Key result
Exercise attenuates fructose-induced cardiac dysfunction in animal models by improving myocardial structure and diastolic function.
Why the study?
Excessive fructose consumption and sedentary lifestyles contribute to cardiometabolic disease, but human studies examining exercise-mediated cardioprotection remain limited.
Does physical exercise improve or prevent fructose-induced cardiac dysfunction in animal models?
Does physical exercise improve or prevent fructose-induced cardiac dysfunction in animal models?
Exercise is a promising non-pharmacological strategy to counteract cardiac dysfunction induced by excessive fructose consumption, primarily through metabolic and structural adaptations.
Hypothesis-generating for exercise in fructose-related cardiomyopathy; human trials needed before clinical consideration.
Excessive fructose consumption, mainly driven by industrial sweeteners, combined with increasingly sedentary lifestyles, has contributed substantially to the global rise in cardiometabolic diseases. Although the evolutionary balance between fructose intake and energy expenditure has been disrupted, it may be restored through targeted lifestyle interventions. This review examines the cardioprotective potential of physical exercise in the context of high fructose intake. Owing to the limited number of human studies, we analyzed 30 animal studies identified in PubMed, focusing on underlying cellular and molecular mechanisms and their possible relevance to lifestyle interventions in humans with impaired cardiometabolic health. Regarding fructose metabolism, exercise has been observed to reduce intestinal fructose absorption, increase hepatic fructose oxidation, suppress fructose-stimulated de novo lipogenesis, and decrease serum uric acid level, thereby attenuating the harmful effects of fructose on the heart. Consistent with these metabolic adaptations, across diverse exercise protocols in trained fructose-fed animals, consistent improvements in myocardial structure, diastolic function, cardiac electrical stability, neurohumoral regulation, and coronary blood flow were observed. These beneficial effects are associated with exercise-induced modulation of key pathways involved in oxidative stress, inflammation, energy substrate metabolism, mitochondrial biogenesis, insulin signaling, cardiac renin-angiotensin system, and nitric oxide synthesis. Notably, these benefits are observed predominantly with low- to moderate-intensity aerobic exercise, although high-intensity interval training is also worth considering. Collectively, the available evidence supports exercise as a promising non-pharmacological strategy for counteracting excessive fructose consumption-induced cardiac dysfunction and underscores the need for well-designed studies in human populations.
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Stojiljković et al. (2026) conducted a review in Fructose-induced cardiac dysfunction (n=30). Physical exercise was evaluated. Physical exercise attenuates fructose-induced cardiac dysfunction in animal models by improving myocardial structure, diastolic function, and modulating key metabolic and inflammatory pathways.
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