Obesity and metabolic syndrome (MetS) have become a growing problem for public health and clinical practice, given their increased prevalence due to the rise of sedentary lifestyles and excessive caloric intake from processed food rich in fat and sugar. There are several definitions of MetS, but most of them describe it as a cluster of cardiovascular and metabolic alterations such as abdominal obesity, reduced high-density lipoprotein (HDL) and elevated low-density lipoprotein (LDL) cholesterol, elevated triglycerides, glucose intolerance, and hypertension. Diagnosis requires three out of these five criteria to be present. Despite the increasing prevalence of MetS, the understanding of its pathophysiology and relationship with disease is still limited. Indeed, the pathological consequences of MetS components have been reported individually, but investigations that have studied the effect of the combination of MeS components on organ pathological remodeling are almost nonexistent. On the other hand, animal models are a powerful tool in understanding the mechanisms that underlie pathological processes such as MetS. In the first part of the review, we will briefly overview the advantages, disadvantages and pathological manifestations of MetS in porcine, canine, rodent, and rabbit diet-induced experimental models. Then, we will focus on the different dietary regimes that have been used in rabbits to induce MetS by means of high-fat, cholesterol, sucrose or fructose-enriched diets and their effects on physiological systems and organ remodeling. Finally, we will discuss the use of dietary regimes in different transgenic strains and special rabbit breeds.

Background: Our aim was to determine the differences in short-term heart rate variability (HRV) between patients with metabolic syndrome (MS) and healthy controls. Methods: We searched electronic databases for primary works with short-term HRV recordings (≤30 min) that made comparisons between individuals with MS versus healthy controls. This systematic review and meta-analysis (MA) was performed according to PRISMA guidelines and registered at PROSPERO (CRD42022358975). Results: Twenty-eight articles were included in the qualitative synthesis and nineteen met the criteria for the MA. Patients with MS showed decreased SDNN (−0.36 [−0.44, −0.28], p < 0.001), rMSSD (−7.59 [−9.98, −5.19], p < 0.001), HF (−0.36 [−0.51, −0.20], p < 0.00001) and LF (−0.24 [−0.38, −0.1], p = 0.001). In subsequent subanalyses, we found a decrease in SDNN (−0.99 (−1.45, −0.52], p < 0.001), rMSSD (−10.18 [−16.85, −3.52], p < 0.01) and HF (−1.04 [−1.97, −0.1] p < 0.05) in women. In men, only LF showed a significant lower value (−0.26 [−0.5, −0.02], p < 0.05). We could not perform MA for non-linear variables. Conclusions: Patients with MS showed changes in time-domain analyses, with lower values in SDNN and rMSSD. Regarding frequency-domain analyses, MS patients showed a decrease in HF and LF When sex was used as a grouping variable, the MA was only possible in one of both sexes (men or women) in rMSSD and LF/HF. Lastly, when data for both men and women were available, subanalyses showed a different behavior compared to mixed analyses for SDNN, HF and LF, which might point towards a different impact of MS in men and women.

Background: Our aim was to determine the impact that metabolic syndrome (MS) produces in long-term heart rate variability (HRV), quantitatively synthesizing the results of published studies to characterize the cardiac autonomic dysfunction in MS. Methods: We searched electronic databases for original research works with long-term HRV recordings (24 h) that compared people with MS (MS+) versus healthy people as a control group (MS−). This systematic review and meta-analysis (MA) was performed according to PRISMA guidelines and registered at PROSPERO (CRD42022358975). Results: A total of 13 articles were included in the qualitative synthesis, and 7 of them met the required criteria to be included in the MA. SDNN (−0.33 [−0.57, 0.09], p = 0.008), LF (−0.32 [−0.41, −0.23], p < 0.00001), VLF (−0.21 [−0.31, −0.10], p = 0.0001) and TP (−0.20 [−0.33, −0.07], p = 0.002) decreased in patients with MS. The rMSSD (p = 0.41), HF (p = 0.06) and LF/HF ratio (p = 0.64) were not modified. Conclusions: In long-term recordings (24 h), SDNN, LF, VLF and TP were consistently decreased in patients with MS. Other parameters that could be included in the quantitative analysis were not modified in MS+ patients (rMSSD, HF, ratio LF/HF). Regarding non-linear analyses, the results are not conclusive due to the low number of datasets found, which prevented us from conducting an MA.

Background/Objectives: Heart rate variability (HRV) is a reliable, non-invasive marker of autonomic nervous system function and is often impaired in individuals with metabolic syndrome (MetS). Physical exercise has emerged as an effective strategy to improve autonomic modulation; however, the comparative effects of different training modalities on HRV in individuals with MetS remain unclear. This systematic review and meta-analysis aimed to evaluate the impact of various exercise interventions on HRV and to identify which training types yield the most significant improvements. Methods: A systematic search was conducted in PubMed and Scopus up to April 2025. Eligible studies (n = 16) included adults with obesity and MetS (n = 752) who underwent structured exercise interventions with HRV assessments pre- and post-intervention. Standardized mean differences were calculated using random effects models. Subgroup analyses were performed based on training modality (endurance training [ET], resistance training [RT], high-intensity interval training [HIIT], and concurrent training [CT]). Results: Sixteen studies of moderate to high quality were included, with eleven studies eligible for meta-analysis. ET and HIIT significantly improved time-domain indices (Root mean square of differences of successive R-R intervals —rMSSD—, Standard deviation of the R-R interval series —SDNN—) and frequency-domain parameters (high-frequency —HF—), suggesting enhanced parasympathetic activity. RT showed inconsistent effects, while CT improved long-term HF and total power (TP). Non-linear indices were the least reported due to insufficient data. Conclusions: Physical exercise—particularly ET and HIIT—appears to enhance cardiac autonomic modulation in individuals with obesity and MetS. These findings support incorporating targeted training strategies into clinical practice to optimize cardiovascular health in these populations.

La ciencia de contar historias: distintos niveles de integración narrativa en innovación docente aplicada a la Fisiología Humana.

Metabolic syndrome (MetS) drives cardiac remodeling and fibrosis, contributing to diastolic dysfunction and heart failure with preserved ejection fraction, but chamber-specific mechanisms remain poorly defined. New Zealand White rabbits were fed a high-fat/high-sucrose diet for 28 weeks to induce experimental MetS. Systemic phenotype, cardiac structure (echocardiography), myocardial fibrosis (Picrosirius red histology), myosin/collagen gene expression (qRT-PCR), and chamber-specific proteomics were assessed across left/right atria and ventricles. The model reproduced central obesity, glucose intolerance, dyslipidemia, and mild hypertension, with concentric left ventricular hypertrophy and selective ventricular fibrosis, as follows: increased collagen in left ventricle (LV) and right ventricle (RV), unchanged in atria. Ventricular α-myosin heavy-chain gene expression was upregulated, while collagen I and α-smooth muscle actin transcripts showed ventricular-specific downregulation. Proteomics revealed atrial metabolic and cytoskeletal adaptations with minimal extracellular matrix involvement; ventricles displayed early profibrotic cues (galectin-3 in LV), metabolic inefficiency (impaired glycolysis/ATP production in LV; lipid oxidation shift in RV), and diminished provisional matrix support. Conclusions: concentric LV hypertrophy and great vessel enlargement occurred without systolic/diastolic dysfunction; ventricular-selective fibrosis, α-myosin heavy-chain upregulation, type I collagen/α-smooth muscle actin downregulation, and chamber-specific proteomic changes showed atrial adaptation versus ventricular early profibrotic/metabolic inefficiency.