The increase in blood pressure and heart rate during exercise is denoted the exercise pressor reflex. When evoked by static handgrip unmyelinated skeletal muscle afferents comprising mechanoreceptors and metaboreceptors are activated and produce regional changes in blood volume and blood flow related to sympathetic activation and parasympathetic withdrawal which are incompletely characterized in humans. We studied 16 healthy subjects aged 20-27 years using segmental impedance plethysmography validated against dye dilution and venous occlusion plethysmography. To study the reflex during exercise static handgrip while supine was performed for two minutes without post exercise ischemia. Measurements of heart rate and blood pressure variability and coherence analyses were used to examine baroreflex-mediated cardiac autonomic effects.

During handgrip systolic blood pressure increased from 12010 to 14814 mmHg while heart rate increased from 608 to 82 12 bpm. Heart rate variability decreased while blood pressure variability increased and transfer function amplitude was therefore reduced from 182 to 82 ms/mmHg. This was associated with a profound reduction the coherence between BP and HR (from .760.10 to .26.05) indicative of uncoupling of heart rate regulation by the baroreflex. Cardiac output increased by approximately 18% associated with a 4.5% increase in central blood volume and an 8.5% increase in total peripheral resistance suggesting an increase in cardiac preload, and contractility. There was a reciprocal decrease in splanchnic blood volume with smaller decreases in pelvic and leg volumes associated with increased splanchnic, pelvic and calf peripheral resistance and evidence for splanchnic venoconstriction.

We conclude that the exercise pressor reflex is primarily driven by increased cardiac output related to enhanced preload due mostly to splanchnic blood mobilization, and to enhanced contractility. The effect of the baroreflex on cardiac regulation is reduced during supine static pressor reflex activation.



The left panels show representative heart rate (upper panel) and blood pressure (lower panel) from an actual subject during static handgrip. The right panels show changes in heart rate and mean arterial blood pressure averaged over all subjects: heart rate is shown in the upper panel and mean arterial blood pressure is shown in the lower panel. Measurements are shown for 1 minute and 2 minutes after the onset of handgrip as well as during the recovery phase. *=P<0.05 compared to baseline.





The figure shows percent changes from baseline in thoracic, splanchnic, pelvic, and calf blood volumes during handgrip averaged over all subjects at 1 minute and 2 minutes after starting handgrip and during recovery. The largest percent changes (increases) occur in the thoracic (central) blood segment with smaller reciprocal decreases in splanchnic segment.
Smaller yet are changes in the pelvic and calf segments. *=P<0.05 compared to baseline.



The figure shows percent changes in segmental blood flow. From top down changes in thoracic, splanchnic, pelvic and leg (calf) are shown in order. Blood flow increases for the central thoracic, pelvic and calf  segments but is relatively unchanged for the splanchnic segment. *=P<0.05 compared to baseline.



The figure shows percent changes in segmental arterial resistance . From top down changes in thoracic, splanchnic, pelvic and leg (calf) are shown in order. Total peripheral resistance (thoracic resistance) was increased by the second minute of handgrip and was increased in splanchnic, pelvic and calf segments during the entire handgrip period. All resistances returned to baseline during recovery. *=P<0.05 compared to baseline.

Our most significant findings are that central blood volume increases and cardiac output increases during evocation of the exercise pressor reflex. This is produced in large part through emptying of the splanchnic vascular bed by venoconstriction and arterial vasoconstriction. We observed about a 4.5% increase in central blood volume with a 2.5% decrease in splanchnic volume. Since the splanchnic vascular bed receives approximately 25% of the cardiac output and contains approximately 25% of it comes as no great surprise that the splanchnic vasculature is able to rapidly transfer its blood to the central circulation  Relatively smaller but directionally similar decreases in segmental blood volume occur within the pelvic and calf segments. The finding of splanchnic emptying at relatively constant splanchnic blood flow implies the active participation of venoconstriction. In addition, there is an increase in total peripheral resistance and therefore cardiac afterload. Given the magnitude of the increment in cardiac output, the increase in central blood volume, and the increase in end-systolic pressure this may imply an increase in cardiac contractility.




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