overactivity reflects deterioration in clinical status and cardiorespiratory reflex control in chronic heart failure.
Piepoli, "Muscle ergoreceptor
overactivity reflects deterioration in clinical status and cardiorespiratory reflex control in chronic heart failure," Circulation, vol.
In patients with chronic lung diseases, an elevated VE/VC[O.sub.2] slope is attributed to the effects of increased physiological dead space, ventilation-perfusion mismatching, and the abnormally elevated chemoreceptor and ergoreceptor
sensitivity that are present at rest and deteriorate during exercise .
Nerve endings that are sensitive to metabolites exist in skeletal muscles and have been named ergoreceptors
.  Ergoreceptors
are intramuscular afferents and are functionally differentiated into mechanoreceptors and chemoreceptors.
The potential candidates underlying the reduced sympathetic nerve activity by AET include afferent autonomic control coordinated by arterial baroreceptors, cardiopulmonary receptors, ergoreceptors
, and chemoreceptors [143-145].
The stimulation of ergoreceptors
sensitive to accumulation of metabolites within respiratory skeletal muscle reflexively increases sympathetic outflow, which limits the increase of blood flow to working muscle, causing reduced perfusion of locomotor muscles and leading to fatigue (3-5).
The mechanism may relate to the release of ergoreceptors
, afferent nerve activity and increased [beta]-endorphin production/release that are stimulated by needle insertion into skin and muscle.
They activate what are known as ergoreceptors
in the muscle that signalize to the body that the muscle cannot sustain the workload.
Unpleasant perceptions of effort during exercise can therefore arise from various chemoreceptors, ergoreceptors
and thermoreceptors in the body, but the perceptions most relevant to catastrophic neuronal dysfunction are probably oppressive feelings of heat and breathlessness, which build until they become imperatives to reduce exercise intensity.