Haruka Murakami

Effects of exercise training of 8 weeks and detraining on plasma levels of endothelium-derived factors, endothelin-1 and nitric oxide, in healthy young humans.

Vascular endothelial cells produce nitric oxide (NO), which is a potent vasodilator substance and has been proposed as having antiatherosclerotic property. Vascular endothelial cells also produce endothelin-1 (ET-1), which is a potent vasoconstrictor peptide and has potent proliferating activity on vascular smooth muscle cells. Therefore, ET-1 has been implicated in the progression of atheromatous vascular disease. Because exercise training has been reported to produce an alteration in the function of vascular endothelial cells in animals, we hypothesized that exercise training influences the production of NO and ET-1 in humans. The purpose of the present study was to examine whether chronic exercise could influence the plasma levels of NO (measured as the stable end product of NO, i.e., nitrite/nitrate [NOx]) and ET-1 in humans. Eight healthy young subjects (20.3 +/- 0.5 yr old) participated in the study and exercised by cycling on a leg ergometer (70% VO2max for 1 hour, 3-4 days/week) for 8 weeks. Venous plasma concentrations of NOx and ET-1 were measured before and after (immediately before the end of 8-week exercise training) the exercise training, and also after the 4th and 8th week after the cessation of training. The VO2max significantly increased after exercise training. After the exercise training, the plasma concentration of NOx significantly increased (30.69 +/- 3.20 vs. 48.64 +/- 8.16 micromol/L, p < 0.05), and the plasma concentration of ET-1 significantly decreased (1.65 +/- 0.14 vs. 1.23 +/- 0.12 pg/mL, p < 0.05). The increase in NOx level and the decrease in ET-1 level lasted to the 4th week after the cessation of exercise training and these levels (levels of NOx and ET-1) returned to the basal levels (the levels before the exercise training) in the 8th week after the cessation of exercise training. There was a significant negative correlation between plasma NOx concentration and plasma ET-1 concentration. The present study suggests that chronic exercise causes an increase in production of NO and a decrease in production of ET-1 in humans, which may produce beneficial effects (i.e., vasodilative and antiatherosclerotic) on the cardiovascular system.

Change in post-exercise vagal reactivation with exercise training and detraining in young men.

Abstract. We studied the effects of aerobic exercise training and detraining in humans on post-exercise vagal reactivation. Ten healthy untrained men trained for 8xa0weeks using a cycle ergometer [70% of initial maximal oxygen uptake (

Age-related reduction of systemic arterial compliance relates to decreased aerobic capacity during sub-maximal exercise.

dot V{rm O}_{2max }

Cross-sectional association of the number of neighborhood facilities assessed using postal code with objectively measured physical activity: the Saku cohort study.

n) for 1xa0h, 3–4xa0days·week–1] and then did not exercise for the next 4xa0weeks. Post-exercise vagal reactivation was evaluated as the time constant of the beat-by-beat decrease in heart rate during the 30xa0s (t30) immediately following 4xa0min exercise at 80% of ventilatory threshold (VT). The

Cytoplasmic transfer of platelet mtDNA from elderly patients with Parkinson's disease to mtDNA-less HeLa cells restores complete mitochondrial respiratory function

dot V{rm O}_{2max }

Relationship between Mitochondrial DNA Polymorphism and the Individual Differences in Aerobic Performance

n and the oxygen uptake at VT had significantly increased after the 8xa0weeks training programme (P<0.0001, P<0.001, respectively). The t30 had shortened after training, and values after 4xa0weeks and 8xa0weeks of training were significantly shorter than the initial t30 (P<0.05, P<0.01, respectively). The change in the t30 after 8xa0weeks of training closely and inversely correlated with the initial t30 (r=–0.965, P<0.0001). The reduced t30 was prolonged significantly after 2xa0weeks of detraining, and had returned almost to the baseline level after a further 2xa0weeks of detraining. These results suggest that aerobic exercise training of moderate intensity accelerates post-exercise vagal reactivation, but that the accelerated function regresses within a few weeks of detraining.