Cardiovascular Diseases and Physical Activity

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The association is also an organizational partner in the National Physical Activity Plan Alliance and has a seat on its board of directors. Authors of the JAMA study say that while more clinical trials could help to better define the relationship between light PA and risk reduction, there's no reason to wait on promoting this type of PA. Research-related stories featured in PT in Motion News are intended to highlight a topic of interest only and do not constitute an endorsement by APTA.

For synthesized research and evidence-based practice information, visit the association's PTNow website. All Rights Reserved. June However, the effects are not consistent in humans, which may be due to the different dietary habits and living conditions [ 41 , 42 ]. It is strongly accepted and reported that exercise leads a high requirement of energy which induces decreasing of plasma TG concentrations [ 43 ].

Blood pressure is elicited by the force exerted by the blood against the blood vessels, which depends on the ejection of the heart and resistance of the blood vessels. Hypertension is another name of high blood pressure, a disease related to heart attack, stroke, heart failure, and other problems [ 44 ]. Exercise always leads to a postexercise hypotension, and both normotensive and hypertensive persons experience a transient reduction in blood pressure.

Study: Light Physical Activity Could Help to Lower Risk of Coronary and Cardiovascular Problems

The reduced magnitude may achieve the point wherein patients with hypertension recover to the normal blood pressure levels. In a meta-analysis, they investigated the effects of acute exercise on blood pressure response. There were significant changes, reduction of 4. So the meta-analysis results confirm the undoubted place of noninvasive therapy method, acute exercise.

The transient reduction only lasts for a few hours and would recover after rest. However, the benefits of physical activity cannot be ignored because of chronic treatment of exercise showing significant changes among subjects.


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The vasodilator activity leads to the decrease of blood pressure. On the contrary, increased blood pressure is caused by vasoconstriction. Moderate-intensity exercise causes a vasodilatory response and decreases the vasoconstricting response and lipid in rat aortas, which exhibits a decrease in diastolic blood pressure [ 46 , 47 ]. In addition to the vascular tone, exercise decreases blood pressure through lowering oxidative stress and inflammation levels. In the spontaneous hypertension rats SHR , exercise normalizes the increased collagen deposition and diminished fenestra size in the internal elastic lamina, meaning that exercise shows the benefit roles in normalizing the increased vascular stiffness and decreased vascular distensibility in both small mesenteric arteries and coronary arteries [ 48 ].

However, high-intensity exercise leads to the opposite effects that increased oxidative stress, elevated blood pressure, and high vasoconstrictor activity are found [ 49 ]. Some studies report that males tend to achieve greater reductions than females from the exercise training [ 50 ].

However, the authors ignore the factors of menstrual cycle in the female subjects which affect the regulation of the autonomic nervous system [ 51 ]. Studying the effects of exercise on circadian rhythms using ambulatory blood pressure monitoring, there are significant reductions of daytime BP, but no obvious changes are observed at nighttime BP [ 44 ].

Blood viscosity in normal conditions is like a Newtonian fluid which is influenced by hematocrit, shear rate of blood flow, vascular caliber, and temperature. Elevated blood viscosity which is associated with blood resistance increases risks of cardiovascular complications. Blood viscosity is decreasing during exercise accompanied by decreased systemic vascular resistance [ 52 ].

More nitric oxide NO is produced attributed to greater shear stress in exercise and promote vasodilation [ 53 , 54 ].

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During exercise, erythrocyte volume is slightly increased; however, a much higher increase of plasma volume is generated which finally results in lower blood viscosity. Decline in plasma fibrinogen level is observed under the effect of exercise which plays important roles in declining erythrocyte aggregation and decreasing blood viscosity [ 55 ]. Platelet is a small volume component in blood which has no cell nucleus generated from megakaryocytes.

Through forming thrombus, the platelets exert primary function of maintaining hemostasis of blood flow. Once an injury occurs, the platelets in the circulation will be activated and aggregated to the interrupted endothelial site to plug the hole [ 56 ]. So abnormality in platelet activation leads to a variety of atherosclerotic diseases mainly through excess thrombosis in small arteries like coronary arteries and blood vessels of the brain [ 57 ].

Exercise training presents an antithrombotic manner through platelet functional regulation. Through enhancing blood flow, exercise enhances endothelial NO production which counteracts platelet activation [ 58 ]. The moderate physical activity decreases both platelet adhesion and aggregation through downregulating intracellular calcium levels and increasing cGMP levels [ 59 ]. It is recommended by government guidelines that physical activity is an effective way to prevent thrombosis [ 60 ]. Exercise is also used to improve chronic complications of deep venous thrombosis, postthrombotic syndrome.

A six-month exercise training markedly increases leg strength, hamstring and gastrocnemius flexibility, and overall fitness [ 61 ]. However, studies showed that the strenuous short-term exercise activated platelets and promoted aggregation of platelets, thus increasing the risk of MI or cardiac arrest. This suggests that acute exhausting exercise may trigger clot formation, but the mechanisms remain to be clarified [ 62 ]. NO is a gaseous signaling molecule playing an irreplaceable role in a variety of biological processes. It is catalyzed by various nitric oxide synthase NOS enzymes by using substrate L-arginine.

Known as an endothelial-derived relaxing factor, NO contributes to not only endothelial-dependent relaxation EDR but also to the maintenance of endothelial function [ 63 ]. The endothelium is a single layer of cells in the intima of vessels separating blood from the tissue.

The functions of the endothelium involve regulating angiogenesis, balancing vasoconstriction and vasodilation, adjusting smooth muscle cell proliferation, and excreting endocrine. The intact endothelium acts an indispensable role in vessel homeostasis [ 64 ]. In a cross-sectional study with healthy individuals, L-arginine was reduced and production of NO was increased after exercise training [ 46 ]. The mechanisms may be partial that exercise training leads to increased blood flow and shear stress, contributing to endothelial NOS eNOS expression, NO release, and artery relaxation.

In blood vessels, PKG activation always induces relaxation and regulates blood pressure. In the heart, PKG works as a brake on stress response signaling [ 65 ]. Increased NO production usually facilitates angiogenesis and vascular permeability. However, chronic exercise improves endothelial function through releasing NO in the aorta. Interestingly, exercise does not affect the vascular function in normal rats administrated with L-arginine but improves vascular function in the aortas from diabetic rats [ 68 ].

In the high fat-induced obese mice, impaired EDR, reduced NO bioavailability, and decreased phosphorylation of eNOS are found in the coronary arteries which can be normalized by exercise. After 4 weeks of exercise training, the eNOS expression did not change, but the phosphorylation of serine residue with an activating impact on eNOS was increased and the phosphorylation at threonine residue with an inhibitory impact on eNOS was decreased.

Through binding to leptin receptors on hypothalamic cells, leptin inhibits hunger, prevents weight gain, and promotes positive energy balance [ 70 ]. So leptin deficiency or leptin resistance promote diabetes, obesity, and other metabolic disorders. Exercise improves leptin resistance and sensitivity, attenuates body weight, and promotes homeostatic control of energy balance through influencing the leptin receptor in the ventromedial hypothalamic nucleus of obese mice [ 71 , 72 ].

It also directly works on leptin receptors to induce NO-dependent vasodilation expressed in endothelial cells [ 73 ]. A decreased leptin sensitivity and hyperleptinaemia are found in obese mice coronary arteries, demonstrating leptin resistance and low leptin sensitivity. Exercise maintains leptin sensitivity of obese mice and preserves leptin receptor, thus exerting endothelial protection [ 74 ]. Exercise facilitates SOCS3 expression and improves leptin resistance in the liver and muscle of high-fat diet-induced rats [ 75 ]. Leptin sensitivity is restored by exercise manifested as facilitating fatty acid toward oxidation and away from triacylglycerol stores [ 76 ].

Shapiro et al. Besides, wheel running for obese rats was insufficient to lower body weight. However, combinational administration of exercise and exogenous leptin dramatically induced weight loss and improved leptin sensitivity [ 78 ]. That means exercise may directly activate leptin signaling pathway or improve leptin sensitivity via coordinating with other therapeutic methods. The autonomic nervous system, regulated by the hypothalamus, consists of sympathetic nervous system, parasympathetic nervous system, and enteric nervous system.

The primary autonomic functions include cardiac regulation, control of respiration, and vasomotor activity, which act largely unconsciously [ 79 ]. Exercise training has beneficial roles in autonomic function, as indicated by improved heart rate recovery HRR and heart rate variability HRV in various populations, such as in sedentary individuals and chronic heart failure patients [ 80 ]. HRR refers to the declining rate of heart rate and is recognized as an indicator of cardiac prognosis [ 81 ].

HRV is defined as consecutive heart beat variations in heart rate of sinus rhythm. Reduced HRV represents attenuation of autonomic regulation of sinoatrial node [ 82 ]. BRS is regulated by sympathetic and parasympathetic autonomic nerves and is downregulated when there is cardiac autonomic neuropathy [ 83 ]. Electrocardiogram is a noninvasive way to determine cardiac conditions.

Physical Activity with Cardiovascular Disease

Elevated R wave amplitudes and widened QT intervals are reliable predictors of autonomic neuropathy. Exercise training lowers heart rate and reduces QT interval and R wave amplitudes on electrocardiogram in the diabetic fatty rat model [ 84 ]. In myocardial-infarcted rats, structural remodeling leads to heterogeneity which causes slow conduction and creates the generation of arrhythmias. However, exercise training increases ratio of parasympathetic over sympathetic tones and decreases probability of ventricular arrhythmias of the MI rats [ 85 ]. The mechanism of exercise-induced improvement of arrhythmia might be related to intrinsic electrophysiological cardioadaptive mechanisms because of decreased action potential duration gradient between epicardial and endocardial cells in the exercise-trained rats [ 86 ].

The mechanisms by which exercise improves autonomic function and preserves neurovascular perfusion might be related to increasing NO bioavailability, lowering angiotensin II AngII levels, and suppressing chronic inflammation [ 87 — 90 ]. It is controversial that some studies show that MI, stroke, ventricular tachycardia, or fibrillation can be elevated during the progress of physical activity, so further studies about the duration, frequency, and intensity need to be specifically investigated.

ROS of physiological levels are responsible for signaling molecules to regulate normal physical activities. ROS overproduction, decreased antioxidant enzymes, and the downstream targets damage the subcellular organelles, thus impairing the cardiovascular system.

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ROS also initiates inflammation with the activation of redox-sensitive transcription factors and promotes expression of inflammatory molecules [ 93 ]. Exercise attenuates oxidative damage in the blood vessel, heart, brain, liver, skeletal muscle, and other organs. Exercise reduces age-related mitochondrial oxidative damage and increases mitochondrial NADH-cytochrome C reductase activity in the heart of aged rats [ 95 ].

By improving the antioxidant enzymes and redox status in many organs and pathologies, the chronic treadmill exercise has an anti-inflammatory effect. In renovascular hypertensive rats, ROS released by vascular endothelial cells impairs EDR by decreasing NO production and facilitating vasoconstriction.

Evidences indicate that exercise reduces ROS, improves endothelial function, and increases levels of elastin, fibrillin, and NO. BRS is improved by physical activity through reducing oxidative stress in the rostral ventrolateral medulla to inhibit the sympathetic nerve [ 98 , 99 ]. In diabetic rats, the overproduction of ROS leads to the abnormal aortic function and metabolic disorder.

Through exercise training, enzymes producing ROS such as p67phox protein decrease and the enzymes taking part in scavenging oxygen-free radicals, like superoxide dismutase SOD 1, SOD2, catalase, and glutathione peroxidase GPX , are normalized, even increased [ 48 , ]. That means, all the proteins taking part in oxidative stress tend to recover to normal levels after exercise treatment [ ]. Exercise increases thioredoxin reductase 1 and decreases thioredoxin-interacting protein TXNIP in blood mononuclear cells and skeletal muscles, which promote antioxidant ability and eliminate free radical [ , ].

TXNIP is a regulator of cellular redox signaling by binding thioredoxin to inhibit the neutralization of ROS, indirectly enhancing the oxidative stress [ ]. Nuclear factor erythroid 2-like factor 2 Nrf2 is reported to be an important transcription factor that performs antioxidant defense mechanisms through Nrf2-ARE signaling to activate antioxidant gene expression [ ].

Based on these risk factors and studies, all major cardiovascular societies recommend that a minimum of 5 days a week of exercise, with at least 30 minutes of moderate-intensity aerobic activity, is needed to prevent CVD [ ]. Because of low-cost, low-risk, and nondrug intervention, the European Society of Cardiology recommended that exercise training should be provided by cardiac rehabilitation programs in patients with non-ST elevation acute coronary syndrome in [ ]. However, the exercise intensity differs between people depending on the physical condition of individuals [ ]. Although lots of studies show a positive correlation between exercise and good health, a thorough physical evaluation is necessary before an intensive exercise training program.

The intensity, mode, duration, and frequency of exercise can strongly affect outcome. Aerobic exercise is defined as using aerobic metabolism to extract energy in muscles, mainly referring to low- to moderate-intensity physical activities. As discussed above, aerobic exercise has favorable effects on lipid metabolism, cardiac remodeling, post-MI heart failure, insulin resistance, and endothelial function. Anaerobic exercise is an activity that synthesize energy sources without using oxygen as energy sources but glycolysis and fermentation.

Anaerobic exercise usually refers to high-intensity training, including sprinting and power lifting. Similar to aerobic exercise, anaerobic exercise also shows positive influences on body mass index and blood pressure [ ]. In some cases, high-intensity training shows more beneficial effects on the cardiovascular system and EDR compared to low-intensity training [ ]. However, there is a paradox of disadvantages about anaerobic exercise training that the elevated mortality and sudden death are brought by high-intensity activity.

A well-recognized viewpoint is that acute strenuous exercise increases the risks for cardiovascular diseases, like MI, by upregulating blood pressure [ 57 ]. In conclusion, intensive exercise should be intermittent especially for a long-term program. Professional supervision and guidance are indispensable when you conduct high-intensity exercise. The general recommended exercise intensity for humans from the American Heart Association to prevent CVD is 30 minutes, 5 times a week to reach at least minutes per week of moderate exercise, or 25 minutes, 3 times a week to reach at least 75 minutes per week of vigorous activity.

Individuals can choose one way of physical activity or combine moderate and vigorous activities. They will also be benefited even if they divide the entire time into several parts of 10 to 15 minutes per day. For those who want to lower the risk for heart attack and stroke, 40 minutes of moderate to vigorous intensity aerobic activity, 3 or 4 times a week, is recommended [ ].

Moderate-intensity exercise is more widely performed among people who are interested in exercise and enjoy rest time. Various studies show that the duration of physical activity but not intensity is the primary factor leading to benefits for humans [ ]. Physical activity is regarded as an efficient way to prevent and counteract age-related changes in muscle and organic function [ ].

As we know, any activity is better than none and it is never too late to start for the elders [ ]. The American College of Sports Medicine and the American Heart Association recommend detailed description for elder people that 30 minutes, 5 times a week, of moderate intensity, or 20 minutes, 3 times a week, of vigorous intensity activity is good for aging-related diseases.

Strength training should be included to enhance muscle groups and prevent falls as exercises with repetitions, twice a week [ ]. For the elders, joining exercise classes to improve balance and prevent falls are strongly suggested [ ]. Exercise is generally safe for older people unless for those elders who already suffered from health problems doing resistance training [ ]. Examples of aerobic exercise include cycling, dancing, hiking, treadmill, climbing stairs, swimming, walking, and any activities the criterion is that you can talk without breathing too hard.

Anaerobic exercise refers to sprinting and power lifting accompanied by accumulation of lactic acid causing muscular fatigue [ ]. However, the definition of moderate and vigorous exercise varies between individuals because the indispensability to measure the level of intensity bases on your fitness and overall health.

Many people are robbed by the thinking all-or-nothing when doing exercise. However, the low-level intensity training program could benefit you as long as you begin to change. Even the easiest activity is better than nothing and whenever you start is not too late [ ]. The existing studies do not provide an exact guidance on the diverse intensity, duration, and frequency of exercise that may be suitable for the different kinds of diseases.

In the future, personalization of exercise will be an irresistible trend. For those young and in healthy condition, it may be optional to consult a doctor before they start an exercise program. However, personalized exercise enables you to perform more specifically based on your present fitness level, interest, age, and gender [ ]. For those old who have been inactive for a long period, it is necessary to consult physicians who will measure some indexes, like cardiorespiratory endurance, muscular strength, muscular endurance, and flexibility, and make graded exercise tests for individuals [ ].

Also, for someone who has a baseline disease, the extreme exercise training seems to trigger the progression of disease. So tailored exercise would bring benefits not only for healthy humans but also for the patients with chronic disease [ ]. For slow disease-related declines of muscle strength, tailored exercise may focus on the training to improve muscle strength and reduce the risk of falls. For those who has type 2 diabetes, body weight control and enhancement of peripheral circulation are the first two goals to realize.

For people with arthritis, tailored exercise helps reduce joint stiffness and enhances muscle strength [ , ]. The systematical and overall exercise guidance from a professional instructor is totally necessary. Personalization of exercise training will be a huge demand and replace the random mode of exercise today. Although we get to know that exercise protects against CVD through attenuating sympathetic activity, arterial pressure, and heart rate, increasing blood flow and endothelial NO production, causing vessel dilation, decreasing inflammatory cytokine and reactive oxygen species formation, the exact mechanisms leading to transcriptional factor changes or transcriptional modifications are not studied.

So future studies may be applied to the mechanisms of protective effects of exercise on the heart and vessels. The authors declare that there is no conflict of interests regarding the publication of this paper. Oxidative Medicine and Cellular Longevity. Indexed in Science Citation Index Expanded. Journal Menu. Special Issues Menu. Subscribe to Table of Contents Alerts.

Table of Contents Alerts. Danyang Tian 1 and Jinqi Meng 2. Abstract This review is aimed at summarizing the new findings about the multiple benefits of exercise on cardiovascular disease CVD. Cardiovascular Diseases: Prevalence and Risk Factors CVD is a class of diseases which are related to the heart or blood vessels including stroke, heart failure, hypertension, coronary artery diseases, heart arrhythmia, peripheral artery disease, and atherosclerosis [ 1 ].

Mechanisms of Action for Physical Exercise Many considerable evidences support the therapeutic and protective effects of exercise on the body, including improvement of insulin sensitivity of diabetic mice, attenuating sympathetic activity, arterial pressure, and heart rate in the spontaneously hypertensive rats [ 24 ]. Insulin Sensitivity and Blood Glucose Control Type 2 diabetes mellitus is a kind of chronic disease characterized by obesity, hyperglycemia, impaired insulin secretion, and insulin resistance [ 26 ].

Lipid Profile Cholesterol is a soft waxy fat that our body needs to function well. Blood Pressure Blood pressure is elicited by the force exerted by the blood against the blood vessels, which depends on the ejection of the heart and resistance of the blood vessels. Blood Viscosity, Platelet Aggregation, and Thrombosis Profile Blood viscosity in normal conditions is like a Newtonian fluid which is influenced by hematocrit, shear rate of blood flow, vascular caliber, and temperature.

Endothelial NO Production NO is a gaseous signaling molecule playing an irreplaceable role in a variety of biological processes. Modulation of Autonomic Function The autonomic nervous system, regulated by the hypothalamus, consists of sympathetic nervous system, parasympathetic nervous system, and enteric nervous system. Antioxidant Defense ROS of physiological levels are responsible for signaling molecules to regulate normal physical activities.

The Recommendations for Physical Activity Because of low-cost, low-risk, and nondrug intervention, the European Society of Cardiology recommended that exercise training should be provided by cardiac rehabilitation programs in patients with non-ST elevation acute coronary syndrome in [ ]. Future Perspectives Many people are robbed by the thinking all-or-nothing when doing exercise.

Conflicts of Interest The authors declare that there is no conflict of interests regarding the publication of this paper. References J. Yong, D. Lin, and X. Hu, Q. Wu, D. Hu, and T. Jiang, F. Mao, Y. Li et al. Ortega, C. Lavie, and S.

Akil and H. Abdelaal, C. Leon and T.

Physical Activity

Grundy, I. Benjamin, G.

Burke et al. Kosiborod, M. Gomes, A. Nicolucci et al. Steenman and G. North and D. Importantly, the influence of regular physical activity on cardiovascular health determinants eg, functional capacity is transient, with a rapid decline on stopping regular physical activity. Further, more substantial health gains are likely to be achieved with appropriate concomitant pharmacological therapy. Notwithstanding the functional and quality-of-life gains, the evidence for survival benefits from habitual physical activity for people with CVD is drawn from studies with some limitations.

Studies mostly involve men undertaking light-to-moderate intensity structured exercise, with varying degrees of supervision, and ongoing medical review. Most studies pre-date the recent major interventional and pharmacological advances in CVD management.

Further research is warranted to confirm the survival benefit with physical activity in those with CVD receiving contemporary medical therapy. The benefits of physical activity clearly far outweigh the risks, with a particularly low prevalence of musculoskeletal injury for walking, gardening and cycling. Where doctors feel unable to provide detailed advice, they may of course refer the patient to tertiary services for advice. Any pre-activity evaluation should involve a medical review, physical examination and a history of physical activity to ensure there is no contraindication to becoming more active.

Further, patients should be taking relevant pharmacological therapies and reducing their overall coronary risk profile, in accordance with national guidelines. If there is uncertainty about the safety of physical activity, or if the patient aspires to regular vigorous exercise, exercise stress testing should be considered, preferably with echocardiography or radionuclide scintigraphy. Supervision may be beneficial to reduce anxiety, monitor symptoms and arrhythmias, and establish appropriate physical activity intensity after an acute cardiovascular event or vessel revascularisation.


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For those with severe or uncontrolled clinical CVD Box 3 , medical evaluation and review of prescription medicines is warranted before beginning physical activity. Concomitantly, clinical advice should be given to cease physical activity when indicated Box 3. Sedentary people should be encouraged to build up gradually from a low intensity to the recommended dose of physical activity. Progression will be slower for those with advanced CVD or comorbidities. Initially, emphasise frequency through the day and number of days followed by duration.

Longer disruptions associated with disease progression or new comorbidities will require greater modulations in dose, including brief abstinence in some cases. For specific practical or special considerations pertaining to engaging in regular physical activity or resumption of sports participation, see the complete guidelines. After an acute cardiovascular event, many people may need outside help to achieve appropriate levels of physical activity. People with well compensated, clinically stable CVD, including those with implantable cardiac devices, and congenital and valvular heart disease, should progress over time to the recommended physical activity dose 13 LOE panel consensus, GOR D.

People with advanced CVD or severely impaired functional status should progress toward the recommended dose of physical activity after first having achieved lower categories of exercise less intense, shorter duration, less frequent interim targets, preferably under supervision 3 LOE panel consensus, GOR D. People who have recently had surgery or angioplasty, with or without stenting for CVD, should be advised to curtail any structured physical activity for several days, or longer in the case of wound infection or a large postprocedural haematoma.

Ideally, these should be implemented under the guidance of an exercise professional and initially supervised. B: Body of evidence can be trusted to guide practice in most situations. C: Body of evidence provides some support for recommendation s , but care should be taken in its application. D: Body of evidence is weak, and recommendation must be applied with caution.

Honorary representatives of the Heart Foundation National Physical Activity Committee who contributed included Professor Bill Bellew health promotion , Professor Adrian Bauman public health; comments provided in absentia and Professor Wendy Brown chair; physical activity. Publication of your online response is subject to the Medical Journal of Australia 's editorial discretion. You will be notified by email within five working days should your response be accepted. Basic Search Advanced search search. Use the Advanced search for more specific terms. Title contains.

Body contains. Date range from. Date range to. Article type. Author's surname. First page. Short reports. Guidelines and statements. Narrative reviews. Ethics and law. Medical education. Position statement. Volume Issue 2. Physical activity for people with cardiovascular disease: recommendations of the National Heart Foundation of Australia.

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