BIOL1008report_540807963

Title
Analyzing the effect of hyperventilation, exercise and normal respiration on breath holding
times
Introduction
Respiration is the exchange of gasses with oxygen(O) entering and the removal of carbon
dioxide (CO₂). The body removes CO₂ from the bloodstream, via diffusion, to the lungs as a
byproduct of cellular respiration causing the urge to breathe and preventing a high
concentration in the blood(pCO₂).

So that this forms a relationship between the concentration of CO₂ in the blood and lungs. The
blood’s general pH ~7.4, is so that high CO₂ causes it to become acidic and low CO₂ makes it
alkali.

Different treatments will affect CO₂ levels in the bloodstream such that holding your breath
causes increased CO₂, depleting O. Different treatments include hyperventilation: excessively
panting with deep recurrent breaths to extinguish CO₂ and preserve O levels and exercise
(physical activity) increases cellular respiration and breathing, increasing CO₂ production. As
opposed to normal ventilation which is more balanced between O & CO₂.

Therefore the breath holding duration is influenced by treatments performed by subjects which
cause changes so I hypothesize that If a person hyperventilates prior to BHT then CO₂ is flushed
out of the body allowing you to hold your breath longer.

Results
The results observed the effect of different treatment groups measured in terms of SE=Standard
error, n-samples size and mean breath holding time. The mean breathing holding time for
individuals who were subjected to hyperventilation prior was 68.74sec (SE=2.920, n=126)
effectively the longest time supporting our hypothesis. Whilst the mean time for normal
ventilation and those who completed exercise was 47.59sec(SE=1.688,n=129) and 16.35
sec(SE=0.670,n=122) respectively (Figure 1).

This supports our hypothesis as CO₂ concentration decreases and is flushed outside prolonging
O’s release . Whilst hyperventilation extended breath holding times to a significant extent, this
is followed by normal ventilation which is more balanced and 20 sec less showing a moderate
pace release of oxygen and buildup of CO₂. This as opposed to exercise which increases the
body's energy demands causing increased cellular respiration and lower breath holding times.

As evident in the ANOVA test demonstrating the profound effect of the varying treatment
groups on the breath holding times (1-way ANOVA:F(2,374)=170.72). Breath holding time(BHT)
was both significantly higher following hyperventilation compared to normal ventilation
compared to exercise (p<0.001) for all groups. This suggests a significant difference in all
treatments on BHT and that the difference is not due to chance.

The ANOVA test displays the significant effect of an independent variable but the Turkey Kramer
test shows us the further analysis of each treatment with each value (p<0.001) and the
significant disparity as between hyperventilation and ventilations means is 21.15 sec and
between ventilation and exercise is 52.39sec. Therefore the independent variable significantly
influenced the dependent variable .
Discussion
The findings from the current study provide evidence that the treatment groups had a
tremendous effect on the BHT of individuals particularly for the longest treatment
hyperventilation, supporting our hypothesis.

The current understanding we have is that ‘hyperventilation increases breath hold time by
lowering the initial tissue CO₂ leaks and so delaying the breaking point”(Heath and Irwin, 1968).
We have learnt the breaking point to be the point at which breathing, an involuntary function,
can no longer be inhibited voluntarily. However our current study allows us to understand that
this breaking point is influenced by ‘chemoreceptors such as a rise in CO₂, drop in O, and drop in
blood pH to become more acidic’ (Skow et al., 2015). And these can be manipulated using
treatment groups proving the hypothesis that hyperventilation can increase BHT.

A study done by Skow et al. (2015) explained the physiology related to longer breath holding
times. Using 7 stages of breathing activities closed circuit rebreathing, hyperventilation,
hypoxia, rebreathing ,etc. This concluded that the stimuli listed above activate central and
peripheral chemoreceptors, relaying information to the brain stem causing an urge to breath
and dyspnea(shortness of breath). However hyperventilation recorded the 2nd highest BHT
similar to our study, as it prolongs the breaking point (Figure 4). This also reveals breath holding
to cause inhibitory lung stretch and a smaller lung volume reservoir to mix atmospheric air thus
arterial blood decreases can breath hold time. This contrasts our study which omitted
physiological details and lacked deeper explanation regarding the most effective treatment on
breath holding time.

Whilst the physiological relationship between BHT & treatment groups remains clear there are
numerous underlying factors that influence the maximum BHT and such future directions can
be incorporated into our study. The phenomenon where panic disorder(PD) patients
experienced shortness of breath and suffocation anxieties and were measured to be lower
end-tidal pCO2 documented by Roth et al (1998), demonstrating the need for future
investigation into subjects' pre-experimental state, which could be done by measuring heart
rate.

There are also further cognitive processes that can substantially influence psychological
processes. A study done by Vigran et al. (2019) found that manipulating the perception of time
using distorted timers by up to 40% faster or slower, delayed the onset of the breaking point, by
affecting the duration of the easy going phase. This proves that future studies could also
manipulate results by measuring patient discomfort through knowledge tests, notifying time
stamps, monitoring chest expansions and further techniques.
Figures

Figure 1: ANOVA test

Figure 2: Post-hoc, Turkey-Kramer test

Figure 3, 7 stage breath hold test showing breath holding times

Reference List

Clark T.J.H., Godfrey S., (1969) The effect of CO₂ on ventilation and breath-holding during
exercise and while breathing through and added resistance The Journal of Physiology, 3:
551-566

J.R.Heath, C.J.Irwin.(1968) An increase in breath-hold time appearing after breath-holding,

Respiration Physiology 4: 73-77

Nicolo A., Gruet M., Sacchetti M. (2023) Editorial: Breathing in sp[ort and exercise: physiology,
pathophysiology and applications. NIH 14: 1347806.

Roth, W. T., Wilhelm, F. H., & Trabert, W. (1998). Voluntary breath holding in panic and
generalized anxiety disorders. Psychosomatic medicine, 6: 671–679.

Skow R.J., Day T.A., Fuller J.E, Bruce D.C., Steinback C.D., (2015) The ins and outs of breath
holding: simple demonstrations of complex respiratory physiology, PubMed 39: 26330043.
https://journals.physiology.org/doi/full/10.1152/advan.00030.2015

Vigran H.J., Kapral G.A, Tytell E.D., Kao M.H. (2019) Manipulating the perception of time affects
voluntary breath-holding duration Physiological Reports 7: 23
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6908740/