Heat stress enhances arterial baroreflex control of muscle sympathetic nerve activity via increased sensitivity of burst gating, not burst area, in humans

David M. Keller, J. Cui, S. L. Davis, D. A. Low, C. G. Crandall

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Abstract

The relationship between muscle sympathetic nerve activity (MSNA) and diastolic blood pressure has been used to describe two sites for arterial baroreflex control of MSNA. By determining both the likelihood of occurrence for sympathetic bursts and the area of each burst for a given diastolic blood pressure, both a 'gating' and an 'area' control site has been described in normothermic humans. Assessing the effect of heat stress on these mechanisms will improve the understanding of baroreflex control of arterial blood pressure under this thermal condition. Therefore, the purpose of this study was to test the hypothesis that heat stress enhances arterial baroreflex control of burst gating and area. In 10 normotensive subjects (age, 32 ± 2 years; mean ± S.E.M.), MSNA (peroneal) was assessed using standard microneurographic techniques. Five minute periods of data were examined during normothermic and whole-body heating conditions. The burst incidence (i.e. number of sympathetic bursts per 100 cardiac cycles) and the area of each burst were determined for each cardiac cycle and were placed into 3 mmHg intervals of diastolic blood pressure. During normotheric conditions, there was a moderate, negative relationship between burst incidence and diastolic blood pressure (slope = 2.49 ± 0.38; r2= 0.73 ± 0.06; mean ± S.E.M.), while area per burst relative to diastolic blood pressure exhibited a less strong relationship (slope = -1.13 ± 0.46; r2=0.45 ± 0.09). During whole-body heating there was an increase in the slope of the relationship between burst incidence and diastolic blood pressure (slope = -4.69 ± 0.44; r2= 0.84 ± 0.03) compared to normothermia (P < 0.05), while the relationship between area per burst and diastolic blood pressure was unchanged (slope = -0.92 ± 0.29; r2= 0.41 ± 0.08) (P= 0.50). The primary finding of this investigation is that, at rest, whole-body heating enhanced arterial baroreflex control of MSNA through increased sensitivity of a 'gating' mechanism, as indicated by an increase in the slope of the relationship between burst incidence and diastolic blood pressure. This occurrence is likely to afford protection against potential decreases in arterial blood pressure in an effort to preserve orthostatic tolerance during heat stress.

Original languageEnglish (US)
Pages (from-to)445-451
Number of pages7
JournalJournal of Physiology
Volume573
Issue number2
DOIs
StatePublished - Jun 1 2006

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Baroreflex
Hot Temperature
Blood Pressure
Muscles
Heating
Incidence
Arterial Pressure
Peroneal Nerve

ASJC Scopus subject areas

  • Physiology

Cite this

Heat stress enhances arterial baroreflex control of muscle sympathetic nerve activity via increased sensitivity of burst gating, not burst area, in humans. / Keller, David M.; Cui, J.; Davis, S. L.; Low, D. A.; Crandall, C. G.

In: Journal of Physiology, Vol. 573, No. 2, 01.06.2006, p. 445-451.

Research output: Contribution to journalArticle

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abstract = "The relationship between muscle sympathetic nerve activity (MSNA) and diastolic blood pressure has been used to describe two sites for arterial baroreflex control of MSNA. By determining both the likelihood of occurrence for sympathetic bursts and the area of each burst for a given diastolic blood pressure, both a 'gating' and an 'area' control site has been described in normothermic humans. Assessing the effect of heat stress on these mechanisms will improve the understanding of baroreflex control of arterial blood pressure under this thermal condition. Therefore, the purpose of this study was to test the hypothesis that heat stress enhances arterial baroreflex control of burst gating and area. In 10 normotensive subjects (age, 32 ± 2 years; mean ± S.E.M.), MSNA (peroneal) was assessed using standard microneurographic techniques. Five minute periods of data were examined during normothermic and whole-body heating conditions. The burst incidence (i.e. number of sympathetic bursts per 100 cardiac cycles) and the area of each burst were determined for each cardiac cycle and were placed into 3 mmHg intervals of diastolic blood pressure. During normotheric conditions, there was a moderate, negative relationship between burst incidence and diastolic blood pressure (slope = 2.49 ± 0.38; r2= 0.73 ± 0.06; mean ± S.E.M.), while area per burst relative to diastolic blood pressure exhibited a less strong relationship (slope = -1.13 ± 0.46; r2=0.45 ± 0.09). During whole-body heating there was an increase in the slope of the relationship between burst incidence and diastolic blood pressure (slope = -4.69 ± 0.44; r2= 0.84 ± 0.03) compared to normothermia (P < 0.05), while the relationship between area per burst and diastolic blood pressure was unchanged (slope = -0.92 ± 0.29; r2= 0.41 ± 0.08) (P= 0.50). The primary finding of this investigation is that, at rest, whole-body heating enhanced arterial baroreflex control of MSNA through increased sensitivity of a 'gating' mechanism, as indicated by an increase in the slope of the relationship between burst incidence and diastolic blood pressure. This occurrence is likely to afford protection against potential decreases in arterial blood pressure in an effort to preserve orthostatic tolerance during heat stress.",
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N2 - The relationship between muscle sympathetic nerve activity (MSNA) and diastolic blood pressure has been used to describe two sites for arterial baroreflex control of MSNA. By determining both the likelihood of occurrence for sympathetic bursts and the area of each burst for a given diastolic blood pressure, both a 'gating' and an 'area' control site has been described in normothermic humans. Assessing the effect of heat stress on these mechanisms will improve the understanding of baroreflex control of arterial blood pressure under this thermal condition. Therefore, the purpose of this study was to test the hypothesis that heat stress enhances arterial baroreflex control of burst gating and area. In 10 normotensive subjects (age, 32 ± 2 years; mean ± S.E.M.), MSNA (peroneal) was assessed using standard microneurographic techniques. Five minute periods of data were examined during normothermic and whole-body heating conditions. The burst incidence (i.e. number of sympathetic bursts per 100 cardiac cycles) and the area of each burst were determined for each cardiac cycle and were placed into 3 mmHg intervals of diastolic blood pressure. During normotheric conditions, there was a moderate, negative relationship between burst incidence and diastolic blood pressure (slope = 2.49 ± 0.38; r2= 0.73 ± 0.06; mean ± S.E.M.), while area per burst relative to diastolic blood pressure exhibited a less strong relationship (slope = -1.13 ± 0.46; r2=0.45 ± 0.09). During whole-body heating there was an increase in the slope of the relationship between burst incidence and diastolic blood pressure (slope = -4.69 ± 0.44; r2= 0.84 ± 0.03) compared to normothermia (P < 0.05), while the relationship between area per burst and diastolic blood pressure was unchanged (slope = -0.92 ± 0.29; r2= 0.41 ± 0.08) (P= 0.50). The primary finding of this investigation is that, at rest, whole-body heating enhanced arterial baroreflex control of MSNA through increased sensitivity of a 'gating' mechanism, as indicated by an increase in the slope of the relationship between burst incidence and diastolic blood pressure. This occurrence is likely to afford protection against potential decreases in arterial blood pressure in an effort to preserve orthostatic tolerance during heat stress.

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