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Influence of exercise intensity on carotid‐cardiac responses at the onset of static exercise in humans
Author(s) -
Young Colin Neal,
Fisher James P,
Ogoh Shigehiko,
Fadel Paul J
Publication year - 2007
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.21.5.a574
Subject(s) - heart rate , cardiology , medicine , blood pressure , baroreflex , intensity (physics) , baroreceptor , expiration , anesthesia , respiratory system , physics , quantum mechanics
Animal studies suggest that the baroreflex‐mediated bradycardia is blunted at exercise onset due to activation of central command. To begin to explore this possibility in humans, heart rate (HR) and mean arterial pressure (MAP) responses to carotid baroreflex (CBR) activation via neck suction (NS) were determined at the immediate onset of varying intensities of handgrip exercise (HG). We reasoned that as exercise intensity increased, central command activation also increased at exercise onset. Eight subjects (25±1 yrs) performed static HG for 1 min at 15, 30, 45 and 60% of maximum voluntary contraction (MVC) while breathing to a metronome set at eupneic frequency. HR, MAP, and respiration were measured continuously. Five second pulses of −60 Torr NS were applied at end expiration at rest, the onset of and after ~40s of HG. Cardiac responses to NS at the onset of 15% (−12±2 bpm) and 30% (−10±2 bpm) MVC HG were not different from rest (−10±1 bpm). However, HR responses to NS were reduced at the onset of 45% and 60% MVC HG (−6±2 and −4±1 bpm, respectively; p<0.001). In contrast, MAP responses to NS were not different from rest at exercise onset at any intensity. Furthermore, both HR and MAP responses to NS applied at ~40s of HG were not different from rest in any trial. These data suggest that CBR control of HR is only attenuated at the onset of higher intensity static HG (≥45% MVC) possibly due to greater activation of central command.

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