Is a decrease in arterial pressure during long-term aerobic exercise caused by a fall in cardiac pump function?

Ten healthy normotensive volunteers demonstrated a progressive decrease (p < 0.01) in systolic and diastolic pressures during 1 hour of aerobic exercise. Cardiac function and structure were assessed by M-mode echocardiography before exercise and, at the same heart rate, after 5 minutes of exercise and after 60 minutes of exercise. After 5 minutes of exercise, heart rate, cardiac output, ejection fraction, fractional fiber shortening, and contractility index significantly increased (p < 0.01, p < 0.05, respectively) and total peripheral resistance decreased (p < 0.01) compared with resting values. When compared with the values at minute 5, there was a decrease (p < 0.01) in cardiac output, ejection fraction, fractional fiber shortening, and contractility index (p < 0.05) and an increase (p < 0.05) in total peripheral resistance after 60 minutes of exercise. We conclude that the gradual decrease in arterial pressure seen with prolonged aerobic exercise is the result of a fall in cardiac pump function (as measured by cardiac output, ejection fraction, fractional fiber shortening, and contractility index), possibly indicating cardiac fatigue.)

Depressed systolic and diastolic cardiac function after prolonged aerobic exercise in healthy subjects.

We studied 11 healthy untrained volunteers (aged 28.9 +/- 4.6 years) during 60 minutes of aerobic ergometric exercise with constant heart rates of 130 to 140 beats/minute. We found a continuous and significant decrease in systolic and diastolic pressure from 175 +/- 18/77 +/- 7 mmHg in the 5th minute to 144 +/- 14/68 +/- 6 mmHg in the 60th minute of exercise. Cardiac function and structure were assessed by M-mode echocardiography before exercise, after 5 minutes and after 60 minutes of exercise at comparable heart rates. The results demonstrated significant decreases in cardiac output, ejection fraction, and diastolic posterior wall velocity and an increase in total peripheral resistance after 60 minutes of exercise. We conclude that the decrease in blood pressure during long-term aerobic exercise in healthy untrained subjects might be at least influenced by a decrease in left ventricular filling and contractility, possibly indicating cardiac fatigue.

Hemodynamic comparison of two nifedipine formulations in patients with essential hypertension.

The hemodynamic and humoral effects and trough-to-peak 24-hour blood pressure responses of 2 nifedipine formulations, capsules and continuous-release once-daily formulation tablets, were evaluated in 10 patients with mild to moderate essential hypertension. Both formulations reduced mean arterial pressure similarly from 120 +/- 3 (baseline) to 107 +/- 2 (p less than 0.005) and 105 +/- 2 mm Hg (p less than 0.005) and total peripheral resistance index from 65 +/- 9 (baseline) to 47 +/- 4 (p less than 0.05) and 45 +/- 3 U/m2 (p less than 0.05), respectively. Renal, splanchnic and total forearm (including skin and skeletal muscle) blood flows were maintained or even increased slightly associated with reductions in regional vascular resistances. Decreases in renal, total forearm and skeletal muscle resistances were significant (p less than 0.05) with the capsules, but the decrease was only significant in renal resistance with the long-acting tablets. Intravascular volume did not expand with reduction in arterial pressure. This antihypertensive effect was not related to baseline plasma renin activity levels or age. Nifedipine tablets provided a better control of mean arterial pressure (66%) than did capsules (44%).

Hemodynamic effects of celiprolol in essential hypertension.

The immediate and short-term (2 week) hemodynamic and humoral effects of the beta-1 antagonist, beta-2 agonist, celiprolol, were compared with those of more prolonged atenolol therapy in 12 patients with essential hypertension. Celiprolol produced an immediate dose-dependent decrease in mean arterial pressure (113 +/- 3 to 102 +/- 2 mm Hg; p less than 0.001) and total peripheral resistance (49 +/- 3 to 38 +/- 1 U/m2; p less than 0.005) that was associated with an increased heart rate (67 +/- 1 to 73 +/- 2 beats/min; p less than 0.01) and cardiac index (2,347 +/- 129 to 2,708 +/- 111 ml/min/m2; p less than 0.01). Both celiprolol and atenolol reduced mean arterial pressure with short-term treatment (p less than 0.01); this was associated with a reduced total peripheral resistance with celiprolol (from 24 +/- 1 to 21 +/- 1 U/m2; p less than 0.02) and was not observed with atenolol. Moreover, in contrast with atenolol, celiprolol did not change heart rate or stroke and cardiac indexes. Splanchnic and forearm vascular resistances decreased with celiprolol (p less than 0.05) but not with atenolol; neither beta-blocking drug altered renal blood flow. These results demonstrate that the hemodynamic effects of celiprolol were strikingly different from atenolol; celiprolol reduced arterial pressure and total peripheral and certain vascular resistances without altering heart rate, cardiac index or regional blood flows. These effects may be explained by celiprolol's cardiac beta-1 receptor inhibitory and peripheral beta-2 receptor agonistic effects.

Antihypertensive therapy in the elderly.

Recent studies have documented that arterial hypertension increases cardiovascular morbidity and mortality even in the geriatric population. Some elderly hypertensive patients, like younger patients, can benefit from antihypertensive therapy. Antihypertensive therapy should be carefully adjusted to suit the cardiovascular pathophysiology of elderly patients.

Effects of antihypertensive therapy on hypertensive heart disease.

Left ventricular hypertrophy (LVH) is a common sequela of long-standing essential hypertension. LVH cannot be considered, however, an adaptive process only serving to normalize wall stress but can be considered one that significantly increases the risk of sudden death, myocardial ischemia, congestive heart failure, and other cardiovascular diseases. Patients with LVH exhibit impaired ventricular filling, ventricular arrhythmias, and myocardial ischemia even in the absence of coronary artery disease. LVH can be prevented or reversed by a variety of antihypertensive agents including calcium channel blockers and angiotensin converting enzyme inhibitors. Calcium channel blockers, more than angiotensin converting enzyme (ACE) inhibitors, suppress ectopic impulse generation, improve ventricular compliance, and alleviate myocardial ischemia while preserving or improving the contractile state. In contrast, ACE inhibitors can be particularly useful in patients with LVH and diminished ventricular contractility and in preventing chamber dilatation after myocardial infarct. These favorable cardiovascular effects of both calcium channel blockers and ACE inhibitors are a reason for optimism that carefully tailored therapy will ultimately diminish the well-documented risk of cardiovascular morbidity and mortality associated with LVH.