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Objective: This study aimed to investigate the acute effects of exercise timing (morning vs. evening) on fat oxidation and energy expenditure in young men, with a focus on interactions between exercise and meal timing.
Methods: Eighteen male college students (23.47 ± 2.11 years) completed a randomized crossover trial under five conditions: sedentary control (SC), exercise before breakfast (EBB), exercise after breakfast (EAB), exercise before dinner (EBD), and exercise after dinner (EAD). Indirect calorimetry (COSMED K5) measured substrate utilization during exercise, post-exercise recovery (0-4 h), and the following morning. Total exercise volume (running distance) was standardized, and energy expenditure was normalized to body weight (kcal/kg).
Results: During the sedentary control test, participants showed similar trends in total energy expenditure. Dring exercise, the EBB group demonstrated significantly higher fat expenditure compared to EAB (P < 0.05), EBD (P < 0.01), and EAD (P < 0.01). Morning exercise overall exhibited superior fat oxidation (P < 0.01). Post-exercise (0-4 h), EBB sustained elevated fat utilization (P < 0.01 vs. EBD/EAD), while EAD showed enhanced fat oxidation the following morning (P < 0.01 vs. EAB).
Conclusion: The findings suggest that exercise timing may influence temporal patterns of fat oxidation, with morning fasting potentially favoring acute lipid utilization, while evening exercise appears to correlate with delayed metabolic adjustments. Although total energy expenditure remained comparable across conditions, the observed shifts in substrate allocation imply a possible circadian-sensitive modulation of energy partitioning. These preliminary observations underscore the need for further investigation to clarify the long-term physiological relevance of such timing-dependent metabolic responses.
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http://dx.doi.org/10.3389/fphys.2025.1574757 | DOI Listing |
J Adv Res
September 2025
School of Public Health and Nursing, Zhejiang Key Laboratory of Medical Epigenetics, Hangzhou Normal University, Hangzhou, China. Electronic address:
Introduction: Metabolic dysfunction-associated steatotic liver disease (MASLD) represents an increasing global health problem in association with obesity and insulin resistance without approved pharmacotherapy. Previous studies revealed malic enzyme 1 (ME1) as a susceptibility gene for metabolic disorders in humans. However, the role and mechanisms of ME1 in regulating hepatic lipid metabolism remain largely unclear.
View Article and Find Full Text PDFFitoterapia
September 2025
Yunnan Key Laboratory of Southern Medicine Utilization, College of Traditional Chinese Medicine, Yunnan University of Chinese Medicine, Kunming 650500, China. Electronic address:
The gut microbiota and its products are recognized as pivotal contributors to the pathogenesis of metabolic-associated fatty liver disease (MAFLD). Shenling Jianpiwei formula (SLJPW), a prescription renowned for its protective effects in intestinal disorders, demonstrates efficacy against MAFLD. However, its underlying mechanisms and chemical composition remain unclear.
View Article and Find Full Text PDFJ Physiol
September 2025
Department of Cell and Molecular Biology, University of Hawaii, Honolulu, HI, USA.
Diagnoses of prediabetes and metabolic syndromes, such as metabolic-associated steatotic liver disease (MASLD), are increasing at an alarming rate worldwide, often simultaneously. A significant consequence of these is high risk of cardiovascular disease, highlighting the need for cardiac-specific therapeutics for intervention during the prediabetic stage. Recent studies have demonstrated that chemogenetic activation of the cardiac parasympathetic system through hypothalamic oxytocin (OXT) neurons provides cardioprotective effects in heart disease models by targeting excitatory neurotransmission to brainstem cardiac vagal neurons.
View Article and Find Full Text PDFExp Physiol
September 2025
Department of Hepatobiliary Surgery, The Affiliated Huaian No.1 People's Hospital of Nanjing Medical University, Huaian, Jiangsu, China.
Hepatic ischaemia-reperfusion (IR) injury is a serious clinical issue, especially in patients with type 2 diabetes mellitus (T2DM). As mitochondria play a critical role in the regulation of IR-induced liver damage, mitochondria-targeted treatment is of the utmost significance for improving outcomes. The present study explored the mitoprotective role of combined ginsenoside-MC1 (GMC1) and irisin administration in diabetic rats with hepatic IR injury.
View Article and Find Full Text PDFJ Endocrinol
September 2025
University of Missouri, Columbia, MO.
Purpose: CL316,243 (CL), a beta 3 adrenergic receptor (B3-AR) agonist has 'exercise mimetic' effects in adipose tissue (AT). CL may also positively affect skeletal muscle (SM), yet the role of estrogen receptor beta (ERβ) in mediating SM-specific effects of CL is not known. We investigated the effects of CL on SM metabolism, as well as the role played by ERβ.
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