The effects of different physical training regimes on the plasma catecholamine values at rest and the density and responsiveness of adrenergic receptors at rest were investigated. The changes during well-defined training periods of swimmers, long-distance runners, weight lifters and wrestlers were compared with untrained male volunteers. The training of swimmers and long-distance runners, building up endurance, resulted in a significantly lower basal plasma norepinephrine (NE) concentration and a significantly or possibly lower ratio NE:EPI (epinephrine). Both values indicated reduced sympathetic activity and resulted also in a significantly lower beta-receptor density and a higher alpha 2-receptor sensitivity compared with the other groups investigated. However, swimming-specific characteristics provoked labile hypertensive blood pressure regulation with an unchanged heart rate in swimmers. Static training of weight lifters, building up power, also led to a lower NE concentration compared with untrained subjects, whereas beta-receptor density was unchanged and alpha 2-receptor density and sensitivity were decreased. Elevated blood pressure values were observed in weight lifters and swimmers due to a reduced baroreceptor sensitivity. The dynamic training of wrestlers affected only basal heart rate and alpha 2-receptor sensitivity, both of which were decreased. Different kinds of physical training caused various adaptations of the basal activity of the autonomic nervous system in which adrenergic receptors also became adapted. In this context, the stronger adrenergic circulatory component of overall sympathetic activity at rest in swimmers and long-distance runners resulted in lower beta-receptor density, and the reduced noradrenergic component sensitized alpha 2-receptors.
We investigated the effects of endurance and high-intensity training periods on the plasma catecholamine (CA) concentration at rest; on the basal alpha- and beta-adrenoceptor density, regulation, and function on circulating cells; and on the cardiovascular adaptation in long-distance runners and swimmers. The findings of each period were compared with those of untrained men. Endurance training of the long-distance runners and the swimmers led both to a reduced sympathetic activity at rest, indicated by lower CA values, and to a lower beta-receptor density and responsiveness on circulating lymphocytes and an increased alpha 2-receptor sensitivity on circulating platelets. During the high-intensity training period beta-receptor density and responsiveness increased, alpha 2-receptor sensitivity normalized, and heart rate as well as blood pressure values increased in both trained groups. The basal sympathetic activity remained reduced, but the norepinephrine-to-epinephrine (NE/EPI) ratio increased. The NE/EPI ratio might play an important part in the regulation of adrenoceptor density during these different training periods. Swimming-specific characteristics caused different physiological impacts compared with running training, but an attenuated baroreceptor sensitivity might be indicated in both intensively trained groups.
We tested the hypothesis that platelet and plasma catecholamine sulfates (CA-S) and platelet catecholamines (CA) reflect the overall sympathoadrenergic activation by exercise of 1 h duration. Ten well-trained subjects performed a low-intensity [62% maximum O2 consumption (VO2max); LI] and a high-intensity exercise test (77% VO2max; HI) and two tests at a similar average power output that consisted of 20 min at 77% VO2max and 40 min at 62% VO2max (HI/LI) and vice versa (LI/HI). Plasma norepinephrine sulfate (NE-S) increased to higher levels after HI than after LI exercise (15.5 +/- 2.1 vs. 8.9 +/- 0.7 nmol/l). Immediately after HI/LI and LI/HI plasma NE-S was similarly increased (9.59 +/- 1.1 vs. 9.96 +/- 1.3 nmol/l), whereas norepinephrine was higher after LI/HI than after HI/LI (23.0 +/- 3.2 vs. 15.7 +/- 2.3 nmol/l). Platelet CA and CA-S were increased only after HI. In conclusion, the plasma NE-S response to exercise parallels the overall sympathetic activation. These results support the hypothesis that plasma NE-S measured immediately after exercise reflects the overall sympathoadrenergic activity over prolonged periods of exercise. Platelet CA and CA-S poorly reflect sympathoadrenergic activation.
Background Autosomal dominant polycystic kidney disease (ADPKD) has numerous extrarenal manifestations. Pericardial effusion (PE) may be an under-recognized complication with a reported prevalence of up to 35%. Our study is the first to systematically evaluate the prevalence of PE and associated risk factors in an ADPKD cohort outside the U.S. Methods Clinically stable ADPKD patients from a specialized outpatient clinic were evaluated retrospectively. Magnetic resonance tomography and computed tomography scans were analysed regarding the presence of PE (≥4 mm). Imaging results were linked to clinical characteristics. Results Out of 286 ADPKD patients, 208 had computed tomography or magnetic resonance imaging suitable for evaluation of PE. In this group, we detected PE in 17 patients (8.2%). The overall prevalence of PE was 6.3% with more females being affected (prevalence of PE 7.8% in female and 3.8% in male patients). PE mean size was 6.8 ± 3.3 mm. The prevalence of autoimmune diseases was higher in the patients with PE (11.8% versus 2.1%, P = 0.022), while presence and size of PE was not associated with signs of rapid progressive disease, ADPKD genotype, patient age, BMI, and other clinical parameters. Exploratory investigation of individual characteristics of PE patients by regression tree analysis suggested renal functional impairment, sex, and proteinuria as candidate variables. Conclusions PE prevalence in our cohort was lower than previously reported and showed a clear female preponderance. Our data suggest that patients with PE size > 10 mm deserve further attention, as they may have additional non-ADPKD related pathologies.
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