Chapter 13 Segmental and descending control of the synaptic effectiveness of muscle afferents

Author(s):  
Pablo Rudomin
Circulation ◽  
1996 ◽  
Vol 93 (5) ◽  
pp. 940-952 ◽  
Author(s):  
Massimo Piepoli ◽  
Andrew L. Clark ◽  
Maurizio Volterrani ◽  
Stamatis Adamopoulos ◽  
Peter Sleight ◽  
...  

1994 ◽  
Vol 77 (4) ◽  
pp. 1907-1912 ◽  
Author(s):  
D. A. Schneider ◽  
M. T. McEniery ◽  
C. Solomon ◽  
J. Jurimae ◽  
M. S. Wehr

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.


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

2008 ◽  
Vol 586 (5) ◽  
pp. 1277-1289 ◽  
Author(s):  
P. G. Martin ◽  
N. Weerakkody ◽  
S. C. Gandevia ◽  
J. L. Taylor

1990 ◽  
Vol 69 (2) ◽  
pp. 407-418 ◽  
Author(s):  
L. B. Rowell ◽  
D. S. O'Leary

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.


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