BAROREFLEX CONTROL OF SINUS NODE DURING DYNAMIC EXERCISE IN HUMANS - EFFECTS OF CENTRAL COMMAND AND MUSCLE REFLEXES

Citation
F. Iellamo et al., BAROREFLEX CONTROL OF SINUS NODE DURING DYNAMIC EXERCISE IN HUMANS - EFFECTS OF CENTRAL COMMAND AND MUSCLE REFLEXES, American journal of physiology. Heart and circulatory physiology, 41(3), 1997, pp. 1157-1164
Citations number
42
Categorie Soggetti
Physiology
ISSN journal
03636135
Volume
41
Issue
3
Year of publication
1997
Pages
1157 - 1164
Database
ISI
SICI code
0363-6135(1997)41:3<1157:BCOSND>2.0.ZU;2-3
Abstract
This study evaluated the influence of central command and muscle affer ent stimulation (mechanical and chemical) on the integrated arterial b aroreflex control of the sinus node during dynamic exercise. Twenty-tw o healthy men performed voluntary knee extension and electrically indu ced dynamic knee extension under free-flow and arrested-flow (n = 18) conditions. Systolic arterial pressure (SAP) and pulse interval (PI) w ere measured continuously and noninvasively. The arterial baroreflex w as evaluated by analyzing the slopes of sequences of three or more con secutive beats characterized by the SAP and PI of the following beat; both increased or decreased in a linear fashion. Compared with rest, b oth voluntary exercise and electrically induced exercise under arreste d-flow conditions resulted in a maintained baroreflex sensitivity (BRS ; 11.7 +/- 1.2 vs. 9.6 +/- 0.7 and 11.3 +/- 1.4 vs. 9.8 +/- 1.5 ms/mmH g, respectively; not significant), with an apparent rightward shift in the regression line relating SAP to PI. Electrically induced exercise under free-flow conditions resulted in a significant decrease in BRS (12.1 +/- 1.4 vs. 8.8 +/- 0.8 ms/mmHg; P < 0.05). These data suggest t hat the central command and muscle chemoreflex act to preserve the BRS , possibly ''resetting'' the baroreceptor-cardiac response relationshi p, whereas stimulation of mechanosensitive receptors appears capable o f modifying the integrated baroreflex control of sinus node function i n humans. The first two mechanisms seem, however, to overwhelm the lat ter to maintain BRS, thus permitting a concomitant increase in arteria l pressure and heart rate.