8.1 - Exercise Pressor Reflex Flashcards
Discuss the alam and Smirk paper (1938+1937) regarding BP??
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
Discuss the alam and Smirk (1937+1938) papers!??
Same experimental design, with occlusion cuff to induce ischaemia (>SBP).
1.5 minutes of X2 calf raises
HR remained elevated until cuff deflated
Discuss Alam and Smirk (1937+1938) in regards to spinal cord lesion??
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.
Coote (1971) investigated the EPR in an animal model, what did he find?
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.
Coote repeated the 1971 experiment but also cut the dorsal roots, what happened??
This meant there was no sensory feedback
Results showed increased tension but no CV response
Discuss the animal experiment from McCloskey and Mitchell (1972)??
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
McCloskey and Mitchell (1972) repeated their experiment, but instead blocked the type III + IV afferents with local anaesthetic (lidocaine) what did they show?
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
What did Coote and Perez-Gonzalez (1970) state about muscle afferent fibre types??
That group I and II do not contribute to the CV response to exercise.
Discuss Adreani (1997)??
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
What did Kauffman and Hayes (2001) state from looking at their cat model??
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
What did Kauffman and Hayes (2002) state about the action potential response ??
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.
Discuss Pryor et al (1990) using a McArdles model to investigate EPR??
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.
Discuss the evidence for polymodal nature of afferents from Sinoway and Li (2002)??
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).
Discuss the quantity of the group III polymodal response (Hayes, 2005)???
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.
Discuss the group III polymodal response in man (Bell, 2005)??
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