The effect of intensive resistance exercise and excessive fructose intake on metabolic and physiological responses.

IF 3.9 2区医学 Q2 NUTRITION & DIETETICS

Nutrition & Metabolism Pub Date : 2025-05-23 DOI:10.1186/s12986-025-00943-y

Chien-Hua Chen, Shun-Hsi Tsai, Hao-Chien Cheng, Yu-Ting Su, Hung-Wen Liu

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引用次数: 0

Abstract

Background: Muscle-derived uric acid (UA) precursors combined with fructose ingestion may increase liver UA production. Temporary hyperuricemia could impact metabolic and physiological responses over a 24-h period. This study examined the effects of intensive resistance exercise (RE) combined with excessive fructose intake on metabolic and physiological responses.

Methods: Twelve healthy young males participated in four trials: RE with fructose intake (EF), RE with water intake (EW), control (no exercise) with fructose intake (CF), and control with water intake (CW). Blood UA, glucose, lipids, blood pressure, and markers of kidney and liver function were measured during fasting and at 0, 0.5, 1, 2, 4, and 24 h before and after exercise.

Results: UA levels in the EF and EW trials were significantly higher than those in the CF and CW trials at all post-exercise time points. The next morning, UA levels in the EF trial remained above 7 mg/dL. Increased glucose levels at 0 and 0.5 h post-exercise and increased creatinine (CRE) levels immediately post-exercise were observed. RE reduced the area under the curve for the estimated glomerular filtration rate (eGFR) and increased systolic blood pressure, mean arterial blood pressure, and the UA/CRE ratio the next morning. Fructose intake increased glutamate pyruvate transaminase (GPT) levels 24 h post-exercise. CRE showed a positive correlation with UA levels, while eGFR was negatively correlated with UA levels in the RE trials. Additionally, GPT levels correlated positively with UA following fructose intake.

Conclusion: Intensive RE combined with excessive fructose intake induced a notable increase in UA levels. This increase in UA levels appeared to be associated with temporary fluctuations in markers related to renal function.

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高强度抗阻运动和过量果糖摄入对代谢和生理反应的影响。

背景：肌肉源性尿酸（UA）前体与果糖摄入联合可增加肝脏UA生成。暂时性高尿酸血症可影响24小时内的代谢和生理反应。本研究探讨了高强度抗阻运动（RE）结合过量果糖摄入对代谢和生理反应的影响。方法：12名健康年轻男性参加4项试验：果糖摄入（EF）、水摄入（EW）、果糖摄入（CF）对照组（不运动）和水摄入对照组（CW）。在禁食期间以及运动前后0、0.5、1、2、4和24小时测量血尿酸、血糖、血脂、血压和肾功能和肝功能指标。结果：在运动后各时间点，EF和EW试验的UA水平均显著高于CF和CW试验。第二天早上，EF试验中的UA水平保持在7mg /dL以上。观察到运动后0和0.5小时血糖水平升高，运动后立即肌酐（CRE）水平升高。RE减少了估计肾小球滤过率（eGFR）曲线下的面积，增加了收缩压、平均动脉压和次日早晨的UA/CRE比。果糖摄入增加运动后24小时谷氨酸丙酮酸转氨酶（GPT）水平。在RE试验中，CRE与UA水平呈正相关，而eGFR与UA水平呈负相关。此外，GPT水平与果糖摄入后的尿酸呈正相关。结论：高强度RE联合过量果糖摄入可导致UA水平显著升高。UA水平的增加似乎与肾功能相关标志物的暂时波动有关。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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来源期刊

Nutrition & Metabolism 医学-营养学

CiteScore

8.40

自引率

0.00%

发文量

审稿时长

4-8 weeks

期刊介绍： Nutrition & Metabolism publishes studies with a clear focus on nutrition and metabolism with applications ranging from nutrition needs, exercise physiology, clinical and population studies, as well as the underlying mechanisms in these aspects. The areas of interest for Nutrition & Metabolism encompass studies in molecular nutrition in the context of obesity, diabetes, lipedemias, metabolic syndrome and exercise physiology. Manuscripts related to molecular, cellular and human metabolism, nutrient sensing and nutrient–gene interactions are also in interest, as are submissions that have employed new and innovative strategies like metabolomics/lipidomics or other omic-based biomarkers to predict nutritional status and metabolic diseases. Key areas we wish to encourage submissions from include: -how diet and specific nutrients interact with genes, proteins or metabolites to influence metabolic phenotypes and disease outcomes; -the role of epigenetic factors and the microbiome in the pathogenesis of metabolic diseases and their influence on metabolic responses to diet and food components; -how diet and other environmental factors affect epigenetics and microbiota; the extent to which genetic and nongenetic factors modify personal metabolic responses to diet and food compositions and the mechanisms involved; -how specific biologic networks and nutrient sensing mechanisms attribute to metabolic variability.