Obesity is associated with a disturbed adipose tissue (AT) function characterized by adipocyte hypertrophy, an impaired lipolysis and pro-inflammatory phenotype, which contributes to insulin resistance (IR). We investigated whether AT phenotype in different AT depots of obese individuals with and without type 2 diabetes mellitus (T2DM) is associated with whole-body IR. Subcutaneous (SC) and visceral (V) AT biopsies from 18 lean, 17 obese and 8 obese T2DM men were collected. AT phenotype was characterized by ex vivo measurement of basal and stimulated lipolysis (mature adipocytes), adipocyte size distribution (AT tissue sections) and AT immune cells (flow cytometry). In VAT, mean adipocyte size, CD45+ leukocytes and M1 macrophages were significantly increased in both obese groups compared to lean individuals. In SCAT, despite adipocyte hypertrophy, no significant differences in immune cell populations between groups were found. In SCAT, multiple linear regression analysis showed that none of the AT phenotype markers independently contributed to HOMA-IR while in VAT, mean adipocyte size was significantly related to HOMA-IR. In conclusion, beside adipocyte hypertrophy in VAT, M1 macrophage- or B-cell-mediated inflammation, may contribute to IR, while inflammation in hypertrophic SCAT does not seem to play a major role in IR.

IntroductionLow-to-moderate intensity exercise improves muscle contractile properties and endurance capacity in multiple sclerosis (MS). The impact of high intensity exercise remains unknown.MethodsThirty-four MS patients were randomized into a sedentary control group (SED, n = 11) and 2 exercise groups that performed 12 weeks of a high intensity interval (HITR, n = 12) or high intensity continuous cardiovascular training (HCTR, n = 11), both in combination with resistance training. M.vastus lateralis fiber cross sectional area (CSA) and proportion, knee-flexor/extensor strength, body composition, maximal endurance capacity and self-reported physical activity levels were assessed before and after 12 weeks.ResultsCompared to SED, 12 weeks of high intensity exercise increased mean fiber CSA (HITR: +21±7%, HCTR: +23±5%). Furthermore, fiber type I CSA increased in HCTR (+29±6%), whereas type II (+23±7%) and IIa (+23±6%,) CSA increased in HITR. Muscle strength improved in HITR and HCTR (between +13±7% and +45±20%) and body fat percentage tended to decrease (HITR: -3.9±2.0% and HCTR: -2.5±1.2%). Furthermore, endurance capacity (Wmax +21±4%, time to exhaustion +24±5%, VO2max +17±5%) and lean tissue mass (+1.4±0.5%) only increased in HITR. Finally self-reported physical activity levels increased 73±19% and 86±27% in HCTR and HITR, respectively.ConclusionHigh intensity cardiovascular exercise combined with resistance training was safe, well tolerated and improved muscle contractile characteristics and endurance capacity in MS.Trial RegistrationClinicalTrials.gov NCT01845896

Immune cell accumulation in adipose tissue (AT) is associated with the development of AT inflammation, resulting in metabolic dysfunction. Circulating immune cell patterns may reflect immune cell accumulation in expanding AT. However, data linking human leukocytes in blood and AT is lacking. We investigated whether blood immune cell populations are associated with their counterparts in subcutaneous (scAT) or visceral AT (vAT). Flow cytometry was performed on blood, scAT and vAT from 16 lean and 29 obese men. Circulating natural killer (NK)-cells, classical monocytes and nonclassical monocytes were higher in obese individuals. vAT, but not scAT, of obese individuals contained more inflammatory CD11c+ “M1” macrophages and NK cells compared to lean individuals. Blood classical monocytes were associated with CD11c+ macrophages in vAT but not scAT. This association was unrelated to expression of the adhesion molecules CD11b and CD11c or of the chemokine receptor CX3CR1 on these monocytes. Other AT immune cells were not associated with their respective counterparts in blood. Finally, CD11c+ macrophages and CD4+ T-cells in vAT were associated with their counterparts in scAT. In conclusion, blood classical monocytes reflect CD11c+ macrophages in vAT.

Twenty-four weeks of mild-to-moderate-intensity combined endurance and resistance training was not able to improve glycemic control in this cohort of persons with MS. Future research is warranted to investigate the influence of higher exercise intensities on glucose tolerance, in an attempt to remediate metabolic deficits and to decrease the prevalence of comorbidities in MS.

Twelve weeks of high intensity aerobic exercise in combination with resistance training improved glucose tolerance in persons with MS.

Introduction Exercise training is strongly recommended as a therapeutic approach to treat individuals with heart failure. High-intensity exercise training modalities still controversial in this population. The study aims to preliminary assess the consequences of high-intensity exercise training modalities, aerobic interval training (HIIT) and progressive high circuit-resistance training (CRT), on primarily endothelial function and cardiorespiratory fitness, and secondly on muscle strength and physical performance in heart failure patients. Methods This preliminary multicentric randomized controlled trial comprised 23 heart failure patients, aged 56 ± 10 years old, mainly New York Heart Association classification I and II (%), hemodynamically stable, who compromise at least 36 exercise sessions of a randomly assigned intervention (HIIT, CRT or control group). Endothelial function, cardiopulmonary exercise testing, muscle strength and physical performance were completed at baseline and post-intervention. Results Although no effects on endothelial function; both HIIT and CRT modalities were able to produce a positive effect on V˙O2 peak (HIIT = +2.1±6.5, CRT = +3.0±4.2 and control group = -0.1± 5.3 mL/kg/min, time*group p-value<0,05) and METs (HIIT = +0.6±1.8, CRT = +0.9±1.2 and control group = 0±1.6, time*group p-value<0,05). Only HIIT increased isokinetic torque peak (HIIT = +8.8±55.8, CRT = 0.0±60.7 and control group = 1.6±57.6 Nm) matched p-value<0,05. Regarding the physical performance, the CRT modality reduced chair stand test completion time (HIIT = -0.7±3.1, CRT = -3.3±3.2 and control group = -0.3±2.5 s, matched p-value<0,05 and HIIT improved global physical performance(time*group p<0,05). Conclusion This preliminary study trends to indicate for the first time that high-intensity interval training promotes a jointly superior effect compared to progressive high intensity circuit-resistance training by improving cardiorespiratory fitness, muscular strength, and physical performance. Further research with larger cohort is necessary. Clinical trial registration number ReBEC RBR-668c8v.

Exercise-onset Vo(2) kinetics during submaximal endurance exercise are significantly slowed in mildly disabled persons with MS, suggesting low skeletal muscle oxidative capacity. Using mean response time testing, rehabilitation interventions for this reduction in exercise capacity can be assessed and targeted.

Natriuretic peptides have long been known for their cardiovascular function. However, a growing body of evidence emphasizes the role of natriuretic peptides in human substrate and energy metabolism, thereby connecting the heart with several insulin-sensitive organs like adipose tissue, skeletal muscle and liver. Obesity may be associated with an impaired regulation of the natriuretic peptide system, also indicated as a natriuretic handicap. Evidence points towards a contribution of this natriuretic handicap to the development of obesity, type 2 diabetes mellitus and cardiometabolic complications, although the causal relationship is not fully understood. Nevertheless, targeting the natriuretic peptide pathway may improve metabolic health in obesity and type 2 diabetes mellitus. This review will focus on current literature regarding the metabolic roles of natriuretic peptides with emphasis on lipid metabolism and insulin sensitivity. Furthermore, it will be discussed how exercise and lifestyle intervention may modulate the natriuretic peptide-related metabolic effects.