Hypertension: Protective Effects of Physical Exercise on Cognition Function, Arterial Function and Brain Health

Marinei Lopes Pedralli; Eduardo Barbosa; Pedro Guimarães Cunha

doi:10.2991/artres.k.191203.003

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Volume 25, Issue 3-4, December 2019, Pages 81 - 86

Hypertension: Protective Effects of Physical Exercise on Cognition Function, Arterial Function and Brain Health

Authors

Marinei Lopes Pedralli¹^{, *}^{, †}^{, ‡}, Eduardo Barbosa²^{, 3}, Pedro Guimarães Cunha⁴^{, 5}^{, 6}

¹Department of Physical Exercise, Faculdade do Vale do Araranguá (FVA), Araranguá, Santa Catarina, Brazil

²Instituto de Cardiologia do Rio Grande do Sul/Fundação Universitária de Cardiologia (IC/FUC), Laboratório de Investigação clínica (LIC- IC/FUC), Porto Alegre, Rio Grande do Sul, Brazil

³Liga de Combate à Hipertensão de Porto Alegre, Porto Alegre, Rio Grande do Sul, Brazil

⁴Center for the Research and Treatment of Arterial Hypertension and Cardiovascular Risk, Internal Medicine Department, Hospital Senhora da Oliveira, Guimarães/Minho University, Portugal

⁵Life and Health Science Research Institute (ICVS) and School of Medicine, University of Minho, Portugal

⁶ICVS/3B’s - Portugal, Government Associate Laboratory, Braga/Guimarães, Portugal

^†

PRÓ-SQUALUS-PROJETO CARCHARIAS (Organização para a Pesquisa e a Conservação de Esqualos no Brasil) - Health and Quality of Life Department, Torres, Rio Grande do Sul, Brazil

^‡

Grupo de Pesquisa em Ciência e Saúde Coletiva (GPCSC/FVA), Araranguá, Santa Catarina, Brazil

^*Corresponding author. Email: marinei.lopespedralli@gmail.com; marinei.lopes@fva.com.br

Corresponding Author

Marinei Lopes Pedralli

Received 1 December 2019, Accepted 1 December 2019, Available Online 17 December 2019.

DOI: 10.2991/artres.k.191203.003 How to use a DOI?
Keywords: Hypertension; cognition; exercise; vascular health; rehabilitation
Abstract: Systemic Arterial Hypertension (SAH) is a chronic condition that requires clinical treatment and is associated with increased risk of cognitive impairment and dementia. Therefore, strategies with fewer side effects and less invasive procedures are required. Evidence supports that Physical Exercise (PE) has antihypertensive effects and has proven to be an efficient and complementary tool for managing hypertension, reducing cardiovascular disease risk factors, and improving cerebral perfusion in the majority of healthy populations. Much of this cardiovascular-protective effect of PE is probably due to pluripotent effects on the vasculature, including regulation of vascular tone, energy metabolism, microvascular recruitment, and endothelial function (reducing oxidative stress and preserving NO availability). These factors are speculated to work synergistically, thereby reducing systolic and diastolic blood pressure and are directly related to improved cerebrovascular function. However, few studies have specifically examined the potential positive effects of PE on the brain in hypertensive individuals. In this brief review, we discuss the potential effect of different PE modalities (aerobic, resistance, and combined) that may act as an effective preventive or therapeutic strategy for reducing blood pressure in hypertensives and, consequently, mitigate the association between hypertension, cognitive impairment and risk of dementia.
Copyright: © 2019 Association for Research into Arterial Structure and Physiology. Publishing services by Atlantis Press International B.V.
Open Access: This is an open access article distributed under the CC BY-NC 4.0 license (http://creativecommons.org/licenses/by-nc/4.0/).

1. INTRODUCTION

1.1. Systemic Arterial Hypertension and Cognitive Function

It is estimated that Systemic Arterial Hypertension (SAH) affects more than 40% of adults worldwide [1] and is strongly associated with coronary artery disease, stroke, and heart failure [2]. Blood Pressure (BP) rises with age; High BP (HBP) affects 50% of adults aged ≥60 years, and has a lifetime prevalence of 90% [3]. The World Health Organization estimates that suboptimal BP (>115 mmHg systolic BP) is responsible for 62% of cerebrovascular disease [4]. Numerous studies have demonstrated that SAH increases the risk of cognitive impairment, Alzheimer’s Diseases (AD) and vascular dementia [5–16], contributing to the increased burden of the disease worldwide, whose prevalence is achieving alarming figures [17]. Dementia in high-income countries ranks mainly between 3rd and 6th place as a cause of disability adjusted life years over the last 25 years [18].

The Atherosclerosis Risk in Communities Cohort (ARIC) study [19] has followed 13.476 individuals for 20 years, trying to understand the influence that increased BP, registered in mid-life (48–67 years old), might have in the development of cognitive dysfunction in later stages of life. The investigators were able to show that subjects exposed to SAH and pre-hypertension in mid-life had a higher (6.5% and 4.8%, respectively) cognitive function in various domains using a complete neurocognitive assessment (especially executive dysfunction). In fact, the trajectories of cognitive function in individuals with SAH demonstrated faster decline in global cognition and several cognitive domains [20], including worse performance in the executive function and information processing speed [21].

Furthermore, SAH is associated with subtle neurocognitive deficits [22,23] which may be potentiated by one’s lifestyle, like obesity [24], smoking [25], sedentary behavior [26], stress [27] and may further increase the risk of dementia [28]. Taken together, this background is associated with an increased chance SAH individuals have for developing vascular dementia, especially those who have been exposed to this condition for years [29].

A more comprehensive understanding of modifiable dementia risk factors should be based on interventions that can potentially prevent or delay the onset of the condition, and the possible target periods for intervention would extend from prenatal period to old age [30]. The Lancet Commission on dementia concluded that up to 35% of all cases may be attributable to potentially modifiable risk factors including physical inactivity, SAH, obesity, diabetes, smoking, hearing loss, education, depression and social isolation [31]. As such, there is strong, ongoing demand for evidence-based strategies that prevent, delay, or reverse age-associated increases in BP and cognitive decline [32–38]. Indeed, the need for new approaches is expected to grow as the burden of age- and accelerated aging-associated cardiovascular dysfunction and disease continues to rise [39]. An alternative therapeutic approach to HBP [35–38,40], vascular health [41–45] and cognitive dysfunction [29,46], is physical exercises [39].

Physical Exercises (PEs), in particular, has pluripotent effects on the vasculature, including regulation of the vascular tone [47], Cerebral Blood Flow (CBF) [48], endothelial function [42,49], microvascular recruitment [50], energy metabolism [51], vessel insulin actions [52], and antihypertensive effects [36–38,53], all important factors for brain health. PE might be an effective intervention to mitigate the association between SAH and cognitive impairment. In this brief review, we discuss the potential of PE to act as an effective preventive or therapeutic strategy for preventing or restoring SAH, and link it to cognition function and brain health. The focus will be primarily on studies in humans.

2. PHYSICAL EXERCISE AS A MEDIATOR IN SYSTOLIC ARTERIAL HYPERTENSION

Guidelines [54–56] recommend that SAH individuals perform at least 30 min of moderate intensity Aerobic Exercise (AE) ≥3–5 days a week (but preferably every day), supplemented by dynamic Resistance Training (RT). Cornelissen and Smart [57] showed that AE training [moderate to high intensity, <210 min/week or 40–60% Hear Rate (HR) reserve] contributed to reduce Systolic BP (SBP) and Diastolic BP (DBP) (8.5 and 5.1 mmHg, respectively; p < 0.001 for both comparisons) in hypertensive subjects. Wen and Wang [58] have observed decreased SBP (by 7 mmHg) and DBP (by 5 mmHg) in essential hypertensive patients. The study conducted by Moriguchi et al. [59] found that AE training at 50% VO₂max twice a week over a period of 3 months promoted benefits in Flow-Mediated Dilatation (FMD) from 5.2% (pre-training) to 8.7% (post-training; p < 0.001) in hypertensive individuals. Also, there was a reduction in SBP (14.5 mmHg) and DBP (9.6 mmHg) in the study. Vigorous AE training intensities may be considered in patients with HBP. Molmen-Hansen et al. [60] observed that AE performed by hypertensive individuals for 12 weeks improved FMD (before: 6.5 ± 3.7 and after: 10.7 ± 5.0%; p < 0.001) only in the group that practiced AE in high intensities (alternating between 60–70% and 90–95% of HR reserve). Ashor et al. [61] showed significantly reduced Pulse Wave Velocity (PWV) in hypertension subgroups analyses −0.66 (−1.23 to −0.10 m/s; p < 0.02). A significantly higher reduction in PWV after AE intervention in participants with stiffer arteries (PWV > 8 m/s) was also shown.

Cornelissen et al. published a set of meta-analyses on the effects of RT on BP in 2005 [36], 2011 [38], and 2013 [37]. In the 2005 publication, data from nine Randomized Clinical Trials (RCTs) 110 were pooled, and the investigators concluded that RT reduced SBP (by 3.2 mmHg and DBP at 3.5 mmHg). Subsequent meta-analysis (2011) showed that isometric RT (handgrip) may be more effective in reducing BP levels (SBP: 13.5 mmHg and DBP: 6.1 mmHg) than dynamic RT (SBP: 2.8 mmHg and DBP: 2.7 mmHg). In 2013, the meta-analysis confirmed the superiority of isometric RT in reducing SBP (10.9 mmHg) and DBP (6.2 mmHg); however, only four studies for isometric training were analysed [57]. Similar findings for the efficacy of isometric exercise were reported in another meta-analysis [62,63]. A reduction in SBP of 3.0 mmHg and DBP of 3.0 mmHg was observed. MacDonald et al. [63] conducted a meta-analysis with 64 controlled studies (71 interventions) to determine the efficacy of dynamic RT as a stand-alone antihypertensive therapy. Participants (N = 2344) were white (57%), middle-aged (47.2 ± 19.0 years), and overweight (26.8 ± 3.4 kg/m²) adults with SAH (126.7 ± 10.3/76.8 ± 8.7 mmHg); 15% were on antihypertensive medication. Overall, moderate-intensity dynamic RT [65–70% of One-Repetition Maximum (1RM)] was performed 2.8 ± 0.6 days/week for 14.4 ± 0.9 weeks and elicited small-to-moderate reductions in SBP (3.0 mmHg) and DBP (2.1 mmHg) compared with controls (p < 0.001). HBP reductions occurred among samples with higher resting SBP/DBP: ≈6/5 mmHg for hypertension, ≈3/3 mmHg for prehypertension, and ≈0/1 mmHg for normal BP (p < 0.023) [63]. On the other hand, study conducted by Moraes et al. [64] show that middle-aged, stage 1 hypertensive patients without antihypertensive medication (reaching 153 ± 6/93 ± 2 mmHg SBP/DBP after a 6-week medication washout period), submitted to a 12-week conventional RT program (3 sets of 12 repetitions at 60% 1 RM, 3 times a week on nonconsecutive days) reduced SBP (16 mmHg; p < 0.001), DBP (12 mmHg; p < 0.01) and mean BP (13 mmHg; p < 0.01) to prehypertensive values. Moreover, the benefits of BP reduction achieved with RE training remained unchanged for up to 4 weeks without exercise. Similarly, in the study Beck et al. [65] observed reduction in SBP (9.6 mmHg) and DBP (8 mmHg), in young unmedicated prehypertensive after 8 weeks dynamic RT protocol (2 sets of 8–12 repetitions at 60% 1 RM, 3 times a week) and improvement in FMD from 6.2% to 8.30%, concomitant with reduction in the Endothelin-1 level (ET-1). Thus suggesting the effectiveness of the RT in improving the endothelial artery function and oxidant/antioxidant balance in young prehypertensive. Both studies demonstrate the potential usefulness of conventional moderate-intensity (60% 1RM,) RT in the treatment of stage 1 hypertensive patients.

The evidence discussed earlier suggests the antihypertensive effects of isolated AE training (5–8 mmHg) and dynamic RT training (≈2–3 mmHg) for the same population [35–38,63]. Thus, it would be logical to think that combined exercises (AE + RT) performed in a single session or within a couple of hours one from another, which is referred to as concurrent [66] exercise or combined aerobic and resistance exercise [67], could enhance the antihypertensive effect. The Combined Training (CT) conferred the antihypertensive benefit to SAH individuals ≈15–9 mmHg [68] compared with prehypertension ≈2–7–4 mmHg [69], older men with SAH (12–24 mmHg) from BP at rest, respectively. Stewart et al. [70] reported average reductions of 5.3 and 3.7 mmHg for SBP and DBP, respectively, in hypertensive older adults who completed a concurrent training protocol for 6 months. When the training frequency amounted to three weekly sessions, the training intensity ranged from 50–80% of 1RM and 60–90% HRmax and training duration per session averaged 40–90 min. However, the aortic stiffness, indexed by aortofemoral PWV, was unchanged [70]. Son et al. [71] showed that 12 weeks of combined moderate (60–70% HR reserve) aerobic and resistance exercise training is a useful exercise modality for improving brachial-ankle PWV (Δ1.11 ± 0.63 m/s, p < 0.05), both SBP (Δ13.5 ± 1.58 mmHg, p < 0.05) and DBP (Δ11 ± 1.34 mmHg, p < 0.05), and functional capacity (Δ4.4 ± 3.89, p < 0.05) in postmenopausal women with stage 1 hypertension.

3. PHYSICAL EXERCISE, COGNITION FUNCTION, ARTERIAL FUNCTION AND BRAIN HEALTH

Lifestyle habits, including PE, associated with 35% reduction in CVD risk factors and mortality [72] are promising approaches for the prevention of neurocognitive decline [33,73], and physically active (PA) individuals are less likely to develop dementia [74,75]. Evidence suggests that AE improves brain structural integrity – brain volume [76], neurocognitive performance [34] associated with increased attention, executive function, and memory [77]. In addition, PE promotes several molecular and structural adaptations in different neurotrophils in the human brain such as Brain Derived Neurotrophic Factor (BDNF) [78,79], which mediates neuronal survival, plasticity, and synapse reinforcement [79]. It has been observed that PE training is associated with higher CBF, higher metabolic activity in the hippocampus, and better memory compared with the control group that did not exercise [80,81]. Also, PE is associated with increased length, complexity, and density of some types of neuron dendrites [82], and greater integrity of the Blood–Brain Barrier (BBB) [83]. Taking together, it is suggested that PE promotes several molecular and structural adaptations that can improve cognitive functioning [84,85].

Additionally, the cause and effect relationship between PE and cerebral perfusion [86] may be attributed to hemodynamics effects, including BP [35–38,63], endothelial function [41,49,50,65,87,88] and arterial remodeling [42,43,61,89–92]. PE provides benefits not only to the vascular beds that are involved during the session, but also to those in non-working sites or limbs [93,94]. This phenomenon could be explained by the increased shear stimuli in non-working limbs during an exercise bout [95]. The proposed mechanisms through which PE may prevent the development and treatment of SAH are presented in Table 1. It is speculated that these factors work synergistically, thereby reducing systolic and diastolic BP and improvement in vascular function. It is plausible that PE training may contribute to improved CBF in hypertensive individuals.

Reduction	Improvement
Vascular resistance	Endothelial function
Arterial stiffness	Arterial compliance
Intima-media thickness	Arterial lumen diameter
Renin-angiotensin system activity	Angiogenesis and arteriogenesis
Sympathetic activity	Parasympathetic activity
Oxidative stress	Renal function
Inflammation	Sodium handling
Body weight/body mass	Insulin sensitivity/glucose handling
Psychosocial stress	Baroreflex sensitivity
Vascular responsive to adrenergic- and endothelin-receptor stimulation	Nitric oxide (NO)

Table 1

Proposed mechanisms through which PE may treat and prevent the development of hypertension

Summary of mechanisms through which PE promotes vascular adaptation, adapted from Green et al. [96] and Diaz et al. [97].

4. PERSPECTIVES AND CONCLUSION

Therefore, despite the lack of direct evidence showing a relationship between exercise and cognitive function in hypertensive individuals, drawing upon the available literature, there is evidence to support that exercise has antihypertensive effects and benefits on vascular function. In addition, it is plausible to assume that the role of exercise in modifying cardiovascular risk factors may prevent cognitive decline and potentially reduce the risk of dementia in hypertensive individuals.

Although some studies have shown that PE can improve cerebrovascular function and cerebrovascular structure, RCTs focusing on hypertensive individuals are needed. Further research is needed to show how different modalities of physical training (AE, dynamic RT, isometric RT and combined exercises) and their characteristics (frequency, intensity, type and time) act on cerebrovascular structure and function and their implications for cognitive function in this population. Brain function and structure may be assessed by different techniques such as arterial spin marking or Functional Magnetic Resonance Imaging (fMRI), which provides a noninvasive quantitative measure of BF in specific brain regions. fMRI has been used as an approach to examine CBF in regions of interest associated with cognitive dysfunction and dementia. In addition, it may allow a broader understanding of the potential effect of PE training acting as a preventive or therapeutic strategy as well as preventing or restoring impaired brain perfusion and potentially impaired cognitive function with advancing age in hypertensive patients.

CONFLICTS OF INTEREST

The authors declare they have no conflicts of interest.

AUTHORS’ CONTRIBUTION

MLP, EB and PGC conceived and performed the systematic review. MLP, EB and PGC provided physical exercise, hypertension and cognitive function. MLP wrote the manuscript with input from all authors.

FUNDING

No funds or grants were received for the preparation of this manuscript.

ABBREVIATIONS

SAH,: systemic arterial hypertension;

BP,: blood pressure;

AD,: Alzheimer’s diseases;

PE,: physical exercise;

CBF,: cerebral blood flow;

AE,: aerobic exercise;

RT,: resistance training;

SBP,: systolic blood pressure;

DBP,: diastolic blood pressure;

VO₂max,: maximum volume of oxygen;

FMD,: flow-mediated dilation;

HR,: heart rate;

PWV,: pulse wave velocity;

1RM,: one-repetition maximum;

CT,: combined training;

CVD,: cardiovascular disease;

PA,: physically active;

BDNF,: brain derived neurotrophic factor;

BBB,: blood-brain barrier;

ON,: nitric oxide;

METs,: metabolic equivalent of task;

RCTs,: randomized clinical trials;

ASL,: spin marking;

fMRI,: functional magnetic resonance.

Footnotes

Peer review under responsibility of the Association for Research into Arterial Structure and Physiology

REFERENCES

[1]AA Leung, SS Daskalopoulou, K Dasgupta, K McBrien, S Butalia, KB Zarnke, et al., Hypertension Canada’s 2017 Guidelines for diagnosis, risk assessment, prevention, and treatment of hypertension in adults, Can J Cardiol, Vol. 33, 2017, pp. 557-76.

[2]PA James, S Oparil, BL Carter, WC Cushman, C Dennison-Himmelfarb, J Handler, et al., 2014 evidence-based guideline for the management of high blood pressure in adults: report from the panel members appointed to the Eighth Joint National Committee (JNC 8), JAMA, Vol. 311, 2014, pp. 507-20.

[3]RB D’Agostino, RS Vasan, MJ Pencina, PA Wolf, M Cobain, JM Massaro, et al., General cardiovascular risk profile for use in primary care: the Framingham Heart Study, Circulation, Vol. 117, 2008, pp. 743-53.

[4]JA Whitworth, 2003 World Health Organization (WHO)/International Society of Hypertension (ISH) statement on management of hypertension, J Hypertens, Vol. 21, 2003, pp. 1983-92.

[5]Z Guo, L Fratiglioni, L Zhu, J Fastbom, B Winblad, and M Viitanen, Occurrence and progression of dementia in a community population aged 75 years and older: relationship of antihypertensive medication use, Arch Neurol, Vol. 56, 1999, pp. 991-6.

[6]C Tzourio, C Dufouil, P Ducimetière, and A Alpérovitch, Cognitive decline in individuals with high blood pressure: a longitudinal study in the elderly. EVA Study Group. Epidemiology of Vascular Aging, Neurology, Vol. 53, 1999, pp. 1948-52.

[7]M Tadic, C Cuspidi, and D Hering, Hypertension and cognitive dysfunction in elderly: blood pressure management for this global burden, BMC Cardiovasc Disord, Vol. 16, 2016, pp. 208.

[8]TM Hughes and KM Sink, Hypertension and its role in cognitive function: current evidence and challenges for the future, Am J Hypertens, Vol. 29, 2016, pp. 149-57.

[9]C McDonald, MS Pearce, SR Kerr, and JL Newton, Blood pressure variability and cognitive decline in older people: a 5-year longitudinal study, J Hypertens, Vol. 35, 2017, pp. 140-7.

[10]C Iadecola, K Yaffe, J Biller, LC Bratzke, FM Faraci, PB Gorelick, et al., Impact of hypertension on cognitive function: a scientific statement from the American Heart Association, Hypertension, Vol. 68, 2016, pp. e67-e94.

[11]M Kivipelto, EL Helkala, T Hänninen, MP Laakso, M Hallikainen, K Alhainen, et al., Midlife vascular risk factors and late-life mild cognitive impairment: a population-based study, Neurology, Vol. 56, 2001, pp. 1683-9.

[12]LH Kuller, OL Lopez, WJ Jagust, JT Becker, ST DeKosky, C Lyketsos, et al., Determinants of vascular dementia in the Cardiovascular Health Cognition Study, Neurology, Vol. 64, 2005, pp. 1548-52.

[13]SL Seliger, DS Siscovick, CO Stehman-Breen, DL Gillen, A Fitzpatrick, A Bleyer, et al., Moderate renal impairment and risk of dementia among older adults: the Cardiovascular Health Cognition Study, J Am Soc Nephrol, Vol. 15, 2004, pp. 1904-11.

[14]D Gąsecki, M Kwarciany, W Nyka, and K Narkiewicz, Hypertension brain damage and cognitive decline, Curr Hypertens Rep, Vol. 15, 2013, pp. 547-58.

[15]B Haring, C Wu, LH Coker, A Seth, L Snetselaar, JE Manson, et al., Hypertension, dietary sodium, and cognitive decline: results from the women’s health initiative memory study, Am J Hypertens, Vol. 29, 2016, pp. 202-16.

[16]WS Aronow, Hypertension and cognitive impairment, Ann Transl Med, Vol. 5, 2017, pp. 259.

[17]KA Walker, MC Power, and RF Gottesman, Defining the relationship between hypertension, cognitive decline, and dementia: a review, Curr Hypertens Rep, Vol. 19, 2017, pp. 24.

[18]CJL Murray, RM Barber, KJ Foreman, A Abbasoglu Ozgoren, F Abd-Allah, SF Abera, et al., Global, regional, and national disability-adjusted life years (DALYs) for 306 diseases and injuries and healthy life expectancy (HALE) for 188 countries, 1990–2013: quantifying the epidemiological transition, Lancet, Vol. 386, 2015, pp. 2145-91.

[19]RF Gottesman, ALC Schneider, M Albert, A Alonso, K Bandeen-Roche, L Coker, et al., Midlife hypertension and 20-year cognitive change: the atherosclerosis risk in communities neurocognitive study, JAMA Neurol, Vol. 71, 2014, pp. 1218-27.

[20]J Birns, R Morris, N Donaldson, and L Kalra, The effects of blood pressure reduction on cognitive function: a review of effects based on pooled data from clinical trials, J Hypertens, Vol. 24, 2006, pp. 1907-14.

[21]S Köhler, MAE Baars, P Spauwen, S Schievink, FRJ Verhey, and MJP van Boxtel, Temporal evolution of cognitive changes in incident hypertension: prospective cohort study across the adult age span, Hypertension, Vol. 63, 2014, pp. 245-51.

[22]E Duron and O Hanon, Hypertension, cognitive decline and dementia, Arch Cardiovasc Dis, Vol. 101, 2008, pp. 181-9.

[23]E Duron and O Hanon, Vascular risk factors, cognitive decline, and dementia, Vasc Health Risk Manag, Vol. 4, 2008, pp. 363-81.

[24]SR Waldstein and LI Katzel, Interactive relations of central versus total obesity and blood pressure to cognitive function, Int J Obes (Lond), Vol. 30, 2006, pp. 201-7.

[25]JA Ambrose and RS Barua, The pathophysiology of cigarette smoking and cardiovascular disease: an update, J Am Coll Cardiol, Vol. 43, 2004, pp. 1731-7.

[26]JI Recio-Rodriguez, MA Gomez-Marcos, MC Patino-Alonso, M Romaguera-Bosch, G Grandes, M Menendez-Suarez, et al., Association of television viewing time with central hemodynamic parameters and the radial augmentation index in adults, Am J Hypertens, Vol. 26, 2013, pp. 488-94.

[27]M Utsugi, Y Saijo, E Yoshioka, T Sato, N Horikawa, Y Gong, et al., Relationship between two alternative occupational stress models and arterial stiffness: a cross-sectional study among Japanese workers, Int Arch Occup Environ Health, Vol. 82, 2009, pp. 175-83.

[28]MF Elias, PK Elias, LM Sullivan, PA Wolf, and RB D’Agostino, Lower cognitive function in the presence of obesity and hypertension: the Framingham heart study, Int J Obes Relat Metab Disord, Vol. 27, 2003, pp. 260-8.

[29]LJ Trigiani and E Hamel, An endothelial link between the benefits of physical exercise in dementia, J Cereb Blood Flow Metab, Vol. 37, 2017, pp. 2649-64.

[30]E Eggink, EP Moll van Charante, WA van Gool, and E Richard, A population perspective on prevention of dementia, J Clin Med, Vol. 8, 2019. pii: E834.

[31]G Livingston, A Sommerlad, V Orgeta, SG Costafreda, J Huntley, D Ames, et al., Dementia prevention, intervention, and care, Lancet, Vol. 390, 2017, pp. 2673-734.

[32]H Joosten, MEA van Eersel, RT Gansevoort, HJG Bilo, JPJ Slaets, and GJ Izaks, Cardiovascular risk profile and cognitive function in young, middle-aged, and elderly subjects, Stroke, Vol. 44, 2013, pp. 1543-9.

[33]JA Blumenthal, PJ Smith, S Mabe, A Hinderliter, PH Lin, L Liao, et al., Lifestyle and neurocognition in older adults with cognitive impairments: a randomized trial, Neurology, Vol. 92, 2019, pp. e212-e23.

[34]PJ Smith, JA Blumenthal, BM Hoffman, H Cooper, TA Strauman, K Welsh-Bohmer, et al., Aerobic exercise and neurocognitive performance: a meta-analytic review of randomized controlled trials, Psychosom Med, Vol. 72, 2010, pp. 239-52.

[35]LS Pescatello, HV MacDonald, GI Ash, LM Lamberti, WB Farquhar, R Arena, et al., Assessing the existing professional exercise recommendations for hypertension: a review and recommendations for future research priorities, Mayo Clin Proc, Vol. 90, 2015, pp. 801-12.

[36]VA Cornelissen and RH Fagard, Effect of resistance training on resting blood pressure: a meta-analysis of randomized controlled trials, J Hypertens, Vol. 23, 2005, pp. 251-9.

[37]VA Cornelissen, R Buys, and NA Smart, Endurance exercise beneficially affects ambulatory blood pressure: a systematic review and meta-analysis, J Hypertens, Vol. 31, 2013, pp. 639-48.

[38]VA Cornelissen, RH Fagard, E Coeckelberghs, and L Vanhees, Impact of resistance training on blood pressure and other cardiovascular risk factors: a meta-analysis of randomized, controlled trials, Hypertension, Vol. 58, 2011, pp. 950-8.

[39]I Lourida, E Hannon, TJ Littlejohns, KM Langa, E Hyppönen, E Kuźma, et al., Association of lifestyle and genetic risk with incidence of dementia, JAMA, Vol. 322, 2019, pp. 430-7.

[40]LP Santos, RS Moraes, PJ Vieira, GI Ash, G Waclawovsky, LS Pescatello, et al., Effects of aerobic exercise intensity on ambulatory blood pressure and vascular responses in resistant hypertension: a crossover trial, J Hypertens, Vol. 34, 2016, pp. 1317-24.

[41]DJ Green, A Maiorana, G O’Driscoll, and R Taylor, Effect of exercise training on endothelium-derived nitric oxide function in humans, J Physiol, Vol. 561, 2004, pp. 1-25.

[42]DHJ Thijssen, DJ Green, and MTE Hopman, Blood vessel remodeling and physical inactivity in humans, J Appl Physiol (1985), Vol. 111, 2011, pp. 1836-45.

[43]H Tanaka, Effects of regular exercise on arterial stiffness, LS Pescatello (editor), Effects of exercise on hypertension: from cells to physiological systems, Humana Press, New York, 2015, pp. 185-201.

[44]DR Seals, RE Kaplon, RA Gioscia-Ryan, and TJ LaRocca, You’re only as old as your arteries: translational strategies for preserving vascular endothelial function with aging, Physiology (Bethesda), Vol. 29, 2014, pp. 250-64.

[45]DR Seals, EE Nagy, and KL Moreau, Aerobic exercise training and vascular function with ageing in healthy men and women, J Physiol, Vol. 597, 2019, pp. 4901-14.

[46]M Angevaren, G Aufdemkampe, HJJ Verhaar, A Aleman, and L Vanhees, Physical activity and enhanced fitness to improve cognitive function in older people without known cognitive impairment, Cochrane Database Syst Rev, 2008, pp. CD005381.

[47]JN Barnes and AT Corkery, Exercise improves vascular function, but does this translate to the brain?, Brain Plast, Vol. 4, 2018, pp. 65-79.

[48]SJE Lucas, PN Ainslie, CJ Murrell, KN Thomas, EA Franz, and JD Cotter, Effect of age on exercise-induced alterations in cognitive executive function: relationship to cerebral perfusion, Exp Gerontol, Vol. 47, 2012, pp. 541-51.

[49]ML Pedralli, B Eibel, G Waclawovsky, MI Schaun, W Nisa-Castro-Neto, D Umpierre, et al., Effects of exercise training on endothelial function in individuals with hypertension: a systematic review with meta-analysis, J Am Soc Hypertens, Vol. 12, 2018, pp. e65-e75.

[50]DH Thijssen, EA Dawson, MA Black, MT Hopman, NT Cable, and DJ Green, Brachial artery blood flow responses to different modalities of lower limb exercise, Med Sci Sports Exerc, Vol. 41, 2009, pp. 1072-9.

[51]RB Teixeira, JCB Marins, PRS Amorim, I Teoldo, R Cupeiro, MOC de Andrade, et al., Evaluating the effects of exercise on cognitive function in hypertensive and diabetic patients using the mental test and training system, World J Biol Psychiatry, Vol. 20, 2019, pp. 209-18.

[52]FO Maher, RM Clarke, A Kelly, RE Nally, and MA Lynch, Interaction between interferon γ and insulin-like growth factor-1 in hippocampus impacts on the ability of rats to sustain long-term potentiation, J Neurochem, Vol. 96, 2006, pp. 1560-71.

[53]LS Pescatello, HV MacDonald, L Lamberti, and BT Johnson, Exercise for hypertension: a prescription update integrating existing recommendations with emerging research, Curr Hypertens Rep, Vol. 17, 2015, pp. 87.

[54]LS Pescatello, R Arena, D Riebe, and PD Thompson, ACSM’s Guidelines for Exercise Testing and Prescription 9th Ed. 2014, J Can Chiropr Assoc, Vol. 58, 2014, pp. 328.

[55]YN Boutcher and SH Boutcher, Exercise intensity and hypertension: what’s new?, J Hum Hypertens, Vol. 31, 2017, pp. 157-64.

[56]D Hansen, J Niebauer, V Cornelissen, O Barna, D Neunhäuserer, C Stettler, et al., Exercise prescription in patients with different combinations of cardiovascular disease risk factors: a consensus statement from the EXPERT working group, Sports Med, Vol. 48, 2018, pp. 1781-97.

[57]VA Cornelissen and NA Smart, Exercise training for blood pressure: a systematic review and meta-analysis, J Am Heart Assoc, Vol. 2, 2013, pp. e004473.

[58]H Wen and L Wang, Reducing effect of aerobic exercise on blood pressure of essential hypertensive patients: a meta-analysis, Medicine (Baltimore), Vol. 96, 2017, pp. e6150.

[59]J Moriguchi, H Itoh, S Harada, K Takeda, T Hatta, T Nakata, et al., Low frequency regular exercise improves flow-mediated dilatation of subjects with mild hypertension, Hypertens Res, Vol. 28, 2005, pp. 315-21.

[60]HE Molmen-Hansen, T Stolen, AE Tjonna, IL Aamot, IS Ekeberg, GA Tyldum, et al., Aerobic interval training reduces blood pressure and improves myocardial function in hypertensive patients, Eur J Prev Cardiol, Vol. 19, 2012, pp. 151-60.

[61]AW Ashor, J Lara, M Siervo, C Celis-Morales, and JC Mathers, Effects of exercise modalities on arterial stiffness and wave reflection: a systematic review and meta-analysis of randomized controlled trials, PLoS One, Vol. 9, 2014, pp. e110034.

[62]GA Kelley and KS Kelley, Progressive resistance exercise and resting blood pressure: a meta-analysis of randomized controlled trials, Hypertension, Vol. 35, 2000, pp. 838-43.

[63]HV MacDonald, BT Johnson, TB Huedo-Medina, J Livingston, KC Forsyth, WJ Kraemer, et al., Dynamic resistance training as stand-alone antihypertensive lifestyle therapy: a meta-analysis, J Am Heart Assoc, Vol. 5, 2016. pii: e003231.

[64]MR Moraes, RF Bacurau, DE Casarini, ZP Jara, FA Ronchi, SS Almeida, et al., Chronic conventional resistance exercise reduces blood pressure in stage 1 hypertensive men, J Strength Cond Res, Vol. 26, 2012, pp. 1122-9.

[65]DT Beck, JS Martin, DP Casey, and RW Braith, Exercise training improves endothelial function in resistance arteries of young prehypertensives, J Hum Hypertens, Vol. 28, 2014, pp. 303-9.

[66]F Keese, P Farinatti, L Pescatello, and W Monteiro, A comparison of the immediate effects of resistance, aerobic, and concurrent exercise on postexercise hypotension, J Strength Cond Res, Vol. 25, 2011, pp. 1429-36.

[67]BA Dolezal and JA Potteiger, Concurrent resistance and endurance training influence basal metabolic rate in nondieting individuals, J Appl Physiol (1985), Vol. 85, 1998, pp. 695-700.

[68]ES Dos Santos, RY Asano, IG Filho, NL Lopes, P Panelli, D da Cunha Nascimento, et al., Acute and chronic cardiovascular response to 16 weeks of combined eccentric or traditional resistance and aerobic training in elderly hypertensive women: a randomized controlled trial, J Strength Cond Res, Vol. 28, 2014, pp. 3073-84.

[69]I Shaw, BS Shaw, GA Brown, and JF Cilliers, Concurrent resistance and aerobic training as protection against heart disease, Cardiovasc J Afr, Vol. 21, 2010, pp. 196-9.

[70]KJ Stewart, AC Bacher, KL Turner, JL Fleg, PS Hees, EP Shapiro, et al., Effect of exercise on blood pressure in older persons: a randomized controlled trial, Arch Intern Med, Vol. 165, 2005, pp. 756-62.

[71]WM Son, KD Sung, JM Cho, and SY Park, Combined exercise reduces arterial stiffness, blood pressure, and blood markers for cardiovascular risk in postmenopausal women with hypertension, Menopause, Vol. 24, 2017, pp. 262-8.

[72]G Schuler, V Adams, and Y Goto, Role of exercise in the prevention of cardiovascular disease: results, mechanisms, and new perspectives, Eur Heart J, Vol. 34, 2013, pp. 1790-9.

[73]PJ Smith, JA Blumenthal, MA Babyak, L Craighead, KA Welsh-Bohmer, JN Browndyke, et al., Effects of the dietary approaches to stop hypertension diet, exercise, and caloric restriction on neurocognition in overweight adults with high blood pressure, Hypertension, Vol. 55, 2010, pp. 1331-8.

[74]EB Larson, L Wang, JD Bowen, WC McCormick, L Teri, P Crane, et al., Exercise is associated with reduced risk for incident dementia among persons 65 years of age and older, Ann Intern Med, Vol. 144, 2006, pp. 73-81.

[75]S Rovio, I Kåreholt, EL Helkala, M Viitanen, B Winblad, J Tuomilehto, et al., Leisure-time physical activity at midlife and the risk of dementia and Alzheimer’s disease, Lancet Neurol, Vol. 4, 2005, pp. 705-11.

[76]SJ Colcombe, KI Erickson, PE Scalf, JS Kim, R Prakash, E McAuley, et al., Aerobic exercise training increases brain volume in aging humans, J Gerontol A Biol Sci Med Sci, Vol. 61, 2006, pp. 1166-70.

[77]A Deslandes, H Moraes, C Ferreira, H Veiga, H Silveira, R Mouta, et al., Exercise and mental health: many reasons to move, Neuropsychobiology, Vol. 59, 2009, pp. 191-8.

[78]RH Lipsky and AM Marini, Brain-derived neurotrophic factor in neuronal survival and behavior-related plasticity, Ann N Y Acad Sci, Vol. 1122, 2007, pp. 130-43.

[79]WJ Tyler and LD Pozzo-Miller, BDNF enhances quantal neurotransmitter release and increases the number of docked vesicles at the active zones of hippocampal excitatory synapses, J Neurosci, Vol. 21, 2001, pp. 4249-58.

[80]KI Erickson and AF Kramer, Aerobic exercise effects on cognitive and neural plasticity in older adults, Br J Sports Med, Vol. 43, 2009, pp. 22-4.

[81]KI Erickson, MW Voss, RS Prakash, C Basak, A Szabo, L Chaddock, et al., Exercise training increases size of hippocampus and improves memory, Proc Natl Acad Sci U S A, Vol. 108, 2011, pp. 3017-22.

[82]BD Eadie, VA Redila, and BR Christie, Voluntary exercise alters the cytoarchitecture of the adult dentate gyrus by increasing cellular proliferation, dendritic complexity, and spine density, J Comp Neurol, Vol. 486, 2005, pp. 39-47.

[83]L Buttler, MT Jordão, MG Fragas, A Ruggeri, A Ceroni, and LC Michelini, Maintenance of blood-brain barrier integrity in hypertension: a novel benefit of exercise training for autonomic control, Front Physiol, Vol. 8, 2017, pp. 1048.

[84]MLM Rêgo, DAR Cabral, EC Costa, and EB Fontes, Physical exercise for individuals with hypertension: it is time to emphasize its benefits on the brain and cognition, Clin Med Insights Cardiol, Vol. 13, 2019, pp. 1-10.

[85]AC Whittaker, M Delledonne, T Finni, P Garagnani, C Greig, V Kallen, et al., Physical Activity and Nutrition INfluences In ageing (PANINI): consortium mission statement, Aging Clin Exp Res, Vol. 30, 2018, pp. 685-92.

[86]L De Wit, D O’Shea, M Chandler, T Bhaskar, J Tanner, P Vemuri, et al., Physical exercise and cognitive engagement outcomes for mild neurocognitive disorder: a group-randomized pilot trial, Trials, Vol. 19, 2018, pp. 573.

[87]ML Pedralli, G Waclawovsky, A Camacho, MM Markoski, I Castro, and AM Lehnen, Study of endothelial function response to exercise training in hypertensive individuals (SEFRET): study protocol for a randomized controlled trial, Trials, Vol. 17, 2016, pp. 84.

[88]TH Westhoff, N Franke, S Schmidt, K Vallbracht-Israng, R Meissner, H Yildirim, et al., Too old to benefit from sports? The cardiovascular effects of exercise training in elderly subjects treated for isolated systolic hypertension, Kidney Blood Press Res, Vol. 30, 2007, pp. 240-7.

[89]JN Cook, AE DeVan, JL Schleifer, MM Anton, MY Cortez-Cooper, and H Tanaka, Arterial compliance of rowers: implications for combined aerobic and strength training on arterial elasticity, Am J Physiol Heart Circ Physiol, Vol. 290, 2006, pp. H1596-H600.

[90]MY Cortez-Cooper, AE DeVan, MM Anton, RP Farrar, KA Beckwith, JS Todd, et al., Effects of high intensity resistance training on arterial stiffness and wave reflection in women, Am J Hypertens, Vol. 18, 2005, pp. 930-4.

[91]N Nualnim, K Parkhurst, M Dhindsa, T Tarumi, J Vavrek, and H Tanaka, Effects of swimming training on blood pressure and vascular function in adults >50 years of age, Am J Cardiol, Vol. 109, 2012, pp. 1005-10.

[92]AL Spence, HH Carter, LH Naylor, and DJ Green, A prospective randomized longitudinal study involving 6 months of endurance or resistance exercise. Conduit artery adaptation in humans, J Physiol, Vol. 591, 2013, pp. 1265-75.

[93]CA DeSouza, LF Shapiro, CM Clevenger, FA Dinenno, KD Monahan, H Tanaka, et al., Regular aerobic exercise prevents and restores age-related declines in endothelium-dependent vasodilation in healthy men, Circulation, Vol. 102, 2000, pp. 1351-7.

[94]Y Higashi, S Sasaki, S Kurisu, A Yoshimizu, N Sasaki, H Matsuura, et al., Regular aerobic exercise augments endothelium-dependent vascular relaxation in normotensive as well as hypertensive subjects: role of endothelium-derived nitric oxide, Circulation, Vol. 100, 1999, pp. 1194-202.

[95]H Tanaka, S Shimizu, F Ohmori, Y Muraoka, M Kumagai, M Yoshizawa, et al., Increases in blood flow and shear stress to nonworking limbs during incremental exercise, Med Sci Sports Exerc, Vol. 38, 2006, pp. 81-5.

[96]DJ Green, MTE Hopman, J Padilla, MH Laughlin, and DHJ Thijssen, Vascular adaptation to exercise in humans: role of hemodynamic stimuli, Physiol Rev, Vol. 97, 2017, pp. 495-528.

[97]KM Diaz and D Shimbo, Physical activity and the prevention of hypertension, Curr Hypertens Rep, Vol. 15, 2013, pp. 659-68.

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Journal: Artery Research
Volume-Issue: 25 - 3-4
Pages: 81 - 86
Publication Date: 2019/12/17
ISSN (Online): 1876-4401
ISSN (Print): 1872-9312
DOI: 10.2991/artres.k.191203.003 How to use a DOI?
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ris enw bib

TY  - JOUR
AU  - Marinei Lopes Pedralli
AU  - Eduardo Barbosa
AU  - Pedro Guimarães Cunha
PY  - 2019
DA  - 2019/12/17
TI  - Hypertension: Protective Effects of Physical Exercise on Cognition Function, Arterial Function and Brain Health
JO  - Artery Research
SP  - 81
EP  - 86
VL  - 25
IS  - 3-4
SN  - 1876-4401
UR  - https://doi.org/10.2991/artres.k.191203.003
DO  - 10.2991/artres.k.191203.003
ID  - Pedralli2019
ER  -

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