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Mechanical Function of Cardiac Fibre Bundles is Partly Protected by Exercise in Response to Diet-induced Obesity in Rats.
Applied Physiology, Nutrition, and Metabolism ( IF 2.4 ) Pub Date : 2020-06-20 , DOI: 10.1139/apnm-2020-0275 Kevin Boldt 1, 2 , Jaqueline Lourdes Rios 1, 2 , Venus Joumaa 1, 2 , Walter Herzog 1, 2, 3
Applied Physiology, Nutrition, and Metabolism ( IF 2.4 ) Pub Date : 2020-06-20 , DOI: 10.1139/apnm-2020-0275 Kevin Boldt 1, 2 , Jaqueline Lourdes Rios 1, 2 , Venus Joumaa 1, 2 , Walter Herzog 1, 2, 3
Affiliation
Applied Physiology, Nutrition, and Metabolism, Ahead of Print.
Decrements in contractile function resulting from obesity are thought to be major reasons for the link between obesity and cardiovascular disease, while exercise has been shown to improve cardiac muscle contractile function. The purpose of this study was to evaluate cardiac contractile properties following obesity induction and the potential protective effect of exercise. Twelve-week-old rats (n = 30) were organized into either a chow diet or a high-fat, high-sucrose (HFHS) diet group. Following 12 weeks of obesity induction the HFHS group animals were stratified and grouped into sedentary (HFHS+Sed) and exercise (HFHS+Ex) groups for an additional 12 weeks. Following 24 weeks of diet intervention, with 12 weeks of aerobic exercise (25 m/min, 30 min/day, 5 days/week) for the HFHS+Ex group, skinned cardiac fibre bundle testing was used to evaluate cardiac contractile properties. Body fat and mass were significantly greater in the HFHS-fed animals compared with the chow controls (p < 0.043). Hearts from rats in the HFHS+Sed group had significantly greater mass (p < 0.03), significantly slower maximum shortening velocity (p = 0.001), and tended to have lower calcium sensitivity (p = 0.077) and a lower proportion of α-myosin heavy chain composition (p = 0.074) than the sedentary chow animals. However, 12 weeks of moderate aerobic exercise partially prevented these decrements in contractile properties. Novelty Cardiac muscle from animals exposed to an obesogenic diet for 24 weeks had impaired contractile properties compared with controls. Obesity-induced impairment of contractile properties of the heart were partially prevented by a 12-week aerobic exercise regime.
中文翻译：
心脏纤维束的机械功能部分受到运动以应对大鼠饮食引起的肥胖的保护。
应用生理学、营养学和代谢，提前出版。
肥胖导致的收缩功能下降被认为是肥胖与心血管疾病之间存在联系的主要原因，而运动已被证明可以改善心肌收缩功能。本研究的目的是评估肥胖诱导后的心脏收缩特性和运动的潜在保护作用。12 周大的大鼠 (n = 30) 被分为食物组或高脂肪、高蔗糖 (HFHS) 饮食组。在 12 周的肥胖诱导之后，HFHS 组动物被分层并分组为久坐 (HFHS+Sed) 和运动 (HFHS+Ex) 组，再持续 12 周。HFHS+Ex 组进行 24 周的饮食干预后，进行 12 周的有氧运动（25 m/min、30 min/天、5 天/周），剥皮心脏纤维束测试用于评估心脏收缩特性。与饲料对照相比，HFHS 喂养的动物的体脂和体重明显更大（p < 0.043）。HFHS+Sed 组大鼠心脏的质量显着更大 (p < 0.03)，最大缩短速度显着减慢 (p = 0.001)，钙敏感性较低 (p = 0.077) 和 α-肌球蛋白比例较低重链组成 (p = 0.074) 比久坐的松狮动物。然而，12 周的适度有氧运动在一定程度上阻止了这些收缩特性的下降。与对照组相比，暴露于致肥胖饮食 24 周的动物的心肌收缩性能受损。
更新日期：2020-06-20
Decrements in contractile function resulting from obesity are thought to be major reasons for the link between obesity and cardiovascular disease, while exercise has been shown to improve cardiac muscle contractile function. The purpose of this study was to evaluate cardiac contractile properties following obesity induction and the potential protective effect of exercise. Twelve-week-old rats (n = 30) were organized into either a chow diet or a high-fat, high-sucrose (HFHS) diet group. Following 12 weeks of obesity induction the HFHS group animals were stratified and grouped into sedentary (HFHS+Sed) and exercise (HFHS+Ex) groups for an additional 12 weeks. Following 24 weeks of diet intervention, with 12 weeks of aerobic exercise (25 m/min, 30 min/day, 5 days/week) for the HFHS+Ex group, skinned cardiac fibre bundle testing was used to evaluate cardiac contractile properties. Body fat and mass were significantly greater in the HFHS-fed animals compared with the chow controls (p < 0.043). Hearts from rats in the HFHS+Sed group had significantly greater mass (p < 0.03), significantly slower maximum shortening velocity (p = 0.001), and tended to have lower calcium sensitivity (p = 0.077) and a lower proportion of α-myosin heavy chain composition (p = 0.074) than the sedentary chow animals. However, 12 weeks of moderate aerobic exercise partially prevented these decrements in contractile properties. Novelty Cardiac muscle from animals exposed to an obesogenic diet for 24 weeks had impaired contractile properties compared with controls. Obesity-induced impairment of contractile properties of the heart were partially prevented by a 12-week aerobic exercise regime.
中文翻译：
心脏纤维束的机械功能部分受到运动以应对大鼠饮食引起的肥胖的保护。
应用生理学、营养学和代谢，提前出版。
肥胖导致的收缩功能下降被认为是肥胖与心血管疾病之间存在联系的主要原因，而运动已被证明可以改善心肌收缩功能。本研究的目的是评估肥胖诱导后的心脏收缩特性和运动的潜在保护作用。12 周大的大鼠 (n = 30) 被分为食物组或高脂肪、高蔗糖 (HFHS) 饮食组。在 12 周的肥胖诱导之后，HFHS 组动物被分层并分组为久坐 (HFHS+Sed) 和运动 (HFHS+Ex) 组，再持续 12 周。HFHS+Ex 组进行 24 周的饮食干预后，进行 12 周的有氧运动（25 m/min、30 min/天、5 天/周），剥皮心脏纤维束测试用于评估心脏收缩特性。与饲料对照相比，HFHS 喂养的动物的体脂和体重明显更大（p < 0.043）。HFHS+Sed 组大鼠心脏的质量显着更大 (p < 0.03)，最大缩短速度显着减慢 (p = 0.001)，钙敏感性较低 (p = 0.077) 和 α-肌球蛋白比例较低重链组成 (p = 0.074) 比久坐的松狮动物。然而，12 周的适度有氧运动在一定程度上阻止了这些收缩特性的下降。与对照组相比，暴露于致肥胖饮食 24 周的动物的心肌收缩性能受损。
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