High-Intensity Interval Training Attenuates Inflammation in Cardiorenal Syndrome Induced by Renal Ischemia–Reperfusion Injury in Rats

TL;DR

High-intensity interval training in rats reduces inflammation and cardiac damage caused by kidney injury.

Contribution

This study shows that prior high-intensity interval training can partially protect against cardiorenal injury in rats.

Findings

HIIT reduced markers of kidney and heart injury in rats.

HIIT attenuated systemic inflammation and cardiac caspase-3 and TNF-α expression.

Renal ischemia–reperfusion caused dysfunction, inflammation, and heart damage in rats.

Abstract

Acute kidney injury (AKI), a common complication of renal and cardiovascular procedures, induces systemic inflammation that can lead to secondary cardiac injury. This study examined whether prior high-intensity interval training (HIIT) could modulate biochemical and histological markers of cardiac injury following renal ischemia–reperfusion (I/R). Thirty male Sprague–Dawley rats were assigned to Sham, Renal I/R, and HIIT groups; one rat in the I/R group and two in the HIIT group did not survive. Serum analyses included creatinine, CK, troponin I, LDH, and inflammatory cytokines. Renal injury was assessed using tubular and glomerular injury scores, and cardiac injury was evaluated by myocardial injury scoring, TUNEL staining, and expression of caspase-3, TNF-α, and Bax. Renal I/R induced renal dysfunction, systemic inflammation, and myocardial damage. Prior HIIT significantly reduced creatinine, CK, troponin I, LDH, inflammatory cytokines, and cardiac caspase-3 and TNF-α expression. Overall, HIIT provided partial protection against renal I/R-induced systemic and cardiac alterations, primarily by attenuating inflammation, and should be considered a potential—rather than definitive—preconditioning strategy requiring further investigation.

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