Control of breathing during dynamic exercise by thin fiber muscle afferents

2010 ◽  
Vol 109 (4) ◽  
pp. 947-948 ◽  
Author(s):  
Marc P. Kaufman
Keyword(s):  
Muscle Afferents ◽  
Dynamic Exercise ◽  
Control Of Breathing ◽  
Thin Fiber

scholarly journals Cyclooxygenase blockade attenuates responses of group III and IV muscle afferents to dynamic exercise in cats

2006 ◽  
Vol 290 (6) ◽  
pp. H2239-H2246 ◽  
Author(s):  
Shawn G. Hayes ◽  
Angela E. Kindig ◽  
Marc P. Kaufman
Keyword(s):  
Muscle Afferents ◽  
Group Iv ◽  
Dynamic Exercise ◽  
Triceps Surae ◽  
Afferent Activity ◽  
Mesencephalic Locomotor Region ◽  
Thin Fiber ◽  
Group Iii ◽  
Triceps Surae Muscles ◽  
Stimulation Of

Cyclooxygenase products accumulate in statically contracting muscles to stimulate group III and IV afferents. The role played by these products in stimulating thin fiber muscle afferents during dynamic exercise is unknown. Therefore, in decerebrated cats, we recorded the responses of 17 group III and 12 group IV triceps surae muscle afferents to dynamic exercise, evoked by stimulation of the mesencephalic locomotor region. Each afferent was tested while the muscles were freely perfused and while the circulation to the muscles was occluded. The increases in group III and IV afferent activity during dynamic exercise while the circulation to the muscles was occluded were greater than those during exercise while the muscles were freely perfused ( P < 0.01). Indomethacin (5 mg/kg iv), a cyclooxygenase blocker, reduced the responses to dynamic exercise of the group III afferents by 42% when the circulation to the triceps surae muscles was occluded ( P < 0.001) and by 29% when the circulation was not occluded ( P = 0.004). Likewise, indomethacin reduced the responses to dynamic exercise of group IV afferents by 34% when the circulation was occluded ( P < 0.001) and by 18% when the circulation was not occluded ( P = 0.026). Before indomethacin, the activity of the group IV, but not group III, afferents was significantly higher during postexercise circulatory occlusion than during rest ( P < 0.05). After indomethacin, however, group IV activity during postexercise circulatory occlusion was not significantly different from group IV activity during rest. Our data suggest that cyclooxygenase products play a role both in sensitizing group III and IV afferents during exercise and in stimulating group IV afferents during postexercise circulatory occlusion.

High concentrations of 17β-estradiol attenuate the exercise pressor reflex in male cats

2003 ◽  
Vol 94 (4) ◽  
pp. 1431-1436 ◽  
Author(s):  
Petra M. Schmitt ◽  
Marc P. Kaufman
Keyword(s):  
Spinal Cord ◽  
Muscle Afferents ◽  
Central Command ◽  
Physiological Level ◽  
Thin Fiber ◽  
Exercise Pressor Reflex ◽  
17Β Estradiol ◽  
Pressor Reflex ◽  
High Concentrations ◽  
Decerebrate Cats

Previously, intravenous injection of 17β-estradiol in decerebrate male cats was found to attenuate central command but not the exercise pressor reflex. This latter finding was surprising because the dorsal horn, the spinal site receiving synaptic input from thin-fiber muscle afferents, is known to contain estrogen receptors. We were prompted, therefore, to reexamine this issue. Instead of injecting 17β-estradiol intravenously, we applied it topically to the L7 and S1 spinal cord of male decerebrate cats. We found that topical application (150–200 μl) of 17β-estradiol in concentrations of 0.01, 0.1, and 1 μg/ml had no effect on the exercise pressor reflex, whereas a concentration of 10 μg/ml attenuated the reflex. We conclude that, in male cats, estrogen can only attenuate the exercise pressor reflex in concentrations that exceed the physiological level.

Activation of thin-fiber muscle afferents by a P2X agonist in cats

2004 ◽  
Vol 96 (3) ◽  
pp. 1166-1169 ◽  
Author(s):  
Ramy L. Hanna ◽  
Marc P. Kaufman
Keyword(s):  
Pyridoxal Phosphate ◽  
Muscle Afferents ◽  
Group Iv ◽  
Triceps Surae ◽  
Disulfonic Acid ◽  
P2 Receptor ◽  
Thin Fiber ◽  
Group Iii ◽  
Decerebrate Cats ◽  
Stimulation Of

The responses of group III and IV triceps surae muscle afferents to intra-arterial injection of α,β-methylene ATP (50 μg/kg) was examined in decerebrate cats. We found that this P2X3 agonist stimulated only three of 18 group III afferents but 7 of 9 group IV afferents ( P < 0.004). The three group III afferents stimulated by α,β-methylene ATP conducted impulses below 4 m/s. Pyridoxal phosphate-6-azophenyl-2′,4′-disulfonic acid, a P2-receptor antagonist, prevented the stimulation of these afferents by α,β-methylene ATP. We conclude that P2X3 agonists stimulate only the slowest conducting group III muscle afferents as well as group IV afferents.

scholarly journals Responses of group III and IV muscle afferents to dynamic exercise

1997 ◽  
Vol 82 (6) ◽  
pp. 1811-1817 ◽  
Author(s):  
Christine M. Adreani ◽  
Janeen M. Hill ◽  
Marc P. Kaufman
Keyword(s):  
Receptive Fields ◽  
Muscle Afferents ◽  
Group Iv ◽  
Dynamic Exercise ◽  
Triceps Surae ◽  
Group Iii ◽  
Low Levels ◽  
Triceps Surae Muscles ◽  
Decerebrate Cats ◽  
Stimulation Of

Adreani, Christine M., Janeen M. Hill, and Marc P. Kaufman.Responses of group III and IV muscle afferents to dynamic exercise. J. Appl. Physiol. 82(6): 1811–1817, 1997.—Tetanic contraction of hindlimb skeletal muscle, induced by electrical stimulation of either ventral roots or peripheral nerves, is well known to activate group III and IV afferents. Nevertheless, the effect of dynamic exercise on the discharge of these thin fiber afferents is unknown. To shed some light on this question, we recorded in decerebrate cats the discharge of 24 group III and 10 group IV afferents while the mesencephalic locomotor region (MLR) was stimulated electrically. Each of the 34 afferents had their receptive fields in the triceps surae muscles. Stimulation of the MLR for 1 min caused the triceps surae muscles to contract rhythmically, an effect induced by an α-motoneuron discharge pattern and recruitment order almost identical to that occurring during dynamic exercise. Eighteen of the 24 group III and 8 of the 10 group IV muscle afferents were stimulated by MLR stimulation. The oxygen consumption of the dynamically exercising triceps surae muscles was increased by 2.5-fold over their resting levels. We conclude that low levels of dynamic exercise stimulate group III and IV muscle afferents.

Femoral arterial injection of adenosine in humans elevates MSNA via central but not peripheral mechanisms

1997 ◽  
Vol 83 (4) ◽  
pp. 1045-1053 ◽  
Author(s):  
D. A. Maclean ◽  
B. Saltin ◽  
G. Rådegran ◽  
L. Sinoway
Keyword(s):  
Sympathetic Nerve Activity ◽  
Muscle Sympathetic Nerve Activity ◽  
Muscle Afferents ◽  
The Other ◽  
Onset Latency ◽  
Nerve Activity ◽  
Thin Fiber ◽  
Inflated Cuff ◽  
Baseline Values ◽  
Phenylephrine Infusion

MacLean, D. A., B. Saltin, G. Rådegran, and L. Sinoway. Femoral arterial injection of adenosine in humans elevates MSNA via central but not peripheral mechanisms. J. Appl. Physiol. 83(4): 1045–1053, 1997.—The purpose of the present study was to examine the effects of femoral arterial injections of adenosine on muscle sympathetic nerve activity (MSNA) under three different conditions. These conditions were adenosine injection alone, adenosine injection after phenylephrine infusion, and adenosine injection distal to a thigh cuff inflated to arrest the circulation. The arterial injection of adenosine alone resulted in a fourfold (255 ± 18 U/min) increase above baseline (73 ± 12 U/min; P< 0.05) in MSNA with an onset latency of 15.8 ± 0.8 s from the time of injection. The systemic infusion of phenylephrine resulted in an increase ( P < 0.05) in mean arterial pressure of ∼10 mmHg and a decrease ( P < 0.05) in heart rate of 8–10 beats/min compared with baseline values before phenylephrine infusion. After adenosine injection, the onset latency for the increase in MSNA was delayed to 19.2 ± 2.1 s and the magnitude of increase was attenuated by ∼50% (123 ± 20 U/min) compared with adenosine injection alone ( P < 0.05). When a cuff was inflated to 220 mmHg to arrest the circulation and adenosine was injected into the leg distal to the inflated cuff, there were no significant changes in MSNA or any of the other measured variables. However, on deflation of the cuff, there was a rapid increase ( P < 0.05) in MSNA, with an onset latency of 9.1 ± 0.9 s, and the magnitude of increase (276 ± 28 U/min) was similar to that observed for adenosine alone. These data suggest that ∼50% of the effects of exogenously administered adenosine are a result of baroreceptor unloading due to a drop in blood pressure. Furthermore, the finding that adenosine did not directly result in an increase in MSNA while it was trapped in the leg but that it needed to be released into the circulation suggests that adenosine does not directly stimulate thin fiber muscle afferents in the leg of humans. In contrast, it would appear that adenosine exerts its effects via some other chemically sensitive pool of afferents.

scholarly journals Cyclooxygenase products sensitize group III and IV muscle afferents to dynamic exercise

2006 ◽  
Vol 20 (4) ◽  
Author(s):  
Shawn G Hayes ◽  
Angela E Kindig ◽  
Marc P Kaufman
Keyword(s):  
Muscle Afferents ◽  
Dynamic Exercise ◽  
Group Iii

scholarly journals Femoral artery ligation increases the responses of thin-fiber muscle afferents to contraction

2015 ◽  
Vol 113 (10) ◽  
pp. 3961-3966 ◽  
Author(s):  
Audrey J. Stone ◽  
Steven W. Copp ◽  
Jennifer L. McCord ◽  
Marc P. Kaufman
Keyword(s):  
Femoral Artery ◽  
Muscle Afferents ◽  
Group Iv ◽  
Artery Ligation ◽  
Thin Fiber ◽  
Group Iii ◽  
Exercise Pressor Reflex ◽  
Hindlimb Muscles ◽  
Static Contraction ◽  
Pressor Reflex

Previous evidence has shown that ligating the femoral artery for 72 h resulted in an exaggerated exercise pressor reflex. To provide electrophysiological evidence for this finding, we examined in decerebrated rats whose femoral arteries were either freely perfused or ligated for 72 h the responses of thin-fiber (i.e., groups III and IV) afferents to static contraction of the hindlimb muscles. We found that contraction increased the combined activity of group III and IV afferents in both freely perfused ( n = 29; baseline: 0.3 ± 0.1 imp/s, contraction: 0.8 ± 0.2 imp/s; P < 0.05) and ligated rats ( n = 28; baseline: 0.4 ± 0.1 imp/s, contraction: 1.4 ± 0.1 imp/s; P < 0.05). Most importantly, the contraction-induced increase in afferent activity was greater in ligated rats than it was in freely perfused rats ( P = 0.005). In addition, the responses of group III afferents to contraction in ligated rats ( n = 15; baseline 0.3 ± 0.1 imp/s, contraction 1.5 ± 0.2 imp/s) were greater ( P = 0.024) than the responses to contraction in freely perfused rats ( n = 18; baseline 0.3 ± 0.1 imp/s, contraction 0.9 ± 0.2 imp/s). Likewise, the responses of group IV afferents to contraction in ligated rats ( n = 13; baseline 0.5 ± 0.1 imp/s, contraction 1.3 ± 0.2 imp/s) were greater ( P = 0.048) than the responses of group IV afferents in freely perfused rats ( n = 11; baseline 0.3 ± 0.1 imp/s, contraction 0.6 ± 0.2 imp/s). We conclude that both group III and IV afferents contribute to the exaggeration of the exercise pressor reflex induced by femoral artery ligation.

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