Chronic cold exposure causes left ventricular hypertrophy that appears to be physiological.

IF 2.8 2区 生物学 Q2 BIOLOGY
Journal of Experimental Biology Pub Date : 2024-10-15 Epub Date: 2024-10-17 DOI:10.1242/jeb.247476
McKenna P A Burns, Caroline R Reges, Spencer W Barnhill, Kenna N Koehler, Brandon C Lewis, Alyssa T Colombo, Nick J Felter, Paul J Schaeffer
{"title":"Chronic cold exposure causes left ventricular hypertrophy that appears to be physiological.","authors":"McKenna P A Burns, Caroline R Reges, Spencer W Barnhill, Kenna N Koehler, Brandon C Lewis, Alyssa T Colombo, Nick J Felter, Paul J Schaeffer","doi":"10.1242/jeb.247476","DOIUrl":null,"url":null,"abstract":"<p><p>Exposure to winter cold causes an increase in energy demands to meet the challenge of thermoregulation. In small rodents, this increase in cardiac output leads to a profound cardiac hypertrophy, 2-3 times that typically seen with exercise training. The nature of this hypertrophy and its relevance to winter mortality remains unclear. Our goal was to characterize cold-induced cardiac hypertrophy and to assess its similarity to either exercise-induced (physiological) hypertrophy or the pathological hypertrophy of hypertension. We hypothesized that cold-induced hypertrophy will most closely resemble exercise-induced hypertrophy, but be another unique pathway for physiological cardiac growth. We found that cold-induced hypertrophy was largely reversed after a return to warm temperatures. Further, metabolic rates were elevated while gene expression and mitochondrial enzyme activities indicative of pathology were absent. A gene expression panel comparing hearts of exercised and cold-exposed mice further suggests that these activities are similar, although not identical. In conclusion, we found that chronic cold led to a phenotype that most closely resembled physiological hypertrophy, with enhanced metabolic rate, without induction of fetal genes, but with decreased expression of genes associated with fatty acid oxidation, suggesting that heart failure is not a cause of winter mortality in small rodents and identifying a novel approach for the study of cardiac growth.</p>","PeriodicalId":15786,"journal":{"name":"Journal of Experimental Biology","volume":null,"pages":null},"PeriodicalIF":2.8000,"publicationDate":"2024-10-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11529882/pdf/","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Journal of Experimental Biology","FirstCategoryId":"99","ListUrlMain":"https://doi.org/10.1242/jeb.247476","RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2024/10/17 0:00:00","PubModel":"Epub","JCR":"Q2","JCRName":"BIOLOGY","Score":null,"Total":0}
引用次数: 0

Abstract

Exposure to winter cold causes an increase in energy demands to meet the challenge of thermoregulation. In small rodents, this increase in cardiac output leads to a profound cardiac hypertrophy, 2-3 times that typically seen with exercise training. The nature of this hypertrophy and its relevance to winter mortality remains unclear. Our goal was to characterize cold-induced cardiac hypertrophy and to assess its similarity to either exercise-induced (physiological) hypertrophy or the pathological hypertrophy of hypertension. We hypothesized that cold-induced hypertrophy will most closely resemble exercise-induced hypertrophy, but be another unique pathway for physiological cardiac growth. We found that cold-induced hypertrophy was largely reversed after a return to warm temperatures. Further, metabolic rates were elevated while gene expression and mitochondrial enzyme activities indicative of pathology were absent. A gene expression panel comparing hearts of exercised and cold-exposed mice further suggests that these activities are similar, although not identical. In conclusion, we found that chronic cold led to a phenotype that most closely resembled physiological hypertrophy, with enhanced metabolic rate, without induction of fetal genes, but with decreased expression of genes associated with fatty acid oxidation, suggesting that heart failure is not a cause of winter mortality in small rodents and identifying a novel approach for the study of cardiac growth.

长期暴露在寒冷环境中会导致左心室肥大,这似乎是生理性的。
冬季寒冷会导致能量需求增加,以应对体温调节的挑战。在小型啮齿类动物中,心脏输出量的增加会导致严重的心脏肥大,通常是运动训练的 2-3 倍。这种肥大的性质及其与冬季死亡率的关系仍不清楚。我们的目标是描述寒冷诱导的心脏肥大的特征,并评估其与运动诱导的(生理性)肥大或高血压病理肥大的相似性。我们假设,寒冷诱导的肥大与运动诱导的肥大最为相似,但却是生理性心脏生长的另一种独特途径。我们发现,恢复到温暖温度后,冷诱导的肥大在很大程度上被逆转。此外,新陈代谢率升高,而表明病理变化的基因表达和线粒体酶活性却不存在。比较运动小鼠和暴露在寒冷环境中的小鼠心脏的基因表达面板进一步表明,这些活动虽然不完全相同,但很相似。总之,我们发现慢性寒冷导致的表型最接近生理性肥大,代谢率提高,没有诱导胎儿基因,但与脂肪酸氧化相关的基因表达减少,这表明心力衰竭不是小型啮齿类动物冬季死亡的原因,并为研究心脏生长提供了一种新方法。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
求助全文
约1分钟内获得全文 求助全文
来源期刊
CiteScore
5.50
自引率
10.70%
发文量
494
审稿时长
1 months
期刊介绍: Journal of Experimental Biology is the leading primary research journal in comparative physiology and publishes papers on the form and function of living organisms at all levels of biological organisation, from the molecular and subcellular to the integrated whole animal.
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
确定
请完成安全验证×
copy
已复制链接
快去分享给好友吧!
我知道了
右上角分享
点击右上角分享
0
联系我们:info@booksci.cn Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。 Copyright © 2023 布克学术 All rights reserved.
京ICP备2023020795号-1
ghs 京公网安备 11010802042870号
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术官方微信