Hyperbaric oxygen attenuates fructose-induced tachycardia and electrical remodeling in a rat model

Aim: To investigate the arrhythmogenic potential of a high-fructose diet (HFD) in a rat model and evaluated the capacity of adjunctive hyperbaric oxygen (HBO) therapy to mitigate resulting cardiac electrophysiological disturbances. Methods: Thirty-two adult male Wistar rats were randomly allocated into four groups (n=8 each): Control, high-fructose diet (HFD), hyperbaric oxygen (HBO), and HFD+HBO. The HFD groups received a 60 kcal% fructose-enriched diet for 10 weeks. HBO was administered during the final two weeks (weeks 9–10) at 2.4 atmospheres absolute (ATA) with 100% oxygen for 60 minutes daily. At the end of the experimental period, standard limb-lead electrocardiograms (ECGs) were recorded under light anesthesia. Heart rate, RR interval, PR interval, QRS duration, QT interval, QTc, and QRS complex frequency were analyzed. Data were evaluated using one-way ANOVA followed by Fisher’s LSD post hoc test, with p<0.05 considered statistically significant. Results: The HFD group developed significant tachycardia, evidenced by a reduced RR interval and an increased QRS complex count compared to controls (p<0.05). Furthermore, the HFD group exhibited a shortened PR interval, indicating accelerated atrioventricular conduction (p<0.05). HBO administration significantly attenuated the HFD-induced tachycardia, normalizing both RR interval and QRS count (p<0.05 vs. HFD group). However, HBO did not fully reverse the shortened PR interval. No significant differences were observed in QRS duration, QT interval, or P-wave duration among the groups. Conclusion: Hyperbaric oxygen effectively ameliorates the diet-induced tachycardia, supporting its potential role as a therapeutic intervention to stabilize cardiac electrical activity in the context of metabolic stress. These findings highlight a direct link between dietary fructose excess and pro-arrhythmic cardiac remodeling, while proposing HBO as a novel protective strategy.