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Control of Respiration

Pearson
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The control of respiration is tied to the principle of homeostasis. Recall that the body maintains homeostasis through homeostatic control mechanisms, which have three basic components: receptors, control centers, and effectors. Let’s see how this applies to the respiratory system. The principle factors which control respiration are chemical factors in the blood. Changes in arteriole PCO2, PO2 and pH are monitored by sensory receptors called chemoreceptors. The chemoreceptors send sensory input to respiratory centers in the brain stem, which determine the appropriate response to the changing variables. These centers then send nerve impulses to the effectors, the respiratory muscles, to control the force and frequency of contraction. This changes the ventilation, the rate and depth of breathing. Ventilation changes restore the arterial blood gases and pH to their normal range. The basic rhythm of breathing is controlled by respiratory centers located in the medulla and pons of the brainstem. Within the medulla, a group of neurons in the ventral respiratory group sets the basic rhythm by automatically initiating inspiration. The inspiratory neurons send nerve impulses along the phrenic nerves to the diaphragm and along the intercostal nerves to the external intercostal muscles. Let’s see how inspiratory neurons initiate inspiration. The nerve impulses to the diaphragm and the external intercostals muscles continue for a period of about two seconds. This stimulates the inspiratory muscles to contract, initiating inspiration. A second group of neurons in the ventral respiratory group now fires, inhibiting the inspiratory neurons for about three seconds, which allows the muscles to relax. The elastic recoil of the lungs and chest wall leads to expiration. The automatic rhythm generated by these two groups of neurons alternately inhibiting each other produces a normal resting breathing rate ranging between 12 and 15 breaths per minute. Let’s look more closely at how the central chemoreceptors respond to carbon dioxide. The most important factor controlling the rate and depth of breathing. Carbon dioxide readily diffuses from the blood into the brain. Here carbon dioxide combines with water to form carbonic acid, which dissociates into hydrogen ions and bicarbonate ions. The hydrogen ions stimulate the central chemoreceptors, which send nerve impulses to the respiratory centers in the medulla. Did you notice that as carbon dioxide increases so does the number of hydrogen ions, which in turn lowers the pH. The central chemoreceptors actually respond to this pH change caused by the blood PCO2. Can you guess what changes will occur if a person hyperventilates, that is, breathes deeper and faster than necessary for normal gas exchange? During hyperventilation carbon dioxide is exhaled lowering the PCO2. This drives the chemical reaction to the left decreasing the hydrogen ion concentration and increasing pH. Since the PCO2 is low, the central chemoreceptors send fewer impulses to the respiratory centers. Since the pH is high, the peripheral chemoreceptors also send fewer impulses to the respiratory centers, which send fewer nerve impulses to the respiratory muscles, thereby further decreasing breathing rate and depth and returning the arterial gases and pH to normal levels. In addition, several other factors influence ventilation. These factors include voluntary control, pain and emotions, pulmonary irritants, and lung hyperinflation. Pain and strong emotions, such as fear and anxiety, act by way of the hypothalamus to stimulate or inhibit the respiratory centers. Laughing and crying also significantly alter ventilation. Dust, smoke, noxious fumes, excess mucus, and other irritants stimulate receptors in the airways. This initiates protective reflexes, such as coughing and sneezing, which forcibly remove the irritants from the airway. By sending signals from the cerebral cortex to the respiratory muscles, we can voluntarily change our breathing rate and depth when holding our breath, speaking, or singing. However, chemoreceptor input into the respiratory centers will eventually override conscious control and force you to breathe. Stretch receptors in the visceral pleura and large airways send inhibitory signals to the inspiratory neurons during very deep inspirations, protecting against excessive stretching of the lungs. This is known as the inflation, or Hering-Breuer, reflex. Now let’s look at the changes in ventilation during exercise. Ventilation increases during strenuous exercise, with a depth increasing more than the rate. Remarkably, It appears that changes in PCO2 and PO2 do not play a significant role in stimulating this increased ventilation. Although, the precise factors which stimulate increased ventilation during exercise are not fully understood, they probably include: learned responses, neural input from the motor cortex, receptors in muscles and joints, increased body temperature, circulating epinephrine and norepinephrine, and pH changes due to lactic acid. Let’s explore these factors. Ventilation increases within seconds of the beginning of exercise, probably in anticipation of exercise, a learned response. It also increases because the motor areas of the cerebral cortex, which stimulate the muscles, also stimulate the respiratory centers. Proprioceptors in moving muscles and joints stimulate the respiratory centers, as does an increase in body temperature. Circulating epinephrine and norepinephrine secreted by the adrenal medulla stimulates the respiratory centers. Lactic acid produced by exercising muscles is another stimulus.
The control of respiration is tied to the principle of homeostasis. Recall that the body maintains homeostasis through homeostatic control mechanisms, which have three basic components: receptors, control centers, and effectors. Let’s see how this applies to the respiratory system. The principle factors which control respiration are chemical factors in the blood. Changes in arteriole PCO2, PO2 and pH are monitored by sensory receptors called chemoreceptors. The chemoreceptors send sensory input to respiratory centers in the brain stem, which determine the appropriate response to the changing variables. These centers then send nerve impulses to the effectors, the respiratory muscles, to control the force and frequency of contraction. This changes the ventilation, the rate and depth of breathing. Ventilation changes restore the arterial blood gases and pH to their normal range. The basic rhythm of breathing is controlled by respiratory centers located in the medulla and pons of the brainstem. Within the medulla, a group of neurons in the ventral respiratory group sets the basic rhythm by automatically initiating inspiration. The inspiratory neurons send nerve impulses along the phrenic nerves to the diaphragm and along the intercostal nerves to the external intercostal muscles. Let’s see how inspiratory neurons initiate inspiration. The nerve impulses to the diaphragm and the external intercostals muscles continue for a period of about two seconds. This stimulates the inspiratory muscles to contract, initiating inspiration. A second group of neurons in the ventral respiratory group now fires, inhibiting the inspiratory neurons for about three seconds, which allows the muscles to relax. The elastic recoil of the lungs and chest wall leads to expiration. The automatic rhythm generated by these two groups of neurons alternately inhibiting each other produces a normal resting breathing rate ranging between 12 and 15 breaths per minute. Let’s look more closely at how the central chemoreceptors respond to carbon dioxide. The most important factor controlling the rate and depth of breathing. Carbon dioxide readily diffuses from the blood into the brain. Here carbon dioxide combines with water to form carbonic acid, which dissociates into hydrogen ions and bicarbonate ions. The hydrogen ions stimulate the central chemoreceptors, which send nerve impulses to the respiratory centers in the medulla. Did you notice that as carbon dioxide increases so does the number of hydrogen ions, which in turn lowers the pH. The central chemoreceptors actually respond to this pH change caused by the blood PCO2. Can you guess what changes will occur if a person hyperventilates, that is, breathes deeper and faster than necessary for normal gas exchange? During hyperventilation carbon dioxide is exhaled lowering the PCO2. This drives the chemical reaction to the left decreasing the hydrogen ion concentration and increasing pH. Since the PCO2 is low, the central chemoreceptors send fewer impulses to the respiratory centers. Since the pH is high, the peripheral chemoreceptors also send fewer impulses to the respiratory centers, which send fewer nerve impulses to the respiratory muscles, thereby further decreasing breathing rate and depth and returning the arterial gases and pH to normal levels. In addition, several other factors influence ventilation. These factors include voluntary control, pain and emotions, pulmonary irritants, and lung hyperinflation. Pain and strong emotions, such as fear and anxiety, act by way of the hypothalamus to stimulate or inhibit the respiratory centers. Laughing and crying also significantly alter ventilation. Dust, smoke, noxious fumes, excess mucus, and other irritants stimulate receptors in the airways. This initiates protective reflexes, such as coughing and sneezing, which forcibly remove the irritants from the airway. By sending signals from the cerebral cortex to the respiratory muscles, we can voluntarily change our breathing rate and depth when holding our breath, speaking, or singing. However, chemoreceptor input into the respiratory centers will eventually override conscious control and force you to breathe. Stretch receptors in the visceral pleura and large airways send inhibitory signals to the inspiratory neurons during very deep inspirations, protecting against excessive stretching of the lungs. This is known as the inflation, or Hering-Breuer, reflex. Now let’s look at the changes in ventilation during exercise. Ventilation increases during strenuous exercise, with a depth increasing more than the rate. Remarkably, It appears that changes in PCO2 and PO2 do not play a significant role in stimulating this increased ventilation. Although, the precise factors which stimulate increased ventilation during exercise are not fully understood, they probably include: learned responses, neural input from the motor cortex, receptors in muscles and joints, increased body temperature, circulating epinephrine and norepinephrine, and pH changes due to lactic acid. Let’s explore these factors. Ventilation increases within seconds of the beginning of exercise, probably in anticipation of exercise, a learned response. It also increases because the motor areas of the cerebral cortex, which stimulate the muscles, also stimulate the respiratory centers. Proprioceptors in moving muscles and joints stimulate the respiratory centers, as does an increase in body temperature. Circulating epinephrine and norepinephrine secreted by the adrenal medulla stimulates the respiratory centers. Lactic acid produced by exercising muscles is another stimulus.