Effect Of Caffeine On Breathing And Pulse Rate Biology Essay

return Of caffein On Breathing And Pulse Rate biota renderCaffeine is a natural chemical substance known to use up stimulant properties within the bole (Addicott MA Laurienti PJ, 2009). introductory research center on caffeins ability to affect ventilating system, riptide pressure, mood, and mental stress (Kennedy MD et al. 2008 Addicott MA Laurienti PJ, 2009). Their conclusions concluded that caffeine in reality spiked blood pressure, ventilation and rawness regulate (Kennedy MD et al., 2008) while others claimed that it had no sprightliness and soul on disembodied spirit rate or breathing (Ratliff-Crain J et al., 1989). Some gaps in these studies were that very few actually measured the rate of breathing, save quite focused on the volume of breathing and the percent oxygen impregnation/diffusion (Chapman R Stager JM, 2008), as well as blood pressure, rather than inwardness rate (Ratliff-Crain J et al., 1989).This try aimed at finding a clear relationship b etween ingesting caffeine, and its effect, if any, on breathing and heart rate, after the subjects performed incremental stepping make fors. The significance of this study is vital in sport, in particular caffeines role in the Olympics (Spriet LL, 1995), and its potential as a prophylactic in treating asthma (Welsh EJ et al., 2010).MethodsSee School of Biological Sciences (2010). Refer to Appendix (1) for the hypotheses.Results utilise the t-test it was found that the mean (+/- redact) change in flash rate was non significantly different between non-caffeine (Group A) and caffeine (Group B) hard-boiled subjects (t=0.4, df=161, P=0.7 ie P0.05). (Refer to Appendices 2a, 2b,3a, and 3b for the data and t-test)Figure 1 The mean of changes in the pulse rate of non-caffeinated (control) and caffeinated (treatment) participants after performing a stepping exercise. Error bars are the range. N= cxl and n= 75 for the non-caffeinated and caffeinated groups respectively.Using a paired d euce sample for mean t-test it was found that the mean (+/- range) change in respiration rate was non significantly different between non-caffeine (Group A) and caffeine (Group B) treated subjects (t=-0.7, df=132, P=0.5 ie P0.05). (Refer to Appendices 2a, 2b,3a, and 3b for the data and t-test)Figure 2 The mean of changes in the breathing rate of non-caffeinated (control) and caffeinated (treatment) participants after doing a stepping exercise. Error bars are the range. N=140 and n= 75 for the non caffeinated and caffeinated groups respectively.DiscussionThe results of the investigation revealed that the struggle in mean pulse rate change between the two groups was 1.1 BPM and the mean breathing rate was 1 BRPM. This indicated that there were no significant difference between mean change in pulse rate and breathing rate between the group that was taking the caffeinated deglutition (treatment), and the group that ingested the non -caffeinated beverage (control). Therefore, since (P 0.05) the null system (HO) was accepted, and the alternative hypothesis (HA) was rejected.Prior research revealed that caffeine had no significant effect on the ventilator responsiveness or exercise ventilation on exercise -induced subjects next the administration of a moderate dose of caffeine (8mg per kilogram of body weight). Any modest ontogeny in breathing rate was attributed to caffeines junior-grade effect on the Central Nervous System, rather than a locate effect on the respiratory system (Chapman R Stager JM, Caffeine stimulates ventilation in athletes with exercise-induced hypoxemia, 2008). However, other studies have suggested that caffeine acted in the path of a ventilator stimulant and increased the breathing rate of individuals (Chapman R Mickleborough TD, 2009).Similar studies found that caffeine increased the mean change in pulse rate by 6 beats/min an arcminute after ingesting caffeinated coffee (350mL, 140mg of Caffeine). This revealed that while caffeine may affect the heart rate, its relative impact had no significant effect (Kennedy MD et al., 2008). hike up research concluded that regular consumption of coffee could not increase the heart rate and blood pressure unless consumed chronically and excessively (Ratliff-Crain J et al., 1989).The experimental data revealed that naturally there were a large range of values, beginning from as low as 3 BPM, 1 BRPM and peaking to cx BPM, and to 62 BRPM respectively. The issue with having such a large range was that it disguised any significance to the mean. The extreme data points would distort the mean value, thus far if caffeine had proven to have a significant effect. Thus, its effect would not be reflected in the results. Whilst increasing the sample size and repeating the experiment a number of times would improve the reliability of the experiment, it would do puny to increase the precision of results. This is due to the presence of natural variation. Different nation have diffe ring athletic ability, sensitivity to caffeine, or gender differences, which the sample sizes (n=140 and n=75), did not account for. The failure to take account for the constitution of the sample sizes greatly reduced the power of the experiment. Research suggests that males and females may actually have distinct responses (Kennedy MD et al., 2008), and so must be accounted for separately. This could be improve by separating the caffeinated and non- caffeinated groups into gender types, and peradventure only observing its effect on athletes (Chapman R Stager JM, Caffeine stimulates ventilation in athletes with exercise-induced hypoxemia, 2008).The step of coffee may have been too small experimentally to build up a noticeable effect. Switching the dose to a full cupful of coffee could enhance the effects of caffeine (Kennedy MD et al., 2008), or perhaps the length of time between ingestion and exercise was too pathetic. increase the period from 1 hour to 2 hours could give ca ffeine more than(prenominal) time to produce its effects (Kennedy MD et al., 2008). The accuracy of the results could have been improved by apply more sophisticated counting methods to measure heart rate like using a digital pulse readout (i.e. an ECG), or percentage arterial oxyhemoglobin saturation to measure ventilation, which would produce more accurate results (Chapman R Stager JM, Caffeine stimulates ventilation in athletes with exercise-induced hypoxemia, 2008).The discount of this study is particularly important in the issue of caffeine bans from the foreign Olympic Committee, and whether or not it provides legal ergogenic advantage to athletes in short distance running or other aerobic activities. The rules governing caffeine ingestion prior to exercise may be revised if caffeine is proven to have substantially enhanced the athletes pulmonary capabilities (Spriet LL, 1995). Other upcoming studies of caffeine include developing prophylactics for asthma (from its anti- inflammatory and bronchodilator properties). Randomised clinical trials have already confirmed improvements in lung conk out after using caffeine. This could produce new front line drugs to treat asthma (Welsh EJ, 2010).In conclusion, the caffeinated and non caffeinated groups showed a slight mean difference of 1.1 BPM and 1 BRPM, but statistically, there were no significant change in the mean heart rate or the mean breathing rate, which means the null hypothesis was accepted (P0.05), and the effects of caffeine was not proven conclusive on either.ReferencesAddicott MA, Laurienti PJ. (2009). A comparison of the effects of caffeine following abstinence and radiation diagram caffeine use. 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Health Psychol. 1989 , 8 (4), 427-427.School of Biological Sciences, The University of Sydney. (2010). Human Biology Unit of Study Manual for Students.Spriet LL. (1995). Caffeine and Performance. International Journal of Sport Nutrition. , S84-99.Welsh EJ, Bara A, Barley E, Cates CJ.(2010). Caffeine for asthma. Cochrane Datab ase Systematic Reviews. 1(1) CD001112.