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
120±10 to 148±14 mmHg while heart rate increased from 60±8 to 82 ±12 bpm.
Heart rate variability decreased while blood pressure variability increased
and transfer function amplitude was therefore reduced from 18±2 to 8±2
ms/mmHg. This was associated with a profound reduction the coherence between
BP and HR (from .76±0.10 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
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
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
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.