Is the inner ear in humans really part of the respiratory system?

[zonotikk]

There are these papers which strongly imply that the inner ear hair cells, and not the medulla, is primarily the driving factor in the CO2 drive reflex

https://www.ncbi.nlm.nih.gov/pubmed/21130842

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3988803/

But every fMRI study done on chemoreceptors has shown only areas of the brain and carotid bodies light up in response to CO2. I could not find any fMRI study papers showing that the inner ears light up in response to CO2 or any histological evidence that the hair cells of the inner ear are chemosensitive and play a larger role in chemosensation than the brain like these studies are trying to imply. It is said the central chemoreceptors in the brain contribute to 85% of the CO2 drive reflex and the peripheral chemoreceptors contribute 15%, which seems to leave little room for the inner ear hair cells to play such a vital and significant part (53% of the respiratory drive was lost when both ears were damaged).

The papers in question were trying to link SIDs to inner ear damage.

[mistermack]

Is it inevitable that sensing of CO2 in the inner ear should show up in the same area of the brain as hearing? 

I would have thought that it would be quite unsurprising if it showed up in the same area as other indicators of raised CO2. 

 

I find the question interesting, as my father had quite severe sleep apnea, he would apparently stop breathing when he was dozing for scary time intervals. I prodded him awake on a few occasions, and he just opened his eyes and asked what was wrong. ( he did suffer a series of strokes before his death ). 

Sleep apnea is linked to airway obstruction like snoring, just as SIDs is linked to babies' sleeping position or blankets etc. so maybe SIDs and Sleep Apnea could be linked in some way by inner ear conditions.  It's obvious that the CO2 build up doesn't quickly cause breathing to restart in Apnea sufferers.

I've tested myself for sleep apnea a few times, using a homemade rig, a tiny microphone taped just under my nose recording the sound of breathing to a visual sound wave display. Fairly easy to do. I never got a significant pause, like my father did, which was a relief. I should have another go, I haven't done it for a long time.

Edit :

I just looked up the Eustachian tube, and it's stated that it is normally collapsed, and only opens when you swallow. So if the inner ear is important for CO2 response, you would think that it's going to be dependent on how often you swallow. Unless the CO2 in the inner ear is more responsive to blood levels than airway levels. 

Edited October 7, 2019 by mistermack

[CharonY]

1 hour ago, zonotikk said:

There are these papers which strongly imply that the inner ear hair cells, and not the medulla, is primarily the driving factor in the CO2 drive reflex

I'd have to read the papers a bit more carefully, but after an initial screen it seems to me that the response is not driven primarily by CO2 sensing, but rather that hypoxia-hypercarbia somehow results in depolarization which then triggers movement. What they primarily show is that injuries prevent these responses. To reconciliate these findings with existing lit on the dive reflex I would be wondering (because this is not my area of expertise) what the usual measures are used to assess the reflex vs the measures the authors used in their study. I.e. how does the arousal response that was tested by Allen et al. to the dive reflex? It may very well be that different aspects are tested and hence, the numbers do not add up to a whole. 

 

[zonotikk]

1 hour ago, CharonY said:

I'd have to read the papers a bit more carefully, but after an initial screen it seems to me that the response is not driven primarily by CO2 sensing, but rather that hypoxia-hypercarbia somehow results in depolarization which then triggers movement. What they primarily show is that injuries prevent these responses. To reconciliate these findings with existing lit on the dive reflex I would be wondering (because this is not my area of expertise) what the usual measures are used to assess the reflex vs the measures the authors used in their study. I.e. how does the arousal response that was tested by Allen et al. to the dive reflex? It may very well be that different aspects are tested and hence, the numbers do not add up to a whole. 

 

The movement response is not my interest, but more so the fact that mice with damaged inner ears did not breathe faster in response to high CO2 levels during sleep, which implies reduced chemosensation.

[CharonY]

In the 2014 paper it appears that they claim an increase in the ventilatory response whereas respiratory rate change was not significant. I am no animal physiologist, so I am wondering what are the expected values? I would have assumed that there is a significant change in the respiratory rate so I am wondering what the actual consequences of ventilatory responses alone would be. From a quick look I also failed to detect the baseline values of genta-treated mice so I wonder whether there was a baseline shift.

[zonotikk]

Here's a paper which includes a review of the above studies (see section 5.2)
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3812300/

[StringJunky]

I read something about  the connection with SIDS and inner ear damage in babies. Perhaps the key point not noted is cardiac regulation is only controlled this way in the infant stage until the main regulatory mechanism/sensors matures and kicks in; I cannot remember where those sensors are. In the animal studies, this transfer to the other regulatory mechanism may occur at a different time or may even not be controlled by the inner ear at any time in animal's early development; different physiology. Hence, perhaps, the apparent anomaly.

Edited October 8, 2019 by StringJunky