Lecture 13: CV response to exercise 3 Flashcards
- what happens to impulse frequency at level of baroreceptors when blood pressure increases?
- what is MSNA response as BP increases (spontaneously)?
- what is the arterial/sympathetic baroreflex sensitivity?
- impulse frequency increases! more action potentials because receptors on carotid sinus nerve are more stimulated
- DECREASE MSNA response (decrease burst incidence)! bc if BP increases, then baroreflex will decrease SNS in order to bring BP down
- sensitivity = magnitude of change in MSNA elicited by a given change in BP –> sensitivity = slope of relationship –> steep slope = big sensitivity = how good you respond to BP changes
*ie aging ppl have less baroreceptor sensitivity bc arteries are older –> less good response to changing in BP
what is the baroreflex operating point?
- OP is the point of maximum slope (or highest gain) of stimulus response curve, and represents MAP that arterial baroreflex is trying to achieve/regulate to
(- OP is the point at which the arterial baroreflex regulates arterial pressure.
- It’s a variable point that can change over a wide range of pressures, and is determined by inputs from the central and peripheral nervous systems) –> GOOGLE
explain the arterial baroreflex “resetting” during exercise
3 figures
A) central command resets baroreflex to operating point 2 (HORIZONTAL SHIFT) by acting on neuron pool receiving baroreceptor afferents (in brainstem!)
*any perturbation of pressure around original OP is poorly corrected bc pressure falls on insensitive region of new curve
B) VERTICAL SHIFT signifies that muscle chemoreflex raises SNA without changing OP bc the stimulus acts only on Efferent arm of reflex (not on the central neurons controlling the reflex)
C) A + B illustrates a diagonal shift of the curve –> combined effects of both stimuli
- what mechanisms reset OP of arterial baroreflex to a new lower/higher level in an ________ ______-dependent manner?
- feedforward (central command + mechano receptors) + feedback mechanisms (metaboreflex) drive the resetting of OP to a higher level in an exercise intensity-dependent manner
*each increase in exercise intensity (light, moderate to heavy) –> diagonal shift in OP
- arterial baroreflex resetting creates what? explain
- creates a pressure error! difference btw operating point and BP that hasnt changed yet
- ie when arterial baroreflex OP is rest at onset of exercise, there is suddenly a different btw OP (target MAP) and the prevailing or actual MAP (ie pressure error), which has not changed
- ie MAP OP increases from 100 to 120 mmHg at onset of exercise, even though MAP remains at 100 mm Hg = pressure error of 20 mmHg
- proof of concept that arterial baroreflex is reset upwards (vs what was the initial hypothesis?)
- intact aortic baroreceptors vs isolated and denerved aortic baroreceptors: what happens to a) arterial pressure b) HR and CO
and why?
1980s: ppl thought that baroreflex would shut down during exercise
a) INTACT: initial decrease in BP (bc TVK increases more than CO) –> than arterial pressure remains steady around 120 mmHg bc baroreceptors are reset
DENERVED: initial decrease in BP –> than increasing BP! extreme elevations due to intense vasoconstriction even in exercising muscles! = decrease TVK = increase MAP
*“resting” (bc in denerved, we set baroreceptor at a constant BP = no resetting)) carotid sinus pressure must have been interpreted centrally as a progressively increasing hypotensive stimulus (compared to increasing BP in muscles (i think)) –> with each workload/intensity dependant resetting of arterial baroreflex –> evidence for upwards resetting of baroreflex during exercise
vascular conductance is controlled by which 2 factors? explain
- SYMPATHETIC NERVOUS SYSTEM ACTIVITY
- increase in SNS constricts blood vessel and decreases conductance (vasoconstriction)
- decrease in SNS activity allows vessel to relax and increases conductance (vasodilation)
*increase/decrease in SNS = blanket response! –> acts overall in body! - LOCAL FACTORS
- associated with exercising muscle –> important during exercise!
- when vasocilator influences > vasoconstrictor influences, VK and BF increase
- sympatholysis (local attenuation of SNS mediated vasoconstriction)
what is sympatholysis?
local attenuation of SNS-mediated vasoconstriction –> important determinant of exercising muscle blood flow and O2 delivery
*2 forces at play in exercise: SNS vasoconstriction and local factor vasodilation
sympathetic restraint of skeletal MBF during submaximal exercise
- what happens to dogs when submaximal treadmill running? at increasing workloads? MAP, CO, TVK, HR
- VS when injected with smtg that inhibits MSNA mechanisms eliciting ____________
- as expected, as workload increased, progrssive increases in MAP, CO, TVK and HR occured!
- MSNA mechanisms elicit vasoconstriction –> if you block a-adrenergic receptors in exercising muscle –> removes sympathetic vasoconstrictor influence –> increase muscle VK and MBF!!!
does the sympathetic nervous system restrain vasodilation in exercising muscle?
CONCLUSION?
YES!
- experiment: if you blocked MSNA –> more vascular conductance bc less vasoconstriction!
- the extent of functional SNS vasoconstriction increases with exercise intensity
CONCLUSION: you need metabolites to accumulate locally in order to have vasodilation and increase blood flow! SNS alone during exercise will not do any good (bc only vasoconstricts) –> only time it does good, is telling baroreceptors to go up!
is microneurography good at quantifying MSNA at A)rest B)when hand is put in cold water C) continued cold water
- what is the thing we want?
A) at rest: beautiful MSNA signal
B) subject tenses up when hand is placed in water –> increase MSNA, vasoconstriction –> motor units appear (even if no exercise) –> reduced signal to noise ratio)
C) MSNA signal becomes impossible to analyze due to abundance of motor units in purple (filtered signal) –> imagine how exercise would look (NOT GOOD)
- we want a very good signal-to-noise ratio (SNR) form MSNA) + very little else (no activity from other neurons travelling in same nerve, including motor units!)
VS if vasoconstriction –> motor units are innervated = bad signals
4min isometric dorsiflexion of ankle + 6 min post-exercise ischemia (to isolate metaboreflex)
- what happened to MSNA to contracting muscle within 1 min of static exercise?
- what happened to MSNA to contracting muscle during post-exercise ischemia?
CONCLUSIONS (3)
- prompt increase in MSNA!
- post-exercise ischemia had no effect/reduction in MSNA in the contracting muscle/active limb vs increase MSNA in non-contracting muscle –> indicates LACK of role of metaboreflex in increase in MSNA in active limb (bc you would expect metabolites to increase MSNA)
- instead, MSNA parallels voluntary effort of exercise, implicating central command
CONCLUSION:
- central command is the primary mechanism responsible for increasing MSNA to contracting muscle
- the metaboreflex is not expressed in the contracting muscle
- MSNA can be controlled independently between limbs
implications of study showing that metaboreflex doesn’t contribute to increase in MSNA
- why is increase in sympathetic vasocontrictor drive important for non-contracting muscle (1) vs contracting muscle (2)
- for the first time, it was shown that MSNA to the contracting muscle increase/decrease/remains constant for duration of isometric voluntary contraction AND that what is NOT exhibited?
- increase in vasoconstriction to non-contracting muscle is important for regulation of systemic blood pressure - increase of sympathetic outflow to contracting muscle is important for limiting vasodilation and hyperemia during exercise
- MSNA to contracting muscle remains at constant level above rest + muscle metaboreflex is NOT exhibited in contracting muscle
SUMMARY of CV response to exercise
1. feedforward regulation (2): what does they do?
- graded to what? highly dependent on what?
2. feedback regulation (2) –> what do they do?
- FEEDFORWARD:
- central command and muscle mechanoreflex initiate “best guess” change in CO and peripheral vasoconstriction
- graded to exercise intensity + highly dependent on active muscle groups - FEEDBACK:
a) muscle metaboreflexes sens muscle metabolic stress –> evoke increases in CO + peripheral vasoconstriction to elevate arterial BP and attempt to improve muscle blood flow
b) baroreflexes sense MAP and are RESET to a higher operating BP with increasing exercise intensity –> baroreflexses retrains exercising muscle blood flow below that which would occur based on local vasodilatory influences on muscle vascular conductance
MAP regulation competes with what? which will dominate? potential compromise to what?
MAP regulation competes with local exercising muscle blood flow regulation
- MAP will dominate = potential compromise to muscle O2 delivery during exercise! implications for exercise tolerance/performance
