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May 14, 2026Physiology0 citations

High FRAT diet: impact of binge drinking and Western diet on myocardial mechanics

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MWMelinda WetzelIAIhsan Shawki AkiliCMCorina Miko

Key Result

Binge drinking alone suppressed twitch force and myocyte contractility, reduced left-ventricular calcium sensitivity, and increased extracellular matrix passive stiffness in mice.

Key Points

  • The study aims to investigate the combined effects of a Western diet and binge drinking on myocardial function.
  • Mice were exposed to a Control or Western diet for 6 weeks.
  • Binge drinking simulated with 20% ethanol for ~5 hours/day, 4 days/week for 14 weeks.
  • Left-ventricular slices assessed for twitch force, passive mechanics, and cardiomyocyte function.
  • Binge drinking reduced twitch force and myocyte contractility.
  • Left-ventricular passive stiffness decreased, while extracellular matrix stiffness increased.
  • Evidence suggests binge drinking alone can lead to heart disease.

Structured PICO

P
Population
Male and female mice
I
Intervention
Exposure to 20% ethanol for ~5 hours/day, 4 days/week to simulate binge drinking for 14 weeks, following 6 weeks of either a Control or novel Western (high-fat/sugar, low-fiber) diet
C
Comparator
Control diet without binge drinking
O
Outcome
Myocardial mechanics including twitch force, passive mechanics, extracellular matrix stiffness, myofilament calcium sensitivity, and cardiomyocyte shorteningsurrogate

Binge drinking alone impairs myocardial contractility and alters passive stiffness in a murine model, suggesting direct cardiotoxic effects.

Limitations

  • Analysis of the role of Western diet and Western diet plus binge drinking are forthcoming

Abstract

Both alcohol and diet are well-established to cause heart disease, typically characterized by susceptibility to electrical abnormalities, dilation, and reduced cardiac contractility. Despite this, the combination impact of poor diet and alcohol on myocardial function remains poorly characterized. Further, even less is known about the impacts of a poor diet combined with the most common type of immoderate alcohol consumption, binge drinking. Thus, we set out to determine whether combining an unhealthy Western diet and binge drinking impacted the myocardial function of male and female mice provided. We exposed mice to either a Control or novel Western (high-fat/sugar, low-fiber) diet for 6 weeks and then added exposure to 20% ethanol for ~5 hours/day, 4 days/week to simulate binge drinking for 14 weeks. We used left-ventricular slices to assess myocardial twitch force, passive mechanics, extracellular matrix stiffness, myofilament calcium sensitivity and assessed cardiomyocyte shortening in isolated ventricular myocytes. Notably, binge drinking had minimal effect on cardiac hypertrophy, but both twitch force and myocyte contractility were suppressed. Binge drinking tended to reduce the passive stiffness of the left-ventricle and reduced left-ventricular calcium sensitivity, however passive stiffness derived from the extracellular matrix was increased. Analysis of the role of Western diet and Western diet plus binge drinking are forthcoming. Taken together these results indicate binge drinking alone causes evidence of heart disease and it is expected that combining the Western diet and binge drinking will result in more significant evidence of disease. This abstract was presented at the American Physiology Summit 2026 and is only available in HTML format. There is no downloadable file or PDF version. The Physiology editorial board was not involved in the peer review process.

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Cite This Study

Wetzel et al. (2026) studied Heart disease / myocardial mechanics. Western diet and binge drinking (20% ethanol) vs. Control diet was evaluated on Myocardial twitch force, passive mechanics, extracellular matrix stiffness, myofilament calcium sensitivity, and cardiomyocyte shortening. Binge drinking alone suppressed twitch force and myocyte contractility, reduced left-ventricular calcium sensitivity, and increased extracellular matrix passive stiffness in mice.

synapsesocial.com/papers/6a05680ea550a87e60a206c5https://doi.org/10.1152/physiol.2026.41.s1.2297555
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