The gut microbiota is responsible for recovering energy from food, providing hosts with vitamins, and providing a barrier function against exogenous pathogens. In addition, it is involved in maintaining the integrity of the intestinal epithelial barrier, crucial for the functional maturation of the gut immune system. The Western diet (WD)—an unhealthy diet with high consumption of fats—can be broadly characterized by overeating, frequent snacking, and a prolonged postprandial state. The term WD is commonly known and intuitively understood. However, the strict digital expression of nutrient ratios is not precisely defined. Based on the US data for 1908–1989, the calory intake available from fats increased from 32% to 45%. Besides the metabolic aspects (hyperinsulinemia, insulin resistance, dyslipidemia, sympathetic nervous system and renin-angiotensin system overstimulation, and oxidative stress), the consequences of excessive fat consumption (high-fat diet—HFD) comprise dysbiosis, gut barrier dysfunction, increased intestinal permeability, and leakage of toxic bacterial metabolites into the circulation. These can strongly contribute to the development of low-grade systemic inflammation. This narrative review highlights the most important recent advances linking HFD-driven dysbiosis and HFD-related inflammation, presents the pathomechanisms for these phenomena, and examines the possible causative relationship between pro-inflammatory status and gut microbiota changes.

Iron is an indispensable nutrient for life. A lack of it leads to iron deficiency anaemia (IDA), which currently affects about 1.2 billion people worldwide. The primary means of IDA treatment is oral or parenteral iron supplementation. This can be burdened with numerous side effects such as oxidative stress, systemic and local-intestinal inflammation, dysbiosis, carcinogenic processes and gastrointestinal adverse events. Therefore, this review aimed to provide insight into the physiological mechanisms of iron management and investigate the state of knowledge of the relationship between iron supplementation, inflammatory status and changes in gut microbiota milieu in diseases typically complicated with IDA and considered as having an inflammatory background such as in inflammatory bowel disease, colorectal cancer or obesity. Understanding the precise mechanisms critical to iron metabolism and the awareness of serious adverse effects associated with iron supplementation may lead to the provision of better IDA treatment. Well-planned research, specific to each patient category and disease, is needed to find measures and methods to optimise iron treatment and reduce adverse effects.

The most effective type of training to improve cardiometabolic parameters in overweight subjects is unknown. This meta-analysis compared the effect of endurance, strength and combined training on glucose, insulin metabolism and the lipid profile of overweight and obese adults. The Cochrane, PubMed, Scopus and Web of Science databases were searched to identify randomised trials assessing the effect of training intervention on fasting and 2 h glucose and insulin levels, glycated haemoglobin (HbA1c), homeostatic model assessment of insulin resistance (HOMA), C-peptide, total cholesterol (TC), low- (LDL-C) and high-density lipoprotein cholesterol and triglycerides (TG). Forty-six studies were included showing that endurance training more favourably reduced HbA1c (p = 0.044), and LDL-C (p = 0.021) than strength training. Endurance-strength training more effectively decreased glucose (p = 0.002), HbA1c (p = 0.032), HOMA (p = 0.002), TC (p = 0.039), LDL-C (p = 0.046), HDL (p = 0.036) and TG levels (p = 0.025) than strength training. Combined training significantly reduced the HOMA index (p = 0.009) and TG levels (p = 0.039) compared with endurance training. Endurance and endurance-strength training have a more favourable effect on glucose and insulin homeostasis and lipid profile than strength training in overweight and obese adults. However, the results from this meta-analysis should be interpreted cautiously due to significant heterogeneity among included studies.

Sleep is a fundamental biological process in athletes, indispensable for tissue regeneration, exercise adaptation, and injury prevention. Disruptions in sleep architecture and duration have been consistently associated with diminished physical performance and adverse health outcomes, impairing muscular strength, power output, and endurance capacity, and concurrently compromising cognitive function. On a physiological level, insufficient sleep disrupts endocrine homeostasis, elevating cortisol levels and reducing anabolic hormones such as testosterone and growth hormone. At the molecular level, sleep loss promotes the upregulation of pro-apoptotic gene expression and exacerbates pro-inflammatory signalling pathways. Optimal sleep duration and quality represent a critical “regenerative window”, essential for enhancing athletic performance and safeguarding physiological resilience. Ensuring adequate sleep among athletes can be effectively achieved through educational, behavioural, and nutritional interventions outlined in this review.

Preliminary evidence suggests that conjugated linoleic acid (CLA) may reduce body weight and affect body composition. The present study assessed the effect of CLA supplementation on body fat composition in overweight and obese women, while also evaluating the liver safety of CLA use. Seventy-four obese or overweight women were randomly assigned to receive 3 g/day CLA or placebo for 12 weeks. Body composition (dual-energy X-ray absorptiometry) and liver function (¹³C-methacetin breath test and serum liver enzymes) were assessed before and after the trial. Patients receiving CLA experienced a significant reduction of total body fat expressed as mass (p = 0.0007) and percentage (p = 0.0006), android adipose tissue (p = 0.0002), gynoid adipose tissue (p = 0.0028), and visceral adipose tissue (p = 4.2 × 10⁻⁹) as well as a significant increase in lean body mass to height (p = 6.1 × 10⁻¹¹) when compared to those receiving a placebo. The maximum momentary 13C recovery changes and end-point values were significantly higher in the CLA group when compared to the placebo group (p = 0.0385 and p = 0.0076, respectively). There were no significant changes in alanine aminotransferase, asparagine aminotransferase, and gamma-glutamyl transpeptidase activities between the groups. In conclusion, CLA supplementation was well tolerated and safe for the liver, which shows beneficial effects on fat composition in overweight and obese women.

Limited data suggested that inclusion of a strength component into endurance exercises might intensify the beneficial effect of training. However, the available data is limited. Therefore, we aimed to compare the effect of endurance and endurance-strength training on anthropometric parameters, endothelial function, arterial stiffness, antioxidant status, and inflammatory markers in abdominally obese women without serious comorbidities. A total of 101 women were recruited and randomly divided into endurance (n = 52) and endurance-strength (n = 49) groups. During the three-month intervention, both groups performed supervised sixty-minute training three times a week. All studied parameters were measured pre- and post-intervention period. In total, 85 women completed the study. Both training significantly decreased anthropometric parameters. Besides, endurance training decreased endothelial nitric oxide synthase, central aortic systolic pressure, pulse wave velocity, glutathione (GSH), total antioxidant status (TAS), interleukin (IL) 8, matrix metalloproteinase (MMP) 9, and tumor necrosis factor alpha, while endurance-strength training decreased MMP-2 concentrations, and increased IL-6, monocyte chemoattractant protein-1, and MMP-9 levels. We observed significant differences between groups for GSH, TAS, and MMP-9 levels. In summary, endurance and endurance-strength training did not differ in the impact on endothelial function and arterial stiffness. However, endurance training significantly depleted the antioxidant defense, simultaneously reducing MMP-9 levels. The study was retrospectively registered with the German Clinical Trials Register within the number DRKS00019832.