scholarly journals Impact of Group III/IV Afferent Feedback on Breathing Pattern During Incremental Cycling Exercise to Peak Capacity in Patients with COPD

Author(s):  
M. Martin ◽  
M. Frenette ◽  
J.S. Bussières ◽  
F. Maltais
2015 ◽  
Vol 100 (3) ◽  
pp. 302-311 ◽  
Author(s):  
Thales C. Barbosa ◽  
Igor A. Fernandes ◽  
Nisval Magalhães-Jr ◽  
Ismar L. Cavalcanti ◽  
Niels H. Secher ◽  
...  

1981 ◽  
Vol 59 (7) ◽  
pp. 700-706 ◽  
Author(s):  
C. von Euler

Current concepts of the basic neural control system and its modulation by afferent inputs are reviewed. It is emphasized that, in analogy with locomotion, the central pattern generator (CPG) for automatic metabolic respiration does not depend on any afferent feedback from receptors sensitive to the movements of the "pump," or the streams of pumped air, for its production of a rhythmic motor output provided the CPG receives some "drive" inputs above threshold and adequate bias.The operation of a variety of reflexes and feedback loops is of fundamental importance, however, for adapting the breathing pattern to the varying requirements for gas exchange and to the many behavioural, nonmetabolic demands on the breathing apparatus which are competing with its primary metabolic control functions. The presentation is focussed also on available evidence that the respiratory CPG exerts powerful modulations on the transmission in these reflex pathways controlling the pattern of breathing and adjusting it to the various metabolic and behavioural demands. Mechanisms for "gating," "phasic gain changes," and "phase-dependent reflex reversal" are exemplified.


2018 ◽  
Vol 596 (19) ◽  
pp. 4789-4801 ◽  
Author(s):  
Simranjit K. Sidhu ◽  
Joshua C. Weavil ◽  
Taylor S. Thurston ◽  
Dorothea Rosenberger ◽  
Jacob E. Jessop ◽  
...  

2017 ◽  
Vol 128 (1) ◽  
pp. 44-55 ◽  
Author(s):  
Simranjit K. Sidhu ◽  
Joshua C. Weavil ◽  
Tyler S. Mangum ◽  
Jacob E. Jessop ◽  
Russell S. Richardson ◽  
...  

2014 ◽  
Vol 306 (12) ◽  
pp. R934-R940 ◽  
Author(s):  
Matthew J. Rossman ◽  
Ryan S. Garten ◽  
Massimo Venturelli ◽  
Markus Amann ◽  
Russell S. Richardson

Greater peripheral quadriceps fatigue at the voluntary termination of single-leg knee-extensor exercise (KE), compared with whole-body cycling, has been attributed to confining group III and IV skeletal muscle afferent feedback to a small muscle mass, enabling the central nervous system (CNS) to tolerate greater peripheral fatigue. However, as task specificity and vastly differing systemic challenges may have complicated this interpretation, eight males were studied during constant workload trials to exhaustion at 85% of peak workload during single-leg and double-leg KE. It was hypothesized that because of the smaller muscle mass engaged during single-leg KE, a greater magnitude of peripheral quadriceps fatigue would be present at exhaustion. Vastus lateralis integrated electromyogram (iEMG) signal relative to the first minute of exercise, preexercise to postexercise maximal voluntary contractions (MVCs) of the quadriceps, and twitch-force evoked by supramaximal magnetic femoral nerve stimulation (Qtw,pot) quantified peripheral quadriceps fatigue. Trials performed with single-leg KE (8.1 ± 1.2 min; 45 ± 4 W) resulted in significantly greater peripheral quadriceps fatigue than double-leg KE (10 ± 1.3 min; 83 ± 7 W), as documented by changes in the iEMG signal (147 ± 24 vs. 85 ± 13%), MVC (−25 ± 3 vs. −12 ± 3%), and Qtw,pot (−44 ± 6 vs. −33 ± 7%), for single-leg and double-leg KE, respectively. Therefore, avoiding concerns over task specificity and cardiorespiratory limitations, this study reveals that a reduction in muscle mass permits the development of greater peripheral muscle fatigue and supports the concept that the CNS tolerates a greater magnitude of peripheral fatigue when the source of group III/IV afferent feedback is limited to a small muscle mass.


2020 ◽  
Vol 27 (17) ◽  
pp. 1862-1872
Author(s):  
Luca Angius ◽  
Antonio Crisafulli

Exercise intolerance and early fatiguability are hallmark symptoms of chronic heart failure. While the malfunction of the heart is certainly the leading cause of chronic heart failure, the patho-physiological mechanisms of exercise intolerance in these patients are more complex, multifactorial and only partially understood. Some evidence points towards a potential role of an exaggerated afferent feedback from group III/IV muscle afferents in the genesis of these symptoms. Overactivity of feedback from these muscle afferents may cause exercise intolerance with a double action: by inducing cardiovascular dysregulation, by reducing motor output and by facilitating the development of central and peripheral fatigue during exercise. Importantly, physical inactivity appears to affect the progression of the syndrome negatively, while physical training can partially counteract this condition. In the present review, the role played by group III/IV afferent feedback in cardiovascular regulation during exercise and exercise-induced muscle fatigue of healthy people and their potential role in inducing exercise intolerance in chronic heart failure patients will be summarised.


2020 ◽  
Vol 48 (4) ◽  
pp. 209-216
Author(s):  
Markus Amann ◽  
Hsuan-Yu Wan ◽  
Taylor S. Thurston ◽  
Vincent P. Georgescu ◽  
Joshua C. Weavil

2010 ◽  
Vol 109 (4) ◽  
pp. 966-976 ◽  
Author(s):  
Markus Amann ◽  
Gregory M. Blain ◽  
Lester T. Proctor ◽  
Joshua J. Sebranek ◽  
David F. Pegelow ◽  
...  

We investigated the role of somatosensory feedback on cardioventilatory responses to rhythmic exercise in five men. In a double-blind, placebo-controlled design, subjects performed the same leg cycling exercise (50/100/150/325 ± 19 W, 3 min each) under placebo conditions (interspinous saline, L3–L4) and with lumbar intrathecal fentanyl impairing central projection of spinal opioid receptor-sensitive muscle afferents. Quadriceps strength was similar before and after fentanyl administration. To evaluate whether a cephalad migration of fentanyl affected cardioventilatory control centers in the brain stem, we compared resting ventilatory responses to hypercapnia (HCVR) and cardioventilatory responses to arm vs. leg cycling exercise after each injection. Similar HCVR and minor effects of fentanyl on cardioventilatory responses to arm exercise excluded direct medullary effects of fentanyl. Central command during leg exercise was estimated via quadriceps electromyogram. No differences between conditions were found in resting heart rate (HR), ventilation [minute ventilation (V̇e)], or mean arterial pressure (MAP). Quadriceps electromyogram, O2 consumption (V̇o2), and plasma lactate were similar in both conditions at the four steady-state workloads. Compared with placebo, a substantial hypoventilation during fentanyl exercise was indicated by the 8–17% reduction in V̇e/CO2 production (V̇co2) secondary to a reduced breathing frequency, leading to average increases of 4–7 Torr in end-tidal Pco2 ( P < 0.001) and a reduced hemoglobin saturation (−3 ± 1%; P < 0.05) at the heaviest workload (∼90% maximal V̇o2) with fentanyl. HR was reduced 2–8%, MAP 8–13%, and ratings of perceived exertion by 13% during fentanyl vs. placebo exercise ( P < 0.05). These findings demonstrate the essential contribution of muscle afferent feedback to the ventilatory, cardiovascular, and perceptual responses to rhythmic exercise in humans, even in the presence of unaltered contributions from other major inputs to cardioventilatory control.


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