Unlike noradrenaline, the sympathetic neurotransmitter which overflows to the circulation, adrenaline (ADR) is a secreted hormone, with a low plasma concentration, and plasma concentration for biological action a log order lower than that of noradrenaline. The venous drainage of the left adrenal medulla into the left renal vein does expose this vein to uniquely high plasma ADR concentrations and possible risk of thrombosis at high rates of ADR secretion. There is typically a different timeframe for adrenal medullary and sympathetic nervous system responses: ADR release is short term in contrast with sympathetic activation persisting for years in heart failure and hypertension. The historic view of Walter Cannon, subject to recent review, that the sympathoadrenal system is a unified biological system, was deconstructed further with demonstration of frequent mismatching of adrenal medullary and sympathetic nervous responses. Under gravity stimulation with standing, there is prompt sympathetic activation without ADR release. In many diseases, notably obesity, hypertension, heart failure and depressive illness, an activated sympathetic nervous system and silent adrenal medulla coexist. The therapeutic corollary of this is that ADR blockade is much less commonly needed clinically than pharmacological antagonism of the sympathetic nervous system.

PURPOSE: The purpose of this study was to compare common carotid artery (CCA) stiffness at rest and immediately following brief aerobic exercise between young males of moderate and high cardiorespiratory fitness (CRF). METHODS: Accordingly, heart rate (HR), blood pressure (BP), arterial diameter, conventional parameters of arterial stiffness (Petersons’ elastic modulus [Ep], β1 stiffness index) and novel two-dimensional (2D) strain imaging indices (global circumferential strain, strain rate and β2 stiffness index) were assessed in the CCA pre and immediately post 5-min of aerobic exercise (40% peak exercise capacity) in twenty-two young healthy males (age: 21 ± 2 years). Moderate and high CRF groups demonstrated mean V†o2 peak data of 49 ± 8 and 66 ± 6 mL kg-1min-1, respectively (P .05). However, whilst there was a similar increase in CCA wall deformation as indicated by global circumferential strain following exercise (pre vs. post, moderate: 9.12 ± 2.6% vs. 9.36 ± 2.4%; high: 10.19 ± 2.9% vs. 11.34 ± 2.9%, both P > .05), CCA wall deformation was significantly faster in the high-fit group only, as reflected by increased systolic circumferential strain rate (moderate: 1.09 ± 0.3 vs. 1.17 ± 0.2 1/s, P > .05; high: 1.14 ± 0.2 vs. 1.35 ± 0.3 1/s, P = .049). CONCLUSION: Using novel 2D strain imaging, this study shows that young high-fit individuals may exhibit different arterial wall dynamics compared to their lower-fit counterparts following a short bout of aerobic exercise. The increase in global circumferential strain rate following exercise in high-fit individuals may reflect a greater ability to buffer the significant rise in pulse-pressure and blood flow that occurs in response to exercise.

Key points During cardiac contraction, left ventricular (LV) mechanics play an important role in equalising transmural fibre stress and ensuring efficient ejection of blood. The factors responsible for altered LV mechanics in humans with high aerobic exercise capacity are unknown but are believed to be related to changes in LV structure or heart rate. We performed a comprehensive assessment of LV mechanics and cardiovascular function at rest and during dynamic exercise in individuals with moderate and high aerobic exercise capacity. Our novel data indicate that there is no direct association between altered LV mechanics in humans with high aerobic fitness and classic indicators of cardiovascular adaptation. The findings provide evidence of a previously unknown type of physiological LV adaptation that may have important implications for exercise training in various healthy and diseased populations.

Background Although heart rate variability (HRV) at 0.1 Hz has been proposed as a noninvasive clinical measure of cardiac sympathetic nerve firing, this premise has not been sufficiently validated by comparison with techniques such as microneurography and the measurement of norepinephrine spillover from the heart that more directly reflect presynaptic sympathetic activity. Methods and Results We compared the three techniques under conditions of effective cardiac sympathetic denervation, pure autonomic failure (n=4), dopamine 83-hydroxylase deficiency (n= 1), and after cardiac transplantation (n=9) as well as in the context of sympathetic nervous activation in cardiac failure (n= 15) and with aging (n= 10). Age-matched comparisons were made in each case with healthy individuals drawn from a pool of 52 volunteers. In pure autonomic failure and early after transplantation, cardiac norepinephrine spillover was negligible, and HRV was low. Late after transplantation, however, cardiac norepinephrine spillover returned to normal levels, and HRV remained low. In comparison to younger

Radiotracer methods were used to measure the rates of regional release of adrenaline and noradrenaline into plasma in man. This was done as a partial test of a theory of essential hypertension pathogenesis which envisages an important cotransmitter function for neuronally released adrenaline. In healthy resting men no release of adrenaline could be detected from the heart, lungs or liver. Adrenaline was released into the right renal vein but an adrenal medullary source is suspected. With the relatively limited activation of the cardiac sympathetic outflow which accompanied mental challenge and isometric exercise, cardiac adrenaline release remained undetectable. During supine bicycle exercise, which increased cardiac noradrenaline release 10–30 fold, to a mean value of 197ng/min, cardiac adrenaline release averaged 2.36 ng/min. In two clinical conditions associated with persistently elevated plasma adrenaline concentrations, cardiac failure and adrenaline-secreting phaeochromocytoma, regional release of adrenaline was clearly evident. Thus, in normal man during exercise, and in patients with cardiac failure at rest, adrenaline is released from non-adrenal sources, and probably from sympathetic nerves. Whether neuronal adrenaline release of the degree found would be sufficient to facilitate noradrenaline release, augment sympathetically-mediated cardiovascular responses and contribute to the development of arterial hypertension remains to be tested.