Greater sympathetic drive has been established in the early stages of essential hypertension, suggesting that neurohormonal dysregulation may be key to its aetiology and progression.
The two systems are usually in balance, although it's hardly surprising that YAU athletes experienced increased sympathetic drive even before the beginning of their race.
Diminished capacity within the right frontal region may be expressed in poor regulatory control over anger and hostility and over sympathetic drive.
We proposed that anger regulation and concurrent regulatory control over sympathetic drive suffer in hostile, violent-prone men due to diminished capacity within right frontal systems.
Finally, we were aware of the potential influence of antihypertensive medication (calcium blocking agents, beta blocking agents) that may alter sympathetic drive and thereby uptake of 123I mIBG.
However, increases in sAA activity have been found previously in both cervical- and thoracic-level athletes with SCI and non-spinal injured controls following strenuous exercise, which further questions sAA as a true indicator of central sympathetic drive [22].
Further, hypertensive patients exhibiting chronic inhibition of the sympathetic drive have increased circulating adiponectin [36].
An injection of melanotan II, the central melanocortin receptor (Mcr) agonist, provokes a differential sympathetic drive of WAT and BAT reflected by an increased norepinephrine turnover [19].
Adults born with VLBW have a higher heart rate suggesting an elevated cardiac sympathetic drive [11], whereas other studies suggest a lower muscle sympathetic nerve activity [36].
Conditions such as fasting or cold exposure normally stimulate WAT's sympathetic drive and decreases leptin synthesis/release in mice [10], [11], reducing leptin expression in isolated adipocytes [42].
For them, the feeling of fatigue or depression may be due to lack of sympathetic drive.
