Sensing vascular distension in skeletal muscle by slow conducting afferent fibers

Neurophysiological basis and implication for respiratory control

Philippe Haouzi, Bruno Chenuel, Andrew Huszczuk

Research output: Contribution to journalReview article

74 Citations (Scopus)

Abstract

This review examines the evidence that skeletal muscles can sense the status of the peripheral vascular network through group III and IV muscle afferent fibers. The anatomic and neurophysiological basis for such a mechanism is the following: 1) a significant portion of group III and IV afferent fibers have been found in the vicinity and the adventitia of the arterioles and the venules; 2) both of these groups of afferent fibers can respond to mechanical stimuli; 3) a population of group III and IV fibers stimulated during muscle contraction has been found to be inhibited to various degrees by arterial occlusion; and 4) more recently, direct evidence has been obtained showing that a part of the group IV muscle afferent fibers is stimulated by venous occlusion and by injection of vasodilatory agents. The physiological relevance of sensing local distension of the vascular network at venular level in the muscles is clearly different from that of the large veins, since the former can directly monitor the degree of tissue perfusion. The possible involvement of this sensing mechanism in respiratory control is discussed mainly in the light of the ventilatory effects of peripheral vascular occlusions during and after muscular exercise. It is proposed that this regulatory system anticipates the chemical changes that would occur in the arterial blood during increased metabolic load and attempts to minimize them by adjusting the level of ventilation to the level of muscle perfusion, thus matching the magnitudes of the peripheral and pulmonary gas exchange.

Original languageEnglish (US)
Pages (from-to)407-418
Number of pages12
JournalJournal of Applied Physiology
Volume96
Issue number2
DOIs
StatePublished - Feb 1 2004

Fingerprint

Blood Vessels
Skeletal Muscle
Muscles
Perfusion
Pulmonary Gas Exchange
Adventitia
Venules
Arterioles
Muscle Contraction
Ventilation
Veins
Injections

All Science Journal Classification (ASJC) codes

  • Physiology
  • Physiology (medical)

Cite this

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Sensing vascular distension in skeletal muscle by slow conducting afferent fibers : Neurophysiological basis and implication for respiratory control. / Haouzi, Philippe; Chenuel, Bruno; Huszczuk, Andrew.

In: Journal of Applied Physiology, Vol. 96, No. 2, 01.02.2004, p. 407-418.

Research output: Contribution to journalReview article

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AB - This review examines the evidence that skeletal muscles can sense the status of the peripheral vascular network through group III and IV muscle afferent fibers. The anatomic and neurophysiological basis for such a mechanism is the following: 1) a significant portion of group III and IV afferent fibers have been found in the vicinity and the adventitia of the arterioles and the venules; 2) both of these groups of afferent fibers can respond to mechanical stimuli; 3) a population of group III and IV fibers stimulated during muscle contraction has been found to be inhibited to various degrees by arterial occlusion; and 4) more recently, direct evidence has been obtained showing that a part of the group IV muscle afferent fibers is stimulated by venous occlusion and by injection of vasodilatory agents. The physiological relevance of sensing local distension of the vascular network at venular level in the muscles is clearly different from that of the large veins, since the former can directly monitor the degree of tissue perfusion. The possible involvement of this sensing mechanism in respiratory control is discussed mainly in the light of the ventilatory effects of peripheral vascular occlusions during and after muscular exercise. It is proposed that this regulatory system anticipates the chemical changes that would occur in the arterial blood during increased metabolic load and attempts to minimize them by adjusting the level of ventilation to the level of muscle perfusion, thus matching the magnitudes of the peripheral and pulmonary gas exchange.

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