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During moments of rest, the respiratory system maintains a steady, rhythmic pattern directed by the brain's respiratory centers. This regulated pace ensures that the oxygen supply adequately meets the body's tissue requirements. However, there are occasions when the respiratory system needs to adjust its functions to match the body's increased demand for oxygen.
Respiratory Rate and Control of Ventilation
Breathing typically occurs involuntarily, but there are instances where one can consciously control it, like when swimming underwater, singing, or blowing bubbles. The rate of breathing is governed by respiratory centers situated in the pons and medulla oblongata, primarily responding to alterations in carbon dioxide, oxygen, and blood pH levels.
A child's normal breathing rate undergoes changes from birth to adolescence. An infant might breathe 30 to 60 times per minute, while a 10-year-old might average 18 to 30 breaths per minute. As they reach adolescence, their normal breathing rate aligns more closely with that of adults, around 12 to 18 breaths per minute.
Neural Control of Ventilation
The regulation of ventilation involves an intricate coordination among various brain regions, which signal the muscles responsible for pulmonary ventilation to contract (Figure 36, Table 6). This coordination typically leads to a regular and rhythmic pattern of breathing, ensuring adequate intake of oxygen and effective removal of carbon dioxide from the body.

Figure 35 | Neural Control of Respiration |60 This illustration depicts the hierarchical neural control of respiration, highlighting the key brainstem centers and their connections to respiratory muscles. At the top, a simplified brain diagram shows the location of the pons and medulla oblongata, the primary regions involved in respiratory regulation. An inset image provides a magnified view of these brainstem structures. Within the pons, the pneumotaxic center and apneustic center, collectively known as the pontine respiratory group (PRG), are shown. The PRG modulates respiratory rhythm and depth. In the medulla oblongata, the dorsal respiratory group (DRG) and the ventral respiratory group (VRG) are depicted. The DRG primarily controls inspiration, while the VRG is involved in both inspiration and expiration, especially during forceful breathing. Descending pathways from these brainstem centers are illustrated, showing their connections to the respiratory muscles. These include the diaphragm, the primary muscle of inspiration, as well as the external and internal intercostal muscles, which assist in breathing by expanding and contracting the rib cage. Accessory respiratory muscles, shown on the left, are recruited during increased respiratory demand. The red lines indicate the neural pathways, with (+) symbols denoting excitatory signals, indicating that these pathways stimulate muscle contraction. The inset shows inhibitory signals (-) indicating that the pontine respiratory group modulates the medullary respiratory centers.
Neurons that innervate the respiratory muscles play a crucial role in controlling and regulating pulmonary ventilation. The primary brain centers responsible for this process are located in the medulla oblongata and the pontine respiratory group (Figure 35). The medulla oblongata contains the dorsal respiratory group (DRG) and the ventral respiratory group (VRG). The DRG helps maintain a steady breathing rhythm by stimulating the diaphragm and intercostal muscles to contract during inhalation. When DRG activity decreases, it ceases to prompt these muscles, allowing them to relax, thereby causing exhalation. DRG initiates breathing through intrinsic nerve activity, acting like a pacemaker for respiration. It generates a ramp signal, which begins with a weak impulse that gradually strengthens in a ramp-like manner over approximately 2 seconds. This steady increase in nerve activity stimulates the diaphragm to contract and initiate inhalation. After 2 seconds, the ramp signal ceases abruptly for about 3 seconds, which stops diaphragm excitation and allows the lungs to undergo passive elastic recoil, leading to exhalation. Following this period, a new inspiratory cycle begins as the DRG reactivates, maintaining a rhythmic breathing pattern. In contrast, the VRG is involved in forced breathing. Neurons within the VRG stimulate the accessory muscles for forced inhalation and exhalation, facilitating these specific breathing actions.
The pontine respiratory group includes the apneustic and pneumotaxic centers, essential parts of the breathing control mechanism. The apneustic center, a dual cluster of neuronal cell bodies, stimulates the neurons in the DRG, regulating the depth of inspiration, particularly for deeper breaths. On the other hand, the pneumotaxic center, comprising a network of neurons, suppresses the activity of the neurons in the DRG. It facilitates the relaxation phase after inspiration, thereby managing the overall rate of breathing.
The respiratory system’s neural connections are organized into afferent and efferent pathways that facilitate breathing regulation. Afferent pathways carry sensory signals to the respiratory centers from various receptors. Chemoreceptor and baroreceptor signals travel through cranial nerves IX and X, while signals from thermoreceptors, pain receptors, and proprioceptors also contribute to respiratory adjustments based on temperature, pain, and body position. Efferent pathways carry motor signals from the brain to the respiratory muscles. These signals descend through the anterior portion of the lateral column of the spinal cord, reaching the cervical and thoracic segments. The phrenic nerve, originating from spinal levels C3 to C5, innervates the diaphragm, and the intercostal nerves, from T1 to T11, supply the intercostal muscles. Together, these pathways coordinate respiratory muscle activity to maintain effective breathing.10
The brain centers respond to systemic stimuli like carbon dioxide, oxygen, and pH levels in the blood. The primary stimulant for the medulla oblongata and pons is carbon dioxide concentration, not oxygen. Chemoreceptors, namely the central and peripheral receptors, sense these chemical changes. Central chemoreceptors are located on the ventrolateral surface of the medulla oblongata. They are sensitive primarily to changes in the pH of the cerebrospinal fluid, which reflects carbon dioxide levels in the blood. When blood carbon dioxide levels rise, it diffuses across the blood-brain barrier into the CSF, where it forms hydrogen ions and lowers the pH. This decrease in pH stimulates the central chemoreceptors to increase the respiratory rate and depth, helping to expel excess carbon dioxide and restore pH balance. Conversely, decreased carbon dioxide in the blood causes decreased hydrogen ions, resulting in shallower and slower breathing. Furthermore, peripheral chemoreceptors located in the aortic arch and carotid arteries are sensitive to hydrogen ion levels in the blood, adjusting ventilation to reduce carbon dioxide levels and balance hydrogen ions, thus regulating pH. They also sense drastic changes in dissolved oxygen. A significant drop in dissolved oxygen triggers these receptors to increase the respiratory rate. However, most oxygen is carried by hemoglobin, and these receptors sense dissolved oxygen only.
The peripheral chemoreceptors that are situated in the carotid bodies and aortic bodies, respond differently to changes in blood gases. They respond to decreased PaO2 and changes in pH. Moreover, the hypoxic drive originating from the peripheral chemoreceptors is crucial in advanced hypoxic states, where these receptors sustain respiration when other respiratory centers are unresponsive to direct chemical stimulation. Additionally, various brain regions, such as the hypothalamus and the limbic system, interact with the respiratory centers. The hypothalamus and other limbic regions influence breathing rates in response to emotions, pain, and changes in body temperature. For example, increased body temperature often leads to heightened respiratory rates. Feelings of excitement or fight-or-flight responses also prompt increased breathing rates. In chronic acidosis, the pH of cerebrospinal fluid is maintained close to normal through adjustments in bicarbonate ion concentrations, regulated by an ion pump at the blood-brain barrier.
Pulmonary Reflexes
The Hering-Breuer inflation reflex, attributed to Josef Breuer and Ewald Hering, is a protective reflex that prevents excessive lung inflation. Pulmonary stretch receptors, present in the airway smooth muscles, respond to overstretching of the lung during deep inhalation. When activated, they send signals via the vagus nerve to the inspiratory area in the brainstem, inhibiting further inspiration and allowing expiration (Figure 36). However, the exact role of this reflex in normal breathing patterns is not entirely clear. It appears inactive during shallow breathing but is activated when lung volumes reach around 800 ml above functional residual capacity, potentially preventing alveolar overdistention.
Apart from these slowly adapting receptors, rapidly adapting receptors are found between the epithelial cells of the respiratory tract, primarily in larger airways, and respond rapidly to sudden mechanical stimuli. Their strategic locations make them sensitive to inhaled irritants or gases, leading to protective reflex actions such as coughing, bronchoconstriction, or hyperventilation.
C-fiber endings, also known as J receptors, are found near the pulmonary-capillary region. They are sensitive to various substances and are activated by factors like pulmonary congestion, edema, and microembolism. These endings respond to specific chemical agents, contributing to bronchoconstriction or dilation.61
Nasal airways contain receptors connected to the trigeminal and olfactory nerves. Stimulating these receptors leads to sneezing. Similarly, mechanical or chemical stimulation of the larynx, trachea, or bronchi triggers the cough reflex, which involves a deep inhalation followed by forced expiration to clear the airways of irritants.
Hiccups, sudden diaphragm spasms with glottis closure, are controlled by a mechanism separate from regular respiratory rhythm. Each of these reflexes plays a critical role in maintaining airway integrity and responding to potential threats or irritants encountered in the respiratory tract.
Figure 36 | Overview of the Regulation of Breathing | The cycle of inspiration and expiration is influenced by higher brain centers and multiple reflex pathways. Reflexes originating from the lungs, airways, cardiovascular system, muscles, joints, and skin provide sensory feedback to modulate respiration. Additionally, arterial and central chemoreceptors detect changes in blood gases, such as oxygen and carbon dioxide levels, and contribute to respiratory control. The cycle of breathing directly regulates the activity of respiratory muscles to maintain proper ventilation and gas exchange. Dashed and solid arrows indicate direct and indirect regulatory pathways in respiratory control.
Hyperpnea
Hyperpnea refers to the increased rate and depth of breathing that accommodates the higher oxygen demand required during certain conditions like exercise or specific diseases that target the respiratory system. It is distinct from hyperventilation, which leads to low blood carbon dioxide levels and higher blood pH and is not necessarily related to meeting the cellular need for oxygen. During exercise, the muscles require more oxygen. While one might expect hyperpnea to be triggered by this increased demand, it actually precedes a drop in oxygen levels in the muscles which suggests that other mechanisms, apart from a decline in oxygen levels, are at play. The exact triggers behind exercise-related hyperpnea remain unclear but involve various factors related to the nervous system and the brain's respiratory centers.
The decision to engage in physical activity initiates a psychological stimulus that influences the brain's respiratory centers. Additionally, the activation of motor neurons controlling the muscles involved in the activity also stimulates these centers. The movement and stretching detected by proprioceptors located in the muscles, joints, and tendons represent another signal to the brain's respiratory centers. These neural factors align with the rapid and immediate rise in ventilation observed at the start of exercise and the subsequent swift decrease upon its conclusion, indicating a strong correlation between neural inputs and changes in ventilation throughout the activity.
|
System Component |
Function |
|---|---|
|
Medullary Respiratory Center |
Sets the basic rhythm of breathing |
|
Ventral Respiratory Group |
Generates the breathing rhythm and integrates data coming into the medulla |
|
Dorsal Respiratory Group |
Integrates input from the stretch receptors and the chemoreceptors in the periphery |
|
Pontine Respiratory Group |
Influences and modifies the function of the medulla oblongata |
|
Aortic Body |
Monitors blood pCO2 and pO2 |
|
Carotid Body |
Monitors blood pCO2, pO2 and pH |
|
Hypothalamus |
Monitors emotional state and body temperature |
|
Cortical Areas of the Brain |
Control voluntary breathing |
|
Proprioceptors |
Send impulses regarding joint and muscle movements |
|
Pulmonary Irritant Reflexes |
Protect the respiratory zones from foreign material |
|
Inflation Reflex |
Protects the lungs from overinflating |
High Altitude Effects
At higher altitudes, the reduced atmospheric pressure affects the ability of the body to achieve the same level of oxygen saturation compared to lower altitudes. While the proportion of oxygen in the atmosphere remains constant at approximately 21 percent, the decreased pressure causes a decline in the partial pressure of oxygen. Consequently, individuals at higher altitudes find it more challenging to achieve the same level of oxygen saturation as those at sea level. The reduced atmospheric pressure impacts the saturation of hemoglobin in the blood. At 19,000 feet above sea level, hemoglobin saturation can be around 67 percent, contrasting with the approximately 98 percent saturation observed at sea level.
|
Example Location |
Altitude (Feet Above Sea Level) |
Atmospheric Pressure (mmHg) |
Partial Pressure of Oxygen (mmHg) |
|---|---|---|---|
|
New York City, New York |
0 |
760 |
159 |
|
Boulder, Colorado |
5,000 |
632 |
133 |
|
Aspen, Colorado |
8,000 |
565 |
118 |
|
Pike’s Peak, Colorado |
14,000 |
447 |
94 |
|
Denali (Mt. McKinley), Alaska |
20,000 |
350 |
73 |
|
Mt. Everest, Tibet |
29,000 |
260 |
54 |
At higher altitudes, the diminished partial pressure of oxygen reduces the diffusion of oxygen across the respiratory membrane, leading to a decreased saturation of hemoglobin. However, despite this reduced saturation, the body's tissues continue to receive a sufficient oxygen supply, particularly during periods of rest. This phenomenon is attributed to two primary mechanisms.
Primarily, the volume of oxygen molecules entering the tissues from the blood is almost equivalent between sea level and high altitudes. Although hemoglobin saturation is greater at sea level, only a quarter of the oxygen molecules are actually released into the tissues. Conversely, at high altitudes, a larger proportion of oxygen molecules is liberated into the tissues.
Furthermore, at high altitudes, erythrocytes produce an increased amount of BPG, which facilitates the detachment of oxygen from hemoglobin. However, strenuous physical activities like skiing or hiking at high altitudes may provoke altitude sickness due to the diminished oxygen reserves in the blood. At sea level, a significant reserve of oxygen is present in venous blood, which muscles can utilize during physical exertion.
Given the considerably lower oxygen saturation at higher altitudes, this venous reserve becomes small, contributing to symptoms indicative of diminished blood oxygen levels. In response to the oxygen-deprived environment at high altitudes, the body increases erythropoietin secretion, resulting in a higher count of red blood cells.62
12.8: Control of Breathing is shared under a CC BY-NC-SA license and was authored, remixed, and/or curated by LibreTexts.
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