8.1 - Exercise Pressor Reflex Flashcards

1
Q

Discuss the alam and Smirk paper (1938+1937) regarding BP??

A

After the handgrip exercise, blood pressure remained elevated until the cuff is deflated.
The reflex response here is due to the accumulation of metabolites produced by exercise

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2
Q

Discuss the alam and Smirk (1937+1938) papers!??

A

Same experimental design, with occlusion cuff to induce ischaemia (>SBP).
1.5 minutes of X2 calf raises
HR remained elevated until cuff deflated

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3
Q

Discuss Alam and Smirk (1937+1938) in regards to spinal cord lesion??

A

The participant has the same muscular power in both legs, with no afferents feedback in the insensitive leg.
1.5 minutes of calf raises - 1 set in insensitive leg, 1 set in normal leg.
BP raised in both legs during exercise (role of CC?? - as no afferent feedback)
- in PECO, BP drops in the insensitive leg, and was sustained in the normal leg.

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4
Q

Coote (1971) investigated the EPR in an animal model, what did he find?

A

Cut the ventral roots (motor nerves) of L7+S1 and connected them to stimulating electrodes.

Therefore no CC but was afferent feedback
The electrodes were stimulated and muscle tension and cv response was measured - the results showed increased tension, HR and MAP.

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5
Q

Coote repeated the 1971 experiment but also cut the dorsal roots, what happened??

A

This meant there was no sensory feedback

Results showed increased tension but no CV response

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6
Q

Discuss the animal experiment from McCloskey and Mitchell (1972)??

A

Induced a muscle contraction and recorded the CV response
Put a direct current anodal block (think it was dorsal.) on group I + II fibres (so no feedback).

Repeated contractions showed no change in CV response , which provides evidence that type I+II afferents do not contribute to the CV response

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7
Q

McCloskey and Mitchell (1972) repeated their experiment, but instead blocked the type III + IV afferents with local anaesthetic (lidocaine) what did they show?

A

Showed no CV response to the induced muscular contraction . The stimulation and recording sites prove the efficacy of pharmalogical blocks
Also showed no BP response to the induced contraction -> an extended BP response during occlusion

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8
Q

What did Coote and Perez-Gonzalez (1970) state about muscle afferent fibre types??

A

That group I and II do not contribute to the CV response to exercise.

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9
Q

Discuss Adreani (1997)??

A

Looked at decerebrate cats and stimulated either the hypothalamic or mesenphalic locomotor regions (MLR) and induced locomotion - with conduction velocity of 20m/s.
- the group 3 afferents discharged in sync with muscle contraction

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10
Q

What did Kauffman and Hayes (2001) state from looking at their cat model??

A

They blocked the group III mechanoreceptor discharge with galdolinium, injected into the arterial supply of the contracting muscles.

  • this resulted in a reduction in the ex-induced CV response (⬇️MAP⬇️HR) for both a static contraction (mech and metabolic stimulus) and for a tendon stretch (mechanical stimulus)
  • the ventilation response was only greater in the first 5s in static contraction
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11
Q

What did Kauffman and Hayes (2002) state about the action potential response ??

A

Showed the action potential response of group III afferents was abolished by galdolinium , results also showed no change in the firing rates of group IV afferents.

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12
Q

Discuss Pryor et al (1990) using a McArdles model to investigate EPR??

A

Had participants perform static handgrip contractions
Results showed myophosphorylase deficiency led to no increase in MSNA activity , an attenuated BP response and a similar HR response.

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13
Q

Discuss the evidence for polymodal nature of afferents from Sinoway and Li (2002)??

A

Looked at decerebrate cats by performing a 2kg muscle stretch in the triceps surface - then electrical stimulation of the L7/S1 roots.
Provided a femoral artery injection with either saline/ATP/P2X Receptor agonist/P2X receptor blockade.

The P2X antagonist PPADS reduces the effect of ATP by 78%.
Worth noting the nerve ending location is important - the interstitial space close to lymphatics and blood vessels (polymodal), close to collagen (mechanically sensitive).

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14
Q

Discuss the quantity of the group III polymodal response (Hayes, 2005)???

A

Used decerebrate cat:- tendon stretch (just mechanic), static contraction (mechanical and metabolic).
Afferent conduction velocity was measured at the dorsal root (30 group III, 11 group IV).

In static contraction - in group III -> 60% response, group IV -> 73% response
In tendon stretch - in group III -> 43% response, group IV -> 27% response
Of the group III that responded to static contraction ~40% responded to both.

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15
Q

Discuss the group III polymodal response in man (Bell, 2005)??

A

Subjects performed isometric plantar flexion at 20-80% MVC.
Thigh cuff occlusion occurred - at 60s PECO, the calf cuff is inflated by a compression stimulus -> a constant stimulus should elicit a constant CV response.

The mechanical reflex influenced by local muscular metabolic conditions - led to higher BP to greater preceding exercise intensity

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16
Q

What’s the background to the work of Hayes (2007)?

A

lactic acid stimulates acid sensing ion channel (ASIC) - and is blocked by amiloride.
Capsaicin stimulates the TRPV1.

17
Q

Discuss the methods and findings of Hayes (2007)??

A

Wanted to investigate dosages of amiloride in decerebrate cats.
Provided static contraction or tendon stretch to arterial injections of LA and capsaicin.

Found that 0.5ug/kg amiloride attenuate the pressor response to LA, but not to capsaicin or to tendon strength. Also found amiloride blocked the group III response to lactic acid and showed an attenuated response to tendon stretch and static contraction

Low dose amiloride did not attenuate response of group III afferents to the tendon stretch
Low dose amiloride blocked group IV response to lactic acid and static contraction - evidence that lactic acid via ASIC contributes to the EPR.

18
Q

Koba et al (2011) looked at the metabolic by products of contraction in decerebrate rats, what did he find??

A

Looked at TRPA1 - which is stimulated by metabolic by-products of contraction (AA metabolites, bradykinin) and investigated RSNA.
Provided injection of either a TRPA1 agonist or TRPA1 antagonist.

Data showed TRPA1 stimulation increases RSNA, blockade of TRPA1 attenuates RSNA during contractions ~10-30 seconds.

Lactic acid does not stimulate TRPA1 (capsaicin does)
TRPA1 stimulation via contraction by-products contributes to the EPR.

19
Q

Kindig (2006) looked at ATP in decerebrate cats, what did they find ??

A

ATP activates group III and IV p2 receptors. Wanted to investigate whether PPAD’s (p2 receptor antagonist) attenuates the EPR to post-contraction circulatory occlusion.
Had a static contraction looking at 23 group III afferents and 17 group IV afferents (In triceps surae).
Results showed when the P2 receptor was blocked with PPADS, there was an attenuated response to both group III and IV afferents to static contraction (freely perfused and circulation occluded).
PPADS prevented the responses of group IV afferents to post-contraction circulatory occlusion

20
Q

Knowing that P2 receptors invoke the EPR, what did Cui (2011) find???

A

Looked at the p2 receptor in man and measured BP, HR and MSNA. Provided a P2 antagonist (pyroxidine) or saline and had participants perform a static isometric handgrip (30% MVC) to failure.

Results showed after the pyroxidine, MSNA and MAP responses during the last minute of handgrip were significantly less than that in the pre-pyroxidine trial.
There was no difference in the MSNA response to handgrip task, also showed that MSNA and MAP reponses to PECO after pyroxidine were significantly less than in the pre-infusion trial.

21
Q

What did Cui (2011) conclude??

A

P2 receptor antagonism was associated with attenuated MSNA and BP.
- no difference in RPE and HR
- a cold pressor test invoked the same MSNA and blood pressure response for saline and pyridoxine infusion
All provides evidence that P2 receptors are involved in EPR in man.