associated with a twofold greater risk of developing cardiovascular disease than those without. Recent research has shown that there are alterations in cardiac structure and function in NAFLD in the absence of overt cardiac disease. This study aimed to investigate exercise as a therapeutic tool to decrease cardiac risk in NAFLD. Patients and Methods: Twenty adults with NAFLD were randomised to 12 weeks of high intensity intermittent training or continue standard care. Cardiac structure and function were assessed using high resolution cardiac magnetic resonance imaging and tagging at 3.0T. High energy phosphate metabolism was assessed using 31 P-spectroscopy to measure PCr/ATP ratio. People with a history of discrete cardiac events or potential cardiac symptoms were excluded from the study. Liver fat was assessed using 1 H-magnetic resonance spectroscopy. The intervention group undertook exercise 3 times per week. Results: Exercise improved diastolic function in adults with NAFLD. E/A ratio increased with exercise (1.16±0.47 to 1.49±0.62; p = 0.022) but not in control (1.48± 0.98 to 1.17 ±0.46; p = 0.346) as did the early diastolic filling rate (exercise: 261.2±70.8 to 315.3±93.6 ml/s; p = 0.008, control: 276.2±86.2 to 281.9±75.3 ml/s; p = 0.757). Exercise also decreased peak cardiac torsion (exercise: 7.78±2.49 to 6.34±1.84deg; p = 0.048. control: 5.48±0.96 to 6.50±2.16deg; p = 0.300) but had no effect on cardiac structure, systolic function, or cardiac energetics. Conclusions: A 12-week high intensity intermittent exercise programme improves cardiac diastolic function and torsion in adults with NAFLD. Clinical care teams should consider high intensity intermittent exercise as part of their therapeutic regimen to modify the excess risk of cardiovascular disease associated with NAFLD.