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Cardiac repolarization and autonomic regulation during short-term cold exposure in hypertensive men: an experimental study.

ABSTRACT: The aim of our study was to assess the effect of short-term cold exposure, typical in subarctic climate, on cardiac electrical function among untreated middle-aged hypertensive men.We conducted a population-based recruitment of 51 hypertensive men and a control group of 32 men without hypertension (age 55-65 years) who underwent whole-body cold exposure (15 min exposure to temperature -10°C, wind 3 m/s, winter clothes). Conduction times and amplitudes, vectorcardiography, arrhythmias, and heart rate variability (autonomic nervous function) were assessed.Short-term cold exposure increased T-peak to T-end interval from 67 to 72 ms (p<0.001) and 71 to 75 ms (p<0.001) and T-wave amplitude from 0.12 to 0.14 mV (p<0.001) and from 0.17 to 0.21 mV (p<0.001), while QTc interval was shortened from 408 to 398 ms (p<0.001) and from 410 to 401 ms (p<0.001) among hypertensive men and controls, respectively. Cold exposure increased both low (from 390 to 630 ms2 (p<0.001) and 380 to 700 ms2 (p<0.001), respectively) and high frequency heart rate variability (from 90 to 190 ms2 (p<0.001) and 150 to 300 ms2 (p<0.001), respectively), while low-to-high frequency-ratio was reduced. In addition, the frequency of ventricular ectopic beats increased slightly during cold exposure. The cold induced changes were similar between untreated hypertensive men and controls.Short-term cold exposure with moderate facial and mild whole body cooling resulted in prolongation of T-peak to T-end interval and higher T-wave amplitude while QTc interval was shortened. These changes of ventricular repolarization may have resulted from altered cardiac autonomic regulation and were unaffected by untreated hypertension.ClinicalTrials.gov NCT02007031.

SUBMITTER: Hintsala H

PROVIDER: S-EPMC4077657 | biostudies-literature | 2014

REPOSITORIES: biostudies-literature

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Cardiac repolarization and autonomic regulation during short-term cold exposure in hypertensive men: an experimental study.

Hintsala Heidi H Kenttä Tuomas V TV Tulppo Mikko M Kiviniemi Antti A Huikuri Heikki V HV Mäntysaari Matti M Keinänen-Kiukaannemi Sirkka S Bloigu Risto R Herzig Karl-Heinz KH Antikainen Riitta R Rintamäki Hannu H Jaakkola Jouni J K JJ Ikäheimo Tiina M TM

PloS one 20140701 7

<h4>Objectives</h4>The aim of our study was to assess the effect of short-term cold exposure, typical in subarctic climate, on cardiac electrical function among untreated middle-aged hypertensive men.<h4>Methods</h4>We conducted a population-based recruitment of 51 hypertensive men and a control group of 32 men without hypertension (age 55-65 years) who underwent whole-body cold exposure (15 min exposure to temperature -10°C, wind 3 m/s, winter clothes). Conduction times and amplitudes, vectorca ...[more]

PMID: 24983379

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Project description:ObjectiveObesity and type-2 diabetes (T2D) are metabolic diseases that represent a critical health problem worldwide. Metabolic disease is differentially associated with fat distribution, while visceral white adipose tissue (VAT) is particularly prone to obesity-associated inflammation. Next to their canonical function of immune suppression, regulatory T cells (Tregs) are key in controlling adipose tissue homeostasis. Towards understanding the molecular underpinnings of metabolic disease, we focus on how environmental-metabolic stimuli impinge on the functional interplay between Tregs and adipose tissue. Here, cold exposure or beta3-adrenergic signaling are a promising tool to increase energy expenditure by activating brown adipose tissue, as well as by reducing local inflammation within fat depots by supporting immunosuppressive Tregs. However, in humans, the underlying mechanisms that enable the environmental-immune crosstalk in the periphery and in the respective tissue remain currently unknown.MethodsWe used combinatorial approaches of next generation humanized mouse models and in vitro and in vivo experiments together with beta3-adrenergic stimulation to dissect the underlying mechanisms of human Treg induction exposed to environmental stimuli such as cold. To test the translational relevance of our findings, we analyzed samples from the FREECE study in which human subjects were exposed to individualized cooling protocols. Samples were analyzed ex vivo and after in vitro Treg induction using qRT-PCR, immunofluorescence, as well as with multicolor flow cytometry and cell sorting.ResultsIn vivo application of the beta3-adrenergic receptor agonist mirabegron in humanized mice induced thermogenesis and improved the Treg induction capacity of naïve T cells isolated from these animals. Using samples from the human FREECE study, we demonstrate that a short-term cold stimulus supports human Treg induction in vitro and in vivo. Mechanistically, we identify BORCS6 encoding the Ragulator-interacting protein C17orf59 to be significantly induced in human CD4+ T cells upon short-term cold exposure. Strong mTOR signaling is known to limit successful Treg induction and thus likely by interfering with mTOR activation at lysosomal surfaces, C17orf59 improves the Treg induction capacity of human naïve T cells upon cold exposure.ConclusionsThese novel insights into the molecular underpinnings of human Treg induction suggest an important role of Tregs in linking environmental stimuli with adipose tissue function and metabolic diseases. Moreover, these discoveries shed new light on potential approaches towards tailored anti-inflammatory concepts that support human adipose tissue homeostasis by enabling Tregs.

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Cardiac repolarization and autonomic regulation during short-term cold exposure in hypertensive men: an experimental study.

Publications

Cardiac repolarization and autonomic regulation during short-term cold exposure in hypertensive men: an experimental study.

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