|
 
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| REVIEW ARTICLE |
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| Year : 2020 | Volume
: 17
| Issue : 1 | Page : 11-20 |
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Therapeutic exercise for hypertension: An update for exercise prescribers
Mubarak Muhammad1, Jibril M Nuhu2, Tasneem M Hassan3, Sani S Baba4, Mustapha I Radda4, Mubarak M Mutawakkil5, Majida A Musa5
1 Department of Physiology, College of Medicine, University of Ibadan, Ibadan, Nigeria
2 Department of Physiotherapy, College of Health Sciences, Bayero University, Kano, Nigeria
3 Department of Physiotherapy, Aminu Kano Teaching Hospital, Kano, Nigeria
4 Department of Human Physiology, College of Health Sciences, Bayero University, Kano, Nigeria
5 Department of Pharmacology and Therapeutics, College of Health Sciences, Bayero University, Kano, Nigeria
| Date of Submission | 12-Oct-2019 |
| Date of Decision | 13-Dec-2019 |
| Date of Acceptance | 09-Jan-2020 |
| Date of Web Publication | 30-Jun-2020 |
Correspondence Address:
Dr. Mubarak Muhammad
Department of Physiology, College of Medicine, University of Ibadan, Ibadan
Nigeria
 Source of Support: None, Conflict of Interest: None  | Check |
DOI: 10.4103/njc.njc_24_19
Hypertension (HTN) remains the most common noncommunicable disease that constitutes the greatest public health problem worldwide, with the management involving pharmacological and nonpharmacological means. Therapeutic exercise is an important first-line intervention for a number of chronic diseases and has been recommended both as a measure for prevention and as an adjunctive nonpharmacological intervention for HTN, however; exercise prescription to hypertensive patients is still low, especially among primary healthcare professionals. This study examined from evidence-based literature the various aspects of therapeutic exercise and HTN to successfully stimulate the integration of exercise for HTN management in clinical settings, especially at the primary healthcare level. The paper reviewed published articles on exercise and HTN on Google Scholar, PubMed, and ScienceDirect using search terms “exercise” and “hypertension.” Studies identified in this review were summarized to further enrich literature with data and provide an update to exercise prescribers on exercise and HTN. This study revealed and identified three key aspects that need to be strengthened for successful integration of exercise for HTN management in all clinical settings: adequate and routine pre-exercise screening and monitoring; well-informed prescription of therapeutic exercise by qualified exercise professionals; and sufficient knowledge about potential interaction between exercise and antihypertensive medications.
Keywords: Exercise, exercise prescription, hypertension, hypertension treatment, therapeutic exercise
How to cite this article:
Muhammad M, Nuhu JM, Hassan TM, Baba SS, Radda MI, Mutawakkil MM, Musa MA. Therapeutic exercise for hypertension: An update for exercise prescribers. Nig J Cardiol 2020;17:11-20 |
How to cite this URL:
Muhammad M, Nuhu JM, Hassan TM, Baba SS, Radda MI, Mutawakkil MM, Musa MA. Therapeutic exercise for hypertension: An update for exercise prescribers. Nig J Cardiol [serial online] 2020 [cited 2023 May 30];17:11-20. Available from: https://www.nigjcardiol.org/text.asp?2020/17/1/11/288647 |
| Introduction | |  |
Hypertension (HTN) is the most common noncommunicable disease that constitutes the greatest public health problem in both economically developing and developed countries,[1],[2],[3],[4],[5] and it is identified to be the main important cardiovascular disease (CVD) risk factor[6],[7] and recently determined to be the overall number one global risk factor for disease.[8] HTN is defined as a chronic elevation of blood pressure (BP) level ≥140 mmHg systolic and/or 90 mmHg diastolic and/or taking antihypertensive medication.[9],[10],[11] It is classified based on etiology as either essential (primary or idiopathic) or secondary HTN. While primary HTN accounts for over 90%–95% of all cases of HTN,[12] being a systemic HTN that results from dysregulation of normal homeostatic control mechanisms of BP in the absence of detectable known secondary causes, secondary HTN accounts for <5% of cases of HTN, and it is associated with an underlying disorder that ranges from renal disorders, endocrinal disorders, and pharmacological causes.[13],[14] The etiological factors of HTN are complex, involving interactions between genetic predisposition and a range of environmental factors that include sodium retention, obesity, high caloric intake, and decreased energy expenditure.[15],[16] The exact mechanisms by which these environmental factors increase BP are not fully clarified, but it seems that a high caloric intake and decreased energy expenditure produce sympathetic hyperactivity.[16]
Despite HTN being highly preventable, it is responsible for a significant proportion of global morbidity and mortality.[17] Therapeutic exercise plays a pivotal role not only in the management but also in the primary prevention for a wide range of chronic diseases. The use of appropriate therapeutic exercise is globally a general consensus both as a measure for prevention and as an adjunctive nonpharmacological intervention in all treatment guidelines for HTN.[18],[19],[20],[21],[22],[23] The main clinical guidelines such as the World Health Organization and the International Society of HTN (ISH),[24],[25],[26] the World HTN League,[27] the European Society of HTN,[28] the American Society of HTN (ASH) and the ASH/ISH,[29] the American College of Sports Medicine,[30] the Joint National Committee (5–8) on the Detection, Evaluation, and Treatment of High BP,[31],[32],[33],[34] the American College of Cardiology (ACC),[35] the American Heart Association ACC,[36] the Canadian HTN Education Program,[37] the Malaysian Society of HTN,[38] and the International Forum for HTN Control and Prevention in Africa,[39] all recognize the significant role of exercise in the prevention and management of HTN.
HTN guidelines represent evidence-based best practices aimed at improving HTN diagnosis, evaluation, treatment, and control. These guidelines are updated over the course of time to make available updated knowledge on HTN for healthcare professionals and to identify deficiencies in the HTN management approach to achieve the ultimate goal of adequate HTN control.[5] Recently, a high level evidence from network meta-analysis of 391 randomized controlled trials (RCTs) assessing exercise and medication effects on systolic BP (SBP) found that the SBP-lowering effect of exercise among hypertensive populations was similar to that of commonly used antihypertensive drugs.[40]
Despite considerable volume of literature and professional recommendations on the value of exercise as an antihypertensive lifestyle therapy, exercise prescription to hypertensive patients is still low, especially among primary care physicians.[41] This might be due to substantial shortcomings in knowledge about the BP-lowering benefits of exercise, such as evidence of biomarkers that predict the degree of the BP response to exercise and evidence of exercise intervention dependent upon specific patient clinical characteristics such as sex, race/ethnicity, medication use, adiposity, and cardiometabolic profile.[42] Therefore, there is continued need to enrich the literature with information about therapeutic exercise for HTN. This review discusses summary of the literature and provides updated information to exercise prescribers on exercise and HTN.
| Methodology | | |
This was narrative review study that searched for published articles on exercise and HTN. Search terms “exercise” and “hypertension” were used, and three scientific search engine databases consisting of Google Scholar, PubMed, and ScienceDirect were considered. All types of studies ranging from systematic reviews to RCTs, cohort studies, case–control studies, case series and case reports, editorials, and expert opinion were considered.
| Mechanism Underlying the Antihypertensive Effect of Exercise | | |
BP directly depends proportionately upon two important fundamental physiologic factors termed cardiac output (CO) (for SBP) and total peripheral resistance (TPR, for diastolic BP [DBP]). CO, being the amount of blood ejected by the heart per unit time, depends on stroke volume and heart rate (HR) while TPR is the cumulative resistance offered by the arterioles of the body to the blood flow from systemic arterial to venous compartment. Any of the factors such as antihypertensive medications and therapeutic exercise that may mediate BP will ultimately affect either of the aforementioned basic physiologic factors. The overall typical fashion of BP response to an acute bout of exercise is a gradual increase in SBP, from resting baseline level to exercise demand level through the redistribution of CO, and a decrease or neutral effect on DBP. This response is mediated by changes in the autonomic nervous system and hormonal influences in response to exercise.[43]
The antihypertensive effect of therapeutic exercise is achieved through both acute (immediate) response and chronic (delay) responses of the body.[43],[44],[45] The acute response otherwise known as postexercise hypotension (PEH) is due to reductions in systemic vascular resistance.[43],[44] An acute fall in BP within minutes or hours after exercise that is observed and more pronounced among hypertensive subjects[46],[47] and to a comparably lesser extent among prehypertensive and normotensive individuals[45] is termed as PEH. This PEH phenomenon may lead to 5–7 mmHg decrease in BP that lasts up to 24-h postexercise period and over time lead to potentially beneficial exercise-induced ventricular physiologic hypertrophy.[10],[43],[48] The physiologic mechanism of PEH is mediated by both neural and vascular hemodynamic changes that result in persistent reductions in vascular resistance.[46] The neural mechanism involves sympathoinhibition with the termination of exercise. It is known that during exercise, the baroreflex is reset to a higher operating point and sympathetic activity is increased to accommodate exercise demand level. After exercise, these reflexes are reset to lower pressures such that sympathetic outflow from the central nervous system is lower than pre-exercise level, and one of such decrease in sympathetic outflow effect is decrease in sympathetic vasoconstrictor nerve activity, thereby causing less vascular resistance and TPR for a given pressure after exercise. The vascular mechanism involves a partly contribution from aforementioned reductions in sympathetic outflow to the vascular system after exercise and partly by the release of local vasodilator substances from vascular endothelium after exercise. Prominent vasodilator substance known to be released after acute exercise is nitric oxide and other potential vasodilators such as prostaglandins, adenosine, and adenosine triphosphate that all lead to arteriolar vasodilation such that resistance to blood flow and ultimately TPR are reduced.[46]
The chronic response is unclear, unspecific, and not well explained, but its positive effect on BP has been proposed based on the following mechanisms: changes in sympathetic nervous system activity,[10],[19],[44],[49] changes in renin-angiotensin-aldosterone system (RAAS),[10],[19],[44],[49] improvement in endothelial function,[10],[23],[50] improved insulin sensitivity,[10],[18],[19] increased level of nitric oxide,[44] increased level of prostaglandins,[50] and improve lipoprotein-lipid profile.[18]
Changes in the sympathetic nervous system activity are attributed to exercise effect in improvement and recovery baroreflex sensitivity back to normotensive control levels.[8],[51],[52] One of the key factors contributing to the pathophysiology of HTN is sympathetic overstimulation that results from increased sensitivity of baroreceptors in hypertensive individuals such that the supposedly normal response of the baroreceptors to a decrease in BP to normotensive level became exaggerated and results in baroreceptor-mediated over-stimulatory effect of the sympathetic nervous system on the vasculature to cause exaggerated systemic vasoconstriction and hyper-increase TPR, leading to HTN.[8] Exercise has been suggested to mediate improvement in sensitivity of arterial baroreceptors through the mechanical factors of improving arterial compliance and distensibility or the neural factor that is directly associated with exercise stimulus.[8]
Changes in RAAS are related to exercise-mediated effect in decreasing RAAS-mediated abnormal increase in vasoconstrictor tone to normotensive level.[8],[21] Increase in vasoconstrictor tone has been found to contribute to the pathogenesis of HTN through RAAS-mediated abnormal increase vasoconstrictor tone that translates into increase in TPR, causing HTN. Exercise has been suggested to mediate a decrease in this vasoconstrictor tone through decreasing endothelin-1 endogenous bioavailability and decrease in mRNA and protein expression of the angiotensin II type 1 receptor, which is necessary for the vasoconstrictive effect of angiotensin II.[8]
Improvement in endothelial function by exercise involves improvement of endothelium-dependent relaxation and endothelial adaptation.[8],[11] HTN is known to be associated with endothelial dysfunction that results in impairment in endothelium-dependent vasodilation and thus causing abnormal high systemic vascular resistance and TPR, leading to HTN. This endothelial dysfunction has been found to be the result of oxidative stress, and that reduction of oxidative stress is an important contributor to the improvement of endothelial function observed as a result of exercise.[11]
Improvement and increase in insulin sensitivity are among the proposed mediators of BP response to exercise.[21],[45],[49],[53],[54] One of the insulin-derived action on vascular system is enhanced sympathetic tone, and this when become sustained translate sequentially into increase in sympathetic vasoconstriction tone, TPR and BP. Exercise both diminishes over-secretion of insulin and improves insulin resistance, thus consequently reducing the insulin-derived action on BP as well.[21],[53],[54]
Increase in the levels of nitric oxide and prostaglandins by exercise is closely related by the fact that both nitric oxide and prostaglandins are potent endogenous vasodilator substances that serve to attenuate vascular response to sympathetic vasoconstriction, causing relaxation and vasodilatation of vascular smooth muscle, and ultimately decrease TPR and lower BP.[11],[55] Decreased bioavailability of nitric oxide has also been proposed to be one of the critical factors in the development of HTN. The mechanism is reduction of nitric oxide bioavailability result in reduction in antioxidant potential of nitric oxide, and this promotes elevation of reactive oxygen species and oxidative stress that have been implicated in endothelial dysfunction, hyperactivity of the sympathetic nervous system and disturbances of the RAAS.[11] Improved lipoprotein-lipid profile by exercise is a metabolic change that operates simultaneously with other antihypertensive mechanisms of exercise to favorably affect BP.[49],[54]
| Various Exercise Programs and Their Effects on Blood Pressure | | |
Systematic reviews and meta-analysis represent highest level of evidence-based knowledge and literature, and various systematic reviews and meta-analysis of randomized controlled intervention trials that assessed various exercise programs effect on BP have also been carried out.[20],[56],[57],[58],[59],[60],[61],[62],[63],[64],[65],[66],[67] In a meta-analysis of 44 RCTs carried out by Fagard,[56],[57] the net change in SBP/DBP in response to dynamic aerobic training was significant and averaged −3.4/−2.4 mmHg. Hayashino et al.[58] carried out a systematic review and meta-analysis of 42 RCTs and found the net change in SBP of various structured exercise was −2.42 mmHg in SBP and −2.23 mmHg in DBP in response to various exercise programs among adults with type 2 diabetes. Cornelissen et al.[20] in a meta-analysis of 28 RCTs that assessed the effect of resistance exercise on BP found that resistance exercise induced significant decrease in SBP/DBP by −3.9/−3.9 mmHg among normotensive or prehypertensive study subjects, while there was decrease in SBP/DBP by −4.1/−1.5 mmHg among hypertensive study subjects, which was not statistically significant. Kelley et al.[59] studied the effects of aerobic exercise on resting SBP and DBP in adults in the form of meta-analysis of 47 clinical trials; this study found a statistically significant decrease in resting SBP/DBP by −6/−3 and −2/−1 mmHg in hypertensive and normotensive study subject groups, respectively.
Cornelissen and Smart[62] studied systematic reviews and meta-analysis of various exercise program types such as endurance, dynamic resistance, and isometric resistance exercise on resting BP in adults. This study found that SBP/DBP was reduced by −3.5/−2.5 mmHg after endurance exercise, −1.8/−3.2 mmHg after dynamic resistance exercise, and −10.9/−6.2 mmHg after isometric resistance exercise. Pescatello and Kulikowich[63] carried out a systematic review on aftereffects of dynamic exercise program on ambulatory BP among hypertensive and normotensive study subjects. Dynamic exercise was found to significantly decrease arterial BP at day, night, and 24-h period after the exercise. Cao et al.[64] in a systematic review and meta-analysis aimed at assessing the effectiveness of aerobic exercise on hypertensive patients found that aerobic exercise reduced SBP/DBP by a net difference of −12.26/−6.12 mmHg. Börjesson et al.[65] in systematic reviews with meta-analysis of 27 RCTs found that aerobic exercise resulted in mean reductions SBP/DBP by 10.8/4.7 mmHg. MacDonald et al.[66] systematically reviewed 64 controlled studies on the effect of resistance exercise training on BP among prehypertensive and hypertensive participants. The meta-analysis of this study found reductions in SBP/DBP by 3.0/3.3 mmHg among prehypertensive and 5.7/5.2 mmHg among hypertensive study groups, respectively. Corso et al.[67] carried out meta-analyses of 68 trials which focused on the combination of dynamic resistance and aerobic exercise as antihypertensive therapy. This study found reductions of SBP/DBP of 5.3/5.6 mmHg among hypertensive participants and 2.9/3.6 mmHg in prehypertensive participants.
The experimental studies that assessed the efficacy of various exercise programs and their effects on BP usually involved both hypertensive[68],[69],[70],[71],[72] and other[73],[74],[75] subjects as experimental group that were often screened for exercise before receiving exercise as intervention. Tsai et al.[68] designed aerobic exercise program (treadmill walking/jogging) for three times/week for 30 min of moderate intensity (60%–70% maximal HR reserve) for a total intervention period of 10 weeks. This study found significant reduction in SBP/DBP of −13.1/−6.3 mmHg and −1.5/+6.0 mmHg when compared baseline value and control group, respectively. Dimeo et al.[69] used treadmill exercise program (walking on a treadmill) for three times weekly with a target lactate concentration in capillary blood slightly above the aerobic threshold for a total intervention period of 8–12 weeks. This exercise program significantly decreased SBP and DBP by 6 and 3 mmHg, respectively. Moreau et al.[70] used aerobic exercise program in the form of walking for 3 km/day for a total intervention period of 24 weeks. This study observed a significant decrease in resting SBP of about 11 mmHg, while DBP remained unchanged. Collier et al.[71] designed a comparative study that compared aerobic and resistance exercise programs in which aerobic exercise program consists of treadmill exercise for 3 days/week for 30 min at intensity of 65% of previously determined peak oxygen consumption (VO2peak), and resistance exercise program of three sets of 10 repetitions at 65% of their 10 repetitions maximum 3 days/week both for a total intervention period of 4 weeks. The two exercise programs were observed to significantly reduce SBP and DBP in a similar fashion. Schroeder et al.[72] compared effectiveness of various exercise programs such as aerobic, resistance, and combined training in the form of 3 days/week for 60 min at intensity of 80% of their HR reserve for a total of 8 weeks. The combined training group was observed to cause reduced peripheral and central DBP of −4 and −4 mmHg, respectively.
| Combination of Antihypertensive Medications and Exercise | | |
There are several available antihypertensive medications that can be broadly classified into diuretics (loop diuretics – furosemide, bumetanide; thiazide diuretics – bendroflumethiazide, hydrochlorothiazide; thiazide-like diuretics – indapamide, metolazone; K+-sparing diuretics – spironolactone, amiloride), angiotensin-converting enzyme inhibitors (ACEIs – lisinopril, enalapril, ramipril, captopril, fosinopril, quinapril, benazepril, moexipril, and trandolapril perindopril), angiotensin II receptor blockers (ARBs – losartan, valsartan, candesartan, irbesartan, olmesartan, telmisartan), renin inhibitor (aliskiren), direct-acting vasodilators (hydralazine, diazoxide, nitroprusside, minoxidil), calcium channel blockers (CCBs – dihydropyridines CCB; amlodipine, nifedipine, felodipine, isradipine; nondihydropyridines CCB – diltiazem, verapamil), centrally acting antiadrenergic agents (alpha-2-agonists – clonidine, methyldopa, moxonidine), and peripherally acting antiadrenergic agents (alpha-blockers – prazosin, doxazosin, terazosin; beta-blockers (BB) – atenolol, propranolol, bisoprolol, metoprolol; dual alpha-beta blocker – labetalol, carvedilol; sympathetic nerve-ending blockers – reserpine, guanadrel, metyrosine; ganglionic blocker – hexamethonium).[3],[35],[76],[77]
Among these classes of antihypertensive drugs, the most commonly prescribed antihypertensive drug classes encountered in local settings are ACEIs, ARBs, BB, CCBs, centrally acting antiadrenergic agents (notably alpha-methyldopa), and diuretics.[14]
Antihypertensive medications are usually taken in a life-long treatment fashion. Personnel involved in the management of HTN, including exercise prescribers, must be familiar not only with the hemodynamic changes, which occur when people have HTN, but also with the hemodynamic changes the different drugs cause to make rational decisions about their patients.[3] Antihypertensive medications can interact with exercise prescribed to hypertensive subjects via two-fold; one is through interfering with exercise performance and second is through the side effects of the drugs that may present as associated complaint during exercise.
BB, especially nonselective BB, such as propranolol, leads to loss of β2-mediated action of skeletal muscle vasodilation, which leads to decrease contractility, easy fatigability, and intolerance to exercise, thus interfering with exercise performance.[78] β2-blockade also inhibits release of glucagon from islet alpha cells, and this leads to loss of glucagon-mediated primary function of increasing blood glucose level (through glycogenolysis and gluconeogenesis) during sympathetic stimulation in response to exercise demand and thus promote hypoglycemia that might interfere with exercise performance. Nonselective BB can also induce hypoglycemia unawareness, a situation whereby symptoms of hypoglycemia such as palpitations and elevated HR that patient would otherwise experience becomes masked. This is because hypoglycemia is a potent stimulator of glucagon release and such release becomes inhibited by β2-blockade. Evidence of nonselective BB associated effect in compromising exercise performance was reported in experimental clinical studies and therefore not recommended for combining exercise with such antihypertensive medication.[79],[80] Therefore, BBs are not recommended antihypertensive medication for effective exercise performance, and if exercise must be combined with BB, selective β1-blocker is to be prescribed to prevent β2-mediated interference with exercise performance.[81]
Alpha-blockers are associated with side effects of orthostatic hypotension that can lead to a situation, whereby hypertensive patient experiences vertigo or dizziness on suddenly assuming a standing position or during exercise.[77] This is because the use of α-blockers prevents vasomotor sympathetic outflow to veins on sudden standing up such that venous return to the heart and subsequently CO is reduced. Thus, patients could experience vertigo or blackout as a result of reduced blood flow to the brain, and such episodes that are dependent to the effect of the drug but independent to the effect of the exercise might be reported in patients combining alpha-blockers with exercise.[82],[83]
All diuretics can alter the normal rate and extent of secretion of body fluid ions, and hypokalemia is a side effect of these antihypertensive.[77] Diuretics may induce arrhythmias during exercise in the presence of hypokalemia,[81] and symptoms of arrhythmia need to be noted. It is also important to know that in some patients, BBs and diuretics have an adverse impact on thermoregulatory function; hence, the need to educate patients about the sign and symptoms of heat intolerance. Preferably, it is important to monitor the room temperature when exercising indoor, use the Borg scale as an adjunct to HR to monitor exercise intensity, and extend the cool down period for such patients.[10]
The most frequent side effects of CCBs are derived from cutaneous vasodilation and are primarily manifested by ankle edema.[16] CCBs constitute one of the best options for a combination therapy; however, patients treated with CCBs, BB, and vasodilators should stop exercise gradually as they have an increased likelihood of exaggerated hypotension postexercise.[10],[84],[85]
In athletes and physically active subjects who become hypertensive, the antihypertensive medication chosen should be one that ideally lowers BP not only at rest but also during exertion, not adversely affects exercise capacity, and decreases systemic vascular resistance.[86] ACEIs (or ARBs) and CCBs are the best drugs of choice for the initiation of treatment in these patients; this is because other initiation drug of choice such as diuretics are associated with electrolyte disturbances (risk of hypovolemia or hypokalemia) and/or may be on the doping list for some sports; while BB may decrease exercise performance.[86],[87]
The most popular side effect of ACEI that the patient might complain about is persistent nonproductive dry coughing.[16],[87] This is because ACEIs increase bradykinin level via the inhibition of the breakdown of bradykinin by angiotensin II which serves as added antihypertensive effect of ACEI, as bradykinin is an endogenous vasodilator and serve to additionally contribute to stimulation of nitric oxide production. However, increased bradykinin levels in the lung irritate nerve ending to initiate cough reflex, leading to the dry cough and the promotion of angioedema. The major difference between ARB and ACEI is the absence of an increase in bradykinin levels with the former and therefore is not associated with coughing.[88]
It is worthy of note that commonly prescribed drugs for arthritis and pain relief such as nonsteroidal anti-inflammatory drugs (NSAIDs) interfere with antihypertensive medications. With the exception of nondihydropyridines CCB, NSAIDs reduce the hypotensive effect of all antihypertensive drugs due to sodium/fluid retention.[77] NSAIDs and steroids have been identified as the most important prescription drugs that affect BP; and if the use of NSAIDs is necessarily indicated in patients taken antihypertensive medication, acetaminophen (paracetamol) is typically offered as a possible (if imperfect) substitute.[77]
| Preexercise Screening for Hypertensive Patients | | |
Evaluation of patients with HTN before commencing exercise program focuses more on preexercise evaluation of the cardiovascular status that is routinely assessed through history-taking, physical examination, and/or laboratory tests. The risk of CVD in patients with HTN is determined not only by the level of BP but also by the presence or absence of target organ damage and other risk factors, such as smoking, dyslipidemia, and diabetes.[89] Baster and Baster-Brooks[90] proposed a model of exercise screening based on health s.tatus and age as follows [Figure 1]: | Figure 1: Flowchart for exercise screening based on health status and age adopted from Baster and Baster-Brooks[90]
Click here to view |
- If the patient is prehypertensive with no suspected CVD <50 years, or Grade 1 hypertensive <50 years, patients can safely begin a moderate-intensity exercise program without extensive medical screening
- If the patient is prehypertensive with suspected CVD, or prehypertensive >50 years with no suspected CVD, Grade 2 hypertensive with no suspected CVD <50 years, exercise testing such as stress testing and monitoring is recommended to know how their heart responds to exercise
- If the patient is hypertensive with no suspected CVD >50 years, or hypertensive with suspected CVD, exercise testing and monitoring are recommended.
Hypertensive patients on exercise prescription should always be well informed about any abnormal symptoms such as shortness of breath, dizziness, chest discomfort, or palpitation and immediately report such symptoms. Patients with uncontrolled HTN are generally discouraged from heavy exercise and submaximal exercise testing until drug therapy lower the BP. An exercise SBP higher than 220 mmHg or DBP higher than 100 mmHg is considered abnormal.[90]
Recommendations
Therapeutic exercise is distinct from other related terms, such as physical activity and physical fitness. Physical activity is any bodily movement produced by contraction of skeletal muscles that increases energy expenditure above resting levels and comprises routine daily tasks such as commuting, occupational tasks, or household activities, as well as purposeful health-enhancing movements/activities; physical fitness is the quantifiable attribute an individual has or can achieve that relates to their ability to perform physical activities without undue fatigue and reflects a combination of physical activity behaviors, genetic potential, and the health of various organ systems; while exercise is a component of physical activity that is planned, structured, and repetitive with the intent of improving or maintaining health.[21]
Therapeutic exercise is prescribed and an exercise prescription (Ex Rx) is the process whereby the recommended physical activity program is designed in a systematic and individualized manner in terms of the frequency (how often?), intensity (how hard?), time (how long?), and type (what kind?), otherwise known as the frequency, intensity, time, and type (FITT) principle.[48] Ex Rx such as aerobic exercise (walking) for at least 3 days/week for 30 min of low–moderate intensity (40%–60% HR reserve) is in conformity with the FITT principle because frequency (3 days/week), intensity (low-moderate intensity), time (30 min), and type (aerobic exercise) are clearly well defined. Generally, aerobic exercise type, 30–40 min time, at 60% of predicted maximal HR intensity, most days of the week frequency is the most preferred FITT principle to significantly improve BP and reduce augmentation index.[91] Dynamic resistance and isometric exercise types were the next in the level of evidence after aerobic exercise.[92]
Exercise progression for hypertensive patients should be gradual, avoiding large increases on in any of the FITT components, especially the intensity; a case report progression proposed by Ivan et al.[16] can be an ideal protocol for exercise progression. There is no professional consensus as to single recommended exercise prescription; the recommended FITT of the Ex Rx varies across the professional committees and organizations; the consensus that can be taken from the level of agreement among the various professional recommendations is for adults with pre-established to established HTN to participate in 30 min/day or more of moderate-intensity aerobic exercise on most, if not all, days of the week to total 150 min/week or more.[42]
Unstructured and unmonitored chronically high-intensity extreme exercise has been documented to threat risk development of health-related complication when the balance tilts toward harmful effects.[93] Gastrointestinal complications such as heartburn, diarrhea, gastrointestinal bleeding,[94] exercise-induced rhabdomyolysis,[95] and other cardiotoxicity risks[93],[96],[97],[98] have all been among the documented potential complications. In HTN, potential complication of major interest is cardiotoxicity such as myocardial infarction, especially in patients with cardiac disease,[93],[96] atrial and ventricular enlargement, fibrosis, and propensity for high-grade ventricular arrhythmias.[97] These complications are rare and are often majorly minimized with adequate professional exercise prescription and monitoring.[93]
| Conclusion | | |
Adequate and routine pre-exercise screening and monitoring, well-informed prescription of therapeutic exercise by qualified exercise professionals, and sufficient knowledge about potential interaction between exercise and antihypertensive medications are essential to a successful utilization or administration of exercise for HTN in all clinical settings.
Financial support and sponsorship
Nil.
Conflicts of interest
There are no conflicts of interest.
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