One-year Aerobic Interval Training Improves Endothelial Dysfunction in Patients with Atrial Fibrillation: A Randomized Trial.

Objective To evaluate the effects of one-year aerobic interval training on endothelial dysfunction in patients with atrial fibrillation. Methods Seventy-four patients with atrial fibrillation (53 men, 21 women; mean age 63±6 years old) were randomized into a 1-year continuous aerobic interval training (CT), 6-month detraining after 6 months of aerobic interval training (DT), or medical treatment only (MT) group. Aerobic interval training was performed 3 times a week for 1 year or 6 months, with an exercise intensity of 85-95% of the peak heart rate. The primary outcome was a change in biomarkers of endothelial dysfunction from baseline at six months or at the one-year follow-up. Results Six-month aerobic interval training reduced von Willebrand factor (CT: 103.7±30.7 IU/dL and DT: 106±31.2 IU/dL vs. MT: 145±47.7 IU/dL, p=0.044). Improvements were maintained with continuous aerobic interval training; however, the values increased again to the baseline levels upon detraining (CT: 84.3±39.1 IU/dL vs. DT: 122.2±27.5 IU/dL and MT: 135.9±50.4 IU/dL, p=0.002). Interleukin 1 beta levels decreased after 6 months of aerobic interval training (CT: 0.59±0.1 pg/mL and DT: 0.63±0.09 pg/mL vs. MT: 0.82±0.28 pg/mL, p=0.031), and the improvement was maintained with continuous aerobic interval training and even after detraining (CT: 0.58±0.08 pg/mL and DT: 0.62±0.09 pg/mL vs. MT: 0.86±0.28 pg/mL, p=0.015). Conclusion One-year aerobic interval training improves endothelial dysfunction in patients with atrial fibrillation and is primarily associated with the reduction in circulating thrombogenic and pro-inflammatory factors. A definitive way to sustain these improvements is the long-term continuation of aerobic training.

Treadmill exercise decreases intrastriatal hemorrhage-induced neuronal cell death via suppression on caspase-3 expression in rats.

Intracerebral hemorrhage is one of the most devastating types of stroke. This disease is known to cause severe neurological damage and also has a very high mortality rate. In this study, the effect of treadmill exercise on intrastriatal hemorrhage-induced neuronal cell death was investigated. Intrastriatal hemorrhage was caused by injection of collagenase into the striatum using a stereotaxic instrument. Animals of the exercise group were made to run on a treadmill for 30 min once a day during 10 consecutive days. In the present results, treadmill exercise was shown to suppress the increase in the size of hemorrhage-induced lesions and the increase in caspase-3 expression in the striatum. Based on these results, it is possible that treadmill exercise aids in the recovery from central nervous system sequelae following intracerebral hemorrhage.