Expected results were seen in
subjects 3 and 4 during the breath holding procedures. Breath holding duration
increased after voluntarily hyperventilating for 1 minute, and decreased
drastically after exercising at 200 watts for 90 seconds. It is expected for
breath holding durations to increase in length almost twice after hyperventilation,
due to high oxygen and low carbon dioxide conditions of the body since the
drive for respiration is decreased (7). However, the opposite is
true for breath-holding after exercise. Ventilation needs to increase during and
after exercise to fulfill the body’s needs for oxygen, which is why subjects 3
and 4 were not able to hold for very long after exercising at a relatively high
power output (1). The signals that chemoreceptors send are what is
responsible for our ability to hold our breath for certain periods of time (1).
Chemoreceptors respond to changes in blood pH and carbon dioxide levels (1).
When exercising, the body’s need for oxygen increases, and gets fulfilled by
increasing ventilation. Chemoreceptors in the muscle and lung act upon this
need for oxygen and are activated so this demand is fulfilled (1).
During breath holding after hyperventilation, chemoreceptors are inhibited due
to the body’s sufficient oxygen levels, and are activated later to stimulate
ventilation when the subjects couldn’t hold their breath any longer (1).
Additionally, the role of chemoreceptors is also seen in obstructive lung
diseases as well. In patients with obstructive lung diseases, their partial
pressure and saturation of oxygen are typically lower and their carbon dioxide
concentrations are higher due to decreased air flow, so the body stimulates
chemoreceptors to try to increase ventilation to increase blood oxygen levels (3).
Furthermore, obstructive lung
diseases as well as restrictive lung diseases both have a negative impact on
gas exchange. When there is an obstruction in the airway, there is a decreased
amount of air into the lung and to the alveoli, potentially causing the alveoli
to die, which decreases surface area in the lung (3). Alveoli can
also become swollen and filled with thick mucus, which causes a greater
distance between the alveoli and the blood, as well as increases thickness of
the sheet (3). Additionally, if the airway becomes swollen in a
patient with an obstructive pulmonary disease, the pressure difference
decreases as well (3). These are all negative affects on Fick’s law
of diffusion, and therefore resulting in reduced diffusion and gas exchange. Furthermore,
in restrictive lung diseases, there is evidence that alveoli become scarred and
lungs become very stiff, making it more difficult to inhale or exhale a high
volume of air at a certain time (6). This inevitably leads to
hypoxia and reduced gas exchange as well