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14 Cards in this Set
- Front
- Back
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Muscle Chemoreflex
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Trapping metabolites in limb after exercise prevented normal recovery of MAP
no central command or mechanical activity of skeletal muscle MAP elevated as long as limb is occluded HR shows normal recovery, not due to chemoreflex Strength of chemoreflex related to mass of ischemic muscle Occlusion of resting muscle for up to 1 hour does not affect MAP |
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Exercise with Ischemia
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Exercising muscle made ischemic during & after isometric contractions
Partial recovery of MAP some other factors in addition to metabolites must increase MAP during contraction HR & MAP may be controlled differently |
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Group 3 & 4 Afferents in Chemoreflex
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Spinal cord lesion sensory neuropathy patients
Normal HR & MAP response to static ischemic contractions post exercising ischemic HR & MAP fully recovered Sensory loss does not affect ability to increase MAP during static contraction Sensory loss eliminates pressor response to ischemia after exercise Sensory loss does not affect HR response |
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Chemoreflex During Dynamic Exercise
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Dynamic arm exercise under free flow & ischemia
No increase in MSNA until 40 watts MSNA increases after 1-2 min of exercise, delay due to chemoreflesx Cannot account for increased MAP during exercise MSNA remains elevated during post exercise ischemia (not shown) Threshold at lowest workloads, takes large decrease in blood flow to activates a pressure raising reflex No threshold at highest workloads margin for a flow error is small takes small decrease in blood flow to activate a pressure raising reflex Chemoreflex not tonically active during mild dynamic exercise, activated only when blood flow is below critical level Chemoreflex is tonically active during heavy dynamic exercise any decrease in blood flow activates the reflex |
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Chemoreflex Stimulus Dynamic Exercise
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Increase in MAP occurred at higher levels of blood flow when arterial O2 content is reduced
Increase in MAP occurs at same level O2 delivery with normal & reduced arterial O2 content Suggests O2 delivery below some critical level activates the chemoreflex during dynamic exercise |
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MAP & HR Control
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Control
HR & MAP increase during both exercise conditions HR recovers during post exercise occlusion MAP remains elevated Atropine HR & MAP increase during both exercise conditions HR & MAP both remain elevated during post exercise occlusion |
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Chemoreflex Summary
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Muscle chemoreflex activated by a build up of metabolites within active skeletal muscle due to inadequate muscle blood flow
mismatch between muscle metabolism & blood flow During dynamic exercise chemoreflex appears to be most sensitive to changes (decreases) in oxygen delivery to the active muscle Chemoreflex appears to be able to increase muscle blood flow by as much as 50-75% Although the chemoreflex increases MSNA & MAP during dynamic exercise delay in activation of the reflex is too slow to account for the (almost immediate) increase in MSNA & MAP at the onset of dynamic exercise |
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Baroreflex & Dynamic Exercise
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At the onset of dynamic exercise the exercise pressor response is activated (increased HR, CO, MAP)
SNA increases when HR approaches 100 bpm (40% O2) |
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MAP Response: Dynamic Exercise
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Transition from seated rest to upright exercise
transient fall in MAP sustain increases slightly higher than rest Transition to higher workloads, no fall in MAP Transient fall in MAP thought to be stimulus to increase SNA & MAP during steady state exercise |
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Role of Baroreflex During Exercise
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Fall in MAP = increase in vascular conductance offset by increase in CO or no support from the baroreflex
Baroreflex supports the rise in MAP |
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MAP Increase During Exercise
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Any increase in MAP should be opposed by the baroreflex
Evidence suggests baroreflex is required to allow the rise in MAP Hypothesized that baroreflex is reset to a higher pressure defend higher MAP during exercise resting prevailing pressure perceived as hypotension baroreflex = stimulus to increase SNA to inactive regions Baroreflex also stabilized MAP during mild exercise Baroreflex will oppose further increase in MAP above operating point |
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Baroreflex Resetting During Exercise
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Similar HR & cO responses
Exaggerated MAP response with isolated carotid sinus Vascular conductance increases from rest to exercise at 0% but no further increase at higher workloads powerful vasoconstriction to active muscle & inactive regions Resting CSP perceived as extreme hypotension stepwise resetting of baroreflex in proportion to work rate No change in gain Large increase in RSNA (848%) if normal increase in MAP during exercise is prevented nitroglycerin: powerful vasodilator Upward shift to relationship between HR & MSNA to MAP |
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Chemoreflex & Baroreflex Interaction
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If vasoconstriction is primary regulation of MAP at maximal exercise the cartid sinus hypertension should result in hypotension & release of vasoconstriction
Opposite effects occur less effect of neck suction at highest levels of exercise Chemoreflex gain 50-75% Baroreflex gain 60-70% Following sino aortic denervation chemoreflex gain = 86%, increased by 2.5 fold Baroreflex can reduce the effect of chemoreflex on MAP by 60% |
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Overall Summary
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Gain of the baroreflex is unchanged during exercise
Baroreflex supports the increase in MAP at the onset of exercise due to resetting of the reflex to a higher operating point Baroreflex is responsible for maintaing a stable MAP during mild to moderate exercise The chemoreflex & baroreflex oppose each other during exercise The chemoreflex may be one mechanism to increase muscle blood flow during exercise, but only when muscle blood flow falls below a critical level O2 delivery appears to be the stimulus for the chemoreflex The baroreflex & chemoreflex must counteract mismatches between CO & vascular conductance & vasoconstrict active muscle to maintain MAP during sever dynamic exercise |
