ObjectiveWe previously showed that a training intervention comprising a combination of meditation, exposure to cold, and breathing exercises enables voluntary activation of the sympathetic nervous system, reflected by profoundly increased plasma epinephrine levels, and subsequent attenuation of the lipopolysaccharide (LPS)-induced inflammatory response. Several elements of the intervention may contribute to these effects, namely, two different breathing exercises (either with or without prolonged breath retention) and exposure to cold. We determined the contribution of these different elements to the observed effects.MethodsForty healthy male volunteers were randomized to either a short or an extensive training in both breathing exercises by either the creator of the training intervention or an independent trainer. The primary outcome was plasma epinephrine levels. In a subsequent study, 48 healthy male volunteers were randomized to cold exposure training, training in the established optimal breathing exercise, a combination of both, or no training. These 48 participants were subsequently intravenously challenged with 2 ng/kg LPS. The primary outcome was plasma cytokine levels.ResultsBoth breathing exercises were associated with an increase in plasma epinephrine levels, which did not vary as a function of length of training or the trainer (F(4,152) = 0.53, p = .71, and F(4,152) = 0.92, p = .46, respectively). In the second study, the breathing exercise also resulted in increased plasma epinephrine levels. Cold exposure training alone did not relevantly modulate the LPS-induced inflammatory response (F(8,37) = 0.60, p = .77), whereas the breathing exercise led to significantly enhanced anti-inflammatory and attenuated proinflammatory cytokine levels (F(8,37) = 3.80, p = .002). Cold exposure training significantly enhanced the immunomodulatory effects of the breathing exercise (F(8,37) = 2.57, p = .02).ConclusionsThe combination of cold exposure training and a breathing exercise most potently attenuates the in vivo inflammatory response in healthy young males. Our study demonstrates that the immunomodulatory effects of the intervention can be reproduced in a standardized manner, thereby paving the way for clinical trials.Trial Registration:ClinicalTrials.gov identifiers: NCT02417155 and NCT03240497.
Background Relatives of intensive care unit (ICU) survivors may suffer from various symptoms after ICU admittance of their relative, known as post-intensive care syndrome-family (PICS-F). Studies regarding PICS-F have been performed but its impact in primary care is unknown. Objectives To explore health problems of relatives of ICU survivors in primary care. Methods This is an exploratory prospective cohort study in which we combined data from two hospitals and a primary care research network in the Netherlands. ICU survivors who had been admitted between January 2005 and July 2017 were identified and matched by sex and age with up to four chronically ill (e.g. COPD, cardiovascular disease) patients. In both groups, relatives living in the same household were identified and included in this study. Primary outcome was the number of new episodes of care (International Classification of Primary Care-2) for up to five years. Hazard ratios (HRs) for the total number of new episodes were calculated. Results Relatives of ICU survivors ( n = 267, mean age 38.1 years, 41.0% male) had significantly more new care episodes compared to the reference group ( n = 705, mean age 36.3 years, 41.1% male) 1–2 years (median 0.11 vs. 0.08, HR 1.26; 95% confidence interval (CI) 1.03–1.54) and 2–5 years (median 0.18 vs. 0.13, HR 1.28; 95%CI 1.06–1.56) after ICU discharge. No differences were found in the period before ICU admission. Conclusion Relatives of ICU survivors present more morbidity in primary care than relatives of chronically ill patients up to five years after ICU discharge.
Background - We previously showed that a training intervention encompassing two breathing exercises and exposure to cold enables for voluntary activation of the sympathetic nervous system, reflected by profoundly increased plasma adrenaline levels, and subsequent attenuation of the endotoxin-induced inflammatory response. Herein, we determined the contribution of the different elements of the training, assessed if the training duration is of importance, and whether it can be provided by an independent trainer instead of the well-known individual who devised it. Methods – Forty healthy male volunteers were randomized to either a short or extensive training in both breathing exercises (i.e. cyclic hyperventilation with or without prolonged breath retention) by either the creator of the intervention or an independent trainer. In a subsequent study, 48 healthy male volunteers were randomized to cold exposure training, training in the established optimal breathing exercise, a combination of both, or no training. All 48 subjects were subsequently intravenously challenged with 2 ng/kg lipopolysaccharide to induce endotoxaemia. Results - Both breathing exercises were equally effective in enhancing plasma adrenaline concentrations and this response was also independent from the length of the training or the individual who provided it. Cold exposure training alone did not result in relevant modulation of the endotoxin-induced cytokine response, although flu-like symptoms were markedly reduced compared with the untrained group. Whereas subjects who received training in the breathing exercise alone displayed attenuated plasma levels of pro-inflammatory cytokines IL-6, IL-8, IP-10, MCP-1, MIP-1α, and MIP-1β (-34%, -14%, -48%, -37%, and -28%, respectively) during endotoxemia, combined training resulted in enhanced concentrations of anti-inflammatory IL-10 (+44%) and reduced concentrations of TNF-α, IL-6, IL-8, IP-10, MCP-1, MIP-1α, and MIP-1β (-32%, -35%, -30%, -48%, -29%, -35%, -30%, respectively) compared with untrained individuals. Conclusions - The combination of cold exposure training and a hyperventilation breathing exercise attenuates the in vivo inflammatory response most potently. Our study demonstrates that the immunomodulatory effects of the intervention can be reproduced in a standardized manner, thereby paving the way for clinical trials. Trial registration - Both studies described in this manuscript are registered at www.clinicaltrials.gov (breathing exercises study: NCT02417155; experimental human endotoxaemia study: NCT03240497).
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