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1 Department of Integrative Physiology University of North Texas Health Science Center at Fort Worth, TX 76107, USA
2 School of Sport and Exercise Sciences, University of Birmingham, Edgbaston, Birmingham B15 2TT, UK
3 Copenhagen Muscle Research Centre, Department of Anaesthesia, Rigshospitalet, University of Copenhagen, DK-2100, Copenhagen, Denmark
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 µg 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 ß-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 ß-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.
(Received 4 February 2005;
accepted after revision 2 May 2005;
first published online 12 May 2005)
Corresponding author S. Ogoh: Department of Integrative Physiology, University of North Texas Health Science Center, 3500 Camp Bowie Boulevard, Fort Worth, TX 76107, USA. Email: sogoh{at}hsc.unt.edu
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