supine position (13.1 +/- 5.6 bpm)
standing position (8.5 +/- 3.8 bpm).
Thus in the normal population 95% of people’s HR raised:
laying flat 2-24bpm
Standing 1- 16bpm
This video documents a rise of 68-92 bpm, laying reclined. The following day sitting knees up in a crouch position, resting 59 went up to 94bpm, a raise of 36bpm). Once PEM improved, EG able to move more under 100bpm, the repeat test of 7 swallows of water elevated heart rate 20bpm only (Resting 63- peak 83- dropped back to 61). This return to bradycardia is noted as part of normal parasympethic compensation.
The parasympathetic nervous system slows heart rate through the action of the vagus nerve. The response relies on the vagus nerve, which may be lacking tone, or inflamed? in ME/CFS/fibro. Thus in PEM there is sympathetic dominance, the HR isn’t slowed by the parasympathetic response, the parsympathetic response may not occur and the heart rate may continue to elevate beyond the third swallow. This may likely be inflammation, as if it was just a lack of tone it would presumably be constant across time, not just in crashes. This seems to be readily documentable evidence of vagus nerve problems, specific to PEM.