Purpose:To assess the validity and the reliability of short-term resting heart-rate variability (HRV) measures obtained using the Polar S810 heart-rate monitor and accompanying software.Methods:Measures of HRV were obtained from 5-min R to R wave (RR) interval data for 19 males and 14 female

Aims/hypothesis Cardiac disease remains the leading cause of mortality in type 2 diabetes, yet few strategies to target cardiac dysfunction have been developed. This randomised controlled trial aimed to investigate high intensity intermittent training (HIIT) as a potential therapy to improve cardiac structure and function in type 2 diabetes. The impact of HIIT on liver fat and metabolic control was also investigated. Methods Using an online random allocation sequence, 28 patients with type 2 diabetes (metformin and diet controlled) were randomised to 12 weeks of HIIT (n = 14) or standard care (n = 14). Cardiac structure and function were measured by 3.0 T MRI and tagging. Liver fat was determined by ¹H-magnetic resonance spectroscopy and glucose control by an OGTT. MRI analysis was performed by an observer blinded to group allocation. All study procedures took place in Newcastle upon Tyne, UK. Results Five patients did not complete the study and were therefore excluded from analysis: this left 12 HIIT and 11 control patients for the intention-to-treat analysis. Compared with controls, HIIT improved cardiac structure (left ventricular wall mass 104 ± 17 g to 116 ± 20 g vs 107 ± 25 g to 105 ± 25 g, p < 0.05) and systolic function (stroke volume 76 ± 16 ml to 87 ± 19 ml vs 79 ± 14 ml to 75 ± 15 ml, p < 0.01). Early diastolic filling rates increased (241 ± 84 ml/s to 299 ± 89 ml/s vs 250 ± 44 ml/s to 251 ± 47 ml/s, p < 0.05) and peak torsion decreased (8.1 ± 1.8° to 6.9 ± 1.6° vs 7.1 ± 2.2° to 7.6 ± 1.9°, p < 0.05) in the treatment group. Following HIIT, there was a 39% relative reduction in liver fat (p < 0.05) and a reduction in HbA_1c (7.1 ± 1.0% [54.5 mmol/mol] to 6.8 ± 0.9% [51.3 mmol/mol] vs 7.2 ± 0.5% [54.9 mmol/mol] to 7.4 ± 0.7% [57.0 mmol/mol], p < 0.05). Changes in liver fat correlated with changes in HbA_1c (r = 0.70, p < 0.000) and 2 h glucose (r = 0.57, p < 0.004). No adverse events were recorded. Conclusions/interpretation This is the first study to demonstrate improvements in cardiac structure and function, along with the greatest reduction in liver fat, to be recorded following an exercise intervention in type 2 diabetes. HIIT should be considered by clinical care teams as a therapy to improve cardiometabolic risk in patients with type 2 diabetes. Trial registration: www.isrctn.com 78698481 Funding: Medical Research Council.

Background. Exercise therapy could potentially modify metabolic risk factors and brain physiology alongside improving function post stroke. Objective. To explore the short-term metabolic, brain, cognitive, and functional effects of exercise following stroke. Methods. A total of 40 participants (>50 years, >6 months post stroke, independently mobile) were recruited to a single-blind, parallel, randomized controlled trial of community-based exercise (19 weeks, 3 times/wk, “exercise” group) or stretching (“control” group). Primary outcome measures were glucose control and cerebral blood flow. Secondary outcome measures were cardiorespiratory fitness, blood pressure, lipid profile, body composition, cerebral tissue atrophy and regional brain metabolism, and physical and cognitive function. Results. Exercise did not change glucose control (homeostasis model assessment 1·5 ± 0·8 to 1·5 ± 0·7 vs 1·6 ± 0·8 to 1·7 ± 0·7, P = .97; CI = −0·5 to 0·49). Medial temporal lobe tissue blood flow increased with exercise (38 ± 8 to 42 ± 10 mL/100 g/min; P < .05; CI = 9.0 to 0.1) without any change in gray matter tissue volume. There was no change in medial temporal lobe tissue blood flow in the control group (41 ± 8 to 40 ± 7 mL/100 g/min; P = .13; CI = −3.6 to 6.7) but significant gray matter atrophy. Cardiorespiratory fitness, diastolic blood pressure, high-density lipoprotein cholesterol, physical function, and cognition also improved with exercise. Conclusion. Exercise therapy improves short-term metabolic, brain, physical, and cognitive function, without changes in glucose control following stroke. The long-term impact of exercise on stroke recurrence, cardiovascular health, and disability should now be explored.

Aging is associated with significant changes in both cardiac and vascular structure and function that lower the threshold for clinical signs and symptoms, making older people more susceptible to cardiovascular diseases, morbidity and mortality. Understanding of age-related cardiovascular changes is necessary for effective and efficient prevention and treatment of cardiovascular disease in older people. Cardiac aging is associated with left ventricular remodelling marked by increased mass-to-volume ratio and accompanied by systolic and diastolic myocardial dysfunction, and reduced sensitivity to sympathetic stimuli that compromises myocardial contractility and pumping ability in older people. The vascular age-related remodelling is associated with increased arterial wall thickness, arterial stiffness, and an impaired endothelial vasoreactivity. Over the previous three decades of intensive research in cardiovascular aging, it became apparently clear that lifestyle factors such as physical activity and exercise play an important role in attenuating cardiovascular function decline with aging. This review highlights the effect of age on cardiac and vascular changes and their adaptations to exercise, providing physiological, molecular and cellular mechanisms that underlie diminished cardiovascular response in older age. It further describes cardiovascular differences between the individuals who maintain a physically active lifestyle, and who undergo exercise interventions in later life.