1
Evidence has accumulated that in chronic heart failure vagal activity is decreased.
2
Heart rate and sinus arrhythmia gap were used to express vagal activity indirectly.
3
Group comparisons on vagal activity were controlled for age and body mass index.
4
An inhibition of efferent vagal activity may contribute to the inhibitory effect of GLP-1 on gastric emptying.
5
Thus, the circadian rhythmicity of vagal activity seems to have an important role in the genesis of NSVT.
6
These alterations included low vagal activity, elevated sympathetic activity, and low complexity and adaptability in heart rate control dynamics.
7
By exploiting the spectral paradigm of heartbeat dynamics, cortical and sub-cortical areas functionally linked to vagal activity have been identified.
8
At rest, vagal activity dominates while during different forms of stress the activated sympathetic nervous system markedly modulates secretions and motility.
9
As vagal activity increases, the nervous system slows down, heart rate and blood pressure decrease, and your brain waves show relaxation.
10
Objectives: The goal of this study was to assess the hypothesis that transdermal scopolamine would increase vagal activity in patients after myocardial infarction.