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Objective: A role for microRNAs is implicated in several biological and pathological processes. We investigated the effects of high-intensity interval training (HIIT) and moderate-intensity continuous training (MICT) on molecular markers of diabetic cardiomyopathy in rats. Methods: Eighteen male Wistar rats (260 ± 10 g; aged 8 weeks) with streptozotocin (STZ)-induced type 1 diabetes mellitus (55 mg/kg, IP) were randomly allocated to three groups: control, MICT, and HIIT. The two different training protocols were performed 5 days each week for 5 weeks. Cardiac performance (end-systolic and end-diastolic dimensions, ejection fraction), the expression of miR-206, HSP60, and markers of apoptosis (cleaved PARP and cytochrome C) were determined at the end of the exercise interventions. Results: Both exercise interventions (HIIT and MICT) decreased blood glucose levels and improved cardiac performance, with greater changes in the HIIT group (p < 0.001, η2: 0.909). While the expressions of miR-206 and apoptotic markers decreased in both training protocols (p < 0.001, η2: 0.967), HIIT caused greater reductions in apoptotic markers and produced a 20% greater reduction in miR-206 compared with the MICT protocol (p < 0.001). Furthermore, both training protocols enhanced the expression of HSP60 (p < 0.001, η2: 0.976), with a nearly 50% greater increase in the HIIT group compared with MICT. Conclusions: Our results indicate that both exercise protocols, HIIT and MICT, have the potential to reduce diabetic cardiomyopathy by modifying the expression of miR-206 and its downstream targets of apoptosis. It seems however that HIIT is even more effective than MICT to modulate these molecular markers.
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INTRODUCTION: Preclinical studies provide foundational knowledge to develop new effective treatments for use in clinical practice. Similar to clinical exercise oncology studies, it is also important to monitor, identify and/or avoid cancer-induced complications in preclinical (e.g., murine) exercise oncology studies. This may help close the gap between preclinical and clinical exercise oncology studies. The aim of the present mini review is to provide insight into exercise protocol design in preclinical exercise oncology studies in order to close the preclinical-clinical gap. A secondary aim was to examine exercise-responsive outcomes in the preclinical versus clinical setting. METHOD: We reviewed animal studies in exercise oncology. A literature search was performed in PubMed/Medline and studies in English were screened. RESULTS: We found that the majority of preclinical exercise protocols have not been at least tested clinically. We found some evidence that certain outcomes of preclinical studies (e.g., markers of cellular and molecular adaptation) that translate to clinical studies. However, this translation was dependent on the use, by investigators in their study design, of suitable and applicable preclinical exercise protocols. CONCLUSIONS: Cancer and its treatment-induced complications (e.g., fatigue, cardiac atrophy, cachexia, etc.) have largely been ignored in the exercise protocols of preclinical oncology studies. Preclinical exercise oncology studies should consider the limitations of human exercise oncology studies when conducting gap analysis for their study design to increase the probability that findings related to mechanistic adaptations in exercise oncology will be translatable to the clinical setting. By virtue of paying heed to patient compliance and adverse effects, clinical exercise oncology research teams must design relevant, feasible exercise protocols; researchers in preclinical exercise oncology should also take such factors into consideration in order to help bridge the gap between preclinical and clinical studies in exercise oncology.
