In a healthy athlete undergoing strenuous exercise, what typically happens to the arterial Po2, Pco2, and pH?
Explanation
This question highlights a key concept in exercise physiology: the precise matching of ventilation to metabolic rate, which results in the remarkable stability of arterial blood gases and pH.
Other questions
Where are the aortic bodies, which are peripheral chemoreceptors, primarily located?
What is the rate of blood flow through the chemoreceptor bodies, such as the carotid and aortic bodies?
Due to the extreme blood flow they receive, what type of blood are the peripheral chemoreceptors constantly exposed to?
In which range of arterial Po2 is the impulse rate from a carotid body particularly sensitive to changes?
What are the glandular-like cells within the carotid and aortic bodies that function as chemoreceptors and stimulate afferent nerve endings?
What is the initial event in glomus cells that leads to their stimulation when blood Po2 decreases markedly?
Following depolarization of a glomus cell due to low Po2, what specific ion influx increases the intracellular concentration and stimulates neurotransmitter release?
While early studies suggested dopamine or acetylcholine, what do more recent studies suggest is the key excitatory neurotransmitter released by carotid body glomus cells during hypoxia?
How does the power of the direct effects of increased CO2 and H+ concentration in the respiratory center compare to their indirect effects mediated through peripheral chemoreceptors?
What is the key difference in the speed of response between peripheral chemoreceptor stimulation and central stimulation by CO2?
As long as the arterial Po2 remains greater than 100 mm Hg, and Pco2 and H+ concentrations are kept normal, what is the effect on alveolar ventilation?
When arterial Po2 falls to 60 mm Hg while Pco2 and H+ levels are held constant, by how much does alveolar ventilation approximately increase?
What is the term for the phenomenon where mountain climbers, after ascending slowly over days, breathe much more deeply and can withstand lower atmospheric O2 concentrations?
What is the primary reason for acclimatization, which allows for a greater respiratory response to low O2 after 2 to 3 days?
Due to acclimatization over 2 to 3 days, by how much can alveolar ventilation increase in response to low O2, compared to the initial acute increase?
What do the four red curves in the composite diagram of Figure 42-8 represent?
In the composite diagram shown in Figure 42-8, the green curves were measured at a blood pH of 7.3. How do they compare to the red curves measured at a pH of 7.4?
During strenuous exercise, by how much can oxygen consumption and carbon dioxide formation increase in a healthy athlete?
Given that arterial blood gas and pH values do not change significantly during exercise, what is believed to be the predominant cause of the intense increase in ventilation?
According to the description of Figure 42-10, what happens to alveolar ventilation at the immediate onset of exercise?
What is the initial effect on arterial Pco2 when ventilation increases at the start of exercise?
After the initial changes at the onset of exercise, approximately how long does it take for the amount of CO2 released from the muscles to match the increased ventilation rate, causing arterial Pco2 to return to normal?
As summarized in Figure 42-11, what is the approximate upward shift in the Pco2-ventilation response curve caused by the neurogenic factor during heavy exercise?
What evidence suggests that the neurogenic control of ventilation during exercise may be partly a learned response involving the cerebral cortex?
What is the primary function of the pulmonary irritant receptors located in the epithelium of the trachea, bronchi, and bronchioles?
Where are Lung J receptors located, and what sensation might their excitation cause?
What is the primary effect of acute brain edema, such as that resulting from a brain concussion, on the respiratory center?
What does the text identify as perhaps the most prevalent cause of respiratory depression and respiratory arrest?
Cheyne-Stokes breathing is a type of periodic breathing characterized by a slowly waxing and waning respiration that repeats itself over what time interval?
What is the basic underlying cause of the cyclical pattern in Cheyne-Stokes breathing?
Why does Cheyne-Stokes breathing not typically occur in healthy individuals despite the underlying mechanism being present in everyone?
In which clinical condition is Cheyne-Stokes breathing often seen due to a prolonged delay in blood transport from the lungs to the brain?
What is the second cause of Cheyne-Stokes breathing, which involves an increased negative feedback gain in the respiratory control areas?
During Cheyne-Stokes breathing, the depth of respiration corresponds with the Pco2 level in which location?
What is the medical term for the absence of spontaneous breathing?
In individuals with sleep apnea, what is the typical duration and frequency of the apneic episodes?
What is the underlying cause of obstructive sleep apnea?
What are the physiological consequences that result from the periods of apnea in a person with sleep apnea?
What is the name of the surgical procedure used to treat obstructive sleep apnea by removing excess fat tissue from the back of the throat?
What is the primary cause of 'central' sleep apnea?
What is the estimated percentage of all sleep apnea cases that are accounted for by the 'mixed' type, a combination of obstructive and central mechanisms?
What does the text identify as the most common cause of sleep apnea?
What does the section on 'Voluntary Control of Respiration' state about the ability of a person to control their breathing?
What is the reported world record for voluntary breath-holding (apnea) under static resting conditions without pre-hyperventilating with pure oxygen?
After hyperventilating with pure oxygen and expelling large amounts of CO2, for how long have individuals been able to hold their breath underwater?
To what level can oxygen saturation fall in ultra-elite apnea competitors before unconsciousness limits the breath-hold duration?
Based on the diagram of carotid body glomus cell oxygen sensing (Figure 42-6), what is the direct cause of cell depolarization when PO2 levels fall?
According to the composite diagram showing the effects of Pco2, Po2, and pH on alveolar ventilation (Figure 42-8), what is the effect of decreasing pH from 7.4 to 7.3?
Based on Figure 42-10, what is the immediate response of alveolar ventilation when a 1-minute period of exercise is terminated?