Reflex actions of muscle afferents on fusimotor innervation in decerebrated cats: an assessment of beta contributions

1985 ◽  
Vol 59 (2) ◽  
Author(s):  
S.E. Grill ◽  
W.Z. Rymer
Keyword(s):  
Muscle Afferents ◽  
Fusimotor Innervation

Contribution of Muscle Afferents to the Hemodynamic, Autonomic, and Ventilatory Responses to Exercise in Patients With Chronic Heart Failure

Circulation ◽  
1996 ◽  
Vol 93 (5) ◽  
pp. 940-952 ◽  
Author(s):  
Massimo Piepoli ◽  
Andrew L. Clark ◽  
Maurizio Volterrani ◽  
Stamatis Adamopoulos ◽  
Peter Sleight ◽  
...  
Keyword(s):  
Heart Failure ◽  
Chronic Heart Failure ◽  
Muscle Afferents ◽  
Ventilatory Responses

Ventilatory and hyperkalemic responses to incremental exercise after propranolol treatment

1994 ◽  
Vol 77 (4) ◽  
pp. 1907-1912 ◽  
Author(s):  
D. A. Schneider ◽  
M. T. McEniery ◽  
C. Solomon ◽  
J. Jurimae ◽  
M. S. Wehr
Keyword(s):  
Minute Ventilation ◽  
Plasma Potassium ◽  
Muscle Afferents ◽  
Incremental Exercise ◽  
Co2 Production ◽  
Beta Blockade ◽  
Adrenergic Blockade ◽  
Propranolol Treatment ◽  
Positive Correlations ◽  
And Control

The purpose of the present study was to examine the relationship of plasma potassium (K+) and minute ventilation (VE) during incremental cycling (20 W/2 min) under conditions of beta-adrenergic blockade (80 mg of propranolol) and placebo in six untrained male subjects. No significant differences existed between treatments in O2 uptake, CO2 production, blood lactate, pH, or VE during the submaximal work stages of incremental exercise common to both treatments (20–220 W). During exercise with beta-blockade, plasma K+ concentrations were found to be significantly elevated compared with control levels at every work stage except 20 W. Significant positive correlations between VE and plasma K+ were found during both beta-blockade (r = 0.99) and control conditions (r = 1.00). Although the high correlation between VE and K+ was not altered with beta-blockade, propranolol treatment resulted in a significant reduction in the slope of this relationship during incremental exercise (P < 0.01). These findings suggest that 1) beta-blockade decreases the VE-K+ relationship observed during exercise and 2) K+ stimulation of muscle afferents is not an important signal in the control of exercise ventilation.

Effects of muscle afferents on brain stem reticular and vestibular units

1971 ◽  
Vol 25 (1) ◽  
pp. 179-183 ◽  
Author(s):  
C.D. Barnes ◽  
O. Pompeiano
Keyword(s):  
Brain Stem ◽  
Muscle Afferents

scholarly journals Group III and IV muscle afferents differentially affect the motor cortex and motoneurones in humans

2008 ◽  
Vol 586 (5) ◽  
pp. 1277-1289 ◽  
Author(s):  
P. G. Martin ◽  
N. Weerakkody ◽  
S. C. Gandevia ◽  
J. L. Taylor
Keyword(s):  
Motor Cortex ◽  
Muscle Afferents ◽  
Group Iii

Reflex control of the circulation during exercise: chemoreflexes and mechanoreflexes

1990 ◽  
Vol 69 (2) ◽  
pp. 407-418 ◽  
Author(s):  
L. B. Rowell ◽  
D. S. O'Leary
Keyword(s):  
Blood Flow ◽  
Muscle Blood Flow ◽  
Nervous Activity ◽  
Isometric Exercise ◽  
Muscle Afferents ◽  
Operating Point ◽  
Central Command ◽  
Vascular Conductance ◽  
Muscle Chemoreflex ◽  
Vagal Withdrawal

The overall scheme for control is as follows: central command sets basic patterns of cardiovascular effector activity, which is modulated via muscle chemo- and mechanoreflexes and arterial mechanoreflexes (baroreflexes) as appropriate error signals develop. A key question is whether the primary error corrected is a mismatch between blood flow and metabolism (a flow error that accumulates muscle metabolites that activate group III and IV chemosensitive muscle afferents) or a mismatch between cardiac output (CO) and vascular conductance [a blood pressure (BP) error] that activates the arterial baroreflex and raises BP. Reduction in muscle blood flow to a threshold for the muscle chemoreflex raises muscle metabolite concentration and reflexly raises BP by activating chemosensitive muscle afferents. In isometric exercise, sympathetic nervous activity (SNA) is increased mainly by muscle chemoreflex whereas central command raises heart rate (HR) and CO by vagal withdrawal. Cardiovascular control changes for dynamic exercise with large muscles. At exercise onset, central command increases HR by vagal withdrawal and "resets" the baroreflex to a higher BP. As long as vagal withdrawal can raise HR and CO rapidly so that BP rises quickly to its higher operating point, there is no mismatch between CO and vascular conductance (no BP error) and SNA does not increase. Increased SNA occurs at whatever HR (depending on species) exceeds the range of vagal withdrawal; the additional sympathetically mediated rise in CO needed to raise BP to its new operating point is slower and leads to a BP error. Sympathetic vasoconstriction is needed to complete the rise in BP. The baroreflex is essential for BP elevation at onset of exercise and for BP stabilization during mild exercise (subthreshold for chemoreflex), and it can oppose or magnify the chemoreflex when it is activated at higher work rates. Ultimately, when vascular conductance exceeds cardiac pumping capacity in the most severe exercise both chemoreflex and baroreflex must maintain BP by vasoconstricting active muscle.

scholarly journals Projection to cerebral cortex of Group I muscle afferents from the cat's hind limb

1969 ◽  
Vol 200 (2) ◽  
pp. 353-372 ◽  
Author(s):  
S. Landgren ◽  
H. Silfvenius
Keyword(s):  
Cerebral Cortex ◽  
Hind Limb ◽  
Muscle Afferents ◽  
Group I

Inhibition of inspiratory activity by intercostal muscle afferents

1970 ◽  
Vol 10 (3) ◽  
pp. 358-383 ◽  
Author(s):  
John E. Remmers
Keyword(s):  
Muscle Afferents ◽  
Intercostal Muscle ◽  
Inspiratory Activity
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