Effects of intense and prolonged exercise on insulin sensitivity and glycogen metabolism in hypertensive subjects.

BACKGROUND: The information that insulin sensitivity and glycogen synthesis are reduced in hypertension arises primarily from studies using insulin infusions. Whether glycogen metabolism is actually altered in a physiological condition, such as during and after prolonged exercise, is currently unknown. METHODS AND RESULTS: To examine this issue, 9 hypertensive and 11 normotensive subjects were evaluated on a rest day and after intense and prolonged exercise on a separate day. Insulin sensitivity and hemodynamic variables were measured on both days. On the exercise day, whole-body substrate utilization was assessed and muscle biopsies were taken in the leg at baseline, immediately after exercise, and 2.5 and 4 hours after exercise. Insulin sensitivity at rest was lower in hypertensive than normotensive subjects (P<0.05) and increased after exercise in normotensive (P<0.01) but not in hypertensive (P=NS) subjects. Leg blood flow increased after exercise in both groups but to a lesser extent in hypertensive than normotensive subjects. Baseline glycogen content and maximal glycogen synthase activity were higher in hypertensive than normotensive subjects (P<0.001). Glycogen concentration decreased relatively less (-35 versus -66%) and returned to baseline levels faster in hypertensive subjects after exercise. Hypertensive subjects used approximately 40% less carbohydrates during exercise (P<0.001) at the expense of greater free fatty acid oxidation. CONCLUSIONS: It is concluded that increased intramuscular glycogen storage and resynthesis in hypertension are independent of blood flow and may represent compensatory mechanisms for the reduced insulin sensitivity and carbohydrate metabolism in this condition.

Baroreflex resetting after successful surgical repair of tetralogy of Fallot.

BACKGROUND: Tetralogy of Fallot (TOF) and its surgical repair are associated with alterations in right ventricular systolic and diastolic functions. The cardiopulmonary baroreflex describes the peripheral vasoconstriction response to the volume-unloading deactivation of left and possibly right ventricular receptors. Alterations in cardiac geometry or distensibility and pulmonary vasculature of operated TOF may affect the mechanical stimulation of sensitive cardiopulmonary receptors leading to an impaired baroreflex function. There has to date been no report on the integrity of baroreflex function in postoperative TOF. OBJECTIVE: To characterize the combined cardiopulmonary and baroreflex response of patients successfully operated for TOF in early childhood to central volume unloading using graded lower body negative pressure (LBNP) application. METHODS: Fifteen patients operated on for TOF (mean+/-SEM) 15.7+/-1.4 years previously and 13 healthy age-matched control subjects were submitted to four consecutive 5 min LBNP applications at -10, -20, -30 and -40 mmHg. Forearm blood flow and vascular resistance, left ventricle end-diastolic diameter (LVEDD), arterial blood pressure and heart rate were obtained. RESULTS: TOF exhibited a lower LVEDD (42.7+/-1.5 mm) than control subjects (51.9+/-1.6). The forearm vascular resistance to LVEDD relationship was shifted left and upward in TOF compared with that of control subjects, but the slope of the relationship was not different between groups. LBNP -40 mmHg induced a lesser change in heart rate in TOF (+10.6+/-1.5%) than in control subjects (+14.7 +/-2.4%) and an increase (P<0.05) in diastolic blood pressure in TOF (-2.4+/-2.5%), which was not seen in control subjects (+4.3+/-2.9%). CONCLUSIONS: Young adults successfully operated on for TOF in early childhood exhibit a resetting of the cardiopulmonary baroreflex to operate at smaller LVEDD and at a higher level of forearm vascular resistance. The blunted heart rate response to LBNP -40 mmHg is consistent with previous observations pointing to disturbances in the efferent arm of the baroreflex.

Effects of mild exercise on insulin sensitivity in hypertensive subjects.

Physical exercise increases insulin sensitivity in conditions associated with insulin resistance, such as obesity and diabetes, but little is known in this regard in hypertension. Whether postexercise changes in hemodynamics and/or changes in insulin-induced vasodilatation could contribute to a postexercise increase in insulin sensitivity in hypertensive subjects is unknown. We investigated the effects of acute physical exercise on insulin sensitivity in 10 hypertensive and 10 normotensive subjects during a control evaluation (CTRL), during lower body negative pressure (LBNP), after 30 minutes of mild bicycle exercise (POSTEX), and during LBNP after exercise (POSTEX+LBNP). Insulin-induced vasodilatation was assessed from peak forearm blood flow during the intravenous glucose tolerance test. Cardiac output (4.9+/-0.3 versus 5.3+/-0.4 L/min, mean+/-SEM) and insulin sensitivity (the glucose disappearance rate over insulin area under the curve: 0.91+/-0.07 versus 1.38+/-0.25 min(-1)/[pmol. L(-1)]. minute) were lower (both P<0.05) in hypertensive than in normotensive subjects, respectively. Cardiac output decreased during LBNP, increased during POSTEX, and was similar to control during POSTEX+LBNP in both groups. Insulin sensitivity was unchanged during LBNP, increased during POSTEX, and remained elevated during POSTEX+LBNP in hypertensive subjects, whereas it remained unchanged in normotensives. Peak forearm blood flow was significantly lower in hypertensive than in normotensive subjects, despite higher insulin levels in hypertensives, and was not modified by LBNP or exercise. In conclusion, insulin sensitivity increases after exercise in hypertensive subjects, and the increase in cardiac output does not contribute to this effect. Endogenous insulin-induced vasodilatation is reduced in hypertensive subjects, and this insulin action is not affected by physical exercise.