11.1 Afferent Feedback + Disease Flashcards

1
Q

Discuss the methodology of Fadel (2003) who looked at mcArdles patients??

A

Conflicting evidence occurs that muscle acidosis is not a prerequisite for sympathoexcitation during exercise.
8 mcArdles and 24 control subjects.
Static handgrip ex performed - 2 mins of 33% or 45% of MVC
- 30% MVC to fatigue followed by PECO
Also non ex stimuli to MSNA :- cold pressor test (2min) to activate the cutaneous afferents, - valsava manouver to deactivate the arterial baroreceptors

Measured the CV response (BR and BP) and MSNA (peroneal nerve)

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2
Q

Discuss Fadel’s (2003) results??

A

At rest:- MSNA was 29% higher in patients than controls (significant). The CV response was similar between groups. But considerable variation in MSNA response in controls (28%-478%).

Also showed intensity dependent increases in MSNA, MAP and HR in controls. Only the HR response was intensity dependent in mcArdles patients.

30%MVC to fatigue was the same in both groups.
Large and progressive increases in MSNA in controls were seen that were 7x greater than that in patients

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3
Q

Discuss the summary of Fadel (2003) this needs reviewing.

A

Attenuated MSNA response in patients compared to controls can be seen as shown by burst/min being less for 2min 33%,2min 45% and 30%MVC time to fatigue.

Attenuated BP response to static handgrip in patients compared to controls, HR responses are identical.
MSNA responses to the cold pressor test and valsava were similar in both groups.
Concluded that activation of glycogenolytic pathways is required for metaboreflex-mediated sympathoexcitation during static exercise.

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4
Q

Disucss the methodology of Sterns (1991)??

A

Had 8 controls, 9 CHF patients.
It’s known fanfare resting SNS activity is increased in CHF patients, but it’s ambiguous if SNS activity increases in CHF patients are larger during exercise.

Static handgrip exercise - 30% MVC for 2 mins then PECO.
Measured CV response (BP, HR), MSNA (pn) and pH with NMRS

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5
Q

Disucss the results of Sterns (1991)??

A

Showed MSNA responses during contraction were similar, attenuation in MSNA responses following PECO in the heart failure subjects (15%⬆️CHF compared to 57%⬆️in controls).

The cold pressor test demonstrated normal MSNA in CHF patients (141% vs 215%⬆️)
The NMRS indicated an attenuated EPR response in CHF wasn’t due to reduced H+ production
Concluded generally that skeletal muscle metaboloreceptor responses were impaired in CHF

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6
Q

Discuss Sinoway and Li (2005)??

A

Looked at MSNA responses to a bout of static handgrip for 2 min. The ⬆️ in MSNA at end grip was fairly similar in both groups, however during PHG-CA (circulatory arrest), MSNA remained elevated in controls and fell towards baseline in heart failure subjects.

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7
Q

Discuss the methodology of Carrington (2001) when he looked at AF and CC in CHF???

A

Wanted to examine the role of muscle afferent activity and CC in the CV response to isometric plantar flexion in CHF patients.
Stable CHF patients with age arched controls.
Had electrically invoked (AF only) and voluntary exercise (AF+CC) with each having 2 min contraction @30%MVC with 2 mins of PECO.

Took measures of BP + HR.

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8
Q

Discuss the results of Carrington (2001) after they were compared to the non-age matched controls from prior experiment of Bull, 1989????

A

In electrically evoked contraction: CHF had smaller mean increases of SBP and DBP than controls - not the case during PECO.

In voluntary contraction: control subjects had a greater mean increase in SBP than CHF, again not the case during PECO, suggests role of CC.

Greater mean SBP and DBP increases during voluntary than evoked contraction between the groups - suggests CHF patients may have a relatively desensitised muscle mechanoreceptor reflex.
Results showed that muscle afferent feedback to the pressor response from the triceps surae is low in this age group - look up what age group (both groups).

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9
Q

Very briefly, discuss Piepoli et al (1996) muscle hypothesis of CHF??

A

An initially reduction in LV function activates catabolic and reduces anabolic factors that collectively cause skeletal myopathy.

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10
Q

Discuss the methods of Piepoli et al (1996) who looked at CHF and training???

A

Wanted to investigate afferent sensitivity to skeletal muscle work in CHF and training influences on their activity.
60yr old participants.

Protocol consisted of 2-3 daily sessions for 6 weeks, squeezed hand dynamometer as tightly as possible for 10 seconds (10 reps of this). Followed this by 40 squeezes per min for 5 mins.

The pre and post tests were : MVC/40 contractions per minute @50% MVC/same but with PECO

Took arterial blood before, at peak effort and at 3+8 mins of recovery, also analysed potassium, CO2, oxygen and pH

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11
Q

Discuss the baseline exercise to exhaustion results of Piepoli (1996) - massive study so going to have to break it down

A

The ventilation response was higher for CHF (for handgrip with circulatory occlusion group) and didn’t drop during PECO.

When looking at CHF patients at baseline and post training, longer duration of forearm exercise post training occurs (8-4.8 mins), also showed higher peak work rates (78.5-64.9kg)

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12
Q

Discuss the general results of Piepoli (1996) and their conclusions???

A

In both groups, conditioning reduced systolic and diastolic pressure, Ve, VO2, VCO2 and leg vascular resistance with increased blood flow.

Further, an enhanced contribution of the ergo-receptors to the autonomic, haemodynamic and respiratory responses to exercise in CHF at baseline during PECO.
Training benefits can be seen in both groups. With training, the enhanced ergoreflex seen in CHF during PECOwas bought closer to normal via a reduction of EPR excitation

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13
Q

Disucss the work on SNA and CHF (Silber, 1998)??

A

Exercise induced increases in MSNA and SNA was the same during both groups but during PECO, it remained elevated in CHF.

Results suggestion muscle metaboreflex activation
The mechanisms and distribution of sympathetic outflow during exercise appear to be different from normal

NMRS during RHG demonstrated significant muscle acidosis and Pi accumulation in CHF but not controls.
In CHF patients , RHG exercise leads to premature fatigue and accumulation of muscle metabolites

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14
Q

Disucss the methodology of Momen et al (2004) who looked at renal blood flow???

A

Wanted to look at the relationship between static handgrip and renal bf velocity in CHF patients

3 protocols: 1) 40% MVC to exhaustion followed by 2 min PECO

2) 15 seconds of HG at 10,30,50 + 70% MVC, with 1 min rest between each
3) involuntary biceps contraction - 15-30% MVC was sustained for ~15 seconds

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15
Q

Discuss the results of Momen et al (2004)???

A

Protocol 1: a greater RBV in CHF , the reduction in RBV early in HG more prominent during the early phases of contraction. During PHG-CA, RBV responses were similar between the two groups.

Protocol 2: greater reductions in RBV in CHF than controls

Protocol 3: involuntary and voluntary biceps contractions evoked RVR in ………

Increases in RVR were similar during biceps contractions 19.5% (involuntary), 25.6% (voluntary)

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16
Q

Provide a discussion of Momen et al (2004)??

A

CHF patients have greater renal blood flow reductions during the early phase of static exercise. Provides evidence that the muscle mechanoreflex (not metaboreflex) plays a crucial role in regulating renal blood flow during exercise in CHF.

17
Q

What did Sinoway and Li (2005) say about muscle metaboreflex??

A

Unlikely the muscle metaboreflex played an important role in eliciting the exaggerated renal vasoconstrictor response to exercise in CHF.

Also stated this was seen early in exercise, and no group difference occurs during PECO.

18
Q

What did Zucker et al (2004) state??

A

Looked at radiographs of rabbit medulla showing AT1 binding in normal rabbits and CHF rabbits.

Showed enhanced binding is observed in the NTS and RVLM.

19
Q

What did Middlekauff and Sinoway (2007) argue?

A

They believed that increased mechanoreceptor/metaboreceptor stimulation explains the exaggerated EPR seen in heart failure.
Also discussed the CHF muscle hypothesis. E.g. ‘Which sensory fibres are responsible for the reflex abnormalities during exercise??’