Hesperidin is a prominent flavanone found in citrus fruits that has a broad range of biological effects, including anti-inflammatory and antioxidant capabilities. The study’s objective was to evaluate the effects of hesperidin supplementation on anti-inflammatory and antioxidant parameters such as MDA, TAC, GSH, SOD, and CAT; CRP, TNF-α, IL-6, and IL-4 levels respectively, by analyzing human intervention trials. Google Scholar, PubMed, grey literature databases, and the ClinicalTrials website were scanned to identify eligible studies. For the meta-analysis, eighteen studies were chosen. Hesperidin supplementation had significant lowering effect on not only CRP, IL-6, and IL-4 levels but also MDA level (Meta-regression analysis revealed a non-significant direct relationship between hesperidin dosage and chance in CRP, IL-6, and MDA levels. As a result, it can be said that hesperidin supplementation contributes to the inflammatory and antioxidant response, but this contribution is independent of dosage.

Background: Brain-derived neurotrophic factor (BDNF) is a key regulator of neuroplasticity, cognitive function, and mental health. Exercise is proposed as a non-pharmacological strategy to enhance BDNF; however, findings across neurological and non-neurological disorders remain inconsistent, and the influence of exercise type or dose-related parameters remains unclear. Objective: This meta-analysis evaluated the effects of exercise interventions on peripheral BDNF levels in individuals with neurological (e.g., multiple sclerosis, cognitive impairment, schizophrenia, depression) and non-neurological (e.g., obesity, type 2 diabetes, cancer) disorders, and examined whether outcomes varied by disease category, exercise modality, or dose. Methods: A systematic search of Web of Science, PubMed, ScienceDirect, Scopus, and Cochrane was conducted up to 1 October 2025. Eligible randomized controlled trials (RCTs) and the quality of evidence were assessed using the PEDro scale and the GRADE approach, respectively. Random-effects models were applied, with subgroup analyses (neurological vs. non-neurological; exercise type; duration and assay type), meta-regressions (duration, frequency, session length), and publication bias tests (funnel plot, Begg’s test, Egger’s regression, and trim-and-fill). Results: Nineteen RCTs, including 850 participants, were analyzed. According to low-quality evidence, exercise significantly increased peripheral BDNF (SMD = 1.03, 95% CI: [0.56–1.49, p < 0.0001). Effects did not differ significantly between neurological (SMD = 0.91, 95% CI: 0.31–1.50) and non-neurological (SMD = 1.23, 95% CI: 0.47–1.99) conditions (Q (1) = 0.44, p = 0.51). Subgroup analyses revealed significant improvements for resistance exercise (SMD = 1.57, 95% CI: 0.91–2.23), followed by aerobic (SMD = 1.44, 95% CI: 0.36–2.52) and combined exercise (SMD = 0.55, 95% CI: 0.21–0.89). Meta-regressions showed no moderating effects of duration (β = 0.0101, p = 0.834), weekly frequency (β = 0.1464, p = 0.648), minutes per session (β = −0.0124, p = 0.233) or total weekly minutes (β = 0.0005, p = 0.919) apart from age and baseline BDNF level factors (β = 0.0348, p = 0.020; β = −0.035, p = 0.0258). Publication bias tests indicated minimal publication bias, with adjusted effects remaining robust. Conclusions: Exercise interventions have been shown to increase peripheral BDNF significantly across diverse clinical populations. In particular, resistance and aerobic exercise protocols accounted for the exploratory component, whereas simple dose-related factors did not explain the variability. These findings are consistent with the biological plausibility of exercise-induced neuroplasticity and underscore the need for larger, pre-registered RCTs with harmonized biomarker protocols to strengthen clinical translation. However, the certainty of evidence is limited by small sample sizes and the frequent lack of blinding of participants and assessors across included trials.

Background and Objectives: The hypertrophic adaptation of the diaphragm to inspiratory muscle training (IMT) remains insufficiently characterized, particularly in healthy and athletic populations. To address this gap, we conducted a meta-analysis and meta-regression to evaluate the effects of IMT on diaphragm thickness and identify potential moderating factors. Materials and Methods: A systematic search was conducted across PubMed, MEDLINE, Embase, CINAHL, and SPORTDiscus as well as Google Scholar (gray literature) through November 2025. Eight studies involving 203 healthy participants met the inclusion criteria. A random-effects model was used to calculate pooled effect sizes and meta-regression estimates. Results: IMT produced a statistically significant moderate increase in diaphragm muscle thickness, with a standardized mean difference (SMD) of Hedges’ g = 0.52 (95% CI: 0.19 to 0.85; p < 0.05). Subgroup analyses indicated that IMT with 50% maximal inspiratory pressure (MIP) produces a statistically significant effect (p = 0.0069), whereas fitness status and age did not significantly influence outcomes (p = 0.589 and p = 0.126, respectively). Meta-regression analyses revealed that only baseline MIP value (β = 0.030; 95% CI: 0.009 to 0.050; p = 0.004) was associated with diaphragm hypertrophy. Conclusions: IMT with 50% of MIP elicits meaningful diaphragmatic hypertrophy in healthy individuals. This response appears independent of fitness status or age, but is significantly influenced by baseline inspiratory muscle strength (MIP). These findings support the utility of IMT in enhancing respiratory muscle morphology in health and performance contexts.