Effects of a short residential thermal spa program to prevent work-related stress/burnout on stress biomarkers: The thermstress proof of concept study

Objective Work-related stress is a public health issue. Stress has multiple physical and psychological consequences, the most serious of which are increased mortality and cardiovascular morbidity. The ThermStress protocol was designed to offer a short residential thermal spa program for work-related stress prevention that is compatible with a professional context. Methods Participants will be 56 male and female workers aged 18 years or above. All participants will undergo a 6-day residential spa program comprising psychological intervention, physical activity, thermal spa treatment, health education, eating disorder therapy and a follow-up. On six occasions, participants’ heart rate variability, cardiac remodelling and function, electrodermal activity, blood markers, anthropometry and body composition, psychology and quality of life will be measured using questionnaires and bone parameters. Results This study protocol reports the planned and ongoing research for this intervention. Discussion The ThermStress protocol has been approved by an institutional ethics committee (ANSM: 2016 A02082 49). It is expected that this proof of concept study will highlight the effect of a short-term specific residential thermal spa program on the prevention of occupational burnout and work-related stress. The findings will be disseminated at several research conferences and in published articles in peer-reviewed journals. Trial Registration: ClinicalTrials.gov (NCT 03536624, 24/05/2018

Regional myocardial function abnormalities are associated with macro- and microcirculation dysfunction in the metabolic syndrome: the RESOLVE study

Abnormalities in myocardial and vascular function have been reported in the metabolic syndrome (MetS), but whether these alterations are related remains poorly documented. Our aim was accordingly to investigate interrelationships between macro- and microcirculatory vasoreactivity and left ventricular (LV) myocardial function in MetS patients. Eighty-eight MetS individuals and 44 age- and gender-matched healthy controls were enrolled. LV global longitudinal strain (GLS) was measured using Vector Velocity Imaging. Endothelial-dependent and independent reactivity in macro- and microcirculatory territories was established using flow-mediated dilation and nitrate-mediated dilation of the brachial artery and cutaneous blood flow measured with laser Doppler flowmetry in response to iontophoresis of acetylcholine and sodium nitroprusside, respectively. Carotid intima-media thickness (cIMT) was measured according to the Mannheim consensus. Compared to controls, MetS patients presented with reduced GLS (p < 0.001) increased cIMT and impaired (p < 0.001) endothelial and smooth muscle function of the brachial artery and the forearm skin microcirculation. Highly significant relationships (p < 0.01) were noticed between GLS and vascular outcomes. In addition, cIMT (β = 0.21, p = 0.024) and microcirculatory endothelium-dependent reactivity (β = − 0.20, p = 0.035) were identified as independent predictors of GLS. In MetS, abnormalities in myocardial function and endothelial as well as smooth muscle function of small and large arteries co-exist and are closely associated. This study supports a role for microvascular dysfunction in the pathogenesis of LV myocardial dysfunction

Different modalities of exercise improve macrovascular function but not microvascular function in metabolic syndrome: The RESOLVE randomized trial

Objective To determine which modality of exercise program (endurance and/or resistance dominance) is the most effective for improving vascular function in the micro- and macrocirculation in metabolic syndrome (MetS). Methods Sixty-two MetS patients were enrolled in a 6-month lifestyle intervention program based on diet and exercise training. Each participant was randomly assigned to one of 3 groups categorized by exercise modality (e.g. high-intensity resistance or endurance training, or combined moderate-intensity). Measurements of anthropometrics, biological blood markers, physical fitness and vascular function were performed at baseline, at the end of the 3-week residential program, and at 3 and 6 months after baseline. Brachial artery flow-mediated dilation (FMD) and the response to sublingual nitrate were assessed by high-resolution ultrasound. Microvascular reactivity was evaluated using laser Doppler flowmetry in conjunction with iontophoresis of acetylcholine and sodium nitroprusside. Results Regardless of the training program, FMD significantly increased from baseline to 3 weeks in all groups with no further changes at 3 and 6 months. Changes in central fat, diastolic blood pressure, triglycerides, interleukin-6 and physical fitness were independent predictors of increased FMD. Nitrate-mediated dilation increased from baseline to 3 months and then remained unchanged up to 6 months. Endothelium-dependent and endothelium-independent function of the skin microcirculation did not change significantly in all groups. Conclusions In MetS patients, exercise training, regardless of its endurance or resistance dominance, is able to improve vascular function in large vessels only. Lifestyle intervention programs including exercise training must be encouraged in those with MetS

Left ventricular myocardial dyssynchrony is already present in nondiabetic patients with metabolic syndrome

The presence of left ventricular (LV) dyssynchrony in individuals with metabolic syndrome (MetS), a predictor of type 2 diabetes (T2D), lacks clarity. We compared LV dyssynchrony in MetS individuals with and without T2D, and healthy control subjects using speckle-tracking imaging echocardiography. Ninety-two MetS participants (64 without, 28 with T2D) and 40 control subjects underwent echocardiographic and clinical/biological analyses. LV-dyssynchrony in the longitudinal axis only was present in all MetS individuals, but was not further exacerbated by T2D. Strong associations were found with systemic inflammation, abdominal obesity, and LV mass. Investigations of myocardial dyssynchrony in the nondiabetic MetS stage might facilitate timely and more effective prevention

Long-term cost reduction of routine medications following a residential programme combining physical activity and nutrition in the treatment of type 2 diabetes: a prospective cohort study

Objectives To demonstrate that lifestyle modifications will reduce the cost of routine medications in individuals with type 2 diabetes (T2D), through a mechanism involving glycaemic control. Design A within-trial cost-medication analysis with a 1-year time horizon. Setting Controlled environment within the spa resort of Chatel-Guyon, France. Participants Twenty-nine participants (aged 50-70 years) with T2D. Interventions A 1-year follow-up intervention, beginning with a 3-week residential programme combining high exercise volume (15-20 hours/week), restrictive diet (-500 kcal/day) and education. Participants continued their routine medication, independently managed by their general practitioner. Main outcome measures Number of medications, number of pills, cost of medications and health-related outcomes. Results Twenty-six participants completed the 1-year intervention. At 1 year, 14 patients out of 26 (54%) stopped/decreased their medications whereas only 5 (19%) increased or introduced new drugs (φ2 =6.3, p=0.02). The number of pills per day decreased by 1.3±0.3 at 12 months (p 6.5% in the highest (last) quartile doubled their routine medication costs (66% vs 33%, p=0.037). Conclusions Individuals with T2D reduced routine medication costs following a long-term lifestyle intervention that started with a 3-week residential programme. Combining high exercise volume, restrictive diet and education effectively supported the health of T2D. The main factor explaining reduced medication costs was better glycaemic control, independent of weight changes. Despite limitations precluding generalisability, cost-effective results of reduced medication should contribute to the evidence base required to promote lifestyle interventions for individuals with T2D

Beta-Adrenergic receptors desensitization is not involved in exercise-induced cardiac fatigue: NADPH oxidase-induced oxidative stress as a new trigger

Prolonged strenuous exercise (PSE) induces transient left ventricular (LV) dysfunction. Previous studies suggest that β-adrenergic pathway desensitization could be involved in this phenomenon, but it remains to be confirmed. Moreover, other underlying mechanisms involving oxidative stress have been recently proposed. The present study aimed to evaluate the involvement of both the β-adrenergic pathway and NADPH oxidase (Nox) enzyme-induced oxidative stress in myocardial dysfunction in rats following PSE. Rats were divided into 4 groups: controls (Ctrl), 4-h exercised on treadmill (PSE), and 2 groups in which Nox enzyme was inhibited with apocynin treatment (Ctrl APO and PSE APO, respectively). We evaluated cardiac function in vivo and ex vivo during basal conditions and isoproterenol stress. GSH/GSSG ratio, cardiac troponin I (cTnI) release, and lipid peroxidation (MDA) were evaluated. PSE induced a decrease in LV developed pressure, intrinsic myocardial contractility, and relaxation associated with an increase in plasma cTnI release. Our in vivo and ex vivo results demonstrated no differences in myocardial response to isoproterenol and of effective dose 50 between control and PSE rats. Interestingly, the LV dysfunction was reversed by apocynin treatment. Moreover, apocynin prevented cellular oxidation [GSH/GSSG ratio: PSE APO rats vs. PSE rats in arbitrary units (au): 1.98 ± 0.07 vs. 1.35 ± 0.10; P < 0.001]. However, no differences in MDA were observed between groups. These data suggest that myocardial dysfunction observed after PSE was not due to β-adrenergic receptor desensitization but could be due to a signaling oxidative stress from the Nox enzyme

Paradoxical dissociation between heart rate and heart rate variability following different modalities of exercise in individuals with metabolic syndrome: The RESOLVE study

Aims: To analyse the effects of different modalities of exercise training on heart rate variability (HRV) in individuals with metabolic syndrome (MetS). Methods and results: Eighty MetS participants (aged 50–70 years) were housed and managed in an inpatient medical centre for 21 days, including weekends. Physical activity and food intake/diet were intensively monitored. Participants were randomly assigned into three training groups, differing only by intensity of exercise: moderate-endurance-moderate-resistance (re), high-resistance-moderate-endurance (Re), and moderate-resistance-high-endurance (rE). HRV was recorded before and after the intervention by 24-hour Holter electrocardiogram. Although mean 24-hour heart rate decreased more in Re than re (–11.6 ± 1.6 vs. –4.8 ± 2.1%; P = 0.010), low frequency/high frequency decreased more in re than Re (–20.4 ± 5.5% vs. + 20.4 ± 9.1%; P = 0.002) and rE (–20.4 ± 5.5% vs. –0.3 ± 11.1%; P = 0.003). Very low frequency increased more in Re than re (+121.2 ± 35.7 vs. 42.9 ± 11.3%; P = 0.004). For all HRV parameters, rE ranged between re and Re values. Low frequency/high frequency changes were linked with visceral fat loss only in re (coefficient 5.9, 95% CI 1.9–10.0; P = 0.004). By day 21, HRV parameters of MetS groups (heart rate –8.6 ± 1.0%, standard deviation of R-R intervals + 34.0 ± 6.6%, total power + 63.3 ± 11.1%; P  <  0.001) became closer to values of 50 aged-matched healthy controls. Conclusions: A 3-week residential programme with intensive volumes of physical activity (15–20 hours per week) enhanced HRV in individuals with MetS. Participants with moderate intensity of training had greater improvements in sympathovagal balance, whereas those with high intensity in resistance training had greater decreases in heart rate and greater increases in very low frequency. Modality-specific relationships were observed between enhanced HRV and visceral fat loss. Clinical Trial Registration: URL: http://www.clinicaltrials.gov. Unique identifier: NCT00917917