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Selective attenuation of carotid‐cardiac responses to hypertension at the onset of static handgrip in humans
Author(s) -
Deo Shekhar H,
Young Colin N.,
Fairfax Seth T.,
Fadel Paul J.
Publication year - 2010
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.24.1_supplement.807.6
Subject(s) - baroreflex , medicine , cardiology , heart rate , blood pressure , expiration , cardiac output , anesthesia , respiratory system
Previous studies have indicated that at the onset of exercise cardiac baroreflex function is reduced in an intensity‐dependent manner, which appears to be mediated by a blunted ability to buffer hypertensive challenges. However, whether cardiac baroreflex responses to a hypotensive stimulus are altered at exercise onset is unclear. To examine this, ten subjects (25±1 years) performed multiple 1‐min bouts of static handgrip (HG) at 15 and 60% of maximal voluntary contraction (MVC), while breathing to a metronome set at eupneic frequency. Neck pressure (NP +40 Torr) or neck suction (NS −60 Torr) was applied for 5s at end expiration, to simulate carotid baroreflex (CBR) hypotension and hypertension, respectively at rest, at the onset of HG (<1 s), and at ~40 s of HG. Cardiac responses to NP at the onset of exercise were maintained at both HG intensities, whereas heart rate responses to NS were blunted at exercise onset during 60% MVC HG (−16±2 rest vs. −9±3 bpm 60% MVC; P<0.05) but preserved at 15% MVC. The response range of the carotid‐cardiac baroreflex at the onset of 60% MVC HG was reduced (25±1 rest vs. 18±3 bpm 60% MVC; P<0.05) compared to rest and 15% MVC. Heart rate responses to NP and NS applied at ~40s of 15 and 60% MVC HG were similar to rest. These results suggest that carotid‐cardiac responses to hypertension are selectively contributing to an impaired CBR control of heart rate at the onset of static HG in humans. Support: NIH R01HL093167