Lecture 19 - Control of Blood Flow During Exercise Flashcards
1
Q
How is heart rate raised during exercise?
A
- until approx 30% VO2 max, vagus receives most of the blood (aka blood is sent to the organs)
- after approx 3-% VO2 max, sympathetic (SNS) starts to take over and vagus (PNS) starts to withdraw (to send blood where it is needed)
- SA node innervation = low PNS input at SA node (active at rest/a break/slow down) and high SNS input to SA node (stress responses/speed up)
2
Q
what is an inotrope?
A
- an agent that alters the force of muscle contraction
- positive inotropes = norepinephrine and epinephrine
3
Q
what is inotropy?
A
- an increase in contractility and force
- caused by an increase in norepinephrine and epinephrine
- causes increased cardio muscle tension and therefore a larger SV
- walls of the heart are stretched (elastic potential) so end-diastolic volume is higher than normal
4
Q
how is inotropy affected by exercise?
A
- the increased firing of sympathetic nerves (innervate both the heart and cardiac muscle)
- increase in circulating Epi and Norep
- dependent on intensity (increased intensity causes increased contractility and SV)
5
Q
what are the “central” effects of the muscle pump?
A
- muscle contraction (increased force) pushes blood back to the heart (increased venous return) from the muscle
- increased venous return causes increased stroke volume
6
Q
how is cardiac output distributed during exercise?
A
- most blood is sent to the muscles (at all exercise stages, but not at rest)
- increase in blood sent to muscles as intensity increases
- decrease in blood sent to other organs as intensity increases
7
Q
what are the “peripheral” effects of the muscle pump?
A
- muscle contraction increases arterial flow (modifies deltaP)
- changes in muscle length and tension produce oscillations which change the pressure gradient for capillary perfusion
- vacuum pressure is created (negative pressure in venous system) which helps direct the blood flow
8
Q
what is the diversion of blood flow?
A
- the control of blood flow by the actual vessels themselves
9
Q
how do blood vessels divert blood flow?
A
- vasoconstriction (increased resistance) and vasodilation (decreased resistance)
- resistance = 8n L / pi r^4
- 8n = blood viscosity
- L = length of the vascular system
- r = radius of blood vessel (the only thing that changes, affects resistance)
10
Q
what two factors influence vasoconstriction?
A
- sympathetic vasoconstriction (SNS)
- circulating vasoconstrictors
11
Q
what three factors influence vasodilation?
A
- vasodilator formation in skeletal muscle
- flow-induced vasodilation
- myogenic vasodilation
12
Q
what is vasoconstrictor control?
A
- SNS innervates smooth muscle of arterioles (and the heart)
- SNS innervates the adrenal medulla
13
Q
how does sympathetic activity influence vasoconstriction of actual blood vessel size?
A
- baseline sympathetic activity = vasomotor tone (homeostatic level)
- increase sympathetic activity (more impulses) = increased vasoconstriction
- decreased sympathetic activity = decreased vasoconstriction (cannot cause relaxation, just less constriction, aka increases the magnitude of dilation)
14
Q
how does sympathetic activity influence chemical/hormone levels for vasoconstriction?
A
- increased sympathetic activity = increased catecholamine release
- increased circulating epi and norep = constriction of non-active organs, dilation of active muscles, increased HR, increased metabolism and blood glucose (glycogenolysis and gluconeogenesis)
15
Q
what are the three main types of intrinsic control over vasodilation?
A
- metabolic
- endothelial
- myogenic
