Academic Journal
Moderate-Intensity and High-Intensity Interval Exercise Training Offer Equal Cardioprotection, with Different Mechanisms, during the Development of Type 2 Diabetes in Rats
| العنوان: | Moderate-Intensity and High-Intensity Interval Exercise Training Offer Equal Cardioprotection, with Different Mechanisms, during the Development of Type 2 Diabetes in Rats |
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| المؤلفون: | Sarah D’Haese, Lisa Claes, Iris de Laat, Sven Van Campenhout, Dorien Deluyker, Ellen Heeren, Sibren Haesen, Ivo Lambrichts, Kristiaan Wouters, Casper G. Schalkwijk, Dominique Hansen, BO Eijnde, Virginie Bito |
| المصدر: | Nutrients, Vol 16, Iss 3, p 431 (2024) |
| بيانات النشر: | MDPI AG |
| سنة النشر: | 2024 |
| المجموعة: | Directory of Open Access Journals: DOAJ Articles |
| مصطلحات موضوعية: | type 2 diabetes, diabetic cardiomyopathy, western diet, exercise training, cardioprotection, Nutrition. Foods and food supply, TX341-641 |
| الوصف: | Endurance exercise training is a promising cardioprotective strategy in type 2 diabetes mellitus (T2DM), but the impact of its intensity is not clear. We aimed to investigate whether and how isocaloric moderate-intensity exercise training (MIT) and high-intensity interval exercise training (HIIT) could prevent the adverse cardiac remodeling and dysfunction that develop T2DM in rats. Male rats received a Western diet (WD) to induce T2DM and underwent a sedentary lifestyle ( n = 7), MIT ( n = 7) or HIIT ( n = 8). Insulin resistance was defined as the HOMA-IR value. Cardiac function was assessed with left ventricular (LV) echocardiography and invasive hemodynamics. A qPCR and histology of LV tissue unraveled underlying mechanisms. We found that MIT and HIIT halted T2DM development compared to in sedentary WD rats ( p < 0.05). Both interventions prevented increases in LV end-systolic pressure, wall thickness and interstitial collagen content ( p < 0.05). In LV tissue, HIIT tended to upregulate the gene expression of an ROS-generating enzyme (NOX4), while both modalities increased proinflammatory macrophage markers and cytokines (CD86, TNF-α, IL-1β; p < 0.05). HIIT promoted antioxidant and dicarbonyl defense systems (SOD2, glyoxalase 1; p < 0.05) whereas MIT elevated anti-inflammatory macrophage marker expression (CD206, CD163; p < 0.01). We conclude that both MIT and HIIT limit WD-induced T2DM with diastolic dysfunction and pathological LV hypertrophy, possibly using different adaptive mechanisms. |
| نوع الوثيقة: | article in journal/newspaper |
| اللغة: | English |
| Relation: | https://www.mdpi.com/2072-6643/16/3/431; https://doaj.org/toc/2072-6643; https://doaj.org/article/d368dc365ff742e4ba63dc4e716d2cd6 |
| DOI: | 10.3390/nu16030431 |
| الاتاحة: | https://doi.org/10.3390/nu16030431 https://doaj.org/article/d368dc365ff742e4ba63dc4e716d2cd6 |
| رقم الانضمام: | edsbas.7BD14715 |
| قاعدة البيانات: | BASE |
| DOI: | 10.3390/nu16030431 |
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