Human Anatomy and Physiology: Respiratory and altitude

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To describe the key components that aid in the regulation of the respiratory system and explain the mechanics behind how this system is regulated (via homeostasis) when the human body is at rest at sea level and during exposure for 2 hours to simulated altitude. This simulated altitude will be at ~3500m and 15% O2 level.


Respiration is the exchange of gases between the atmosphere and cells within an organism and can be split into 3 different types of respiration. The main ones to consider when looking at the respiratory process are internal and external respiration.

External Respiration can be described as the process in which an exchange of gases occur where oxygen is transported from the surrounding atmosphere to tissues in the body and CO2 is released by the respiring cells and transported back into the atmosphere (Hickin, S., Chapman, R. and Renshaw, J.). Internal respiration is the transport of O2 from the blood, where it is attached to haemoglobin, to cells that are oxygen deficient (Lee, R.

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The function of the respiratory system is the exchange of gases and ventilation to sustain life by contributing to processes such as metabolism and maintaining the pH of bodily fluids. (Bergan-Roller, H. et al). The main components of the respiratory system can be split into two parts, the upper respiratory tract and the lower respiratory tract. The upper tract consists of the nasal cavity, larynx and trachea responsible for the filtering, warming and humidifying air inhaled so that efficient exchange can occur allowing the sensitive lungs to remain wet.

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The lower respiratory tract includes bronchi/bronchioles and lungs encased by the thoracic cavity. The lungs are the main organs involved in respiration and are where the bronchi airways split into smaller airways before eventually ending with the acinus. The acinus is the site of oxygen transportation from the lungs into the bloodstream and CO2 transportation from the bloodstream into the lungs (Hickin, S., Chapman, R. and Renshaw, J.).

The respiratory system is complex and requires maintenance to continue, referred to as homeostasis. The key variables that the respiratory system must control are the partial pressures of both O2 and CO2 in the blood as well as the pH levels. In this essay we explore how the respiratory system responds to changes in both arteriole PO2/PCO2 and pH when at rest at sea level compared to when exposed to hypoxic environments and how it maintains respiratory control by the homeostatic system.


Homeostasis is defined as the maintenance or regulation of internal variables in a state of constancy within the respiratory system (Asarian, L., Gloy, V. and Geary, N.). For homeostasis to be effective, the regulation of external respiration is essential. This regulation is controlled by a negative feedback loop within the body. When set variables fall outside their set range, receptors throughout the body detect any fluctuations triggering the negative feedback system kick in. This allows the body to counteract any abnormalities in order to return these values to within their correct range preventing any harm. The homeostatic system relies upon the sensitivity of sensors and the effectiveness of effectors to maintain its control. (Edwards, B.). Below we explore the process of homeostatic control both at rest and when acutely exposed to a hypoxic environment.

Homeostatic control at rest – The main variables that the feedback loop controls in the respiratory system are the partial pressures of O2 and CO2 in the arteriole blood referred to as PO2 / PCO2 as well as monitoring the body’s pH. When at rest the PO2 is between 80 – 105 mmHg and the PCO2 equals 35 – 45 mmHg. (Edwards, B.) If the partial pressure of both O2 and CO2 venture outside these limits, the result may be disease or even death. The body counteracts such changes by processes involving the cooperation of the brain and spinal column (Cotes, J., Chinn, D. and Miller, M.) using a network of neurons in the medulla and pons (respiratory centres), both parts of the brain responsible for autonomic activity (Rogers, K.). Throughout the body are a series of sensors that monitor fluctuations outside set limits with the most important being chemoreceptors. These receptors detect changes in the level of O2 and CO2 in the blood changing ventilation levels accordingly to ensure sufficient O2 levels in the blood and maintain an appropriate CO2 level and body pH (Rogers, K.).

When at rest, the mechanics of respiration work by rhythmic control via the medulla that is responsible for breathing. The main stimulus for how we breathe at sea level is the PCO2 with the PO2 playing no role in the breathing rate. The respiratory centres in the brain set strict guidelines for the level of arteriole CO2. When at rest, the arteriole CO2 is equal to this pre-established value meaning the rate of inspiration is constant when at rest at sea level (Rakhimov, A.). Centres in the medulla oblongata are responsible for normal inspiration and expiration. The inspiratory centre controls normal quiet breathing while the expiratory centre is only activated during forced breathing. Pneumotaxic centres control breathing when at rest by continually sending signals to inhibit the inspiratory centre to prevent it from getting too full. At this point stretch receptors trigger the Hering-Breuer reflex that signal for inhibition of the inspiratory centres to allow expiration to occur. Once the lungs deflate, this inhibition stops and the process repeats (McLafferty, E. et al). While there are many internal factors that may cause the respiratory rate to change including pain, body temperature and even coughing or sneezing, external factors can have a great impact too. Inspiration can be influenced by external factors including changes in levels of central excitation such as sleep and exercise. Fluctuations in PCO2 cause a change in ventilation rate to return these values to normal.

Homeostatic control at in acute high-altitude conditions – Upon initial exposure to high altitude, a fall in the external pressure and therefore decrease of atmospheric PO2 (barometric pressure) causes a fall in the partial pressure of oxygen in the alveoli to outside its set range of between 35 – 45 mmHg (Rogers, K.). Without a counter change, the fall in PO2 would result in lower partial pressure of alveolar O2 and a reduction in the arteriole blood saturation of oxygen (SaO2) leading to a decrease in sufficient amounts of oxygen being delivered to tissues in need (Martin, D. and Windsor, J.) Initially, during acute exposure when not enough oxygen is obtained via inspiration and cells struggle to gain the adequate levels of oxygen needed, carbohydrates may be broken down to provide more energy, producing lactate as a bi product. The data from the male subjects shows higher levels of lactate in the blood at between 0.2 – 0.6% compared to when at rest (between 0.1-0.3%) supporting the idea of carbohydrate deconstruction. This occurs until the process of acclimatisation is complete.

At high altitude, due to the fall in atmospheric O2 and therefore the fall in alveolar PO2, the consequence is reduced diffusion of O2 into arterial blood. Furthermore, the pressure gradient between venous CO2 and alveolar CO2 decreases resulting in the excretion of less CO2 from the body producing an increase in alveolar PCO2. This low PO2 and high PCO2 caused by acute exposure to a hypoxic environment triggers a series of responses by the autonomic nervous system (Chawla, S. and Saxena, S.). Acclimatisation begins when chemoreceptors in the body, responsible for detecting the partial pressure of oxygen and carbon dioxide in arterial blood as well as H+ concentrations in the cerebrospinal fluid (Schoene, R), detect the high H+ levels caused by high PCO2 levels and become more sensitive. As a result, these receptors begin to fire more frequently resulting in an increase in chemoreceptor activity. This increased activity by the receptors sends a signal through the nervous system to respiratory receptors in the brain to signal respiratory muscles to work faster resulting in an increase in breathing / ventilation depth and rate (Chawla, S. and Saxena, S.). The data obtained from 6 male subjects shows how the breathing rate was significantly higher in altitude at 3500m where O2 was only 15%, ranging from 68 – 82 BPM compared to between 58 – 68 BPM when at rest at sea level. The increased ventilation rate known as hyperventilation, works to counteract the high levels of CO2 in the blood. This works by expelling the carbon dioxide at a higher rate from the lungs to reduce the CO2 tensions and increase the PO2 by forcing diffusion of oxygen into the arterial blood (Cotes, J., Chinn, D. and Miller, M.). The decrease of PCO2 in the blood caused by diffusion of said CO2 into surrounding cells, causes a change in the increase in the pH as there in less CO2 to be hydrolysed meaning less H+ ions are produced. This change in pH (respiratory alkalosis) is corrected by the kidneys renal system (Speck, D. et al). See Figure 2

Whilst external factors play a role in how well altitude is tolerated, there are genetic components that aid in such tolerance too. The effect of hypoxemia varies and is dependent on internal/external factors such as the rate of ascent and an individual’s genetic. Most evidence for genetic tolerance originates from looking at generations born in higher altitudes and how their genetics appear to have changed over time to be able to adapt to the lower oxygen environment. One genetic component to altitude tolerance is the maximum capacity an individual has for transporting oxygen around their body, VO2max (San, T. et al). Those with a higher VO2max are more likely to regulate their body effectively thereby acclimatising to higher altitude at a faster rate. Another link to genetic tolerance is suggested that those who have less metabolites in their skeletal muscles experience less muscle fatigue therefore have a higher altitude tolerance. An example of some of these metabolites include inorganic phosphates and reactive oxygen species (Guilherme, J. and Silveira, A.).


The set point theory states that when variables fall 0.5 outside of a set range, the body must counteract this change by the process of homeostasis. In this case, when the PO2 and PCO2 stray 0.5 mmHg outside the ranges 80 – 105 and 35 – 45 mmHg retrospectively, the body has a negative feedback system to return the values to their initial readings (Edwards, B.). This feedback system triggers several responses by the autonomic nervous system with the main effects including an increase in both heart rate and cardiac output before resulting in hyperventilation (Zhang, D. et al) as supported from data obtained from the 6 male subjects that showed an increase in both variable values when compared to measurement taken at sea level (see figure 1). The response by the homeostatic system to the decrease in atmospheric pressure from sea level to high altitude is caused by a decrease in arteriole PO2 and increase in PCO2. Sensitive receptors therefore relay a series of signals through the central nervous system to cause an increase in ventilation depth/rate by the increase in breathing rate. The combined increase in both breathing and ventilation rate is what causes an increase heart rate and therefore an increase in cardiac output ensures sufficient amount of oxygen is supplied to support mitochondrial activity (San, T. et al). The result of all these factors combined sees an increase in PO2 and decrease in PCO2 levels to the same as when resting at sea level. This increased ventilation rate and its subsequent effects is the process of acclimatisation to high altitudes. These monitored effects of altitude influence compared to sea level is evidence of a complex homeostatic system and negative feedback loop that is efficient at counteracting changes caused by both internal and external factors to ensure key dynamic consistency.

The physiological data obtained from 6 male subjects measures 6 key variables that are influenced by respiration; Ventilation rate (total volume of air entering lungs), Breathing Rate (number of breaths per minute), Heart Rate (number of beats per minute), Cardiac Output (amount of blood pumped through the circulatory system), Lactate Production and SaO2 levels (arteriole blood saturation of oxygen). When comparing these findings at sea level compared to when at higher altitude, we expect all these values to increase, expect the SaO2 which should see a reduction. This is because the homeostatic system counteracts fluctuations in PCO2 and PO2 by increasing the breathing rate in order to increase the ventilation rate increasing the volume of air inhaled to ensure sufficient amount of oxygen is consumed. Due to their being less oxygen inhaled per breath, the circulatory system must pump oxygen around the body at a higher rate which is why we see an increase in the cardiac output and heart rate. Finally, due to their initially being significantly lower oxygen levels when exposed to the hypoxic environment, lactate is produced from the break down in carbohydrates to support ATP production which is why we see an increase in lactate levels. The reduction in SaO2 levels is due to an there being less oxygen taken into the body due to the decreased pressure gradient between the external o2 concentration and internal pressure. This results in less oxygen binding and transported by haemoglobin in the blood. (See Figure 1 and Table 1 for supporting values).


  • Hickin, S., Renshaw, J. and Chapman, R. (2015). Respiratory System – Crash Course Series, 4th ed. Elsevier Health Science, pp. 3
  • Bergan-Roller, H., Galt, N., Helikar, T. and Dauer, J. (2018). Using concept maps to characterise cellular respiration knowledge in undergraduate students, pp 33-34
  • Asarian, L., Gloy, V. and Geary, N. (2012) Encyclopedia of Human Behavior – Homeostasis, 2nd ed, pp. 324
  • Speck, D., Dekin, M., Frazier, D. and Revelette, R. (1992) Respiratory Control: Central and Peripheral Mechanisms. University Press of Kentucky, pp 163
  • Zhang, D., She, J., Zhang, Z. and Yu, M. (2014). Effects of acute hypoxia on heart rate variability, sample entropy and cardiorespiratory phase synchronization. BioMed Eng OnLine
  • Lee, R. (1943). Respiration in man at high altitudes
  • Schoene, R. (1997). Respiration: Control of breathing at high. pp 407
  • Martin, D. and Windsor, J. (2008). From mountain to bedside: understanding the clinical relevance of human acclimatisation to high-altitude hypoxia. Postgrad Med J, issue 84, pp. 622
  • Chawla, S. and Saxena, S. (2014). RESONANCE: Physiology of High-Altitude Acclimatization. pp 540 – 544
  • San, T., Polat, S., Cingi, C., Eskiizmir, G., Oghan, F. and Cakir, B. (2013). Effects of High Altitude on Sleep and Respiratory System and Theirs Adaptations. ScientificWorldJournal
  • Rogers, K. (2011). The respiratory system (The Human Body). Britannica Educational Publishing, pp. 41-48
  • Cotes, J., Chinn, D. and Miller, M. (2006). Lung Function: Physiology, Measurement and Application in Medicine. 6th ed, Blackwell Publishing Ltd, pp 286-288
  • Edwards, B. (2020). Human Anatomy and Physiology Week 25: Respiratory System. Liverpool John Moores University. 17/02/2020
  • Guilherme, J. and Silveira, A. (2019). Could genetic and epigenetic factors explain hypoxia tolerance and superior muscle performance of Sherpas at high-altitude? The Journal of Physiology. pp.1231
  • McLafferty, E., Johnstone, C., Hendry, C. and Farley, A. (2013). Respiratory System Part 2: Gas Exchange. Nursing Standard, 27(23), pp. 39-40
  • Rakhimov, A. Normal Breathing: the key to vital health. Pp. 51-52
  • Exam 3 Review:  Chapter 22:  ANS Control of Breathing, viewed 09th March 2020,
  • Figure 1 – Mean values and standard deviations for ventilation (L.min-1) and heart rate (Beats.min-1) after 2 hours of exposure to either Sea Level and Altitude
  • Figure 2 – Negative feedback response to increased PCO2 during high altitude exposure (Reference – Exam 3 Review:  Chapter 22:  ANS Control of Breathing)


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Human Anatomy and Physiology: Respiratory and altitude. (2021, Sep 22). Retrieved from

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