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Interaction of semicircular canal stimulation with carotid baroreceptor reflex control of heart rate

The carotid-cardiac baroreflex contributes to the prediction of orthostatic tolerance; experimental attenuation of the reflex response leads to orthostatic hypotension in humans and animals. Anecdotal observations indicate that rotational head movements about the vertical axis of the body can also induce orthostatic bradycardia and hypotension through increased parasympathetic activity. We therefore measured the chronotropic response to carotid baroreceptor stimulation in 12 men during varying conditions of vestibulo-oculomotor stimulation to test the hypothesis that stimulation of the semicircular canals associated with head movements in the yaw plane inhibits cardioacceleration through a vagally mediated baroreflex. Carotid-cardiac baroreflex response was assessed by plotting R-R intervals (ms) at each of 8 neck pressure steps with their respective carotid distending pressures (mmHg). Calculated baroreflex gain (maximal slope of the stimulus-response relationship) was measured under 4 experimental conditions: 1) sinusoidal whole-body yaw rotation of the subject in the dark without visual fixation (combined vestibular-oculomotor stimulation); 2) yaw oscillation of the subject while tracking a small head-fixed light moving with the subject (vestibular stimulation without eye movements); 3) subject stationary while fixating on a small light oscillating in yaw at the same frequency, peak acceleration, and velocity as the chair (eye movements without vestibular stimulation); and 4) subject stationary in the dark (no eye or head motion). Head motion alone and with eye movement reduced baseline baroreflex responsiveness to the same stimulus by 30%. Inhibition of cardioacceleration during rotational head movements may have significant impact on functional performance in aerospace environments, particularly in high-performance aircraft pilots during high angular acceleration in aerial combat maneuvers or in astronauts upon return from spaceflight who already have attenuated baroreflex functions.

Review, Tutorial↗

Augmented baroreflex heart rate gain after moderate-intensity, dynamic exercise

The occurrence of a sustained vasodilation and hypotension after acute, dynamic exercise suggests that exercise may alter arterial baroreflex mechanisms. Therefore, we assessed systemic hemodynamics, baroreflex regulation of heart rate, and cardiac vagal tone after 60 min of cycling at 60% peak oxygen consumption in 12 healthy, untrained men and women (ages 21-28 yr). We derived sigmoidal carotid-cardiac baroreflex relations by measurement of R-R interval changes induced by ramped, stepwise, R-wave-triggered changes in external neck pressure from 40 to -65 mmHg. We estimated tonic cardiac vagal control with power spectral analysis of R-R interval variability in the respiratory frequency band (0.2-0.3 Hz) during frequency- and tidal volume-controlled breathing. Both mean arterial pressure and total peripheral resistance were reduced postexercise [pressure: from 86 +/- 2 (mean +/- SE) to 81 +/- 2 mmHg; resistance: from 23 +/- 2 to 16 +/- 1 units; both P < 0.05]. Cardiac output was increased postexercise (from 3.9 +/- 0.3 to 5.5 +/- 0.5 l/min, P < 0.05). Both slope and range of the carotid-cardiac baroreflex relation were increased postexercise (slope: from 4.7 +/- 0.7 to 6.1 +/- 0.9 ms/mmHg; range: from 186 +/- 23 to 238 +/- 30 ms, P < 0.05). Respiratory R-R interval variability (cardiac vagal tone) was not changed at any time after exercise, whereas heart rate and plasma norepinephrine levels were elevated. Thus moderate-intensity, dynamic exercise increases heart rate and cardiac output, reduces peripheral vascular resistance, and augments baroreflex responsiveness. Our data suggest that augmented baroreflex heart rate gain restrains rather than contributes to postexercise hypotension, which appears to be mediated predominately by vasodilation.

NASA Discipline Cardiopulmonary↗