Heart-rate and blood-pressure variability during psychophysiological tasks involving speech: Influence of respiration

2007 ◽  
Vol 44 (5) ◽  
pp. 767-778 ◽  
Author(s):  
Alessandro Beda ◽  
Frederico C. Jandre ◽  
David I.W. Phillips ◽  
Antonio Giannella-Neto ◽  
David M. Simpson
2005 ◽  
Vol 20 (4) ◽  
pp. 394 ◽  
Author(s):  
V. Papaioannou ◽  
M. Giannakou ◽  
N. Maglaveras ◽  
E. Sofianos ◽  
M. Giala

1992 ◽  
Vol 146 (2) ◽  
pp. 155-164 ◽  
Author(s):  
A. E. HEDMAN ◽  
J. E. K. HARTIKAINEN ◽  
K. U. O. TAHVANAINEN ◽  
M. O. K. HAKUMÄKI

2000 ◽  
Vol 53 (1) ◽  
pp. 17-23 ◽  
Author(s):  
Kathrine Jauregui-Renaud ◽  
Kielan Yarrow ◽  
Ruth Oliver ◽  
Michael A Gresty ◽  
Adolfo M Bronstein

2008 ◽  
Vol 295 (3) ◽  
pp. H1150-H1155 ◽  
Author(s):  
François Cottin ◽  
Claire Médigue ◽  
Yves Papelier

The aim of the study was to assess the instantaneous spectral components of heart rate variability (HRV) and systolic blood pressure variability (SBPV) and determine the low-frequency (LF) and high-frequency baroreflex sensitivity (HF-BRS) during a graded maximal exercise test. The first hypothesis was that the hyperpnea elicited by heavy exercise could entail a significant increase in HF-SBPV by mechanical effect once the first and second ventilatory thresholds (VTs) were exceeded. It was secondly hypothesized that vagal tone progressively withdrawing with increasing load, HF-BRS could decrease during the exercise test. Fifteen well-trained subjects participated in this study. Electrocardiogram (ECG), blood pressure, and gas exchanges were recorded during a cycloergometer test. Ventilatory equivalents were computed from gas exchange parameters to assess VTs. Spectral analysis was applied on cardiovascular series to compute RR and systolic blood pressure power spectral densities, cross-spectral coherence, gain, and α index of BRS. Three exercise intensity stages were compared: below (A1), between (A2), and above (A3) VTs. From A1 to A3, both HF-SBPV (A1: 45 ± 6, A2: 65 ± 10, and A3: 120 ± 23 mm2Hg, P < 0.001) and HF-HRV increased (A1: 20 ± 5, A2: 23 ± 8, and A3:40 ± 11 ms2, P < 0.02), maintaining HF-BRS (gain, A1: 0.68 ± 0.12, A2: 0.63 ± 0.08, and A3: 0.57 ± 0.09; α index, A1: 0.58 ± 0.08, A2: 0.48 ± 0.06, and A3: 0.50 ± 0.09 ms/mmHg, not significant). However, LF-BRS decreased (gain, A1: 0.39 ± 0.06, A2: 0.17 ± 0.02, and A3: 0.11 ± 0.01, P < 0.001; α index, A1: 0.46 ± 0.07, A2: 0.20 ± 0.02, and A3: 0.14 ± 0.01 ms/mmHg, P < 0.001). As expected, once VTs were exceeded, hyperpnea induced a marked increase in both HF-HRV and HF-SBPV. However, this concomitant increase allowed the maintenance of HF-BRS, presumably by a mechanoelectric feedback mechanism.


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