It has been reported that GSR increases in participants who
practice breathing exercises. The reasoning provided was that deep breathing causes a
phasic sympathetic release that increases sweating (Nida et al. 2014). In my work I did compare slow breathing with relaxing music in https://macsphere.mcmaster.ca/handle/11375/25887 and did not find significant differences in GSR between the two groups. A deep breath can elicit a sympathetic discharge that causes an increase in sweating, which
increase the GSR response. So, I wanted to know if we assume that slow breathing reduces sympathetic activity, is GSR a valid measure in this context as respiration itself can effect the GSR activity.
Hi
In my experience some subjects show increased skin responses during paced breathing and these responses are mostly evoked-shaped, that means when they are going to follow a visual cue (in my studies) sometimes there is a SCR right after beginning of inspiration. This I think is mostly due to performing a task and the required cognitive demand. It can be phasic because the task is phasic. Correct comparison should be between two paced breathing condition one with slow rate and one at normal frequency to control the effect of task (paced breathing), though this is not a perfect control but better than nothing. And when you compare so, there is no difference suggesting this is not specific to breathing rate.
The GSR of course is limited in representing ANS activity.
To test whether slow breathing influences sympathetic responses I suggest MSNA. And we always need a control condition.
A deep breath can cause an artifact, a brief rise in conductance, that I have always assumed is caused by friction in the airways. It resembles the effect of a brush of the hand on the skin anywhere on the body. Smokers are more likely to have this happen from deep breathing -- also anyone getting over a cold, or chronic bronchitis.
If it's caused as you suggest by a brief increase in sweating, then that's hard to differentiate from the friction/abrasion hypothesis. It may not matter so much anyway.
If it's caused by a correlation with cognitive demand, interesting -- but could be tested by timing the task performance demand to exhalation instead, just to see what happens.
Interesting discussion! Anyone else?
I've spent a lot of time watching the GSR activity of people both trying to relax and also when speaking. The possibility that inhalation increases sympathetic activity is worth considering, especially since heart rate tends to increase, provoked by sympathetic input (RSA, HRV). But perhaps that's only the heart. I doubt that sympathetic activity across the whole body rises with every inhale.
My assumption all along has been that the GSR rise with inhalation is due to mild friction in the airways. To support this, people with bronchitis and those with sore or sensitive throats after getting over a cold, and also chronic smokers all are more likely to generate this inhalation artifact. Sometimes this makes the data unusable for biofeedback. A laugh, cough, or just clearing the throat will usually tweak the GSR also, and looks just like a scary thought or stressful memory popping up.
To settle this, we'd need an independent and reliable index of sympathetic level, since it's a mass-action phenomenon, unlike the more specific parasympathetic system. Then we could see how that index correlates with GSR rises related to and unrelated to phase of breathing. If it doesn't correlate, then the throat-friction hypothesis is more likely. Let's all think about it.
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