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Exercise Physiology
Control of Blood Flow During Exercise
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2 formulas for cardiac output:
Q
=
HR
x
SV
Q =
MAP
/
TPR
Rise in HR during exercise:
due to innervation of the
SA
node by
SNS
and
PSNS
to increase HR -->
FIRST
!
decrease
PSNS
to increase HR -->
NEXT
!
increase
SNS
PSNS always active at
rest
SNS reserved for
stressful
situations
with exercise -->
inhibit
PSNS vagal nerve, no more
slow
contraction, HR
increases
, then SNS takes over
Increase in contractility during exercise:
inotropy
= alters force of muscle
contraction
positive inotropes =
NE
and
Epi
increase inotrope concentration =
increase
cardiac muscle tension for EDV/preload
during exercise, increase inotropy by... 1) increasing
SNS
; 2) increasing
catecholamines
The muscle pump:
central
effects
muscle
contraction
helps
increase
venous return
propels
blood
from muscles to heart
increase
VR
= increase
SV
How do we increase Q with higher exercise intensity?
there are 5 ways:
decrease
PSNS
increase
SNS
increase
inotropy
increase
catecholamines
mechanical
muscle pump
Distribution of
Q
:
mainly goes to
muscle
during exercise
Muscle pump effect:
peripheral
effect
muscle
contraction
increases arterial flow
when muscles
contract
, they pinch the venous vessels
when muscles
relax
, venous system
opens
up again; causes
negative
pressure
vacuum
effect = opening up of vessels causes blood in
capillaries
to be sucked up into the
venous
system
Diversion of blood flow:
at any pressure, flow through vessels is regulated by
modifications
in local vascular
resistance
resistance =
8
n L / pi r4
Vasoconstriction:
due to
sympathetic
vasoconstriction (SNS --> NE)
due to
circulating
vasoconstrictors
Vasodilation:
due to
vasodilator
formation in
skeletal
muscles
due to flow-induced
vasodilation
due to
myogenic
vasodilation
Vasoconstrictor control:
SNS innervates
smooth
muscle in
arterioles
increase
SNS =
increase
constriction
decrease
SNS =
decrease
constriction
Vasoconstrictor control:
SNS innervates
adrenal
medulla
increase SNS = increase
catecholamines
increase catecholamines = increase
constriction
of non-active tissues
increase catecholamines = increase
HR
and
contractility
increase catecholamines = increase
glycogenolysis
and
gluconeogenesis
NE and Epi (
vasoconstriction
):
NE and Epi constrict non-active vessels
NE and Epi
dilate
active vessels
SNS diverts Q to muscle:
splanchnic and renal blood flow =
decreases
plasma NE =
increases
(has
constricting
effect on kidneys and organs in the splanchnic region)
Vasodilator
control:
three types:
metabolic
--> chemical agents released; cause smooth muscle relaxation (
CO2
,
K
+,
H
+,
lactic
acid)
endothelial
--> dilator substances within endothelium of
arterioles
(
nitric
oxide, etc.)
myogenic
-->
pressure
changes within vessels cause smooth muscle constriction or relaxation (increase pressure outside = decrease pressure inside (
dilation
); decrease pressure outside = increase pressure inside (
constriction
))
Factors influencing Q:
neural
factors
mechanical
factors
vascular
factors
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