The findings suggest that a reduction in insulin sensitivity induces a poor response of sympathetic nervous activity in the postprandial phase and a reduction in postprandial energy expenditure.
These findings suggested that physical activities increase heart rate during sleep, but reduce parasympathetic nervous activity at night. Because both the HF component and RR50 reduce with growth, the exercise-related inhibition of parasympathetic nervous activity may be a developmental stimulus to reach a balanced autonomic nervous pattern in adults.
Diet-induced thermogenesis (DIT) is mainly an insulin-mediated response and the result of fat and glycogen synthesis. We investigated DIT at rest and after exercise to clarify the mechanism of exercise-induced changes in DIT in 6 healthy men (mean age 36 ± 16 years). Subjects exercised for 1 h at 58% of maximal O2 consumption on a bicycle ergometer and then rested for 8 h sitting in a comfortable chair (exercise experiment). On a different day, subjects rested for 8 h without preceding exercising (non-exercise experiment). At 12.30 h, the subjects were given their second meal. DIT to individual meal did not differ significantly between the exercise and non-exercise days. Increased insulin sensitivity and increased free fatty acid oxidation by exercise may facilitate the conversion of glucose to glycogen in muscle. On the other hand, insulin secretion expressed as the ratio of plasma levels of insulin to glucose after the meal was significantly decreased in the exercise experiment (p < 0.05). Study of heart rate variability showed that sympathetic tone, a primary hormonal determinant of glucose metabolism during exercise, was increased and parasympathetic tone was decreased during the recovery period in the exercise experiment (p < 0.05). These findings suggest that changes in DIT are affected by many factors and may be related to the balance between these counteracting factors.
Summary: Magnetocardiograms (MCGs) were recorded by means of a second-derivative SQUID (superconducting quantum interference device) magnetometer in 20 normal subjects and 28 patients with left ventricular overload to analyze the activation sequence of the heart and amplitude of estimated current source. In the normal subjects, the dipole was directed to the left and gradually superiorly 40 ms after the beginning of the QRS wave mainly due to the activation of the left ventricle. In the patients with hypertension, the direction and location of the dipoles were similar to those of the normal subjects, but their dipole moments were increased. In the patients with mitral regurgitation, the dipoles of late QRS were directed more inferiorly than in the normal subjects and their amplitude was increased. In the patients with aortic valve disease, the amplitude of the dipoles was increased markedly and their location was deviated more to the left than the dipoles of the normal subjects. We established the criterion for diagnosis of LVO from the dipole moment of 50 ms of 3.13X 10-3A or more. The sensitivity of this criterion is significantly higher in the diagnosis of left ventricular overload than the electrocardiogram (ECG). The present study shows that the moving dipole method is useful to determine the increased electromotive force in patients with left ventricular overload and that sensitivity in diagnosis of left ventricular overload is increased.
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