Lecture 12: CV response to exercise 2 Flashcards
explain the hemodynamic response to exercise.
1. onset of exercise
2. at around 12sec into exercise
3. over the next 1-2min
- ONSET OF EXERCISE:
MAP decreases initially! –> bc of imbalance btw CO and TVK (or SVR), where immediate increase in TVK (or decrease in SVR) (bc more arterial outflow) is greater than the increase in CO. THUS, both arterial blood volume and MAP decrease
- immediate increase in CO due to immediate increase in HR through parasympathetic withdrawal, with little or no change in CV - 12SEC INTO EXERCISE
- MAP begins to increase, indicating that CO (arterial inflow) is greater than TVK (arterial outflow).
- increases in CO are due to SNS-mediated increases in HR and SV - OVER 1-2min:
- MAP increases to a new steady-state over next 1-2min
- exercising muscle VK (conductance) and blood flow continue to increase, while VK and blood flow to non-exercising tissues decrease
* increase in CO must be greater than increase in muscle VK in order for MAP to increase
what are the 2 feedforward mechanisms for MAP regulation during exercise?
- CENTRAL COMMAND:
- MUSCLE MECHANORECEPTORS:
CENTRAL COMMAND
- where does it originate?
- does what?
- contributes to what?
- CENTRAL COMMAND:
- originates in higher brain centers (motor cortex) where motor command originates
- initiates parasympathetic withdrawal to rapidly increase HR (up to 100 bpm)
- “Resets” arterial baroreflex –> to match exercising BP
MUSCLE MECHANORECEPTORS:
- where does it originate?
- senses what?
- does what?
- contributes to what?
- MUSCLE MECHANORECEPTORS:
- type III myelinated afferents = very fast bc need rapid response to exercise
- sense mechanical (stretch and compression) effects of muscle contraction
- initiates parasympathetic withdrawal to rapidly increase HR (up to 100 bpm)
- contributes to “resetting” of the arterial baroreflex
how to we know that there is a central command contribution to MAP?
- in an attempted forearm contraction in completely paralyzed muscle:
- MAP and HR increase immediately upon attempted contractions
- magnitude of increase in HR and MAP is proportional to attempted contraction intensity
how to we know that there is a muscle mechanoreceptor contribution to MAP?
- took away central command in animal model
- MAP increases immediately upon passive stretch of muscle due to increase in HR and therefore CO –> passive stretch stimulated mechanoreceptors!
- response is abolished by cutting afferent nerves returning from muscle = proves that the mechanoreceptors had smtg to do with MAP response
what are the 2 feedback mechanisms for MAP regulation during exercise?
- MUSCLE METABORECEPTORS
- BAROREFLEX: receptors and afferents
which type of efferent nerves kick in first during exercise + mostly used in high intensity?
vs what does the other type do?
- type III myelinated = fast, kicks in first, high intensity
- type IV unmyelinated –> slow, sustained exercise
MUSCLE METABORECEPTORS
- where does it originate?
- senses what?
- what does it do?
- MUSCLE METABORECEPTORS
- type III (myelinated) and IV (unmyelinated) afferents
- sense metabolic bi-productions of muscle contraction including H+, La-, arachidonic acid, adenosine…
- increases sympathetic vasoconstrictor outflow (vasoconstriction everywhere! not local response).
BAROREFLEX - RECEPTOR AND AFFERENTS
- what is a baroreceptor?
- senses what?
- what does it do? How? Explain inhibitory reflex
BAROREFLEX - RECEPTOR AND AFFERENTS
- baroreceptors are stretch receptors sensing distension in aorta, carotid bodies and heart (aortic arch) due to changes in transmural pressure (Pinside - Poutside)
- increase transmural pressure = increase MAP, and vice versa
- once receptors are activated –> signals CNS through afferent nerves
- “inhibitory” reflex (in normal situation –> increases in baroreceptor afferent firing (ie increased MAP) = increases PNS and decrease SNS activity, which decrease HR and CO and increase TVK (conductance), which decreases MAP. opposite is true
how to we know that there is a muscle metaboreflex contribution to MAP response to exercise?
- anesthetized cats
- recorded what –> what happened in the 2 scenarios?
- anesthetized cats
- recorded directly group III and IV afferents from triceps surae muscles:
a) during static contraction: increase impulses/neural discharge
b) injection of metabolic products of muscular contraction (lactic acid injection into femoral artery) –> causes rapid firing of impulses following lactic acid injection
how to we know that there is a muscle mechano- and metaboreceptor contribution to CV response to rhythmic exercise in humans?
- in humans
- what happened in the 2 scenarios
- takeaway?
- study in humans that had lumbar injection of fentanyl which inhibited feedback from lower limb muscle group III/IV muscle sensory afferent nerves
a) no influence of afferent blockage on central or peripheral hemodynamics at rest (control vs fentanyl both same)
b) throughout exercise with afferent blockage: CO was attenuated (secondary to decrease in HR and SV) + substantial reduction in MAP
TAKEAWAY: contribution of continuous muscle afferent feedback is essential in ensuring appropriate hemodynamic (and ultimately metabolic) response to exercise in humans
explain the arterial baroreflex feedback loop (schéma)
2 steps + 3 results ish
- aortic arch receptors + carotid sinus receptors sense blood pressure –> activates baroreflex afferents innervation –> go to brain stem
- brain stem = central command –> can activate/decrease PNS and SNS activity
a) PNS on heart: Acetylcholine
b) SNS on heart: norepinephrine
c) SNS on blood vessels: Norepinephrine
what is the arterial baroreflex response to hypotension?
3 big steps + 2 separate pathway in between ish
- decrease MAP = error signal
- decrease baroreceptor firing rate –> CV control center (brainstem senses it)
- brainstem will A) increase sympathetic vasomotor outflow and B) decrease parasympathetic outflow
A) increase SNS = increase NE released –> onto a-adrenergic receptors
i) acts on arteriolar smooth muscle = vasoconstriction = decrease total vascular conductance
ii) increases left ventricular contractility = increase CO
iii) acts on SA node = increase HR = increase CO
B) decrease PSNS = decrease Ach released (muscarinic receptors) –> acts on SA node –> increases HR = increase CO
- decrease total vascular conductance + increase CO –> increase MAP –> negative feedback –> normal baroreceptor firing rate
what are the receptors of Ach and NE?
- on which organs fo NE and ACh act on?
NE:
- a-adrenergic receptors:
- peripheral arteries and heart
ACh:
- muscarinic receptors
- acts on the heart
