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Swimming training is superior to running training in inducing physiological cardiac hypertrophy and enhancing myocardial contractility, a response mediated by the PTEN-AKT-S6K1 pathway and specific microRNAs. Novelty: ClaimNovelty.INCREMENTAL. Consensus alignment: ConsensusAlignment.NEUTRAL.

March 3, 2026Open Access

Swimming is superior to running in inducing physiological cardiac hypertrophy and enhancing myocardial performance

Key Points

Swimming training outperformed running training in boosting myocardial mass and cardiac performance, particularly in male Wistar rats.
The study showed that swimming increased papillary muscle shortening velocity and enhanced left ventricular cavity size significantly.

Structured PICO

Does swimming training induce greater physiological cardiac hypertrophy and myocardial performance compared to running training in male Wistar rats?

Population

Male Wistar rats (8-10 weeks old; ~ 250 g)

Intervention

Swimming training (ST) at approximately 75% of VO₂max, performed five days a week, once daily for 60 min for eight weeks

Comparator

Running training (RT) at approximately 75% of VO₂max, performed five days a week, once daily for 60 min for eight weeks, and an untrained (UT) control group

Outcome

Cardiac remodeling (myocardial mass, cardiomyocyte growth, LV cavity size) and myocardial performance (tension and papillary muscle shortening velocity)surrogate

Swimming training is superior to running training for inducing physiological cardiac hypertrophy and enhancing myocardial contractility in a rat model, mediated by the PTEN-AKT-S6K1 pathway.

Abstract

Aerobic exercise training (AET) can induce cardiac hypertrophy, but the specific adaptive response for different types of AET remains unclear. We evaluated nonsingular cardiac remodeling in rats through running (RT) and swimming (ST) training at approximately 75% of VO₂max. Male Wistar rats (8-10 weeks old; ~ 250 g) were divided into untrained (UT), RT, and ST groups. The RT and ST were performed five days a week, once daily for 60 min for eight weeks. Cardiopulmonary fitness was assessed by measuring maximal oxygen consumption and swimming time to exhaustion. Echocardiography evaluated left ventricular parameters, while myocardial mechanics were assessed through the papillary muscle. Histology and Western blotting were performed to evaluate cardiomyocyte size and proteins modulating phosphoinositide 3-kinase (PI3K110α)/AKT1 signaling. Real-time PCR was used to assess the expression of genes and microRNAs involved in myocardial hypertrophy. Both AET protocols enhanced cardiopulmonary capacity, but only the ST group showed increased myocardial mass, cardiomyocyte growth, and LV cavity size, along with greater tension and papillary muscle shortening velocity. A more pronounced alteration in gene expression pattern for proteins modulating PI3K110α/AKT1 signaling was found in the ST group than in the RT group. A similar difference was also found for microRNA 1, 21, 27a, 124, and 144 expressions. ST is more effective than RT in inducing cardiac hypertrophy and enhancing contractility, linked to the PTEN-AKT-S6K1 pathway and increased expressions of microRNAs 1, 21, 27a, 124, and 144. Thus, ST is superior to RT for inducing physiological cardiac hypertrophy.

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