Physiology of Breathing and Ventilation

Lung function, training and exercise performance

Aim

The aim of the first station of the laboratory was to assess pulmonary function using a Peak Flow Meter as well as a Vitalograph in order to determine lung training and exercise performance.  In order to do so the subject performed the experiment using both techniques and the values obtained were recorded and further compared in the discussion section.

Results

Slow Vital Capacity, Peak Expiratory Flow Rate and Peak Flow Meter values were predicted using a nomogram and compared to the recorded measurements of these variables in Figure1. Figure 2 outlines the Slow Vital Capacity, Forced Vital Capacity, Forced Expiratory Volume, their ratio as well as Vitalograph Peak Expiratory Flow Rate and Peak Flow Meter recordings were compared to the same variable recordings of Miguel Indurian, a Spanish road racing cyclist who won Tour de France for 5 consecutive years.

Fig 1. Column chart highlighting the Slow Vital Capacity, Peak Expiratory Flow Rate and Peak Flow Meter values recorded versus predicted from nomogram.

Fig.2 Column chart outlining the Slow Vital Capacity, Forced Vital Capacity, Forced Expiratory Volume, their ratio as well as Vitalograph Peak Expiratory Flow Rate and Peak Flow Meter measurements for the subject in comparison to athlete Miguel Indurian.

Discussion

The predicted and recorded values for the lung function measurements pictured in Figure 1 are similar and appropriate considering textbook values. The Slow Vital Capacity average value ranges from 3-5 l and Peak Expiratory Flow Rate is normally between 10-12 l/sec, which is slightly higher than predicted value. This could be attributed to the subject’s fitness level suggesting that their lung capacity is bigger than an average individual’s of the same sex, height and age.

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The comparison pictured in Figure 2, between the subject and cyclist Miguel Indurian shows clearly that all of the recorded variables are lower in the case of the subject. This observation is to be expected as the lung capacities of professional athletes are either naturally above the normal ranges due to either genetics or training programmes. In this case, the athlete is 1.88 meters which is higher than the subject’s height and could explain the differences in the lung function capacities. Furthermore, the ratio between Forced Expiratory Volume and Forced Vital Capacity can determine the narrowing of the smallest airways (Miller, 2005). In this case, the athlete’s ratio is 10 times bigger in comparison to the subject which suggests a considerable difference in their airway width so there is a possibility that the subject has asthma or another pulmonary disease. To conclude, it is worth mentioning that these are assumptions made on previous literature and textbook values (Levitzky, 1991).

References

Miller, M. (2005). General considerations for lung function testing. European Respiratory Journal, 26(1), pp.153-161.

Levitzky, M. (1991). Pulmonary physiology. New York: McGraw Hill.

                                                The determinants of ventilation

Aim

Station 2 of the respiratory laboratory had the aim to identify the factors that affect ventilation at rest and during exercise in either fasted or fed states. The subject fasted overnight before performing the experiment and using a Douglas bag, fractions of end tidal CO₂ and O₂, blood glucose and heart rate measurements were taken at a resting state. The same measurements were taken at 70 W work using a cycle ergometer rate and subsequently the subject was fed a carbohydrate energy gel and after 30 minutes they performed the exercise at the same work rate. The work rate was increased to 250 W and the same measurements were taken in order to be compared. Using the data collected calculations were performed to determine ventilation values, VO₂, VCO₂, and the Respiratory Exchange Ratio which were included in Table 1 for further discussion.

Results

The results included in Figure 1 are mainly as expected, Ventilation rises with the work rate, Blood glucose is higher after the carbohydrate feed, and both VO₂ and VCO₂ increase with work rate. The ventilation and RER (Respiratory exchange rate) taken at 0W work rate are higher than expected due to altered experimental conditions such as increased temperature, or due to the subject feeling uncomfortable.

Recorded data variables at different exercise states

Fig. 1 Table summarizing recordings of ventilation, work rate, VO₂, VCO₂, blood glucose, RER and heart rateat fasted and fed states.

Fig. 2 Colum chart of RER (Respiratory exchange ratio) at 70W during fasted and fed states.

Fig. 3 Scatter plot and trend line of RER (Respiratory exchange ratio) at 70W and 250W work rate.

Discussion

Figure2 highlights the respiratory exchange ratios at the same exercise rate in fasted and fed conditions and the value of 0.8 for the fasted state suggests that the subject is metabolizing mainly fat and some carbohydrates. The increase of 0.04 for the value at a fed state is not surprising as the subject is now using more carbohydrate as a substrate. Figure 3 pictures the relationship between RER and work rate suggesting that with the increase of the exercise intensity, the substrate used has a higher percentage of carbohydrate. This observation supports previous literature as the contractile elements of skeletal muscle are powered by glucose and muscle glycogen and with increase in exercise intensity carbohydrate is the main energy source being preferred to fat and protein. It is worth mentioning that the carbohydrate used for the feed of the subject was a simple sugar which took a minimum amount of time to fuel the exercise, whereas a more complex form of carbohydrate would require a longer period of time (McArdle et al, 2008).

In conclusion, the experimental results support previous literature on ventilation during exercise but it could be of great meaning to repeat the experiment in different, more appropriate conditions.

References

• McArdle, W., Katch, F. and Katch, V. (2008). Exercise physiology: ENERGY, Nutrition and Human Performance, 8^th Edition

                                                   Station 3 Discussion

Nasal splitting advantages and disadvantages

Part A of the third station of the laboratory included reading scientific literature on nasal splitting and the benefits it could have for athletes. When breathing at rest the majority of normal individuals breathe through their nose exclusively whereas during exercise ventilation increases so the nasal airways can no longer accommodate the amount of air breathed and therefore breathing occurs through oronasal respiration (Chinevere and Faria, 1999). After analysing the suggested papers it was concluded that nasal splitting decrease nasal resistance at rest and throughout isometric exercise but has little to no effect on isotonic exercise performance. Therefore, in sports like weight lifting or rugby nasal splitting can be beneficial, conferring a significant improvement in nasal resistance (Wilde and Ell, 1999).When trying to breathe nasally during exercise the dilator does not make a difference in tidal volumes or in breathing effort sensations. However, it has been shown that external nasal dilators are of great benefit to patients with nasal congestions. They increase the valve cross-sectional and stabilize the lateral nasal wall while decreasing both inspiratory transnasal pressure and resistance. The dilators are a good option for patients suffering with nasal obstruction as they are non –invasive and have a minimum risk for the user (Dinardi et al, 2014). In conclusion, nasal splitting is an unsuccessful method of improving exercise performance but can be of great benefit in ameliorating nasal congestions.

Altitude training

Part B of the laboratory regards altitude training and previous literature that analyses the benefits and disadvantages of this type of elite training. The effect of altitude training in exercise performance has received attention due to impressive achievements of Kenyan athletes which could be correlated to the high peaks of their home country. With altitude exercise capacity diminishes as arterial oxygen pressure is reduced and individuals adapted to these conditions are likely to have improved hypoxia tolerance and a better performance at sea level ( Pedlar et al, 2011)There several strategies when it comes to this type of training but the most common ones are living and training high, living high and training low, living low and training high and intermittent hypoxic training at rest. For all of these strategies  acclimatisation is paramount in order to ensure adequate erythropoietic response to altitude. There are several issues with altitude training which include dehydration, sunburn or even acute mountain sickness which can alter performance but as expected, individual response is variable. It is worth mentioning that not a lot of places in the world are suitable for a strategy such as live high train low so in order to resolve this issue, special altitude houses with lowered O₂ content have been created (Hahn and Gore, 2001). In conclusion, the altitude training plan of action comes with risks but can be of great effect depending on the individual.

• CHINEVERE, T., FARIA, E. and FARIA, I. (1999). Nasal splinting effects on breathing patterns and cardiorespiratory responses. Journal of Sports Sciences, 17(6), pp.443-447.
• Hahn, A. and Gore, C. (2001). The Effect of Altitude on Cycling Performance. Sports Medicine, 31(7), pp.533-557.
• Reis Dinardi, R., Ribeiro de Andrade, C. and da Cunha Ibiapina, C. (2014). External nasal dilators: definition, background, and current uses. International Journal of General Medicine, p.491.
• The BASES Expert Statement on Human Performance in Hypoxia Inducing Environments: Natural and Simulated Altitude
• Wilde, A. and Ell, S. (1999). Effect on nasal resistance of an external nasal splint and isotonic exercise. British Journal of Sports Medicine, 33(2), pp.127-128.

The mechanical control of ventilation

Aim

The aim of Station 4 of the laboratory was to discover how afferent systems affect lung volume and respiratory control centres. In order to do so, expired gas samples from different types of breathing using a neoprene bag were collected The samples were further analysed and for each sample recorded PCO2 and PO2 values.

Results

For the purpose of observing the effect of lung stretch receptors recordings of alveolar gas, gas after breath holding and after re-breathing as well as breath holding whilst applying vibration to the sternum were taken. The average values obtained for PO2 and PCO2 are recorded in the table below.

 Table 1.   Average PO₂  and PCO₂ measured from expired gas at different levels of breath

Re-breathing the air in the neoprene bag followed a much shorter second hold of breath. It was concluded that that the excess of CO2 is the cause of the breaking point during breath holding as carbon dioxide at a high level corresponds to low Ph and signal the need for oxygen.

The pulmonary stretch receptors are found in smooth muscle of the airways and during large inspirations they send action potentials to the inspiratory area in the medulla through the myelinated fibres of the vagus nerve. The stretch receptors inhibit ventilation so they slow respiratory frequency. This is due to the Hering-Breuer reflex, which prevents the over-inflation of the lung (Schweickert and Arroyo, 2015).

Discussion

Previous literature has shown that mechanical stimuli, such as vibration, activate these receptors which delaying the feeling of breathlessness. As a way to stimulate the stretch receptors a physiotherapy vibrator was applied to the subject’s sternum in order to compare the duration of the hold breaths. Research suggests that the amplitude and frequency of these vibrations are critical as they determine the oscillations of the lung tissues but there is no evidence that sternum vibration reaches the airways. Morphological difference between the subjects could have a major impact on the results as muscle distribution and sub-cutaneous fat layers could minimise the effects of the vibration (Binks et al., 2001).

Unfortunately, the period of time of this breath hold has not proven to be longer than the previous ones. This could have been caused by experimental errors such as poor handling of the equipment or the gas analyser. Furthermore, it is worth taking into consideration the conditions under which these measurements have been taken. The subject could have possibly been nervous, or under stress to perform the experiment in front of the class which has probably affected their performance.

In conclusion, the experiment highlights the activity of respiratory centers under different conditions and the results obtained suggest that the excess of CO2 cause the sensation of breathlessness. In order to support previous literature related to the effect of chest wall vibrations the experiment should be repeated under slightly different conditions.

References

Weisman, I., Jorge Ceballos, R. and Bolliger, C. (2002). Clinical exercise testing. Basel, etc.: Karger.

Binks, A., Bloch-Salisbury, E., Banzett, R. and Schwartzstein, R. (2001). Oscillation of the lung by chest-wall vibration. Respiration Physiology, 126(3), pp.245-249.

Simulation of respiratory function

Aim

The aim of Station 5 laboratory is to observe the effects of changes in breathing pattern on blood gas tensions using the MacPuf programme. In order to do so we examined 6 variables: alveolar oxygen pressure, arterial oxygen pressure, arterial oxygen saturation, arterial oxygen content, venous oxygen pressure, venous oxygen content at different oxygen pressures..

Results

Figure 1 pictures the increase of atmospheric, alveolar, arterial and venous PO₂ with the increase of inspired oxygen. Figure 2 highlights the pressure and content of oxygen in arteries and veins at 300 Kpm/min versus 900 Kpm/min whereas Figure 3 compares these values for a fit and an unfit subject at the same work rate. Figure 4 presents the pressure and content of oxygen in arteries and veins with the decrease of inspired oxygen at a work rate of 300 Kpm/min. All of the values have been obtained using simulation of the MacPuff programme and interpreted as performed experiments in the discussion section.

Fig. 1 Atmospheric PO2 (mmHg), Alveolar PO2 (mmHg), Arterial PO2 (mmHg) and Venous PO2 (mmHg) at inspired O₂ of 15%. 21% and 27%.

Fig. 2 Arterial PO2 (mmHg), Venous PO2 (mmHg), Arterial O2 content (ml/100ml) and Venous O2 content (ml/100ml) at work rates of 300 Kpm/min and 900 Kpm/min.

Fig. 3 Arterial PO2 (mmHg), Venous PO2 (mmHg), Arterial O2 content (ml/100ml) and Venous O2 content (ml/100ml) at 300 Kpm/min for a fit and unfit subject.

Fig. 4 Arterial PO2 (mmHg), Venous PO2 (mmHg), Arterial O2 content (ml/100ml) and Venous O2 content (ml/100ml) at 300 Kpm/min at inspired O₂ of 21%, 16%, 10% and 6.5%.

Discussion

The increase of alveolar, arterial and venous PO₂ with the increase of inspired oxygen is expected as atmospheric O₂ pressure is inhaled and further diffused in the blood. Oxygen moves down the pressure gradient from the air level according to the oxygen cascade so the PO₂ values lower going from atmospheric to alveolar, arterial and venous levels (Habler and Messmer, 1997). The pressure and content of oxygen in arteries and veins don’t have a significant change when compared at 300 Kpm/min versus 900Kpm/min. This could be attributed to a small change in the exercise intensity or potentially too short of a period that the subject has performed the more intense exercise. Similarly, the values obtained at the same work rate for the fit and unfit subjects do not present significant differences which could be due to a very short running of the programme so it is recommended that the experiment is repeated for a longer period of time for the results to be valid. The values analysed in Figure 4 replicate the values for pressure and content of oxygen in arteries and veins at increasing altitude. The higher the altitude, the lower the pressure of oxygen so the arterial PO₂ decreases with the decrease of inspired oxygen (Park et al., 2016) .The same trend is observed for the arterial oxygen content and should be for the venous oxygen according to the oxygen cascade. The data collected might not be accurate due to misuse of the Macpuff programme so unfortunately, the data does not support previous literature.

In conclusion, the Macpuff stimulations have proven unsuccessful for part of the experiment so it would be of great use to repeat the laboratory exercise in order to identify the faults in the recording of the data.

References

Habler, O. and Messmer, K. (1997). The physiology of oxygen transport. Transfusion Science, 18(3), pp.425-435.

Park, H., Hwang, H., Park, J., Lee, S. and Lim, K. (2016). The effects of altitude/hypoxic training on oxygen delivery capacity of the blood and aerobic exercise capacity in elite athletes – a metaanalysis. Journal of Exercise Nutrition & Biochemistry, 20(1), pp.15-22.

                                  The chemical control of ventilation

Aim

Station 6 of the respiratory system laboratory classes consisted of a re-breathing experiment with the aim to examine the effect of increasing inspired carbon dioxide concentrations on the chemosensitive afferent systems. Under standard conditions a healthy individual breathes under the influence of PCO_2, the most important factor in the control of ventilation. In order to record the extent to which the two correlate an experiment was performed during normal conditions, using atmospheric gas and in hyperoxic conditions, using 100% O₂ gas. Using a Krogh spirometer and the Spike 2 software the ventilation pattern (L/min BTPS) and alveolar PCO₂ (mmHg) were recorded and plotted against each other (Figure 1) in order to determine the trends and gradient.

Results

        Figure 1.Correlation between alveolar PCO₂ (mmHg) and Ventilation (L/min BTPS) in atmospheric (normoxic) and hyperoxic (100% O₂) conditions pictured in a scatter plot through lines of best fit.

Discussion

The normoxic line of best fit indicates that ventilation rises with te increase of CO₂ in the alveoli as previously suggested by existing literature. In hyperoxic conditions, the trend line also indicates that the higher the PCO₂ the more ventilation increases. Figure1 suggests that ventilation increases at a higher rate in atmospheric conditions in comparison to the rise in hyperoxic conditions . This is probably due to a higher PCO₂ starting point in the atmospheric air, which then diffuses into blood at an alveolar level. Furthermore, the CO₂ partial pressure reaches a higher amount in hyperoxic conditions. For both situations the line is increasing which indicates that as the subject rebreathes, metabolic CO₂ is added to the bag so that the inspired PCO₂ increases gradually causing a rise in the ventilatory response. The relationship between the two variables is regulated by chemoreceptors, which are surrounded by brain extracellular fluid and respond to alterations in the H⁺ concentration. When alveolar PCO₂ rises, carbon dioxide diffuses into the cerebrospinal fluid, releasing H⁺ ions, which stimulate the chemoreceptors. Peripheral chemoreceptors trigger additional stimulus, which enhances the rise in PCO₂ and therefore a rise in ventilation (West, 2012).It is worth mentioning that the subject described the rebreathing experience in hyperoxic conditions uncomfortable and felt light-headed towards the end which could be attributed to the rise in PCO₂ content. The subject was unaware of the nature of the gas in order to prevent any biased results.

In conclusion, the experiment should be performed again, including measurements of PO₂, in order to determine if it has an effect of ventilation as previous literature suggests that higher O₂ content makes the slope of line less. At the same time, reduced PO₂ is meant to increase ventilation so it could be useful to compare the two.

References

West, J. (2012). Respiratory physiology. Philadelphia: Wolters Kluwer Health/Lippincott Williams & Wilkins, pp.128-136.

 Station 2 Discussion

Erythropoietin discussion

Part A of the second discussion session focuses on erythropoietin and the doping controversy around it. Erythropoietin (EPO) is a glycoprotein hormone produced in the kidneys in adults and enhances the production of more red blood cells. Therefore, more oxygen is transported to the muscles improving endurance performance significantly, becoming a popular doping method for elite athletes. The only legal way to get more erythropoietin is by altitude training but unfortunately, many athletes abuse it as it easy to perform and difficult to detect (Hopkins, 2018). Up to date, there is no reliable test for EPO and currently anti-doping authorities use indirect haematological and direct pharmacological approaches (Diamanti-Kandarakis et al., 2005). Both of these techniques face limitations that allow athletes to abuse the administration of recombinant human erythropoietin. The existing blood test does not detect EPO itself but its effects on red blood cells and their density, which can be considered unfair as some individuals have a naturally high volume of red blood cells or alternatively, could achieve a higher haematocrit by training at altitude. The urine test detects the artificial recombinant human erythropoietin using immunoblotting. The main issue with this technique is the short half-life of EPO, of only 3-4 days after the administration, making it inefficient as a detecting technique. In conclusion, the existing approaches to EPO testing are not accurate and lead to illicit practices but novel molecular profiling techniques could soon put an end to EPO doping (Lundby et al, 2012).

Maximal uptake limitations

The second part of the discussion laboratory analyses maximum oxygen uptake and its limiting factors. The main ones refer to cardiac output and skeletal muscle limitations. Maximal cardiac output is thought to be of paramount importance when it comes to VO₂ max differences as there is little variation in maximal heart rate and oxygen extraction. During exercise there is a small amount of oxygen to be extracted from the blood which suggests that blood flow increase is the only improvement to be made when exercising.  Furthermore, previous literature has shown that maximum oxygen uptake is also limited by oxygen carrying capacity, so increasing the haematocrit by blood doping would result in a higher haemoglobin content so therefore an increased oxygen carrying capacity (Basett, 2000). From the skeletal muscle point of view, researchers have discovered that oxygen diffuses between the surface of the red blood cell and the sarcolemma where the pressure of oxygen significantly lowers. However, the experiment was performed on canine skeletal muscle so it is hard to determine if these findings apply to human performance. To conclude, the limiting factors of oxygen uptake have several causes but oxygen carrying capacity seems to be the most significant.

References

Basett, D. (2000). Limiting factors for maximum oxygen uptake and determinants of endurance performance. Medicine & Science in Sports & Exercise, p.70.

Diamanti-Kandarakis, E., Konstantinopoulos, P., Papailiou, J., Kandarakis, S., Andreopoulos, A. and Sykiotis, G. (2005). Erythropoietin Abuse and Erythropoietin Gene Doping. Sports Medicine, 35(10), pp.831-840.

Hopkins, W. (2018). Sportscience In Brief. [online] Sportsci.org. Available at: http://www.sportsci.org/jour/0002/inbrief.html [Accessed 13 Oct. 2018].

Lundby, C., Robach, P. and Saltin, B. (2012). The evolving science of detection of ‘blood doping’. British Journal of Pharmacology, 165(5), pp.1306-1315.

Maughan, R. (1999). Basic and applied sciences for sports medicine. Oxford: Butterworth-Heinemann.