Baroreflex-Mediated Changes in Cardiac Output and Vascular Conductance in Response to Alterations in Carotid Sinus Pressure during Exercise in Humans

Authors

  • Shigehiko Ogoh,

    Corresponding author
    1. Department of Integrative Physiology, University of North Texas Health Science Center at Fort Worth, TX, USA
    • 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@hsc.unt.edu

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  • Paul J. Fadel,

    1. Department of Integrative Physiology, University of North Texas Health Science Center at Fort Worth, TX, USA
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  • Peter Nissen,

    1. Copenhagen Muscle Research Centre, Department of Anaesthesia, Rigshospitalet, University of Copenhagen, DK-2200, Copenhagen, Denmark
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  • Øeivind Jans,

    1. Copenhagen Muscle Research Centre, Department of Anaesthesia, Rigshospitalet, University of Copenhagen, DK-2200, Copenhagen, Denmark
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  • Christian Selmer,

    1. Copenhagen Muscle Research Centre, Department of Anaesthesia, Rigshospitalet, University of Copenhagen, DK-2200, Copenhagen, Denmark
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  • Niels H. Secher,

    1. Copenhagen Muscle Research Centre, Department of Anaesthesia, Rigshospitalet, University of Copenhagen, DK-2200, Copenhagen, Denmark
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  • Peter B. Raven

    1. Department of Integrative Physiology, University of North Texas Health Science Center at Fort Worth, TX, USA
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  • Author's present address
    P. J. Fadel: Department of Internal Medicine, University of Texas Southwestern Medical Center at Dallas, 5323 Harry Hines Boulevard, Dallas, TX 75390-8586, USA.

Abstract

We sought to quantify the contribution of cardiac output (Q) and total vascular conductance (TVC) to carotid baroreflex (CBR)-mediated changes in mean arterial pressure (MAP) during mild to heavy exercise. CBR function was determined in eight subjects (25 ± 1 years) at rest and during three cycle exercise trials at heart rates (HRs) of 90, 120 and 150 beats min−1 performed in random order. Acute changes in carotid sinus transmural pressure were evoked using 5 s pulses of neck pressure (NP) and neck suction (NS) from +40 to −80 Torr (+5.33 to −10.67 kPa). Beat-to-beat changes in HR and MAP were recorded throughout. In addition, stroke volume (SV) was estimated using the Modelflow method, which incorporates a non-linear, three-element model of the aortic input impedance to compute an aortic flow waveform from the arterial pressure wave. The application of NP and NS did not cause any significant changes in SV either at rest or during exercise. Thus, CBR-mediated alterations in Q were solely due to reflex changes in HR. In fact, a decrease in the carotid-HR response range from 26 ± 7 beats min−1 at rest to 7 ± 1 beats min−1 during heavy exercise (P= 0.001) reduced the contribution of Q to the CBR-mediated change in MAP. More importantly, at the time of the peak MAP response, the contribution of TVC to the CBR-mediated change in MAP was increased from 74 ± 14 % at rest to 118 ± 6 % (P= 0.017) during heavy exercise. Collectively, these findings indicate that alterations in vasomotion are the primary means by which the CBR regulates blood pressure during mild to heavy exercise.

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