metaboreceptors

me·tab·o·re·cep·tors

(mĕ-tab'ō-rē-sep'tŏrz)
Peripheral afferent nerve endings that respond to metabolites (lactate, CO2, pH) produced by active muscle.
[metabolism + receptor]
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References in periodicals archive ?
These factors are responsible for the activation of peripheral receptors, such as the mechanoreceptors and metaboreceptors (III and IV fibers) that send information by the afferent pathway to the central nervous system (ventrolateral medullary region), resulting in increased sympathetic discharge to the cardiovascular system (efferent response) (Mitchell, 1990).
The later reduction in post-exercise heart rate is due to the increased parasympathetic activity, which is under the control of the baroreceptors and metaboreceptors (following changes in the subjects' metabolic products, core temperature, catecholamines, and other hormonal factors) (4,32).
The increased work of breathing due to severe obstructive and restrictive breathing in patients with chronic lung disease could lead to sympathetic activation through stimulation of local metaboreceptors.
In the patient who describes work or effort when breathing, the sensation is stimulated by respiratory motor muscle contraction and muscle fatigue and is mediated through a combination of central motor discharge, chest wall receptors, and metaboreceptors located within skeletal muscle, he said at the meeting, which was sponsored by National Jewish Health.
However, prior work has suggested that the activation of type III fibers and metaboreceptors may inhibit the parasympathetic branch of the autonomic nervous system and chemoreflex stimulation, thereby contributing to an increase in human HR (4,5,19).
Inactive recovery from dynamic exercise is associated with cessation of the primary exercise stimulus from the brain and abrupt changes in the stimuli to baro- and metaboreceptors (Rowel, 1993).
Metaboreceptors with sympathetic afferents might be activated by accumulated waste products during exercise (O'Leary, 1993) possibly suggesting an alternative mechanism for sympathetic predominance and elevated HR levels in all four recovery protocols.
Among these, the following should be highlighted: (a) cessation of inhibitory vagal stimuli from the motor cortex (central command) (8); (b) cessation of mechanoreceptor action (7); and (c) the gradual reduction of the stimulation of skeletal muscle metaboreceptors (10).
Metaboreceptors with sympathetic afferents might also be activated by accumulated waste product during exercise (OLeary, 1993) proposing an alternative mechanism for sympathetic predominance.
All this could lead to less metaboreceptor activation in pre-menopausal women who have higher estrogen levels, hence causing less sympathetic neural outflow, which in turn causes a decreased BP rise in response to the handgrip test.