Constricting pythons, known for their ability to consume infrequent, massive meals, exhibit rapid and reversible cardiac hypertrophy following feeding. Our primary goal was to investigate how python hearts achieve this adaptive response after feeding. Isolated myofibrils increased force after feeding without changes in sarcomere ultrastructure and without increasing energy cost. Ca 2+ transients were prolonged after feeding with no changes in myofibril Ca 2+ sensitivity. Feeding reduced titin-based tension, resulting in decreased cardiac tissue stiffness. Feeding also reduced the activity of sirtuins, a metabolically linked class of histone deacetylases, and increased chromatin accessibility. Transcription factor enrichment analysis on transposase-accessible chromatin with sequencing revealed the prominent role of transcription factors Yin Yang1 and NRF1 in postfeeding cardiac adaptation. Gene expression also changed with the enrichment of translation and metabolism. Finally, metabolomics analysis and adenosine triphosphate production demonstrated that cardiac adaptation after feeding not only increased energy demand but also energy production. These findings have broad implications for our understanding of cardiac adaptation across species and hold promise for the development of innovative approaches to address cardiovascular diseases.

中文翻译：

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蟒蛇的餐后心脏肥大是通过力学、表观遗传和代谢重编程来维持的


收缩蟒蛇以其进食频率低、大量进食而闻名，在进食后表现出快速且可逆的心脏肥大。我们的主要目标是研究蟒蛇心脏在进食后如何实现这种适应性反应。孤立的肌原纤维在进食后增加了力量，而肌节超微结构没有变化，也没有增加能量成本。喂养后Ca 2+ 瞬变延长，肌原纤维Ca 2+ 敏感性没有变化。喂养减少了基于肌动蛋白的张力，导致心脏组织硬度降低。喂养还降低了去乙酰化酶（一类与代谢相关的组蛋白脱乙酰酶）的活性，并增加了染色质的可及性。通过测序对转座酶可及的染色质进行转录因子富集分析，揭示了转录因子 Yin Yang1 和 NRF1 在喂养后心脏适应中的突出作用。基因表达也随着翻译和代谢的丰富而改变。最后，代谢组学分析和三磷酸腺苷的产生表明，进食后的心脏适应不仅增加了能量需求，而且增加了能量产生。这些发现对于我们理解跨物种的心脏适应具有广泛的意义，并为开发解决心血管疾病的创新方法带来了希望。