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    Caffeine Habituation, Not CYP1A2 Genotype, Modulates the Acute Effect of Caffeine on Exercise-Induced Hemostatic Responses in Adults with Obesity
    (Lippincott Williams & Wilkins, 2025) Sajedi, Heidar; Aydin, Elif; Keskin, Ozlem; Ercis, Sertac; Akpinar, Selahattin; Khodadadi, Davar
    Purpose: This study aimed to investigate how genotype and caffeine habituation influence the acute effects of caffeine ingestion on exercise-induced hemostatic responses in individuals with obesity. Methods: Using a randomized, double-blind, placebo-controlled crossover design, 40 physically inactive young men with obesity (age, 22.2 +/- 2.3 yr; body mass index, 34.1 +/- 2.7 kgm(-2)) completed two moderate-to-high-intensity concurrent exercise sessions following ingestion of caffeine (3 mgkg(-1)) or placebo. Blood samples were collected at baseline, after exercise, and after 60 min of recovery. Statistical analysis was performed by repeated-measures multivariate analysis of variance. Results: Acute exercise increased platelet count and aggregation, fibrinogen, F1 + 2, tPA antigen, D-dimer, and clot lysis time, regardless of genotype or caffeine habituation status (P < 0.05). PAI-1 antigen remained unchanged after exercise (P > 0.05) but decreased following recovery (P < 0.01). Caffeine resulted in a greater increase in platelet aggregation, fibrinogen, F1 + 2, and clot lysis time, alongside a blunted increase in tPA antigen levels post-exercise in na & iuml;ve consumers (P < 0.05). In contrast, habitual caffeine consumers exhibited a mitigated increase in clot lysis time and a greater post-recovery reduction in PAI-1 antigen following caffeine ingestion (P < 0.001). Caffeine's impact on hemostatic responses to exercise was unaffected by genotype (P > 0.05). Conclusions: Moderate-to-high-intensity concurrent exercise induces a transient prothrombotic state in physically inactive individuals with obesity. Acute caffeine supplementation at a moderate dose modulates the hemostatic responses depending on caffeine habituation status rather than CYP1A2 genotype: it exacerbates the prothrombotic response in na & iuml;ve consumers but attenuates it in habitual consumers.
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    Fasted-State Aerobic Exercise Enhances Cognition and Hippocampal BDNF Signaling in an Alzheimer's Disease Rat Model
    (Springer/Plenum Publishers, 2025) Kirkbir, Fatih; Atasoy, Taner; Khodadadai, Davar; Sajedi, Heidar; Keskin, Ozlem; Babaie, Mohammad
    Alzheimer's disease (AD) is a multifactorial disorder that demands a comprehensive management strategy. Both aerobic exercise training and intermittent fasting (IF) have been shown to ameliorate AD symptoms, yet the impact of exercise in the fasted state remains understudied. This study compared the effects of four weeks of moderate-intensity treadmill running in either a fasted or a normal fed state on cognitive function and hippocampal BDNF signaling in an amyloid-beta (A beta)(1-42)-injected rat model of AD. Twenty-month-old male Wistar rats were allocated into five groups (n = 12 each): AD, AD plus IF (ADIF), AD plus exercise training (ADET), AD plus IF plus exercise training (ADIFET), and control. AD was induced by bilateral intra-hippocampal A beta(1-42) injection. Exercise interventions (fasted or fed) were conducted 5 days/week for 4 weeks. A beta injection significantly impaired learning and memory and reduced hippocampal levels of PKA, CREB, and BDNF (p < 0.001). Both fasting and exercise independently elevated plasma and hippocampal beta-hydroxybutyrate (beta HB) (p < 0.001), with the highest beta HB increase observed in the fasted-exercise group (p < 0.01). All intervention groups (ADIF, ADET, and ADIFET) demonstrated significant improvements in cognitive performance and hippocampal levels of PKA, CREB, and BDNF (p < 0.001). The combined fasting plus exercise group produced greater benefits than either IF or exercise alone (p < 0.05), and exercise alone outperformed fasting alone (p < 0.05). These findings indicate that aerobic exercise in the fasted state offers superior neuroprotective and cognitive benefits, likely via upregulation of beta HB/PKA/CREB/BDNF signaling, highlighting fasted-state exercise as a promising therapeutic approach for AD.