J. Cléroux

Aftereffects of exercise on regional and systemic hemodynamics in hypertension.

Several studies have indicated that a single bout of physical exercise induced a significant antihypertensive effect during the hours after the activity. However, little information is presently available on the underlying hemodynamic changes. We examined 13 essential hypertensive patients and nine normotensive subjects in a randomized, crossover study design during 3 hours after a 30-minute period of upright leg cycling at 50% of peak aerobic capacity and during 3 hours after a 30-minute control period of rest. Blood pressure, heart rate, cardiac output, total peripheral resistance, and regional vascular resistance in the forearm as well as venous plasma catecholamine concentrations were measured repeatedly. After exercise, systolic (-11 +/- 2 mm Hg) and diastolic (-4 +/- 1 mm Hg) blood pressures, total peripheral resistance (-27 +/- 5%), forearm vascular resistance (-25 +/- 6%), and plasma norepinephrine levels (-21 +/- 7%) were significantly (p less than or equal to 0.05) decreased, and cardiac output was increased (+31 +1- 8%) compared with control in hypertensive subjects. In contrast, in normotensive subjects blood pressure, forearm vascular resistance, and plasma norepinephrine were unchanged, and systemic hemodynamics changed to a lesser extent than in hypertensive subjects after exercise. It is concluded that a decrease in regional vascular resistance in skeletal muscles and possibly in the skin in hypertensive patients may contribute importantly to the antihypertensive effect of prior exercise. A decreased sympathetic nervous activity, as seen from lower plasma norepinephrine levels, may be involved in this effect.

Effects of different training intensities on 24-hour blood pressure in hypertensive subjects.

BackgroundIt is generally accepted that physical training decreases blood pressure in hypertensive subjects, but the importance of training intensity has not been established. This study compared the effects of endurance training at different intensities on ambulatory blood pressure and on blood pressure load (percentage of readings above 140/90 and 120/80 mm Hg during the waking and sleeping periods, respectively). Methods and ResultsPreviously sedentary subjects with mild to moderate hypertension were evaluated in a crossover fashion according to a Latin square after a sedentary control period and after training at low and at moderate intensity corresponding to 50%o and 70%o of maximal oxygen uptake, respectively. Each period lasted 10 weeks. After training at moderate intensity, a higher maximal oxygen uptake was found compared with sedentary values but not after training at low intensity. Both training intensities exerted a similar antihypertensive effect of about 5 mm Hg for systolic and diastolic 24-hour blood pressures. However, training at low intensity reduced blood pressure exclusively during the waking hours, whereas training at a moderate intensity reduced blood pressure only during the evening and sleeping hours. Waking blood pressure load decreased from 66% to 49%v after training at low intensity, whereas sleeping blood pressure load decreased from 61% to 34% after training at moderate intensity (both P<.05). ConclusionLow- and moderate-intensity training produce similar 24-hour blood pressure reductions, but each training intensity may interfere with different pathogenic effects associated with different blood pressure profiles.

Antihypertensive effects of amlodipine and hydrochlorothiazide in elderly patients with ambulatory hypertension

Recent studies and authorities have advocated the use of low-dose thiazide diuretics as first-line treatment agents in elderly hypertensives. However, these recommendations were based solely on blood pressure (BP) measured in the clinic. The objective of the present 32-week double-blind study was to compare the effects of hydrochlorothiazide (HCTZ) and amlodipine (AML) in elderly patients with confirmed ambulatory hypertension. After a 4-week placebo washout period, 42 (25 men, 17 women) patients (mean age, 69 years) with clinic sitting diastolic BP of 95 to 114 mm Hg and daytime ambulatory diastolic BP of > or = 90 mm Hg were randomized double-blind to receive AML 5 to 10 mg (n = 21) or HCTZ 12.5 to 25 mg (n = 21) once daily. After 8 weeks of monotherapy, patients in whom clinic diastolic BP remained > or = 90 mm Hg were given combination therapy with the other agent. Amlodipine monotherapy induced significant reductions in clinic, mean 24-h, daytime and sleep systolic/diastolic BPs whereas only clinic BP decreased significantly in patients treated with HCTZ monotherapy. Moreover, 19/21 versus 8/21 patients on AML and HCTZ monotherapies achieved adequate BP control. At the end of the 32-week treatment period, combination therapy in the HCTZ group resulted in statistically significant reductions in clinic as well as in 24-h, daytime and sleep ambulatory BPs that were similar to those observed in the AML monotherapy group. In conclusion, the administration of AML monotherapy induced significant reductions in both clinic and ambulatory BPs in elderly patients whereas only clinic BP was significantly decreased by HCTZ monotherapy. Moreover, the addition of AML to HCTZ in patients inadequately controlled by monotherapy has permitted statistically significant decrements in clinic as well as in ambulatory BP. Consequently, the results of the present study suggest that the use of HCTZ in doses of up to 25 mg daily is inadequate for ambulatory BP control in the elderly despite official recommendations.

Effects of Different Training Intensities on the Cardiopulmonary Baroreflex Control of Forearm Vascular Resistance in Hypertensive Subjects

We recently reported that ambulatory blood pressure decreased during the awake period after training at low intensity but not after training at moderate intensity in subjects with mild to moderate hypertension. The reasons for the failure of moderate-intensity training to reduce blood pressure are not clear. In the present article, we report the effects of different training intensities on cardiopulmonary baroreflex control of forearm vascular resistance, left ventricular function, vascular reactivity, and resistive vessel structure. After moderate-intensity training, the cardiopulmonary baroreflex control of forearm vascular resistance was significantly attenuated, left ventricular performance was enhanced, and vascular reactivity and resistive vessel wall thickness in the calf were reduced compared with values after the control sedentary period. No significant changes in these indexes were found after low-intensity training compared with sedentary values. These results indicate that attenuation of the cardiopulmonary baroreflex control of skeletal muscle vascular resistance after training at moderate intensity may contribute to the lack of antihypertensive effects, as seen from unchanged ambulatory blood pressure levels during the awake period, after training at this intensity. A decreased vascular smooth muscle response to sympathetic nervous stimulation appears to be partly involved in the alteration in the baroreflex control of forearm vascular resistance after moderate-intensity training. Although these findings should be confirmed in a greater number of subjects, the present results point to a key mechanism that might explain why moderate endurance exercise training fails to lower arterial blood pressure in hypertensive subjects.

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.

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 ≈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.

Free and Conjugated Catecholamines in Plasma and Red Blood Cells of Normotensive and Hypertensive Patients

Plasma free and conjugated norepinephrine levels were found to be significantly increased in patients with labile and sustained hypertension whereas epinephrine levels were normal in these patients. While free NE and E levels increased significantly during postural change, conjugated NE and E levels were not altered by this stimulus suggesting that conjugated NE levels could be an index of chronic rather than acute changes in the sympathetic tone. In hypertensive patients, plasma free dopamine levels increased during postural change and conjugated DA levels tended to be higher suggesting a dysfunction in the dopamine metabolism. Red blood cells were also found to contain free and conjugated CA. While conjugated CA levels in red blood cells (RBC) were equal or lower than in the plasma, free CA were found in larger concentrations than in the plasma. In hypertensive patients conjugated CA levels in RBC were similar to those found in normotensive subjects but free NE and E levels were significantly higher in hypertensive patients. These studies demonstrate various abnormalities in the metabolism of CA in hypertensive patients. Each of these could contribute to the maintenance of hypertension by an alteration of the biological expression of the sympathetic tone at the cellular level of these patients.