Observations of the Properties of the Human Respiratory System. April Ramos Dela Fuente. Bill Keenen; Tommy Kham; Grace Park

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1 P a g e 1 Observations of the Properties of the Human Respiratory System April Ramos Dela Fuente Bill Keenen; Tommy Kham; Grace Park NPB 101L - Section 06 - Ailsa Dalgliesh 11/25/14

2 P a g e 2 INTRODUCTION The human respiratory system is generally known for the simple act of breathing. It is not often recognized for its role in other functions such as vocalization or even temperature control. The main role of respiration is its intake of oxygen (O2) for metabolic processes and the elimination of carbon dioxide (CO2), a waste product of metabolism (Sherwood, 461). The two types of respiration are internal and external respiration. Internal respiration, also known as intracellular respiration, refers to the metabolic processes that occur in the mitochondria within a cell. Here, O2 is used to acquire energy from nutrient molecules. As energy is derived, CO2 is produced. (Sherwood, 461). External respiration accounts for the events that occur during the exchange of gases taking place within the lungs. The respiratory system plays an important role in the human body, allowing the exchange of gas to occur between tissues and the external environment (Sherwood, 461). Intracellular respiration governs external respiration. As mentioned before, mitochondria use O2 for metabolic activities. When cells sense a decrease in arterial PO2, they send signals through the afferent nerves to the dorsal respiratory group in the medullary respiratory center to innervate the contraction of inspiratory muscles (Sherwood, 500). The diaphragm, innervated by the phrenic nerve, contracts and moves downwards. External intercostal muscles, innervated by the intercostal nerve, contract and allow the rib cage to elevate and expand. The thoracic volume increases and alveoli can passively enlarge due to the more negative atmospheric pressure. This increase in alveolar volume decreases the alveolar pressure below atmospheric pressure and air flows into the lungs (Sherwood, 470). During expiration, a passive process, the lungs recoil as inspiratory muscles relax. As the lungs recoil, alveolar pressure is greater than atmospheric pressure and air moves out. No muscle is exerted and no energy is required. However, muscles of the abdominal wall can contract and cause further release of air during forced or active expiration (Sherwood, 472). Tidal volume (TV) is the amount of

3 P a g e 3 air normally inhaled and exhaled. The volumes of air that can be forcibly inhaled or exhaled above TV are known as inspiratory and expiratory reserve volumes (IRV, ERV). Residual volume (RV) is the gas remaining after a forced maximal expiration. All four types of volumes make up the total lung capacity (TLC). Functional residual capacity (FRC) is the sum of ERV and RV. Vital capacity is the volume of air that can be expelled which are ERV, IRV, and TV (Sherwood, 479). Ventilation is the movement of air through inhalation and exhalation. Several types of ventilation measured are minute ventilation, dead space ventilation, and alveolar ventilation. Ventilation is regulated by stretch receptors and chemoreceptors. Stretch receptors prevent overexpansion of the lungs. Central chemoreceptors in the medulla detect increases in PCO2 and decreases in ph by sensing an increase in the concentration of hydrogen ions within the cerebrospinal fluid (Rhoades et al, 390). Peripheral chemoreceptors located in the carotid bodies and aortic arch detect local changes rather than global. When a decrease in arterial PO2, decrease in ph, or an increase in PCO2 is detected, these receptors are activated to send signals to increase ventilation rates (Rhoades et al, 390). The purpose of this experiment was to analyze the effects of inspired gas composition, lung volume, and moderate exercise on respiration. IRV and ERV were expected to be more than TV. The largest amount of %CO2 before breath-hold was expected in rebreathing while the smallest amount of %CO2 before breath-hold was expected in hyperventilation.%co2 after breath-hold should have all been similar if subject was holding breath at the same discomfort after each type of ventilation. While a subject increased workload and duration of exercise, ventilation was expected to increase to match the respiratory needs observed during exercise, known as hyperpnea.

4 P a g e 4 MATERIALS AND METHODS Specific details of the procedures from this particular lab can be found in NPB 101L Physiology Lab Manual, Second Edition by Erwin Bautista and Julia Korber. In brief, amounts of O2 and CO2 from the lungs were observed in response to varying types of ventilation and lung volumes. Measurement of static lung volumes were done at a spirometry station using a male subject rested in a seated position. The effects of inspired gas composition and lung volumes on respiration were measured by observing duration of breath-hold and analyzing the %CO2 before and after subject held his breath during normal breathing, re-breathing, and hyperventilation. The effects of increased metabolic activity on respiration were measured by increasing workload on a stationary bicycle by 0.5pka every 2 minutes until 2.0pKa was achieved. Air flow, CO2 expired and respiratory rate (RR) were recorded on BioPac. IRV was calculated on BioPac by determining the change in volume between the peak of the normal inhalation before the maximum inhalation and the peak of the maximum inhalation. ERV was calculated in the same manner by taking the difference between the trough of the maximum exhalation and the trough of the last normal exhalation. TV was determined by taking the absolute value of the area between a peak and trough of a normal breath. Volume capacity (VC) was recorded by taking the absolute value of the area between the peaks of the maximum inhalation to the trough of the maximum exhalation. When observing the relationship between hyperpnea and exercise, mean TV and mean CO2 expired for each workload were calculated using four random values during the last 30 seconds of each particular workload. To calculate minute ventilation (VE), average TV was multiplied to the mean RR. To calculate the minute CO2 production, VE was multiplied to the average end-tidal CO2 (FECO2).

5 P a g e 5 RESULTS Measuring Static Lung Volumes In order to understand static lung volumes, static lung volumes were measured from a male subject. TV is the volume of air that enters and leaves the lung per normal breath and was recorded at being L (Table 1). With maximal inhalation, IRV was observed at L. ERV was observed to be 2.314L during complete forced exhalation. VC was observed to be L. Effects of Inspired Gas Composition and Lung Volume on Respiration The effects of composition of gas inspired on respiration were examined by measuring and analyzing end-tidal CO2 before and after a subject altered their arterial PCO2 during the following ventilation types: normal breathing, re-breathing and hyperventilation. As shown in Table 2, rebreathing had the most %CO2 before breath-hold at 5.45% while hyperventilation had the least %CO2 before breath-hold measured at 2.95%. %CO2 after breath-hold were similar between normal breathing and hyperventilation. %CO2 after breath-hold during re-breathing was slightly higher than the other two values (Figure 1).

6 P a g e 6 The subject had their breath held after normal breathing, re-breathing, and hyperventilation. With normal breathing, subject was able to hold their breath for 57 seconds. As shown in Figure 2, breath-hold after hyperventilation was almost for 70 seconds, about three times longer than the breathhold after re-breathing.

7 P a g e 7 To observe lung volume and its effects on respiration, a subject participated in different inhalations and exhalations and was then asked to hold their breath until they felt absolute discomfort. As illustrated in Figure 3, duration of breath-hold after normal expiration was 39 seconds. Normal inhalation had a close duration of breath-hold at 47 seconds. Forced inhalation had the most significant duration of breath-hold at 132 seconds. After forced exhalation, duration of breath-hold was 27 seconds, the shortest out of all the varying lung volumes.

8 P a g e 8 Exercise Hyperpnea To observe respiratory changes in response to increases in metabolic activity, ventilation responses were recorded during moderate physical activity. As workload increased, TV and CO2 expired (FECO2) increased slightly, remaining close to resting values (Figure 4). RR increased with increases in workload and actually decreased between workloads 1.5pKa and 2.0pKa. Overall, minute ventilation (VE) increased during rises in workload. However, VE decreased from 0.5pKa and 1.0pKa, and again between 1.5pKa and 2.0pKa (Table3). The ventilation parameter that changed the most was minute CO2. At rest, minute CO2 was ml/min. By 2.0pKa, minute CO2 increased to ml/min.

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10 P a g e 10 DISCUSSION In addition to vocalization, temperature control and endocrine functions, the human respiratory system provides the energy needed by the cells within the body. Without external respiration and the exchange of gas within the lungs, essential amounts of oxygen would not be transported to cells properly, increasing carbon dioxide levels and preventing internal respiration to occur smoothly. Studies have shown that exposure to assorted breathing patterns, different gas levels and changes in ventilation generate various responses in respiration. This lab explored static lung volumes, the effects of lung volume and inspired gas composition on respiration, and the concept of hyperpnea during exercise. Static Lung Volumes During a study by Zuurbier et al, VE in resting car passengers ranged from 1.5 to 5.3 L/min. (Zuurbier et al). The determined TV for our subject was L. During the exercise, RR of the subject was 10bpm. By multiplying TV to the RR, the subject had a calculated VE of 6.691L/min. This VE, was within the same range for normal ventilation described in the study by Zuurbier et al. Because dead-space volume (DS) can roughly equal a subject s weight (160lbs), his determined dead-space volume was 160 ml. By multiplying his DS to his RR, his dead space ventilation (VDS) was 1.60L/min. Alveolar ventilation (VA) is equal to the difference between VE and VDS. The VA for the subject was 5.091L/min. IRV and ERV are additional volumes of gas that can be inhaled or exhaled above and beyond TV during force maximal inspiration and expiration (Sherwood, 479). With that being said, both IRV and ERV were expected to be more than TV. In fact, the subject s IRV and ERV were greater than his TV. Also, vital capacity (VC) is the sum of TV, IRV and ERV and yet, as seen in Table 1, VC was less than the three volumes combined. This could have been a result of subject bias due to the subject observing their results as they were being recorded. The subject was sitting across

11 P a g e 11 the computer and saw his breathing being recorded. In addition to these varying volumes, functional residual capacity (FRC) plays an important role in respiration. In addition to allowing air to be readily available for constant gas exchange, FRC also holds the key to why human lungs cannot completely deflate. Since it is the volume of gas that remains in the lungs at the end of every normal TV expiration, FRC prevents the lungs from collapsing after each breath (Sherwood, 479). Effects of Inspired Gas Composition and Lung Volumes on Respiration During the exercise consisting different ventilation methods, there were some differences between the expected end tidal %CO2 before breath-hold compared to the end tidal %CO2 that were actually observed. In normal breathing, it was expected that %CO2 would be lower before breath-hold than after. Based on the results, however, %CO2 was higher before breath-hold than after (Figure 1). Breath-hold during re-breathing should have been higher before breath-hold than after and was demonstrated in our results as well. Lastly, hyperventilation should have shown a lower %CO2 before the breath-hold than after, but in the case of the observed results, the %CO2 was higher before breathhold than after by 0.77% (Table 2). Due to the subject s physiological state and the consistency of the procedure, variations in results could had been encountered. For end tidal %CO2 after breath-holds, it was predicted that the longest breath-hold would be after hyperventilation while the shortest breath-hold would come after rebreathing. It was also predicted the end-tidal CO2 would be the same or similar after normal breathing, re-breathing and hyperventilation. Although end tidal %CO2 results after breath-hold are generally seen around 7%, the results were somewhat consistent. When comparing results shown in Figure 1, there were slight variations between the end-tidal %CO2, but were all still within range of one another. During normal breathing, the end-tidal %CO2 after breath-hold was 2.44%. Similarly, end-tidal %CO2 after breathhold for hyperventilation was 2.18% End-tidal %CO2 after breath-hold for re-breathing was the only

12 P a g e 12 one that was slightly skewed at 3.19%. This may had been caused by an error in data collecting. In regards to re-breathing, there is a usual increase in arterial PCO2. In general, re-breathing will affect arterial gases by increasing PCO2. On the other hand, hyperventilation results in significantly decreasing arterial PCO2. The effects of hyperventilation on arterial gases include quickly lowering normal alveolar CO2 and causing it to exit the body via expired air (McArdle et al, 265). As shown in Figure 2, duration of breath-hold was the longest after hyperventilation and the shortest after re-breathing. This is due to plasma CO2 and how it strongly influences respiratory efforts such as breath holding. Re-breathing increased PCO2 because the subject was inhaling and exhaling the same air in the bag. There was no gas exchange between the air in the bag and the external environment. So as the subject continued to inhale and exhale, greater amounts of CO2 were inspired than O2. During hyperventilation, plasma and arterial PCO2 levels were decreased. Hyperventilation does this by increasing VA greater than the actual ventilation needed for O2 consumption and CO2 elimination during metabolism (McArdle et al 265). Changes in arterial PO2 and PCO2 are monitored by the central and peripheral chemoreceptors. Central chemoreceptors are located in the medulla and sense increases in PCO2. Peripheral chemoreceptors are located in the carotid bodies in the carotid artery and within the aortic arch (Sherwood, 501). They are mostly activated by decreases in arterial PO2 but are also able to sense increases in PCO2. When increases in PCO2 and decreases in arterial PO2 are detected, signals are sent to the dorsal respiratory group, the part of the medulla that causes increases in ventilation rates (O Regan et al). Not only can peripheral chemoreceptors detect fluctuations in arterial PO2 and PCO2, but they also have the ability to detect decreases in ph as well. Chemoreceptors also detect ph to determine respiratory control because the concentration of H + ions is proportional to PCO2. CO2 and H2O react to produce HCO3 - and H + as end products. Build-

13 P a g e 13 up of CO2 results in a build-up of H + ions, decreasing ph. Without an adequate supply of O2, low ph can cause respiratory acidosis. Changes in ph detected by chemoreceptors will stimulate the respiratory center to adjust alveolar ventilation (O Regan et al). Changes in alveolar ventilation will affect arterial ph by either increasing or decreasing the concentration of H + ions affecting respiration. For example, re-breathing will cause an increase in PCO2 resulting in a decrease in ph. On the contrary, hyperventilation will cause a decrease in PCO2, decreasing H + ions and decreasing ph (Sherwood, 581). Exercise Hyperpnea Stretch receptors can be found in the smooth muscle of airways. They are activated when lungs are stretched at large tidal volumes. They send signals down afferent nerve fibers through the vagus nerve to the medullary respiratory center in order to inhibit inspiratory neurons. Before the lungs overinflate, inspiration is interrupted by this negative feedback. This is known as the Hering-Breuer reflex. When tidal volume is large, as seen during exercise, the Hering-Breuer reflex is triggered to prevent the lungs from overinflating (Sherwood, 500). In a study by Wasserman et al, plasma CO2 and O2 tensions were seen to be directly related to the control of respiration and ventilation, demonstrated by the effects of workload intensity on ventilatory response during exercise (Wasserman et al). As observed in their subjects, O2 consumption increased with increases in workload. After a certain duration of continuous exercise, the mean O2 consumption remained consistent over time. Their data indicated that steady states of O2 consumption were related to prolonged time at workload intensities. Similar results were seen during the cycling portion of lab, also demonstrating hyperpnea induced by exercise. Hyperpnea refers to increased ventilation to match increased metabolic demand by body tissues (Rhoades et al, 391). Overall, TV and fraction of expired volume (FECO2) remained constant during the

14 P a g e 14 duration of the cycling exercise (Figure 4). RR and VE increased as well. Minute CO2, the amount of CO2 expired from the lungs per minute, was the respiratory parameter that changed the most during exercise (Figure 4). When looking at TV, there was a slight increase during workloads 0.0pKa and 0.5pKa. However, TV decreased to normal levels after 1.0pKa. This increase and decrease in TV may had been a display of the Hering-Breuer reflex preventing the over inflation of the lungs. In terms of respiratory rate, the subject showed a slow but consistent increase in breaths per minute. However, RR did decrease from 17bpm to 15bpm between workloads 1.5pKa and 2.0pKa. VE decreased at this same interval as well (Figure 4). This may had been due to O2 levels matching the demand for CO2 removal and ventilation rates no longer needing to increase. Due to VE being a product of TV and RR, as either of these parameters increase, VE increases as well. What regulates respiration in an exercising individual is the drive to increase ventilation to match the increase in metabolic activity (Rhoades et al, 390). Hyperpnea matches the demand for CO2 removal by increasing ventilation rate. A dining feature of hyperpnea is increased ventilation with no change in arterial blood PCO2. Therefore, hyperpnea during exercise in independent from the role of chemoreceptors. However, chemoreceptors do regulate respiration in a resting individual. Chemoreceptors will be activated and increase ventilation rates when they sense decreases in arterial PO2 and ph, and increases in PCO2 (Rhoades et al, 390). CONCLUSION As static lung volumes were being observed, IRV and ERV were greater the TV. Although VC is the total of IRV, ERV, and TV, the subject s VC did not equate to the sum of his IRV, ERV, and TV. This may had been due to the subject watching his own breathing be recorded on the computer screen. During normal breathing, end-tidal %CO2 was supposed to be lower before breath-hold than after but data collected showed the opposite. With re-breathing, end-tidal %CO2 was much higher prior to breath-hold than after breath-hold. With hyperventilation, %CO2 was supposed to be much lower

15 P a g e 15 prior to breath-hold than after breath-hold. However, %CO2was seen to be higher before breath-hold than after breath-hold. Differences from what was supposed to be expected were caused by complications during data collection. The longest duration of breath-hold was seen after forced inhalation with a duration of 132 seconds. The shortest duration of breath-hold was 27 seconds, which was done after a forced exhalation. During increases in workload during exercise, hyperpnea came into play by increasing VE to match the demand for O2 used during increased metabolic activity (Dominelli et al). Results from lab provided a greater understanding of the relationship between internal and external respiration demonstrated by static lung volumes, various ventilations, and hyperpnea.

16 P a g e 16 WORKS CITED Bautista, Erwin, and Julia Korber. NPB 101L Physiology Lab Manual. 2nd Edition. N.p.: Cengage Learning, Print. Dominelli, P. B., et al. "Precise mimicking of exercise hyperpnea to investigate the oxygen cost of breathing." Respiratory physiology & neurobiology 201 (2014): Web. 20 Nov McArdle, William D., Frank I. Katch, and Victor L. Katch. Exercise Physiology: Nutrition, Energy, and Human Performance. Baltimore, MD: Lippincott Williams & Wilkins, Print. O'Regan, R. G., and S. Majcherczyk. "Role of peripheral chemoreceptors and central chemosensitivity in the regulation of respiration and circulation." Journal of Experimental Biology (1982): Web. 20 Nov Rhoades, Rodney, and David R. Bell. Medical Physiology: Principles for Clinical Medicine. Philadelphia: Wolters Kluwer Health/Lippincott Williams & Wilkins, Print. Sherwood, Lauralee. Human Physiology: From Cells to Systems. 7th ed. Australia: Thomson/Brooks/Cole, Print. Wasserman, Karlman, Antonius L. Van Kessel, and George G. Burton. "Interaction of physiological mechanisms during exercise." J Appl Physiol 22.1 (1967): Web. 20 Nov Zuurbier, Moniek, et al. "Minute ventilation of cyclists, car and bus passengers: an experimental study." Environ Health 8.48 (2009). Web. 21 Nov

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