Floorball training consists of intense repeated exercise and may offer a motivating and social stimulating team activity in elderly individuals. However, the effect of floorball training in elderly adults on physiological adaptations important for health is not known. Thus, this study examined the effect of floorball training on blood lipids, muscle strength, body composition, and functional capacity of men aged 65-76 years. Thirty-nine recreational active men were randomized into a floorball group (FG; n = 22) or petanque group (PG; n = 17), in which training was performed 1 h twice a week for 12 weeks. In FG and PG, average heart rate (HR) during training was 80% and 57%, respectively, of maximal HR. In FG, plasma low-density lipoprotein (LDL) cholesterol and triglycerides were 11% and 8% lower (P < 0.05), respectively. Insulin resistance determined by homeostatic model assessment (HOMA-IR) was reduced (P < 0.05) by 18%. HR during submaximal cycling was 5% lower (P < 0.05), and maximal voluntary contraction force was 8% higher (P < 0.05). Total and visceral fat content was lowered (P < 0.05) by 5% and 14%, respectively, HR at rest was 8% lower (P < 0.05) and performance in four different functional capacity tests were better (P < 0.05) after compared to before the training period. No changes were observed in PG. In conclusion, 12 weeks of floorball training resulted in a number of favorable effects important for health and functional capacity, suggesting that floorball training can be used as a health-promoting activity in elderly men.

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surrogate marker for arginine vasopressin secretion, with insulin resistance: Influence of adolescence and psychological stress. Peptides, 115,[8][9][10][11][12][13][14] Dette er siste tekst-versjon av artikkelen, og den kan inneholde små forskjeller fra forlagets pdf-versjon. Forlagets pdf-versjon finner du her: http://dx. ABSTRACTIn middle-aged and elderly individuals, circulating copeptin concentrations, a surrogate marker for arginine vasopressin (AVP) secretion, associates with insulin resistance (IR). Whether this association is present in adolescents and young adults is unclear. Because psychological stress associates with higher circulating copeptin concentrations and IR, it has been speculated that increased AVP secretion could be a link between psychological stress and IR. We measured plasma copeptin concentrations in 351 14-16-year-old adolescents and 617 20-28-year-old young adults from the Danish site of the European Youth Heart Study, a population-based cardiovascular risk factor study in adolescents and young adults. IR was determined by the homeostatic model assessment method. Among the young adults, we used symptoms of depression, evaluated by means of the Major Depression Inventory (MDI) scale, as a measure of psychological stress. We applied linear regressions to examine associations, expressed as unstandardized regression coefficients (B) with 95% confidence intervals (CIs), between variables of interest, stratified by age group and adjusting for age, sex and Tanner stages. Copeptin and IR were logtransformed. Among the young adults, copeptin associated with IR (B (95%CI) =0.19 (0.11 to 0.27), P<0.001). This association was not found among the adolescents (B=-0.01 (-0.12 to 0.09), P=0.78). MDI score associated with IR (B=0.010 (0.004 to 0.016), P<0.001) and copeptin (B=0.010 (0.004 to 0.015); P<0.002) in the young adults. Adjusted for copeptin, the strength of the association between MDI score and IR somewhat diminished (to B=0.008). In conclusion, adolescence and psychological stress appear to influence the association between copeptin and IR.

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Endothelin signaling plays an important role in physiology and disease and one of the endothelin receptors, the type B receptor (ETB or EDNRB), is known to be highly plastic, being upregulated in smooth muscle cells by arterial injury and following organ culture in vitro. Herein, we hypothesized that this transcriptional plasticity may arise in part because EDNRB is controlled by ternary complex factors and by the myocardin family coactivator MKL2. In line with this hypothesis we found significant correlations between the ternary complex factors ELK3, FLI1 and EDNRB, and between MKL2 and EDNRB at the mRNA level in human arteries. Overexpression of MKL2 in human coronary artery smooth muscle cells (HCASMC) led to a 30‐ fold induction of EDNRB, and this effect was antagonized by myocardin (MYOCD) which also correlated negatively with EDNRB at the tissue level. Overexpression of ELK3 and FLI1 induced expression of EDNRB, whereas the expression of classical smooth muscle markers was reduced. Depolymerization of actin using latrunculin B (LatB) increased EDNRB on both mRNA and protein levels, and increased calcium responses on stimulation with the ETB‐selective agonist sarafotoxin 6c (S6c) and endothelin 1 (ET‐1). Pretreatment with LatB in organ culture increased S6c and ET‐1‐induced contraction. We also found that ROCK inhibition using Y27632 induced EDNRB expression, and that the effect of LatB is antagonized by MAP‐kinase inhibition. Transcript‐specific primers and promoter reporter assays showed that the EDNRB_2 isoform is regulated by LatB in HCASMC. We finally demonstrate that the mRNA level of EDNRB is increased in rat carotid lesions and human carotid plaques, and that ELK3/FLI1 induction closely parallels EDNRB induction. In all, these studies uncover transcriptional control mechanisms for the endothelin type B receptor (EDNRB) that may explain its plasticity and could be targeted for therapy. Support or Funding Information This study was supported by grants from the Medical Faculty and The Royal Physiographic Society. KKK was supported by Marie Curie ITN Small Artery Remodelling of European Union. This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.

Background Increased potassium intake lowers blood pressure in patients with hypertension, but increased potassium intake also elevates plasma concentrations of the blood pressure‐raising hormone aldosterone. Besides its well‐described renal effects, aldosterone is also believed to have vascular effects, acting through mineralocorticoid receptors present in endothelial and vascular smooth muscle cells, although mineralocorticoid receptors‐independent actions are also thought to be involved. Methods and Results To gain further insight into the effect of increased potassium intake and potassium‐stimulated hyperaldosteronism on the human cardiovascular system, we conducted a randomized placebo‐controlled double‐blind crossover study in 25 healthy normotensive men, where 4 weeks treatment with a potassium supplement (90 mmol/day) was compared with 4 weeks on placebo. At the end of each treatment period, we measured potassium and aldosterone in plasma and performed an angiotensin II (AngII) infusion experiment, during which we assessed the aldosterone response in plasma. Hemodynamics were also monitored during the AngII infusion using ECG, impedance cardiography, finger plethysmography (blood pressure‐monitoring), and Doppler ultrasound. The study showed that higher potassium intake increased plasma potassium (mean±SD, 4.3±0.2 versus 4.0±0.2 mmol/L; P =0.0002) and aldosterone (median [interquartile range], 440 [336–521] versus 237 [173–386] pmol/L; P <0.0001), and based on a linear mixed model for repeated measurements, increased potassium intake potentiated AngII‐stimulated aldosterone secretion ( P =0.0020). In contrast, the hemodynamic responses (blood pressure, total peripheral resistance, cardiac output, and renal artery blood flow) to AngII were similar after potassium and placebo. Conclusions Increased potassium intake potentiates AngII‐stimulated aldosterone secretion without affecting systemic cardiovascular hemodynamics in healthy normotensive men. Registration EudraCT Number: 2013‐004460‐66; URL: https://www.ClinicalTrials.gov ; Unique identifier: NCT02380157.

Obesity is a strong risk factor for hypertension, but the mechanism linking obesity to hypertension is not fully elucidated. In obesity, circulating concentrations of adiponectin are decreased and hypoadiponectinaemia has in some but not all studies been associated with increased risk of hypertension. Due to this inconsistency, we decided to study adiponectin from two aspects in a cross-sectional in vivo study and in an experimental in vitro study. In the cross-sectional study, 103 men with body mass index (BMI) ≥ 30.0 kg/m 2 were studied; 63 had 24-hr ambulatory blood pressure (ABP) ≥ 130/80 mmHg (ObeseHT) and 40 had 24-hr ABP < 130/80 mmHg (ObeseNT). As controls, we studied 27 men with BMI between 20.0 and 24.9 kg/m 2 and 24-hr ABP < 130/80 mmHg (LeanNT). Serum concentrations of adiponectin and body composition using dual-energy X-ray absorptiometry scanning were determined. In vitro, the direct vasomotor response of adiponectin was tested on subcutaneous resistance arteries from human abdominal adipose tissue. The two obese groups had lower adiponectin concentrations compared with LeanNT (p < 0.01) [median (interquartile range)]: ObeseHT 6.5 (5.1-8.3) mg/L; ObeseNT 6.6 (5.2-7.8) mg/L; and LeanNT 9.4 (6.7-12.4) mg/L, with no significant difference in adiponectin concentrations (or body composition) between ObeseHT and ObeseNT (p = 0.67). In vitro, adiponectin did not have any direct vasodilatory effect and adiponectin did not affect angiotensin II-stimulated vasoconstriction. In conclusion, obese hypertensive men have similar serum concentrations of adiponectin as obese normotensive men. In combination with the in vitro data, these findings question a pathogenic role of adiponectin in human hypertension.High body mass index (BMI) caused by excessive growth of adipose tissue is a major risk factor for hypertension [1], but the mechanisms by which excess adipose tissue leads to hypertension are still not fully elucidated [2,3].Over the past decades, it has become increasingly apparent that adipose tissue is not only a passive energy store, but also an active endocrine and paracrine organ that secretes various proinflammatory, vasoactive and metabolic active substances, collectively called adipocytokines or just adipokines [4][5][6][7][8]. Based on both animal and human studies, it has been suggested that these active adipose tissue-derived substances could play a role in overweight-related diseases, such as type 2 diabetes, coronary heart disease (CHD) and hypertension [4][5][6][7][8].Adiponectin, a 244 amino acid protein, which is secreted from adipose tissue, is one of these adipocytokines [4][5][6][8][9][10]. Compared with other adipocytokines, adiponectin is distinct in the sense that lower (hypoadiponectinaemia) rather than higher (hyperadiponectinaemia) circulating concentrations of adiponectin have been associated with increased risk of overweight-related diseases [4][5][6][8][9][10]. Another distinct feature is that adiponectin has been found to be inversely related to anthropometric measures, ...

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