsalva maneuver, is inhibited during whole body heating. Seven individuals (5 men, 2 women) performed three Valsalva maneuvers (each at a 30-mmHg expiratory pressure for 15 s) during normothermia and again during whole body heating (increase sublingual temperature ~0.8°C via water-perfused suit). Each Valsalva maneuver was separated by a minimum of 5 min. Beat-to-beat mean arterial blood pressure (MAP) and heart rate were measured during each Valsalva maneuver, and responses for each phase were averaged across the three Valsalva maneuvers for both, thermal conditions. Baseline MAP was not significantly different between normothermic (88 ± 11 mmHg) and heat stress (84 ± 9 mmHg) conditions. The change in MAP (AMAP) relative to preValsalva MAP during phases IIa and IIb was significantly lower during heat stress (IIa = -20 ± 8 mmHg; IIb = -13 ± 7 mmHg) compared with normothermia (IIa = -1 ± 15 mmHg; IIb = 3 ± 13 mmHg). AMAP from pre-Valsalva baseline during phase IV was significantly higher during heat stress (25 ± 10 mmHg) compared with normothermia (8 ± 9 mmHg). Counter to the proposed hypothesis, the increase in MAP from the end of phase IIa to the end of phase lib during heat stress was not attenuated. Conversely, this increase in MAP tended to be greater during heat stress relative to normothermia (P = 0.06), suggesting that sympathetic activation may be elevated during this phase of the Valsalva while heat stressed. These data show that heat stress does not attenuate this index of vasoconstrictor responsiveness during the Valsalva maneuver.

Original languageEnglish (US)
Pages (from-to)1591-1594
Number of pages4
JournalJournal of Applied Physiology
Volume108
Issue number6
DOIs
StatePublished - Jun 2010

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Valsalva Maneuver
Arterial Pressure
Hot Temperature
Hemodynamics
Heating
Heart Rate
Vasoconstrictor Agents
Vasoconstriction

Keywords

  • Blood pressure control
  • Sympathetic nervous system

ASJC Scopus subject areas

  • Physiology
  • Physiology (medical)

Cite this

Heat stress alters hemodynamic responses during the Valsalva maneuver. / Davis, Scott L.; Crandall, Craig G.

In: Journal of Applied Physiology, Vol. 108, No. 6, 06.2010, p. 1591-1594.

Research output: Contribution to journalArticle

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abstract = "The Valsalva maneuver can be used as a noninvasive index of autonomic control of blood pressure and heart rate. The purpose of this investigation was to test the hypothesis that sympathetic mediated vasoconstriction, as referenced by hemodynamic responses during late phase II (phase IIb) of the Valsalva maneuver, is inhibited during whole body heating. Seven individuals (5 men, 2 women) performed three Valsalva maneuvers (each at a 30-mmHg expiratory pressure for 15 s) during normothermia and again during whole body heating (increase sublingual temperature ~0.8°C via water-perfused suit). Each Valsalva maneuver was separated by a minimum of 5 min. Beat-to-beat mean arterial blood pressure (MAP) and heart rate were measured during each Valsalva maneuver, and responses for each phase were averaged across the three Valsalva maneuvers for both, thermal conditions. Baseline MAP was not significantly different between normothermic (88 ± 11 mmHg) and heat stress (84 ± 9 mmHg) conditions. The change in MAP (AMAP) relative to preValsalva MAP during phases IIa and IIb was significantly lower during heat stress (IIa = -20 ± 8 mmHg; IIb = -13 ± 7 mmHg) compared with normothermia (IIa = -1 ± 15 mmHg; IIb = 3 ± 13 mmHg). AMAP from pre-Valsalva baseline during phase IV was significantly higher during heat stress (25 ± 10 mmHg) compared with normothermia (8 ± 9 mmHg). Counter to the proposed hypothesis, the increase in MAP from the end of phase IIa to the end of phase lib during heat stress was not attenuated. Conversely, this increase in MAP tended to be greater during heat stress relative to normothermia (P = 0.06), suggesting that sympathetic activation may be elevated during this phase of the Valsalva while heat stressed. These data show that heat stress does not attenuate this index of vasoconstrictor responsiveness during the Valsalva maneuver.",
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