Afferent Signals Involved

The symptom of dyspnea is one that relates to the entire control system of respiration. In the biggest picture, dyspnea can be related to difficulty getting mitochondria to undergo oxidative phosphorylation. Both the adequate delivery of oxygen and adequate removal of carbon dioxide relate to the absence or development of dyspnea.

Chemoreceptors
Both of these chemical drives to breathe may directly and proportionally increase dyspnea.

• Hypoxia
• Hypercapnia

Mechanoreceptors of the Respiratory Muscles and Chest Wall
These receptors (particularly the muscle spindles) are fairly well known and understood to mediate dyspnea.

• Chest and wall receptors
  As a group, these are inversely related to dyspnea. Ex. If the chest is allowed to undergo respiratory movement (even with no gas exchange) or likewise with swallowing, the sensation of dyspnea is reduced.
• Muscle spindles
  More common in muscles of the rib cage. It is the muscle spindles that have been recognized to mediate the "length-tension inappropriateness" theory of dyspnea. In summary, muscle stimulation involves activation of both extrafusal fibers (main fibers) as well as intrafusal muscle fibers. Under conditions of load on the respiratory muscles, the inadequate or "inappropriate" shortening of the extrafusal fibers results in stretching of the muscle spindle and spindle efferent discharge increases. This signal may then be centrally processed into the sensation of dyspnea.
• Tendon organs
  More common in the diaphragm, and act in general as load sensors within a muscle.
• Joint receptors
  Provide the center with feedback regarding the movement of the thorax and relative to the drive to move the thorax (breath) may relate to the development of dyspnea.

Lung Receptors

• Irritant receptors
• Stretch receptors
• C-fibers