Wendy L. Wasmund

Role of central command in carotid baroreflex resetting in humans during static exercise

The purpose of the experiments was to examine the role of central command in the exercise‐induced resetting of the carotid baroreflex. Eight subjects performed 30 % maximal voluntary contraction (MVC) static knee extension and flexion with manipulation of central command (CC) by patellar tendon vibration (PTV). The same subjects also performed static knee extension and flexion exercise without PTV at a force development that elicited the same ratings of perceived exertion (RPE) as those observed during exercise with PTV in order to assess involvement of the exercise pressor reflex. Carotid baroreflex (CBR) function curves were modelled from the heart rate (HR) and mean arterial pressure (MAP) responses to rapid changes in neck pressure and suction during steady state static exercise. Knee extension exercise with PTV (decreased CC activation) reset the CBR‐HR and CBR‐MAP to a lower operating pressure (P < 0.05) and knee flexion exercise with PTV (increased CC activation) reset the CBR‐HR and CBR‐MAP to a higher operating pressure (P < 0.05). Comparison between knee extension and flexion exercise at the same RPE with and without PTV found no difference in the resetting of the CBR‐HR function curves (P > 0.05) suggesting the response was determined primarily by CC activation. However, the CBR‐MAP function curves were reset to operating pressures determined by both exercise pressor reflex (EPR) and central command activation. Thus the physiological response to exercise requires CC activation to reset the carotid‐cardiac reflex but requires either CC or EPR to reset the carotid‐vasomotor reflex.

Haemodynamic changes during neck pressure and suction in seated and supine positions

We sought to quantify the contribution of cardiac output (Q) and total vascular conductance (TVC) to carotid baroreflex‐mediated changes in mean arterial pressure (MAP) in the upright seated and supine positions. Acute changes in carotid sinus transmural pressure were evoked using brief 5 s pulses of neck pressure and neck suction (NP/NS) via a simplified paired neck chamber that was developed to enable beat‐to‐beat measurements of stroke volume using pulse‐doppler ultrasound. Percentage contributions of Q and TVC were achieved by calculating the predicted change in MAP during carotid baroreflex stimulation if only the individual changes in Q or TVC occurred and all other parameters remained at control values. All NP and NS stimuli from +40 to −80 Torr (+5.33 to −10.67 kPa) induced significant changes in Q and TVC in both the upright seated and supine positions (P < 0.001). Cardiopulmonary baroreceptor loading with the supine position appeared to cause a greater reliance on carotid baroreflex‐mediated changes in Q. Nevertheless, in both the seated and supine positions the changes in MAP were primarily mediated by alterations in TVC (percentage contribution of TVC at the time‐of‐peak MAP, seated 95 ± 13, supine 76 ± 17 %). These data indicate that alterations in vasomotor activity are the primary means by which the carotid baroreflex regulates blood pressure during acute changes in carotid sinus transmural pressure.

Does Pulsatile and Sustained Neck Pressure or Neck Suction Produce Differential Cardiovascular and Sympathetic Responses in Humans

Although square‐wave sustained and R wave‐triggered pulsatile stimuli have been used to assess carotid baroreflex (CBR) function in humans, it remains unclear whether these different stimulus protocols elicit comparable responses and whether CBR responses adapt during prolonged stimulation. Thus, we measured muscle sympathetic nerve activity (MSNA), heart rate (HR) and mean arterial pressure (MAP) in response to +30 Torr neck pressure (NP) and ‐30 Torr neck suction (NS) delivered for 20 s either as a sustained or pulsatile stimulus. CBR‐mediated changes in MSNA, HR and MAP were similar with sustained and pulsatile stimuli. The time course of MSNA and HR responses identified that significant changes occurred during the initial 5 s and were better maintained over 20 s with NP than with NS. Changes in MAP exhibited a slower onset with the peak increase during NP occurring at 10 s (sustained, 7 ± 1 mmHg; pulsatile, 7 ± 1 mmHg; P > 0.05) and the nadir during NS occurring at 20 s (sustained, ‐7 ± 1 mmHg; pulsatile, ‐9 ± 2 mmHg; P > 0.05). These data demonstrate that sustained and pulsatile NP and NS produce comparable CBR‐mediated responses. Furthermore, despite MSNA and HR returning towards baseline during NS, CBR‐mediated changes in MAP are well maintained over 20 s of NS and NP.

Clinical Effects of a Dietary Antioxidant Silicate Supplement, Microhydrin®, on Cardiovascular Responses to Exercise

Amorphous silicate minerals, often described as rock flour, were once common in natural water sources and abundant in glacial stream waters. Not only do the silica mineral particles bond water and other elements for transport; they also can be adsorbed with reduced hydrogen, which releases electrons, providing antioxidant or reducing potential to surrounding fluids. The purpose of this investigation was to examine the cardiovascular responses during exercise after consumption of a dietary silicate mineral antioxidant supplement, Microhydrin((R)) (Royal BodyCare, Inc., Irving, TX). A clinical trial incorporating a double-blind, placebo-controlled, crossover experimental design was employed. Subjects received either active agent or placebo, four capsules per day, for 7 days before the trial. The trial evaluated six exercise bicycle-trained subjects performing a 40-km bicycling time trial. Ratings of perceived exertion and measurements of oxygen uptake, heart rate, performance workload, and preexercise and postexercise blood lactate concentrations were obtained. Although there were no differences (P >/=.05) in work performed, heart rate, oxygen uptake, and ratings of perceived exertion during the time trial, the postexercise blood lactate concentrations were significantly lower (P </=.05) when the silicate mineral supplement was used, compared with placebo. These data suggest a beneficial effect of Microhydrin on lactate metabolism.

Do vestibular otolith organs participate in human orthostatic blood pressure control

We hypothesized that vestibular otolith organ stimulation contributes to human orthostatic responses. Twelve subjects underwent three 60 degrees upright tilts: (1) with the neck flexed from 0 degrees to 30 degrees relative to the body during 60 degrees tilt, such that the head moved from horizontal to 90 degrees above horizontal (0 to 1 Gz otolith stimulation); (2) with the head and body aligned, such that they tilted together to 60 degrees (0 to 0.87 Gz otolith stimulation); and (3) with the neck flexed 30 degrees relative to the body during supine conditions, and the neck then extended to -30 degrees during 60 degrees body tilting, such that the head remained at 30 degrees above horizontal throughout body tilting (constant 0.5 Gz otolith stimulation). All three tilt procedures increased thoracic impedance, sympathetic nerve activity (N = 8 of 12), arterial pressure, and heart rate relative to supine conditions (all P < 0.04). Within the first 20 s of tilt, arterial pressure increased most obviously in the 0 to 1 Gz otolith condition. Thoracic impedance tended to increase more in otolith-constant conditions, but no dependent variable differed significantly between tilt conditions, and no significant time x tilt interactions emerged. Otolith inputs may contribute to early transient adjustments to orthostasis. However, lack of significant main effects of tilt condition and time x tilt interactions suggests that potential otolith effects on the variables we studied are relatively subtle and ephemeral, or that other mechanisms compensate for a lack of change in otolith input with orthostasis.