The narrative review brings together experimental and clinical research examining the effects of exercise on diabetes-associated heart muscle dysfunction. It identifies several promising biological mechanisms and improvements in selected clinical measures, while highlighting significant gaps between laboratory findings and their application in routine clinical care.
Diabetic cardiomyopathy involves changes in heart muscle metabolism, fibrosis, disrupted calcium handling and ventricular remodelling. Treatment strategies capable of reversing established cardiac injury remain limited, making exercise-based approaches an area of growing research interest.
The review examined how physical training could influence these processes. Experimental studies suggest that exercise can support mitochondrial function and improve the heart's ability to use different energy sources. Training may also help reduce oxidative stress and inflammatory signalling associated with fibrosis.
Other proposed mechanisms include improved calcium regulation and changes in biological pathways involved in cell death. Together, these findings provide a biological basis for considering exercise as part of the management of diabetic cardiomyopathy.
However, the authors caution against interpreting experimental findings as proof of clinical effectiveness. Laboratory evidence alone cannot establish the extent of benefits in patients or determine whether those improvements can be sustained over time. The distinction between a plausible biological mechanism and a proven clinical outcome remains important when assessing the potential of exercise-based interventions.
The clinical evidence reviewed came predominantly from people with Type 2 diabetes who had subclinical or early cardiac abnormalities, rather than clearly characterised populations with established diabetic cardiomyopathy.
Within the available evidence, combined aerobic and resistance training showed potential to improve cardiorespiratory fitness, insulin sensitivity, vascular function and selected measures of left ventricular performance.
High-intensity interval training may provide additional benefits for appropriately selected patients. However, the review stresses that its safety and effectiveness require individual assessment. This limits the scope for recommending a uniform exercise prescription across all patients.
The researchers also identified differences between exercise intervention protocols and inconsistent reporting of exercise doses as important challenges. These variations make it difficult to compare programmes and determine which training approaches deliver the most effective results.
To address these limitations, the authors call for more consistent reporting of exercise intensity using physiologically comparable measures. They also recommend evaluating treatment responses across multiple areas, including cardiac imaging, functional capacity, biomarkers, glycaemic control and adverse events.
Assessing these measures together could help researchers distinguish improvements in physical fitness and metabolic health from actual changes in cardiac function. It would also ensure that potential safety concerns receive appropriate attention when evaluating exercise interventions.
The review concludes that adequately powered clinical trials involving clearly defined patient populations are still necessary to establish the optimal exercise dose and determine whether exercise training can deliver sustained cardiovascular benefits.
While existing findings provide a promising biological and clinical rationale for exercise-based management, establishing its effectiveness in patients with diabetic cardiomyopathy will require more consistent research, clearly defined training protocols and long-term clinical evidence.
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