10.1 - Afferent Feedback And Muscle Properties Flashcards
Discuss the methods of Seals (1991)??
Investigated SNS activation in trained and untrained p’s during acute stress.
Groups were rest/LBNP/ 30%MVC isometric handgrip/ cold pressor test
Measured SNS activity by microneurography of peroneal nerve, measured CV response (HR/MAP)
Discuss the results and their implications from Seals (1991)???
The magnitude of SNS increases between groups from rest to acute stress
A larger SBP drop in untrained vs trained at -10,-15 and -20mmhg during LBNP condition.
During the cold pressor test, athletes had a higher delta change in MSNA compared to untrained.
Large inter-subject variability in MSNA response to acute stress in both groups.
No difference in MSNA at rest
Training induced changes in the vasoconstrictor responses to stimulated orthostasis (LBNP) are not by SNS… therefore by neurotransmitter release or its vascular effects.
Discuss the methodology of Somers (1992)???
Investigated the response of muscle chemoreflex stimulation during isometric exercise post training (5 sessions a week for 6 weeks - 30% MVC until fatigue, with sham training in opposite hand (<0.5kg).
Pre and post training testing: 2 minutes @ 33%MVC, 2 mins PECO, max work to fatigue with measures of MSNA, HR, BP.
Discuss the results of Somers (1992)??
Trained saw a 1,146% ⬆️ in max work to fatigue, untrained only saw a 40% increase.
Showed training attenuated the SNA increases by 73%(111% down to 38% after training).
There was no training effects for HR and BP during isometric handgrip
Further, there was a reduced SNA response to post-ex forearm ischaemia in endurance trained arm.
Concluded, endurance training decreases muscle chemoreflex stimulation during isometric exercise and attenuates the SNA response to IHG.
Discuss the work of White and Carrington (1993)???
Looked at 2 minutes of electrically evoked contractions in the ankle plantar flexor and elbow flexors old and young individuals.
Showed biceps have less of an age related decline in muscle properties.
No difference in the HR response
Elbow flexor contraction elevated in increase in SBP in old participants (rigid arterial tree? Occurs with age)
The TPT: in ankle (128ms OLD to 112ms Y -14%), in elbow (66ms O to 71ms Y +8%)
In ankle plantar flexors a lower diastolic BP response in old relative to young , similar in elbow flexors - perhaps influenced by the relative fast twitch fiber content
Discuss Carrington (1995)??
Wanted to investigate the relationship between the EPR to electrically evoked isometric ankle plantar flexion
- looked at isomyosin composition in LG and SOL in young and old.
There was no association between HR or change in SBP response and the fast isomyosin composition
The change in DBP was association with the fast isomyosin composition of both muscles
Showed a negative relationship between TPT and change in DBP, with older P’s taking longer to reach peak twitch tension .
This suggests the magnitude of the EPR to isometric exercise and the fast isomyosin content of the active muscle are related.
Discuss the methods of Carrington (1999)??
Wanted to investigate the EPR repose to athletic training status, active muscle contractile properties, plantar flexion, electrically invoked and voluntary contractions, 2 mins @30%MVC.
Participants were sprint trained, endurance trained and untrained.
Measured the CV response and time to peak tension
Discuss the results of Carrington (1999)???
Results showed the sprint group were significantly quicker than the distance group, for voluntary MVC, evoked MVC and for time to peak tension.
For voluntary and evoked contractions: the average change in cv response was the same for all groups.
When the sprint forum was divided into 400m and 100m/200m, the 100m athletes showed significant increases of 12mmhg for DBP, 400m saw increases of 19mmhg.
Using the regression data from CARRINGTON (1995) what did he conclude in 1999????
Linked DBP change at the end of test and TPT in untrained subjects, to predict results in current participants.
DBP change and TPT => r=0.78
Some aspect of sprint training , but not endurance training, attenuated the EPR. For sprint 1, the increase in DBP was significantly less.