(Hypertension. 1999;34:720-723.)
© 1999 American Heart Association, Inc.
Scientific Contributions |
From the Hypertension Unit and Cardiovascular Rehabilitation and Exercise Physiology Unit, Heart Institute (InCor), University of São Paulo Medical School, São Paulo, Brazil.
Correspondence to Eduardo M. Krieger, MD, PhD, Unidade de Hipertensão, Instituto do Coração (InCor), HC-FMUSP, Av Dr Enéas de Carvalho Aguiar, 44, São Paulo, SP 05403-000, Brazil. E-mail edkrieger{at}incor4.incor.usp.br
| Abstract |
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Key Words: exercise rats, inbred SHR cardiac output nervous system, sympathetic bradycardia
| Introduction |
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| Training Intensity |
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O2max) or at 85% of
O2max, which we called low-and
high-intensity exercise training regimens, respectively.8
We found that low-intensity exercise training significantly reduced
systolic, diastolic, and mean blood pressure in
SHR. In contrast, high-intensity exercise training caused no change in
blood pressure in SHR. In previous studies, other investigators
demonstrated either that exercise training performed at 55% of
O2max reduced high blood
pressure in men9 or that exercise training performed at
55% of
O2max had a better
effect on blood pressure than did exercise in excess of 75% of
O2 in SHR.10
These results reinforce the idea that low-intensity exercise training
rather than high-intensity exercise training is more effective in
reducing blood pressure in hypertension. | Hemodynamic Alterations |
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-noradrenegic responsiveness. Besides that, in hypertensive
rats12 and humans,13 exercise training
reduced norepinephrine levels, and more recently, other
investigators14 reported that exercise training decreased
muscle sympathetic nerve activity in humans. These
studies12 13 and others15 suggest that the
reduction in total peripheral resistance after exercise
training could be responsible for the decrease in blood pressure in
hypertensive conditions. On the other hand, the rationale for the
concept that exercise training decreases cardiac output came from the
repeated demonstration of the presence of resting bradycardia after
exercise training in rats16 and humans,17
which represents the most valuable marker for exercise training
adaptation. Furthermore, exercise training might reduce stroke volume,
since it is proposed that exercise training may decrease total blood
volume in hypertensive humans.18 To test whether exercise training reduces high blood pressure by provoking a decrease either in total peripheral resistance or in cardiac output, we studied the effects of a 18-week period of low-intensity exercise training on the hemodynamic responses in SHR.8 Cardiac output was evaluated by means of a flow probe implanted around the aortic arch and blood pressure by means of a cannula inserted into the carotid artery. Both parameters were recorded on a beat-to-beat basis at a frequency of 100 Hz for 30 minutes in quiet, conscious, unrestrained rats. Confirming our previous results, low-intensity exercise training significantly reduced high blood pressure in SHR. However, low-intensity exercise training had no effect on total peripheral resistance. In fact, the mechanism by which low-intensity exercise training decreased blood pressure was a reduction in cardiac output due to a lower resting heart rate (Figure 1).
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| Sympathetic Attenuation |
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| Baroreflex Activity During Exercise |
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| Influence of Training on BRS |
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O2max for 12 weeks)
provoked a remarkable recovery of BRS for both bradycardiac and
tachycardiac responses in SHR, which were 65% and 47%
depressed, respectively, when compared with normotensive control
rats.24 In fact, low-intensity exercise training reduced
these depressions to 18% and 17%, respectively, for bradycardiac and
tachycardiac baroreflex responses (Figure 3).
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An increase in vascular compliance was observed in humans25 after exercise training. Increased shear stress during exercise may also enhance the release of endothelial factors.26 All of these mechanisms may increase the sensitivity of the arterial baroreceptor afferents, thus increasing the BRS. In fact, we have observed an increase in baroreceptor gain sensitivity of the baroreceptor function curves in exercise training of normotensive rats.27 However, we cannot exclude the possibility that exercise is associated with other alterations in the central and efferent components of the baroreflex pathway.
| Future Studies |
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| Concluding Remarks |
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Received June 22, 1999; first decision July 9, 1999; accepted July 27, 1999.
| References |
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Duncan JJ, Farr JE, Upton SJ, Hagan RD, Oglesby ME,
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