A number of factors may increase ventilation during exercise Reflexes originating from body movements. Joint and muscle: Receptors excited during muscle contraction reflexly stimulate the respiratory center, abruptly increasing ventilation. 2. Increase in body temperature: Much of the energy generated during muscle contraction is converted to heat rather than to actual mechanical work. Heat-loss mechanisms such as sweating frequently cannot keep pace with the increased heat production. Raised body temperature including fever stimulates ventilation.
3.Epinephrine release: Epinephrine also stimulates ventilation. The level of circulating epinephrine rises during exercise in response to the sympathetic nervous system discharge that accompanies increased physical activity. 4. Impulses from the cerebral cortex: The motor areas of the cerebral cortex, simultaneously stimulate the medullary respiratory neurons and activate the motor neurons of the exercising muscles. Voluntarily person can hold the breath or hyperventilate temporarily , can be override by changes in arterial blood gases.
Protective reflexes: Such as sneezing and coughing, Inhalation of particularly noxious agents govern temporarily respiratory activity. Pain, originating anywhere in the body reflexly stimulates Involuntary modification of breathing. Emotional states, such as laughing, crying, sighing, and groaning, modify respirationdue to connection between limbic system and resp. centers. Hiccups, occur when involuntary, spasmodic contractions of the diaphragm occur, each causing rapid intake of air. During swallowing The respiratory center is reflexly inhibited to close airways to prevent food entering the lungs. Speaking, singing, and whistling: We also control our breathing to perform such voluntary acts.
APNEA & SLEEP APNEA • During apnea person forgets to breath in dyspnea a person is short of breath. • Apnea is the transient interruption of ventilation, with breathing resuming spontaneously. If breathing does not resume, the condition is called respiratory arrest. Because ventilation is normally decreased and the central chemoreceptors are less sensitive to the arterial PCO2 drive during sleep, victims of sleep apnea may stop breathing for a few seconds or up to 1or 2minutes many times in the night. • Mild sleep apnea is not dangerous unless the sufferer has pulmonary or circulatory disease, which can be exacerbated by recurrent bouts of apnea.
SUDDEN INFANT DEATH SYNDROME SUDDEN INFANT DEATH SYNDROME (SIDS): • In exaggerated cases of sleep apnea, the victim may be unable to recover from an apneic period, and death results. • This is the case in sudden infant death syndrome (SIDS), or “crib death,” the leading cause of death in the first year of life. • With this tragic form of sleep apnea, a previously healthy two- to four-month-old infant is found dead in his or her crib for no apparent reason.” • Because the respiratory control mechanisms are immature, either in the brain stem or in the chemoreceptors that monitor the body’s respiratory status. • Poorly developed carotid bodies, the more important of the peripheral chemoreceptorsor abnormal lung development has been suggested.
Role of Respiration In Acid-Base Balance • pH of blood – 7.4 [7.35-7.45] • Lungs and kidneys regulate the pH of body. • Lungs play important role in regulation of pH because they excrete CO2. Respiratory Acidosis • If respiratory center is depressed e.g. brain damage, drugs, it will increase CO2 in the body which will increase H+. • CO2 + H2O H2CO3 H + HCO3 • If H+ ion increases – it will cause Respiratory Acidosis.
Respiratory Alkalosis • If person hyperventilates, it will cause loss of CO2 and H+ ions and pH becomes alkaline [respiratory alkalosis].
Role of respiration in Acid- Base balance • Adjustments in ventilation in response to changes in arterial H+ are important in acid-base balance • Changes in arterial H+ ions concentration cannot influence the central chemoreceptors • However, the aortic and carotid body peripheral chemoreceptors are highly responsive to fluctuations in arterial H+ ions concentration, in contrast to their weak sensitivity to deviations in arterial PCO2 and their unresponsiveness to arterial PO2 until it falls 40% below normal. • Any change in arterial PCO2 brings about a corresponding change in the H+ concentration of the blood as well as of the exercise to keep pace with the increased demand for O2 uptake and CO2 output.