REVISTACIENTIFICAMULTIDISCIPLINARNUCLEODOCONHECIMENTO

Multidisciplinary Scientific Journal

Pesquisar nos:
Filter by Categorias
Accounting
Administration
Aeronautical Sciences
Agricultural Engineering
Agronomy
Architecture
Art
Biology
Chemical engineering
Chemistry
Civil Engineering
Communication
Computer Engineering
Computer science
Cuisine
Dentistry
Education
Electrical engineering
Environment
Environmental Engineering
Ethics
Geography
Health
History
Law
Literature
Lyrics
Marketing
Mathematics
Mechanical Engineering
Naval Administration
Nutrition
Pedagogy
Philosophy
Physical Education
Physics
Production engineering
Production engineering
Psychology
Science of Religion
Social Sciences
Sociology
Technology
Theology
Tourism
Uncategorized
Veterinarian
Weather
Zootechny
Pesquisar por:
Selecionar todos
Autores
Palavras-Chave
Comentários
Anexos / Arquivos

The importance of physical activity in hypertensive subjects

RC: 11879
58 Readings
Rate this post
DOI: ESTE ARTIGO AINDA NÃO POSSUI DOI
SOLICITAR AGORA!

Sections

GARRIDO, Ana Luíza Moraes [1]

NUNES, Caio Victor [2]

COSTA, Débora Caixeta [3]

BARRETO, Genesson dos Santos [4]

ABREU, Karina Fieldkircher [5]

PINHO, Letícia Akemi Sewo de [6]

OLIVEIRA, Lígia Bauer [7]

SANTOS, Matheus Miranda dos [8]

PEREIRA, Pedro Augusto Fleury [9]

GARRIDO, Ana Luíza Moraes;et.al. The importance of physical activity in hypertensive subjects. Multidisciplinary Core scientific journal of knowledge. 07 Edition. 02 year, vol. 03. pp 17-35, October 2017. ISSN: 0959-2448

SUMMARY

Hypertension (SAH) is a multifactorial disease that affects a large part of the adult population and occurs on the loss of the mechanisms responsible for maintaining blood pressure. Studies have found a positive relationship between the practice of physical activities and the reduction of blood pressure in hypertensive patients. In this perspective, conducted a literature review highlighting the influence of physical exercise in the treatment of hypertension. The survey was conducted from virtual databases like PubMed, Scielo and Lilacs, with the keywords: hypertension; high blood pressure; exercise and blood pressure. All the articles found, only those who directly correlated to blood pressure and exercise were included in this work. As a result, it was found that physical activity reduces blood pressure, through awareness of the baroreceptors, release of vasodilators, mitigation of the sympathetic nervous system and the action of Renin-angiotensin-aldosterone system. It was observed that factors such as race, age, obesity and genetic characteristics influence the hypotensive effect of exercise. Finally, it is recommended to hypertensive subjects perform aerobic exercise of low and moderate intensity, complemented by resistance training.

Keywords: Hypertension, high blood pressure, exercise and hypertension, exercise and blood pressure.

INTRODUCTION

Hypertension (SAH) affects about 31 million of people and your Brasil1 prevalence is 15% to 20% of the adult population, and has also a significant prevalence in children and adolescents. Is one of the main risks of cardiovascular mortality and has a high social cost, for it is associated in approximately 40% of cases of early retirement and licence in trabalho2 .3.

SAH occurs on the loss of the mechanisms responsible for maintaining homeostasis of blood pressure, being the main, which will be affected by exercise, the baroreflex system and the Renin-angiotensin-aldosterona4 .5. The baroreflex system works through receptors located in the aorta and carotid arteries and are sensitive to change of arterial6 pressure, while the Renin-angiotensin-aldosterone is a proteolytic cascade that influence the homeostasis of sodium, water and vascular7 .8 .9 tone.

There are two types of hypertension (SAH), the primary and secondary hypertension. SAH occurs in approximately 95 primary% of hypertensive patients, due to an interaction between genetic factors and lifestyle that include salt intake, excessive alcohol consumption, weight and lack of physical activity. The relationship between the sedentary and the highest incidence of cardiovascular disease is well estabelecida10. It is evidenced that, among the brazilian urban population, 37% of men and up to 56% of women present a sedentário11 lifestyle. Already HAS kidney, adrenal abnormalities involves secondary and vasculares12.

High blood pressure is associated with a high incidence of cardiovascular system diseases, such as coronary heart disease, stroke, heart failure, arterial fibrillation, acute renal failure and periférica13 artery disease. Recent studies have found a beneficial relationship between the regular practice of physical exercise and the reduction in mortality from those diseases in individuals hipertensos14 .15.

Factors such as age and ethnicity influence the hypotensive effect of physical exercises. Asian individuals exhibit a reduction of 6.6 mm Hg in diastolic blood pressure, white and black individuals show a lesser reduction when carrying out the same activities. As for the measurement of systolic blood pressure, the Blacks are those with more significant reduction, of 11 mmHg16. In relation to the influence of age, there is evidence that the hypertensive subjects between 40 and 55 years present best answer to exercise físico17.

The practice of physical activities cause important hemodynamic changes and Autonomic influence directly the system cardiovascular18 .19. The main mechanisms responsible for lowering blood pressure after exercise are the decrease in cardiac output and peripheral vascular resistance. The importance of each of these mechanisms varies according to the individual profile hypertensive. In elderly individuals, the reduction of pressure usually happens due to decreased cardiac output, while in younger individuals, this decrease is more linked to the reduction of vascular resistance periférica20 .21 .22.

The Brazilian Society of Cardiology recommends that the hypertensive subjects to perform physical exercises on a regular basis, since undergoing clinical evaluation prévia23. It is important that training is based on results obtained in tests ergométricos, for which there are abnormal responses to exercise, watching the blood pressure (BP). Another way to determine the intensity of the exercise is to evaluate the level achieved in PA esforço24. The proposed physical activity program should increase the intensity and/or duration of exercises in progressive mode, with the purpose of obtaining the blood pressure reduction for values below 140/90mmHg25.

The varieties of training can change your hypotensive effect. A greater reduction in blood pressure as follows: procedures involving major muscle groups, such as cycling or walking/race; training volume larger, more often weekly or longer duration of sessions; and lower intensity exercises (40% to 60% of VO2 peak) 26.

Thus, there is evidence that the regular practice of physical exercises is positive on decrease in blood pressure.  Thus, the objective of the present study is to conduct a review on the influence of physical exercise in the treatment of hypertension.

MATERIALS AND METHODS

This is a literature review study about the importance of physical activity in hypertensive subjects. To this end, we searched articles indexed in Pubmed databases, Scielo and Lilacs. Were used as key words hypertension, high blood pressure, exercise and hypertension, exercise and blood pressure and its similar in English (hypertension, high blood pressure, exercise and hypertension, exercise and blood pressure). Articles found, only those that the reduction in blood pressure associated with the practice of physical exercise were selected.

DISCUSSION

Mechanisms for regulating blood pressure

Adequate tissue perfusion is maintained by the driving force of the movement: the blood pressure (BP), which depends on physical factors such as blood volume and capacitance of circulation and results from the instant combination between the cardiac output, peripheral vascular resistance and the venosa27 capacitance. The adjustment of PA is important as it must be high enough to maintain perfusion without cause structural damage to the heart and the vessels sanguíneos28. Several mechanisms have been identified that regulate blood pressure levels, these being both short as long term.

One of the main mechanisms checked is the Renin-angiotensin-Aldosterone (SRAA). This system is the main regulator of blood pressure at rest and is composed of vasoativos peptides with antihypertensive drugs, which shares hypertensive and act autocrine, paracrine and endocrine. The regulation of this system has been linked to the emergence of cardiovascular disease such as hypertension, myocarditis, coronary artery disease and insufficiency cardíaca29 .30.

In the classic view, the SRAA acts only endocrinamente, the Renin (enzyme released by renal justaglomerular device) cleaves the angiotensinogênio (globulin released by the liver) in angiotensin (a decapeptídeo) which in your time is cleaved in Angiotensin II (ANG II) by Angiotensin-converting enzyme (ACE) inhibitors. This enzyme is present in the vascular surface and your main point anatomofuncional in the pulmonary vascular bed, which receives 100% of debt cardíaco31. The Angiotensin II was considered to be the main component of the hypertensive agent SRAA and believed that she can act just as circulating hormone receptors AT1 and AT2 route. However, there is evidence that the SRAA acts locally in many organs, including acts intracelularmente32. It was found that the ANG II increases the blood volume by stimulating the pituitary gland after releasing the antidiuretic hormone (ADH), which operates in the distal tubules, increasing the reabsorption of water and causing vasoconstrição33. In addition, the ANG II stimulates the release of aldosterone in the adrenal glands and increases the appetite for sodium and water acting directly on the subfornical organ. In the Central nervous system (CNS) to ANG II stimulates the rostral ventrolateral area of the bulb, increasing the release of norepinephrine by the nerve endings simpáticas34. In the peripheral tissues to ANG II reduces the sensitivity of the baroreceptors, which decreases the efficiency of those in control of blood pressure variation

The ANG II activates various cellular processes that induce vasoconstriction, generate reactive oxygen species, vascular inflammation, stimulate the heart and vascular remodeling and aldosterona32 production. In the heart the ANG II stimulates the growth of muscle cells increases lisas35 .37 .38 .39 fibroblastos36 proliferation of .40 and promotes hypertrophy of the miócitos41, in addition to causing vasoconstriction coronariana42.

Other peptides of SRAA have been identified, such as 3, 4 inhibitors inhibitors and angiotensin 1-7 (ANG 1-7). In addition, it was discovered another angiotensin-converting enzyme (ACE 2), which suggests that the SRAA has more physiological functions of anteriormente32 believed.

Some studies suggest that ANG 1-7 exerts cardioprotective role for enhancing vasodilation coronariana43 reduce the concentration of ANG II in miocárdio44 and by decrease of ANG II receptors and reducing your gênica45 expression.

Another important mechanism for regulating blood pressure, natriuretic peptide system that consists of three peptides: type A (ANP), released by Atria; Type B (BNP), released by the ventricles; and type C (CNP), released by endothelial cells. This system promotes diuresis, natriurese, primarily peripheral vasodilation, inhibition of the SRAA system and inhibition of simpática46 activity.

Plasma concentrations of ANP and BNP, besides increasing the response to atrial muscle stretch, seem to be antagonists of the effects of ANG II on vascular tone in the secretion of aldosterone in sodium reabsorption and vascular cell growth. The CNP is found in the brain and in endothelial cells, but their plasma concentrations are baixas47.

In addition to the kidney, cardiovascular and endocrine mechanisms, pressure control is also exercised by neural reflexes involving baroreceptors. The baroreflex system works via vagal afferent pathways and Medullary, through which information reaches the nucleus of the solitary tract. In this nucleus that information is modulated and back to the heart via vagal efferent components fast and can manifest itself in the first subsequent rate and sympathetic efferent slow, that bring the answer with a delay of up to 20 segundos28.

The baroreceptors are the primary mediators of the autonomic nervous system in the control of BP and heart rate, which respond to deformation and stretching of the walls of the vessels where they are located. The carotid sinuses are swelling of the internal carotid arteries that have the thinnest wall and with greater amount of elastic tissue, compared to other walls of arteries. The sensory innervation of the area is provided by branches of the glossopharyngeal nerve (CN IX), while that of aortic baroreceptors is made by branches of the vagus nerve (CN X) 28.

The friendly components of the cardiovascular system are thrilled by projections of a select group of neurons located in the rostral ventrolateral bulb portion (RVL). RVL neurons are controlled by inhibitory projections of neurons located in the ventrolateral bulb flow (CVL). The reflections of the baroreceptors using via inhibitory CVL-RVL for modulation of sympathetic activity in the heart, vessels and adrenal Medulla. The stimulation of baroreceptors excites neurons that project to the nucleus of the solitary tract, that excite neurons in the CVL, increasing your inhibitions about the RVL neurons. The result of this route is a decrease in sympathetic tone to the heart and blood vessels.

In addition to inhibitory projections to the RVL, CVL has projections to the paraventricular and supraópticos, located also in the brainstem, which are responsible for producing the vasopressin. In this way, the baroreflex mechanism that can inhibit the sympathetic tone, as stimulate the production of vasopressin. It was found that the aferências coming from the baroreceptors can promote a brain remodeling will modify the magnitude of the simpático48 tone.

Recent surveys have shown that there is a counterbalance between the baroreflex activity and the SRAA. The ANG II may act on the CENTRAL NERVOUS SYSTEM by increasing sympathetic tone. In addition, as the kidney is modeling both under neural influence (renal nerves), hormonal (SRAA), as they both acting on compensatory natriurese. In this sense, the baroreceptors Act stimulating the excretion of sodium and the SRAA stimulates your reabsorption, due to the release of aldosterone. However, the inhibition of antinatriurétricos effects caused by baroreceptors is relatively weak compared to your simpatoinibitório, which effect will counter the effects of ANG II49 vasoconstrictors.

In addition to the neural and hormonal mechanisms, the integrity of the endothelium of blood vessels is essential for regulating blood pressure. The main functions of the vascular endothelium, which include synthesis of vasodilator substances (endothelium-dependent relaxation factor, prostacyclin, other prostaglandins, nitric oxide, bradykinin and endothelium-derived hyperpolarizing factor), vasoconstritoras, endothelins, cyclical changes, ANG II and reactive oxygen species and role in the modulation of vasoactive substances reception.

In physiological conditions, there is a balance between its vasodilatory substances and vasoconstritoras, so that there is a predominance of relaxing vascular muscle substances, while in pathological situations occurs the predominance of the action of substances constritoras this musculature. Nitric oxide (ON) stands out as a vasodilator substance and is synthesized by L-arginine, event mediated by nitric oxide synthase (NOS). It is assumed that the amount of constitutive in the vascular endothelium is responsible for basal action of ON. The new synthesis is activated by agonists such as acetylcholine, Catecholamines and angiotensin system and also by physical stimuli such as shear stress, which leads to increased intracellular calcium.

Among the substances the endothelin vasoconstritoras, whose production occurs in vascular endothelium and has the participation of angiotensin-converting enzyme endothelin. Its production is stimulated by elements such as adrenaline, ANG II and growth factor beta, in addition to physical factors, such as hypoxia, vessel distension, and shear stress. The endothelin, through interaction with the vascular smooth muscle promotes your contraction.

The reactive oxygen species, generated mainly in situations of oxidative stress, end up generating decreased vasodilation by interacting directly with the ON form peroxynitrite, which has deleterious effects even for playing a radical livre50.

Highlights the action of adenosine on vasculare tone. The receptors for this molecule are divided into A1 and A2. In A1, adenosine acts by reducing the strength of heart contractions, atrioventricular conduction, efferent renal artery constriction. Adenosine causes vasodilation through activation of Adenylate Cyclase, acting in A251 receivers.

Understand the physiological changes caused by exercise

Exercise promotes physiological changes that cause the reduction of blood pressure. During the Aerobic physical activity occurs an increased heart rate and sympathetic nervous system, which promotes a resetting of the baroreceptors to higher levels of pressure. After aerobic exercise, a readjustment of the baroreceptors to smaller levels of PA, which entails a reduction in the activity of the sympathetic nervous system. Consequently, there is a reduction in peripheral vascular resistance and pressure arterial52.

Beyond the acute response to exercise, a fitness training held for four months sparked an improvement in sensitivity of the barorreceptores53. One of the hypotheses for this improvement, is that the increase in arterial compliance due to physical training, may have increased the sensitivity barorreflexa54. According to the mecanoelástico concept, the greater the complacency under the same vascular pulse pressure, the greater the activation of baroreceptors and, consequently, there is a better arterial55 baroreflex control.

A second hypothesis to explain the increased sensitivity of the baroreceptors are endothelial changes that occur after the exercício54. During the year, shear stress occurs in endothelial cells, which increases the release of endothelial factors. These are related to an improvement in barorreceptora activity final56.

The increased sensitivity of the baroreflex may also be connected with the SRAA. Felix et al. showed that three months of exercise in spontaneously hypertensive rats, were able to normalize elevated levels of messenger RNA from angiotensinogênio. This standardization can be a possible mechanism related to improvement in baroreflex control arterial57.

According to the American College of Sports Medicine, the decrease in plasma Renin and ANG II can contribute in controlling PA58. Kiyonga et al. they found that individuals who showed a reduction in plasma Renin after 10 to 20 weeks of physical training, had a greater reduction in PA. In addition, a reduction in Renin and ANG II levels cause a decrease in vasoconstriction, which in your time is related to the reduction in PA due to físico59 training.

The smallest SRAA activation can also be involved in sympathetic nerve activity decrease that occurs in individuals with hypertension after training físico57. It was verified a decrease sympathetic tone in hypertensive individuals, after exercise, due to a reduction in plasma levels of norepinephrine, which is related to reduction of vasoconstriction, peripheral vascular resistance and, consequently, decrease in pressure arterial60.

The mechanisms responsible for the decrease in sympathetic activity after the Aerobic physical training were also related to the restructuring of neural plasticity in the central nervous system. The study of Ichiyama et al. demonstrated that the cardiorrespiratório Center and locomotive system of the brain of mice are profoundly remodelled with physical training. There has been a reduction of total dendritic regions areas of the posterior hypothalamus, lonely tract and the nucleus cuneatus and the authors suggest that many of these areas are responsible for a potential of simpatoexcitação. Thus, the decrease in sympathetic activity could occur due to the decrease of excitatórias61 synapses.

The post-exercise hypotension (HPE) is also related with vasodilating substances. During the exercise, there is a greater need for skeletal muscle blood supply, causing vasodilatação62 mechanism. One of these mechanisms is the increased production of nitric oxide induced by the stress of cisalhamento63. Another study shows that low-intensity aerobic exercise in spontaneously hypertensive rats decrease oxidative stress and, consequently, increase the availability of nítrico64 oxide.

Another possible mechanism of post-exercise vasodilation is the release of adenosine. A survey was conducted in hypertensive subjects using caffeine as blocker of adenosine. It was found that with the blockade of adenosine action there was a reduction in post-exercise hypotension físico65.

Studies show that the regular practice of aerobic exercise can be associated with a reduction in average 6.9 mmHg in systolic and diastolic pressure in mmHg 4.9 individuals hipertensos66. Aerobic training, too, acts in reducing blood pressure levels during the waking state, with an average fall of-5/-7 mmHg in systolic BP/diastólica67. Thus, in some cases, due to hypotension, the aerobic training can promote reducing the dose and/or the number of medicines utilizados68.

Being a disease hypertension resulting both from environmental factors as genetic, it is important to assess that some genes may interact with the hypotensive effect of physical exercise. Are involved in this interaction some genes of the SRAA, the ACE gene I and angiotensinogênio, of the receivers of angiotensin I (ANG I) and ANG II and bradykinin receptor. One of the ACE related polymorphisms occurs on chromosome 17, in the gene responsible for about 50% of the circulating levels of this enzyme. Individuals homozygous for this gene are more circulating levels of ECA, which results in greater production of ANG ll and bigger degradation of bradicinina69.

Factors that influence the hypotensive effect of physical exercise

Some factors may influence on post-exercise hypotension physical (HPE) on hypertensive, being the most important the age, race, some indicators related to obesity and genetic factors, there are no studies that prove great relevance of the influence of the genre in the HPE.

Ishikawa K et al. conducted a survey of an 8-week program of physical activities, with the intent to demonstrate the influence of age on the hypotensive effect of this program. To do so, individuals of different ages participated in the research, and it was observed that changes in systolic and diastolic blood pressure were significantly lower in individuals who were between 50 and 69 years when compared to individuals who had values between 30 and 49 years.

This distinction on the values of blood pressure reduction is not yet entirely clarified, however, there are some hypotheses, one being that the younger individuals may have done the aerobic exercise more intensely than the older ones, even if the duration the activity has been the same. Another possibility is that the younger individuals have a greater reduction in adipose tissue during the 8-week program, which relate to this further reduction in pressure sanguínea70.

Already in relation to factors related to obesity, the study showed that the WB Viegas high values of three indicators of factors obesity (BMI, waist circumference and total cholesterol), negatively affect the resting blood pressure or hypotension induced by physical activity.

This lower hypotensive effect can be related to the fact that visceral fat is linked to insulin resistance and leptin resistance, which causes the activation of the Renin-angiotensin-aldosterone (SRAA). High levels of total cholesterol are also related to SAH, because they promote Endothelial dysfunction through the synthesis of pro-inflammatory factors, SRAA activation, development of atherosclerosis and decreased availability of nitric oxide. So, when there is a vascular damage, there is no efficient action of hypotensive mechanism in response to endothelial física71 activity. Therefore, obesity and hypercholesterolemia may influence blood pressure and the mechanisms that are involved in the reduction of post pressure-exercício72.

About the influence of race, Whelton SP conducted a survey evaluating the difference of HPE in individuals of different breeds, resulting in black individuals, further reduction in systolic blood pressure and, in individuals a greater reduction in Asian blood pressure diastolic blood pressure compared to white guys. In this same study, it was concluded that the effects of aerobic exercise on blood pressure independent of body weight, which contrasts with the WB16 Viegas survey.

With regard to genetic factors, which are closely linked with the ethnic groups, it is noteworthy that mutations related to genes involved in the Renin-angiotensin-aldosterone system, can facilitate the further reduction of the PA, mainly pós aerobic exercise lower intensidade73.

Muszkat, in your study, identified three polymorphisms for the β2 adrenorreceptor, blocking it and affecting, then, vasodilation, damaging the HPE. These polymorphisms are more found in blacks than in whites of Europe, which relates to the raça74 factor.

In this way, it is worth mentioning that the genetic information can and should be taken into account when the prescription of physical activity for individuals with hypertension, and stress the interaction between these environmental factors and genetic analyses, the ones that show, for example, the climate in hot and humid environments, taking residents more susceptible to HAS, since the loss of heat is important, and when you lose large amounts of water and salt through sweating occurs hypovolemia and decrease in capacity for heat dissipation. Thus, individuals genetically adapted to the large appetite for salt and sodium renal conservation increase are better adapted to these environments, evolutionary having a worse response hypotensive exercise físico75.

Identify the modalities of exercise more effective for the reduction in PA

The regular practice of physical activities has the utmost importance in the conduct of drug prevention and treatment of hypertension. According to national and international guidelines, it is necessary that all hypertensive patients perform aerobic exercises, complemented by the resistance, as isolated form or complement the treatment medicamentoso76.

Physical activity is defined as any bodily movement to raise above the basal calorie expenditure. Aerobic exercise is the one that involves activities with the participation of major muscle groups, borrowed from clinical form, in mild to moderate intensity, long duration. Already the resistance exercises are those in which there is muscle contraction of a body segment against a opositora57 force.

Studies have shown an inverse relationship between the practice of physical exercises and PA levels. In relation to aerobic training, there are several studies that have shown significant reductions of systolic/diastolic BP. This reduction is evidenced in both sexes, like don't depend on other factors, such as weight loss and has a magnitude similar to that observed with the medicamentoso66 treatment.

The characteristics of the training can affect your hypotensive effect. The largest reductions are achieved with PA arrangements involving major muscle groups such as walk/run or ciclismo26. In relation to the intensity of the workouts are classified in three ways: low intensity, moderate and intense. The low-intensity exercises are those made between 40% to 60% of VO2 Max, the moderates are held around 60% of VO2 Max and intense are those made up of 80% of VO2 máximo77.

Studies have shown that high-intensity exercises not generate significant reductions of PA, in this way, the intense training shows no hypotensive effect. However, the light and moderate exercise are able to reduce the PA. In relation to low-intensity exercises: in a 3 months training occurred a 15mmHg reduction for systolic blood pressure, blood pressure media 11mmHg and 9mmHg for diastólica78 blood pressure.

It was verified that the mild hypotensive results training better than the moderados79 exercises. However there is controversy in studies, as was verified by Swain and Franklin a decrease in systolic blood pressure after training of moderate intensity, but not after the low intensidade80. Thus, it is not yet clear what the best intensity to obtain the hypotensive effect of aerobic training, but evidence suggests that it is the low intensity. This conclusion is very important for public health, as moderate-intensity exercise programs are much easier for patients with hypertension to start and maintain, compared to high intensity programmes, but these can promote injuries Musculoskeletal, cardiovascular events and require greater supervision médica81.

The duration of the session of aerobic training is a variable that is also related directly with the hypotensive effects of exercise. However, despite this importance, the minimum duration to achieve the hypotensive effect with aerobic training has not yet been determined. A study demonstrated a decrease in systolic and diastolic BP after training with more than 40 minutes, an increase of these pressures after a 10 minutos82 training. In this way, the study suggests that there is a greater hypotensive effect in training with longer duration.

Weekly frequency is also a very important variable. Studies have found a hypotensive response greater than aerobic training performed with 7 than with 3 weekly sessions. Although the largest number of sessions per week can increase the hypotensive effect, this is achieved by the practice of semanais83 sessions 3. Another variable to be analyzed is the aerobic training volume, i.e. minutes of weekly practice. The literature suggests that the largest volume major hipotensores84 effects promotes weekly.

Thus, as the hypotensive effects of aerobic training are evident, they make up the preferential treatment to HAS. In addition, the reduction of systolic diastolic pressure both as a hypertensive patient, when subjected to a physical activity is observed very quickly. This reduction can be observed from 1 to 10 weeks of physical training, besides, the systolic pressure continues to fall between 11 to 20 weeks, while the diastolic blood pressure does not fall with a longer prolonga81.

It is important to note, that the resistance training also reduces the PA systolic/diastolic pressure. However, during the execution of the peak occurs resisted exercise PA quite high, which may represent a risk to the patient, because this peak can lead to disruption of preexisting aneurysms, cerebrovascular accident causing hemorrágico85. Thus, it is necessary to minimize the increase in PA, controlling the characteristics of exercise. So, he's not training for the treatment of hypertension, but rather, a complement to aerobic, due to its benefits for global health.

So, considering the treatment for hypertension, aerobic training is the best choice. It should be performed at least three times a week, for at least 30 minutes of mild to moderate intensity. The resistance training should be done in addition to aerobic two to three times a week, involving the execution of 8 to 10 exercises for the major muscle groups in light intensity and with 10 to 15 repetitions series to moderate fatigue. Between sets and exercises must have a period of 1 to 2 minute intervals. The patient must perform a clinical assessment prior to the commencement of training and exercise testing is recommended for those who have risk factor associated with HAS. It should be emphasized, that in practice, for safety, exercise only starts if the PA is less than 160/105 mmHg86.

CONCLUSION

Based on the literature, it was observed that physical activity promotes a hypotensive effect in hypertensive subjects. This is mainly due to a reduction in sympathetic tone, release of vasodilators, the main ones being nitric oxide and adenosine, awareness of the baroreceptors and reducing the action of Renin-angiotensin-aldosterone system.

Several factors influence this hypotensive effect, the main ones being the breed, age, obesity and genetic traits. In this context, blacks and Asians showed reductions in systolic and diastolic blood pressure in relation to white guys; elderly individuals with HPE showed lower when compared with younger individuals; and patients with obesity high indicative factors presented, also, worse response to HPE. It was observed that some polymorphisms may influence the HPE.

In this sense, for the treatment of HAS, it has been found that the practice that has greater effect is the aerobic training of low and moderate intensity, in addition with resistance training. This training must be performed at least three times a week, for at least 30 minutes of moderate or light intensity, requiring a clinical assessment and treadmill stress test for the prescription of physical training.

REFERENCES

Ministry of health. Department of Informatics of the unified health system (SUS). Brasília; 2016.

1) I national consensus of Cardiovascular Rehabilitation. ARQ Bras Cardiol 1997; 69 (4).

2) III Brazilian Consensus Hypertension-CBHA. Campos do Jordão, SP .12 the Feb. 15, 1998 – SBC.

3) Miyakawa, k. Mechanisms of blood pressure oscillation caused by ischemic central nervous system response. Jpn J Physiol. 1988; 38 (4): 399-425.

Irigoyen MC, 4) Ann-Columbus FM, Krieger EM. Cardiovascular control: reflex regulation and role of the sympathetic nervous system. Rev Bras Hipertens. 2001; 8 ( 1): 55-62.

5 Pramme L, Schächinger H), Frings c. Baroreceptor activity impacts upon controlled but not automatic distractor processing. Biol Psychol. 2015; 110:75-84.

Oparil S, Weber) 6 AM. Hipertensión «El Kidney, Brenner y Rector». Ed: McGraw-Hill Interamericana año 2004:1-4, 77-94.

7) Goldblatt H, Lynch J, Hanzal RF et al. Studies on experimental Hypertension. I: The production of persistent elevation of systolic blood pressure by means of renal ischemia. J Exp Med 1934; 59:347-379.

8) Rigatto KV, M Bohlke, Irigoyen MC. Renin angiotensin system: from Physiology to treatment. Rev Soc Cardiol of Rio Grande do Sul. 2004; 3:1-5.

9) Myers j. Exercise and cardiovascular health. Circulation 2003; 107: e2-e5.

10) Fuchs FD, DM, JP. Antihypertensive efficacy of aerobic fitness. A critical analysis of the experimental evidence. ARQ Bras Cardiol 1993; 61:187-90.10) Fuchs FD, DM, JP. Antihypertensive efficacy of aerobic fitness. A critical analysis of the experimental evidence. ARQ Bras Cardiol 1993; 61:187-90.

11) 2003 European Society of Hypertension-European Society of Cardiology guidelines for the management of arterial hypertension Journal of Hypertension, J Hypertens. 2003 Jun; 21 (6): 1011-53.

12) Lewington S, Clarke R, Qizilbash N, Peto R, Collins R. Age-specific relevance of usual blood pressure to vascular mortality: a meta-analysis of individual data for one million adults in 61 prospective studies. Lancet. 14 Dec 2002; 360 (9349): 1903-13.

13) Jennings GL, Sudhir k. Initial therapy of primary hypertension. Med J Aust 1990; 152:198-203.

14) Grassi G, Seravalle G, Calhoun ad, Boela GB, Mancia G. Physical exercise in essential hypertension. Chest 1992; 101:3125-45.

15) Whelton SP, Chin A, Xin X, He j. Effect of aerobic exercise on blood pressure: A meta-analysis of randomized, controlled trials. Ann Intern Med 2002; 136:493-503.

16) Lesniak KT, Dubbert PM. Exercise and hypertension. Curr Opin Cardiol 2001; 16:356-9.

17) Negrão EC, ED, Basu PC, Roberto Denadai MLDR, Krieger EM. Vagal and sympathetic controls of the heart rate during exercise in trained and sedentary rats. Braz J Med Biol Res 1992; 25:1045-52.

18) Gava NS, Olopade-Silva, Negrão EC, Krieger EM. Low-intensity exercise training attenuates cardiac β-adrenergic tone in spontaneously hypertensive rats during exercise. 1995 hypertension; 26:1129-33.

19) Floras JS, Seals, PE, Ayward Sinkey C, Thoren PN, Mark AL. Post-exercise decreases in blood pressure in borderline hypertensive subjects are be accompained by decreases in mucle sympathetic nerve activity. J Hypertens 1986; 4: S79.

20) Barnett, RMUP Adams MJNN, Braga, AMFW et al. Postexercise blood pressure reduction in elderly hypertensive patients. JACC 2002; 39:676-82.20) Barrios RMUP, Acharya MJNN, Baron AMFW, et al. Postexercise blood pressure reduction in elderly hypertensive patients. JACC 2002; 39:676-82.

21) Hara K, JS Floras. Influence of naloxone on muscle sympathetic nerve activity, systemic and calf haemodynamics and ambulatory blood pressure after exercise in mild essential hypertension. J Hypertens 1994; 13:447-61.
22) IV Brazilian guidelines of hypertension 2002; Cap. 5:13-14-SBC.

23) Bird LC, Ganesh m. cardiovascular Rehabilitation in hypertension. Rev Soc Cardiol Est São Paulo – exercise and heart. São Paulo: 1996 SOCESP; 6:45 -58.

24) Michael OH. Non-pharmacological treatment of hypertension. Lancet 1994; 344:307 (S).

25) Adam LL, Forjaz c. influence of strength and aerobic training volume on lowering blood pressure of hypertensive patients. Rev Bras Ci Mov. 2007; 15:115-22

26) Flues K, influence of baroreceptors settings morphofunctional integrity the spontaneous hypertension in rats heart, 2011. Thesis (doctoral) Faculdade de Medicina da Universidade de São Paulo

27) Anderson m. Reflection of Baroceotores and blood pressure Homeostasis. View HCPA. 2013. 33. 230-37

28) Simões and Silva BC, Frevo NC, Passaglio KT, Sahu RA. Actions of renal angiotensin (1-7). Braz J Med Biol Res. 30 (4): 503-13, 1997

29) Santos RAS, Basu JM, Brosnihan KB, Ferrario CM: The renin angiotensin systen myocardial ischemia in dogs during acute. Hypertension. 15 (Suppl. 2): I121-127, 1990

30) Peach Renin angiotensin system-m.: biochemistry and mechanism of action involved. Physiol Rev. 57:313-70, 197730) Peach Renin angiotensin system-m.: biochemistry and mechanism of action involved. Physiol Rev. 57:313-70, 1977

31) Sanjuliani AF, Torres MRSG, Paula LN, Bassan FB. Renin-angiotensin-Aldosteroa: physiological and pathological bases. 2011. Rev HUPE. 10 (3)

32) CM, Saints Ferrario RA, Brosnihan KB, Block CH, Schiavone MT, Khosla MC, Greene LJ. The hypothesis regarding the function of angiotensin peptides in the brain. Clin Exp Hypertens. 10 Suppl 1:107-21, 1988

33) Andreatta SH, Averil DB, Santos RA, Ferrario CM. The ventrolateral Medulla. The new site of action of the renin-angiotensin system. Hyperteinsion. 1988 Feb; 11 (2Pt2): I163-6

34) Kato H, Suzoki H, Tajima S, Ogata Y, Tominaga T, Sato A, Angiotensin II stimulates Sarota t. collagen synthesis in cultured smooth vascular cells. J Hypertens. 9:17 -22.1991

35) M, Roth M Crabos, Hahn Awa, Erne p. Characterization of angiotensin II receptors in cultured adult rat cardiac fibroblasts. J Clin Invest 93:2372-2378.1994.

36) Sun Y, Ramires FJ, Zhou G, Ganjam VK, Weber KT. Fibrous tissue and angiotensin II. J Mol Cell Cardiol 29 (8): 2001-2012, 1997

37) Kawano (H) YS, Kawano Y, V, Barr M Starnes, Law, Hsueh WA. Angiotensin II has multiple profibrotic effects in human cardiac fibroblasts. Circulation. 101 (10): 1130-1137, 2000
38) Gonzalez, Lopez B, Querejeta R, Diez j. Regulation of myocardial collagen fibrillar by angiotensin II. The role in hypertensive heart disesase? J Mol CellCardiol. 34 (12): 1585-1593, 2002

39) Shivakumar K, Dostal, Boheler K, Baker KM Lakatta EG. Differential response of cardiac fibroblasts from young adults and senescent rats to ANG II. Am J Physiol Heart Circ Physiol. 284 (4): H1454-9, 2003

40) Sadoshima J, Izumo s. angiotensin II induced Molecular characterisation of hypertrophy of cardiac myocytes and hyperplasia of cardíac fibroblasts. Circ Res 73:413-423, 199340) Sadoshima J, Izumo s. angiotensin II induced Molecular characterisation of hypertrophy of cardiac myocytes and hyperplasia of cardíac fibroblasts. Circ Res 73:413-423, 1993

41) Fisher AJ, Santos RAS, Almeida AP. Angiotensi (1-7) improves the post-ischemic isolated rat hearts perfused function in. Braz J Med Biol Res 2002; 35; 90-1083

42) Brosnihan KB, Li P, Ferrario CM. Dilates coronary arteries through canine angiotensin kinins and nitric oxide. Hypertension. 27 (3 Pt 2): 523-8, 1996

43) Mendes, Ferreira AC AJ, Patel SV, Salim RA. Chronic infusion of angiotensin (1-7) reduces angiotensin II levels in rats heart. Regul Pept. 15; 125 (1-3): 29-34, 2005

44) Clark MA, Tallant and, Says DI. Downregulation of the AT1A receiver by pharmacologic concentrations og Angiotensin (1-7). J Cardiovasc Pharmacol 2001; 37 (4): 437-48

45) Vilacorta H, Duarte, Duarte NM, Carrano, Mosque ET, Dohmann HJF, Ferreira EGF. Value of the Pept dieo type B Natriuretic ´ in the diagnosis of congestive heart failure in Patients with Dyspnea in Emergency Unit. ARQ Bras Cardiol 2002; 79 (6): 564-8

46) Luis Carlos AF, BF, Celso B, Paul L, Haissam h. B Type natriuretic peptide and cardiovascular diseases. ARQ Bras Cardiol 2003; 81:529-34
47) Junior RC, Colombari, and Christopher S, Lee or. Hypertension: what you have to say. Rev Bras Hipertens 2006; 8:41-54

48) Thomas EL, Radu I. The Baroreflex to long-term Controller of Pressure Blood. Phisiology 30:148-158, 2015

49) Michel JB, Narayan D, Michel, Poitevin P, Philippe M, Scalbert, and Corman B, Levy BI. Effect of chronic angiotensin converting enzyme inhibition of the aging processes: II-large arteries. Am J Physiol 267: R124-R135, 1994

50) SG File, Hatagima, Silva NLCI. Renin-angiotensin system: it is possible to identify Hypertension susceptibility Genes? ARQ Bras Cardiol 2007; 89 (6): 427-433

51) Dicarlo, s. e.; Bishop, v. n. Central barorreflex resetting as a means of increasing and decreasing blood pressure and sympathetic outflow. Ann N Y Acad Sci, New York, v. 940, n. 1, p. 324-337, Jun 2001.

52) Laterza MC, de Matos LD, Trombetta IC, et al. Exercise training restores baroreflex sensitivity in never-treated hypertensive patients. Hypertension 2007; 49 (in press).

53) Basu, p. c. et al. Exercise training increases baroreceptor gain sensivity in normal and hypertensive rats. Hypertension, Baltimore, v. 36, n. 6, p. 1018-1022, Dec. 2000.

54) Kirchheim HR. Systemic arterial baroreceptor reflexes. Physiol Rev. 1976; 56:100-176.

55) Cameron JD, Dart AM. Exercise training increases systemic arterial compliance total in humans. 1994, 266 (2 Pt 2): H693-701

56) Felix JVC, Michelini LC. Training-induced pressure fall in spontaneously hypertensive rats is associated with reduced angiotensinogen mRNA expression within the nucleus tractus solitarii. Hypertension. 2007; 50:780-85.

57) American College of Sports Medicine. ACSM guidelines for the stress tests and your Prescription. Rio de Janeiro: Guanabara Koogan; 2007

58) Mcallister, r. m. Adaptations in control of blood flow with training: splanchnic and renal blood flows. Med Sci Sports Exerc, Madison, v. 30, n. 3, p. 375-381, 58) Mcallister, r. m. Adaptations in control of blood flow with training: splanchnic and renal blood flows. Med Sci Sports Exerc, Madison, v. 30, n. 3, p. 375-381, Marc. 199859) H, Tanabe Y Urata, Kiyonaga, et al. Antihypertensive and volume-depleting effects of mild exercise on essential hypertension. Hypertension 1987; 9:245-52

60) RM Ichiyama, Gilbert AB, Waldrop, Iwamoto TG GA. Changes in the exercise activation of diencephalic and brainstem areas cardiorrespiratory after training. 2002. 947 (2): 225-33

61) Halliwill, j. r. Mechanisms and clinical implications of post exercise hypotension in humans. Exerc Sport Sci Rev, Baltimore, v. 29, n. 2, p. 65-70, appr. 2001.

62) Goto, c. et al. Different intensities of exercise on effect of endothelium-dependent vaso-dilation in humans. Circulation, Dallas, v. 108, n. 5, p. 530-535, Jul 2003.

63) f. Roque, a. Briones, a. García-round et al. Aerobic exercise reduces oxidative stress and improves changes of small mesenteric vascular and coronary arteries hypertension. Br J Pharmacol. 2013 Feb; 168 (3): 686-703

64) Notarius CF, Morris BL, Floras JS. Caffeine attenuates early post exercise hypotension in middle-aged subjects. Am J Hypertens. 2006; 19 (2): 184-8.

65) Cleroux J, Feldman RD, Petrella Rd. Lifestyle modications to prevent and control hypertension. 4. Recommendations on physical exercise training. Canadian Hypertension Society, Canadian Coalition for High Blood Pressue Preventio and Control, Laboratory Centre for Disease Control Health Canada, t-Hart and Stroke Foundation of Canada. CMAJ. 1999; 160: S21-8

66) Cornelissen VA, Fagard RH. Effects of endurance training on blood pressure, blood pressure-regulating mechanisms, and cardiovascular risk factors. Hypertension. 2005; 46:667-75
67) Cade R, Mars D, H Wagemaker, et al. Effect of aerobic exercise training on patients with arterial systemic hypertension. Am J Med. 1984; 77:785-90.

68) Rigat B, Humberto C, Alhenc-Jarum F, Cambien F, Corvol P, Soubrier F. An insertion/deletion polymorphism in the angiotensin I-converting enzyme gene accounting for half the variance of serum enzyme levels. J Clin Invest 1990; 86:1343-6

69) Ishiwaka k. Influence of Age and Gender on Exercise Training Induced BP Reduction in Systemic Hypertension. 2004

70) Viegas WB, a PIN SKP, Bashir AF, Silva. Obesity Limits the benefits of exercise in reducing BP in hypertensive patients. 2010. View health Cienc Bras. 14 (1): 121-126.

71) Plotnick GD, Coretti MC, Vogel RA. Effect of antioxidant vitamins on the endothelium-dependent transient impairent of brachial artery vasoactivit following a single high-fat meal. JAMA, 1997, 278:1682-1686

72) Pardono and Almeida MB, Bastos AA, Simões HG. Post-exercise hypotension: possible relationship with ethnic and genetic factors. 2012. Rev bras cineantropom 14 performance (3)

73) Muszkat m. di erences Interethnic differences in drug response: the contribution of genetic variability in beta adrenergic receptor and cytochrome P4502C9. Clin Pharmacoler 2007; 82 (2): 215-8.

74) Young JH. Evolution of blood pressure regulation in humans. Curr Hypertens Rep 2007; 9 (1): 13-18

75) Brazilian Society of Cardiology, Brazilian Society of High, Brazilian Society of Nephrology. V Brazilian High blood pressure Guidelines. 5. Ed. Sao Paulo; 2006

76) Adam LL, Forjaz c. influence of strength and Aerobic Training Volume on lowering blood pressure of Hypertensive 2007. 15 (3): 115-122

77) Motoyama M et al. Blood pressure lowering effect of low intensity aerobic training in elderly hypertensive patients. Med Sci Sports Exerc 1998; 30:818-823

78) Tipton CM, Matthes RD, Marcus KD, Rowlett KA, Leininger JR. Influences of exercise intensity, age, and medication on resting systolic blood pressure of SHR populations. J Appl Physiol 1983; 55:1305-1310

79) Swain DP, Franklin BA. Comparison of cardioprotective benefits of moderate intensity aerobic exercise versus whats up, bigger up. Am J Cardiol 2006; 97:141-147

80) Hagberg JM, Park JJ, Brown MD. The Role of Exercise Training in the Treatment of Hypertension 2000; 30 (3): 193-206
81) Arroll B, Hill D, White G, Sharpe N, Beaglehole r. The effect of exercise duration on blood pressure episode. J Hypertension 1994; 12:1413-1415

82) Nelson, Jennings L GL, Esler MD, Komer PI. Effect of changing levels of physical activity on bloodpressure and haemodynamics in essential hypertension. Lancet 1986; 2:473-476
83) Kelley GA, Kelley KS. Progressive resistance exercise and resting blood pressure: a meta-analysis of randomized controlled trials. Hypertension. 2000

84) Vermeer, Rinkel GJ, Algra A. Circadian fluctuations in onset of subarachnoid internal hemorrhage. New data on internal hemorrhage and aneurysmal perimesencephalic and the systematic review. Stroke. 1997; 28:805-8

85) Medina FL, FS, Souza DR, Kanegusuku H, Forjaz CLM. Physical activity: impact on blood pressure. View Bras Hipertens 2010. 17 (2) 103-106

[1] Universidade Federal de Mato Grosso, Cuiabá, the second semester students of medicine

[2] Universidade Federal de Mato Grosso, Cuiabá, the second semester students of medicine

[3] Universidade Federal de Mato Grosso, Cuiabá, the second semester students of medicine

[4] Universidade Federal de Mato Grosso, Cuiabá, the second semester students of medicine

[5] Universidade Federal de Mato Grosso, Cuiabá, the second semester students of medicine

[6] Universidade Federal de Mato Grosso, Cuiabá, the second semester students of medicine

[7] Universidade Federal de Mato Grosso, Cuiabá, the second semester students of medicine

[8] Universidade Federal de Mato Grosso, Cuiabá, the second semester students of medicine

[9] Universidade Federal de Mato Grosso, Cuiabá, the second semester students of medicine

Rate this post

Leave a Reply

Your email address will not be published. Required fields are marked *

POXA QUE TRISTE!😥

Este Artigo ainda não possui registro DOI, sem ele não podemos calcular as Citações!

SOLICITAR REGISTRO
Search by category…
This ad helps keep Education free
There are no more Articles to display