Background/Objectives: Despite the abundant body of evidence linking high-intensity interval training (HIIT) to cardiometabolic markers, little is known about how HIIT affects liver enzymes, particularly in obese adolescents. This study aimed to investigate the effects of HIIT on metabolic dysfunction-associated steatotic liver disease (MASLD)-related biomarkers in overweight/obese adolescent girls. Methods: Thirty-three overweight/obese adolescent girls (age, 17.0 ± 1.15 yr.; body mass index, 33.3 ± 4.77 kg/m²) were randomly assigned to HIIT (n = 17) or control (n = 16) groups. The HIIT group participated in a nine-week HIIT program (three times weekly) without caloric restriction. Maximal aerobic speed, body composition indexes, blood pressure, MASLD-related biomarkers [liver enzymes (alanine aminotransferase (ALT) and aspartate aminotransferase (AST)), plasma lipids, uric acid, platelet count, and homeostasis model assessment index for insulin-resistance (HOMA-IR)] were examined at baseline and after the intervention. Results: Significant “time × group” interactions were found for body composition indexes, systolic blood pressure, maximal aerobic speed, liver enzymes ALT and AST, plasma lipids, glucose, and HOMA-IR. The HIIT program resulted in an increase in maximal aerobic speed (p = 0.035) and a decrease in body composition and plasma lipids (p < 0.01), systolic blood pressure (p = 0.011), ALT (p = 0.013), AST (p = 0.012), and HOMA-IR (p = 0.01), but no significant changes in uric acid and platelet count. None of these markers changed in the control group. Conclusions: HIIT resulted in an improvement in MASLD-related biomarkers. HIIT could be an effective exercise therapy to prevent and reverse MASLD in adolescents with obesity.

The study investigated the effects of high-intensity interval training (HIIT) on cardiorespiratory fitness, hormonal, and psychological markers in adolescents. Twenty-eight healthy male adolescents were randomized to a HIIT group or a non-training control group. HIIT comprises three sessions per week for 10 weeks, alternating 30 s runs at high-intensity and low-intensity. VO_2max was estimated using the incremental running test. Plasma testosterone and cortisol were assessed by ELISA methods. Depression, anxiety, and stress scores were determined using the Depression Anxiety Stress Scales-21. Data were analyzed using two-way ANOVA with repeated measures. Significant “group × time” interactions were detected for VO_2max, testosterone, cortisol, testosterone-to-cortisol ratio, and stress score, but not for anxiety and depression scores. HIIT resulted in increased VO_2max (p < 0.001, d = 1.04), testosterone (p = 0.005, d = 0.52), and testosterone-to-cortisol ratio (p = 0.008, d = 1.05), and decreased cortisol (p = 0.036, d = 1.09) and stress score (p = 0.020, d = 0.98). Ten-week HIIT resulted in an improvement in physical fitness, steroid hormonal balance, and self-reported stress symptoms, but no changes in depressive and anxiety symptoms in comparison to the control group. The findings should be interpreted with caution due to limitations, including the small sample size and the lack of assessment of sex-related differences. Further research is required to elucidate the topic.

Severe Coronavirus disease 2019 (COVID-19) is associated with abnormal innate and adaptive immune responses, as well as systemic alterations, including a shift in lipid network. A case–control study was conducted to describe the systemic lipidomic profile in COVID-19 according to disease severity. Selected polyunsaturated fatty acids (PUFAs), oxylipins, and endocannabinoids were analysed using a targeted liquid chromatography coupled to mass spectrometry in tandem method. Multivariate receiver operating characteristic curve-based model evaluation was performed to define a lipidomic signature for the disease. A total of 135 hospitalized COVID-19 patients, of whom 85 had severe form, and 134 healthy individuals were included. Patients exhibited increased levels of free PUFAs, proinflammatory and pro-resolving oxylipins, and endocannabinoids compared to controls. A combination of five lipid mediators, i.e., prostaglandin D2, prostaglandin E2, thromboxane B2, lipoxin B4, and 2-archidonylglycerol, discriminates patients from control individuals with excellent accuracy [AUC, 0.977 (0.950–0.995)]. The severe form is characterized by an imbalance between proinflammatory and pro-resolving oxylipins and increased endocannabinoids. COVID-19 is associated with a lipid storm that conditions disease severity. Targeting lipid mediators-related metabolic and signalling pathways could be an interesting therapeutic option in severe forms.