lecture 19

Question 1

cardiac output and muscle blood flow

Answer 1

increase in proportion to metbolic rate

what causes the “hypereic” response?

Question 2

graphs

Answer 2

cardiac output rises linearly, just like VO2

SBP higher than normal, and DBP is lower than normal

Question 3

the rise in HR during exercise

Answer 3

• decrease in PNS input to SA node (break/slow down)
• increase SNS input to SA node (accelerate/speed up)

Question 4

the increase in contractility during exercise

Answer 4

• inotropy
  - “inotrope” = agent that alters the force of muscle contraction
  - positive inotropes = norepinephrine and epinephrine
  - increase positive inotrope concentration = increase cardiac muscle tension for a given preload (or EDV) and rate of muscle tnsion development
  - increase inotropy = increase SV
• durign exercise, increase inotropy
  - increase firing of sympathetic nerves innervating ventricle
  - increase circulating catecholamines (Epi and NE)
  - intensity - dependent

Question 5

the muscle pump effect

Answer 5

“central” effects
- muscle contraction helps increase venous return (A —> B)
- propels blood away from muscle and back to heart (increase venous return —> increase stroke volume)

• increase in sympathetic nervous system driv to the heart
• decrease in parasympathetic control of heart
• increase inotropy
• increase circulating catecholamines (Epi and NE)

“peripheral” effects
- muscle contraction increases arterial flow (B —> C)
- changes in muscle length and tension produce cyclic oscillations in intramuscular pressure
- oscillations in arterial and venous pressure change the pressure gradient for capillary perfusion

C —> receives more cardiac output than B

Question 6

distribution of cardiac output

Answer 6

a) absolute values —> mostly muscle
b) relative to total blood volume —> mostly muscle and kidneys

Question 7

the diversion of blood flow

Answer 7

• at any pressure, flow though blood vessels is regulated by modifcations in local vascular resistance

resistance = 8 n L divided by (pie) r^4

• increase r, decrease resistance (vasodilation)
• decrease r, increase resistance (vasconstriction)

vasoconstrction
- sympathetic vasoconstriction
- circulating vasoconstriction

vasodilation
- vasodilator formation in skeletal muscle
- flow-induced vasodilation
- myogenic vasodilation

Question 8

vasoconstrictor control (decrease flow)

Answer 8

• sympathetic nervous system innervates smooth muscle in arterioles
  - baseline sympathetic activity —> vasomotor tone
  - increase sympathetic activity —> increase vasoconstriction
  - decrease sympathetic activity —> decrease vasoconstriction (passive vasodilation)

if we vasoconstrict that decreases r, which increases resistance

• sympathetic nervous system innervates adrenal medulla
  - increase sympathetic activity —> increase catecholamine release
  - inrease circulating epinephrine and norepinephrine leads to:
  - increase vasoconstriction non-ctive tissues (dilation in muscle)
  - increase heart rate and contractility
  - increase glycogenolysis and gluconeogenesis (liver and muscle)

hypothalamus —> nerve impulses —> spinal cord —> adrenal medulla —> catecholamines (epinephrine and norepinephrine)

Question 9

vasodilator control (increase flow)

Answer 9

three types of intrinsic control

1. metabolic
   - chemical agents released as a consequence of metabolim cause smooth muscle relaxation
   - increase CO2, K+, H+, lactic acid
2. endothelial
   - dilator substances produced within endothelium (inner lining) of arterioles in response various stimuli
   - nitric oxide, prostaglandins, endothelium-derived hyperpolrizing factor
3. myogenic
   - pressure changes within the vessels themselves can cause smooth muscle constriction or relaxation