SUMMARY1. Blood pressure, cardiac function and forearm blood flow following voluntary maximal upright bicycle exercise were studied in thirteen normal volunteers in a cross-over design against a control day.2. After exercise there was a short-lived (5-10 min) increase in systolic blood pressure, peak aortic blood velocity and aortic acceleration suggesting a persistence of the positive inotropic influence of exercise.3. Systemic vasodilation, which was seen immediately exercise stopped, lasted at least 60 min. This was associated with a reduction in diastolic blood pressure for the whole hour. After 30 min systolic blood pressure was also reduced. Heart rate and cardiac output were still significantly elevated and systemic vascular resistance still reduced at 60 min post-exercise.4. A non-exercising limb vascular bed (forearm) showed a marked vasodilation for 1 h after predominately leg exercise indicating the presence of a vasodilatory influence affecting vascular beds other than the exercising muscle groups.
BackgroundAtrial fibrillation is associated with higher mortality. Identification of causes of death and contemporary risk factors for all‐cause mortality may guide interventions.Methods and ResultsIn the Rivaroxaban Once Daily Oral Direct Factor Xa Inhibition Compared with Vitamin K Antagonism for Prevention of Stroke and Embolism Trial in Atrial Fibrillation (ROCKET AF) study, patients with nonvalvular atrial fibrillation were randomized to rivaroxaban or dose‐adjusted warfarin. Cox proportional hazards regression with backward elimination identified factors at randomization that were independently associated with all‐cause mortality in the 14 171 participants in the intention‐to‐treat population. The median age was 73 years, and the mean CHADS 2 score was 3.5. Over 1.9 years of median follow‐up, 1214 (8.6%) patients died. Kaplan–Meier mortality rates were 4.2% at 1 year and 8.9% at 2 years. The majority of classified deaths (1081) were cardiovascular (72%), whereas only 6% were nonhemorrhagic stroke or systemic embolism. No significant difference in all‐cause mortality was observed between the rivaroxaban and warfarin arms (P=0.15). Heart failure (hazard ratio 1.51, 95% CI 1.33–1.70, P<0.0001) and age ≥75 years (hazard ratio 1.69, 95% CI 1.51–1.90, P<0.0001) were associated with higher all‐cause mortality. Multiple additional characteristics were independently associated with higher mortality, with decreasing creatinine clearance, chronic obstructive pulmonary disease, male sex, peripheral vascular disease, and diabetes being among the most strongly associated (model C‐index 0.677).ConclusionsIn a large population of patients anticoagulated for nonvalvular atrial fibrillation, ≈7 in 10 deaths were cardiovascular, whereas <1 in 10 deaths were caused by nonhemorrhagic stroke or systemic embolism. Optimal prevention and treatment of heart failure, renal impairment, chronic obstructive pulmonary disease, and diabetes may improve survival.Clinical Trial Registration URL: https://www.clinicaltrials.gov/. Unique identifier: NCT00403767.
Blood pressure falls after a single session of exercise. The duration for which this fall in blood pressure persists is not known. Sustained hypotension after a single session of exercise may have important implications in the treatment of patients with mild hypertension. We studied 24 subjects (12 normotensive subjects and 12 patients with mild or borderline hypertension). Blood pressure was measured in the laboratory for 30 minutes before and for an hour after graded bicycle exercise to maximal voluntary capacity. Subjects then left the hospital and measured their blood pressures at home (three measurements every 2 hours) following a strict measurement protocol for the rest of the day (usually between 8 and 12 hours). These home blood pressure measurements were compared with home blood pressure measurements recorded at the same times on a nonexercise control day. At 30 minutes after the graded maximal exercise test, the hypertensive patients experienced a fall in blood pressure from 142±3.5/93±6.5 mm Hg (mean±SEM) to 124±4.5/79±2.8 mm Hg (/><0.01). For the normotensive subjects, blood pressure after exercise fell from 117±3.1/70±2.1 mm Hg to 109±3.1/ 62±2.8 mm Hg (/»<0.01). Despite these striking blood pressure reductions for the second half hour after exercise, blood pressure measurements recorded at home were not significantly different on the exercise and control days in either group. We conclude that although a single bout of exercise lowers blood pressure for a short (1-hour) period, this hypotension is not sustained. {Hypertension 1991;18:211-215) I n 1922, Schneider and Truesdell reported that standing blood pressures were lower 2 minutes after a step exercise protocol. 1 A subsequent anecdotal report by Fitzgerald 2 suggested that blood pressure in labile hypertension was reduced for 4-10 hours after 25 minutes of jogging. It has been proposed therefore that a single session of exercise once or twice a day may assist in controlling blood pressure purely on the basis of the hypotensive effect after exercise.2 -3 Sustained postexercise hypotension may also significantly affect interventional studies of blood pressure, especially studies involving the effects of exercise training. Indeed, the more recent studies on the effects of physical training on blood pressure have allowed 24-48 hours between the last session of exercise and blood pressure measurement.4 -7 However, despite extensive studies on the acute fall of blood pressure after exercise, the dura- tion of this blood pressure reduction and its possible role in the management of hypertension has not been systematically studied. We therefore examined whether hypotension after exercise persisted for the rest of the exercise day in normotensive and hypertensive subjects. Methods SubjectsWe studied 12 normotensive subjects (26.2±3.2 years of age; eight men and four women) and 12 mild and borderline hypertensive patients (32.4±3.8 years of age; nine men and three women). All patients and subjects had sedentary occupations and participated in occasional ...
1. It is known that acute exercise is often followed by a reduction in , compared with the control day. Systolic and mean pressure also fell (non-significantly) after 45 min; heart rate was significantly elevated for the whole hour of recovery (at 60 min, +7'23 beats min'). No changes in post-exercise blood pressure and heart rate were observed on the days of moderate and minimal exercises. 4. An increase in cardiac index was observed after maximal exercise compared with control (at 60 min, 2'6 + 0'3 vs. 1'9 + 0'2 1 min' m-2). This was entirely accounted for by the persistent increase in heart rate, with no significant alteration in stroke volume after exercise on any day. 5. Systemic vasodilatation was present immediately after maximal exercise compared with control (after a 5 min rest, total peripheral resistance was 17'9 + 3S5 vs.27'8 + 3-4 mmHg (1 min')-' on the control day) and lasted at least 60 min (at 60 min, 23'3 + 3'5 vs. 31'0 + 3'8 mmHg (1 min`)`o n the control day). No significant changes in total peripheral vascular resistance were observed after moderate or minimal exercise days. 6. After this predominantly leg exercise, minimal and moderate loads significantly increased forearm vascular resistance with respect to baseline pre-exercise resistance (at 60 min, +26'7 % and +20'5%, respectively), but there were no significant differences with respect to the control day; maximal leg exercise significantly decreased the forearm vascular resistance for 1 h (at 60 min, -17'2 % vs. baseline pre-exercise value and -46'0 % compared to the control day). This suggests that prolonged forearm vasodilatation occurred only after higher exercise loads.Hypotension has been shown to follow short periods of exercise
The haemodynamic changes during 4 h following maximal upright bicycle exercise were evaluated in six normals in a randomized controlled crossover design. Total peripheral resistance was reduced to 2 h (-6.7 mmHg min l-1, P < 0.05); exercising and non-exercising vascular beds were vasodilated for 2 h (-24.1 and -23.8 mmHg min ml-1 100 ml-1 tissue, respectively, P < 0.05), associated with reductions in systolic (-5.8 mmHg, P < 0.05) and diastolic pressure (-8.3 mmHg, P < 0.05). Rise in cardiac index for 1 h (+0.51 min-1 m-2, P < 0.05) was accounted for by an elevated heart rate (+14.4 beats min-1, P < 0.01) as stroke volume was unchanged. Body temperature was elevated until 40 min (+0.20 degrees C, P < 0.05). The return of all haemodynamic variables to control by 3 h suggests a 3 h limit for a hypotensive effect of exercise. Rise in body temperature is not the only factor responsible for the hypotension.
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