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.

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 PCO2, 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.

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.

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.