Literature DB >> 15890708

Autonomic nervous system influence on arterial baroreflex control of heart rate during exercise in humans.

Shigehiko Ogoh1, James P Fisher, Ellen A Dawson, Michael J White, Niels H Secher, Peter B Raven.   

Abstract

A combination of sympathoexcitation and vagal withdrawal increases heart rate (HR) during exercise, however, their specific contribution to arterial baroreflex sensitivity remains unclear. Eight subjects performed 25 min bouts of exercise at a HR of 90, 120, and 150 beats min-1, respectively, with and without metoprolol (0.16 +/- 0.01 mg kg(-1); mean +/- S.E.M.) or glycopyrrolate (12.6 +/- 1.6 microg kg-1). Carotid baroreflex (CBR) function was determined using 5 s pulses of neck pressure (NP) and neck suction (NS) from +40 to -80 Torr, while transfer function gain (GTF) was calculated to assess the linear dynamic relationship between mean arterial pressure and HR. Spontaneous baroreflex sensitivity (SBR) was evaluated as the slope of sequences of three consecutive beats in which systolic blood pressure and the R-R interval of the ECG either increased or decreased, in a linear fashion. The beta-1 adrenergic blockade decreased and vagal cardiac blockade increased HR both at rest and during exercise (P < 0.05). The gain at the operating point of the modelled reflex function curve (GOP) obtained using NP and NS decreased with workload independent of beta-1 adrenergic blockade. In contrast, vagal blockade decreased GOP from -0.40 +/- 0.04 to -0.06 +/- 0.01 beats min-1 mmHg-1 at rest (P < 0.05). Furthermore, as workload increased both GOP and SBR, and GOP and GTF were correlated (P < 0.001), suggesting that the two dynamic methods applied to evaluate arterial baroreflex (ABR) function provide the same information as the modelled GOP. These findings suggest that during exercise the reduction of arterial baroreceptor reflex sensitivity at the operating point was a result of vagal withdrawal rather than an increase in sympathetic activity.

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Year:  2005        PMID: 15890708      PMCID: PMC1464761          DOI: 10.1113/jphysiol.2005.084541

Source DB:  PubMed          Journal:  J Physiol        ISSN: 0022-3751            Impact factor:   5.182


  47 in total

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Authors:  J T Potts; P B Raven
Journal:  Am J Physiol       Date:  1995-03
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