The two articles below are from American College of Sports Medicine and are position stands. Both of these articles are helpful for the heart patient to understand in the care and prevention of heart conditions. A couple of things to point out to the rehabilitating heart patient would be, the expected drop in blood pressure from exercise is 5-7 mmHg, but can remain lower for quite some time afterwards. This is why you must be alert for dizziness, lightheadedness, fainting, especially after getting up from lying or seated positions.
The article mentions controlled hypertension.Understand you blood pressure as there are levels of hypertension mild moderate and severe. Exercise is not recommended when blood pressure is elevated in the severe ranges. Most should focus their effort in keeping the intensity mild to moderate. This is harder than you think keeping exercise light to moderate, be patient.
The second article, yes there are risks involved with exercise and they can be life threatening. What can you do to lower the risk? The intensity of exercise is important to understand. Learn about MET levels and exercise intensity here after you finish reading the article.
Hypertension (HTN), one of the most common medical disorders, is associated with an increased incidence of all-cause and cardiovascular disease (CVD) mortality. Lifestyle modifications are advocated for the prevention, treatment, and control of HTN, with exercise being an integral component. Exercise programs that primarily involve endurance activity prevent the development of HTN and lower blood pressure (BP) in adults with normal BP and those with HTN. The BP lowering effects of exercise are most pronounced in people with HTN who engage in endurance exercise with BP decreasing approximately 5-7 mm Hg after an isolated exercise session (acute) or following exercise training (chronic). Moreover, BP is reduced for up to 22 h after an endurance exercise bout (e.g., postexercise hypotension), with the greatest decreases among those with the highest baseline BP.
The proposed mechanisms for the BP lowering effects of exercise include neurohumoral, vascular, and structural adaptations. Decreases in catecholamines and total peripheral resistance, improved insulin sensitivity, and alterations in vasodilators and vasoconstrictors are some of the postulated explanations for the antihypertensive effects of exercise. Emerging data suggest genetic links to the BP reductions associated with acute and chronic endurance exercise. Nonetheless, definitive conclusions regarding the mechanisms for the BP reductions following endurance exercise cannot be made at this time.
Individuals with controlled HTN and no CVD or renal complications may participate in an exercise program or competitive athletics, but should be evaluated, treated, and monitored closely. Preliminary peak or symptom-limited exercise testing may be warranted, especially for men over 45 and women over 55 yr planning a vigorous exercise program (i.e., ≥ 60% V̇O2R, oxygen uptake reserve). In the interim, while formal evaluation and management are taking place, it is reasonable for the majority of patients to begin moderate intensity exercise training (40-<60% V̇O2R) such as walking. When pharmacologic therapy is indicated in physically active people it should, ideally: a) lower BP at rest and during exertion; b) decrease total peripheral resistance; and, c) not adversely affect exercise capacity. For these reasons, angiotensin converting enzyme (ACE) inhibitors (or angiotensin II receptor blockers in case of ACE inhibitor intolerance) and calcium channel blockers are currently the drugs of choice for recreational exercisers and athletes who have HTN.
Exercise remains a cornerstone therapy for the primary prevention, treatment, and control of HTN. The optimal training frequency, intensity, time, and type (FITT) need to be better defined to optimize the BP lowering capacities of exercise, particularly in children, women, older adults, and certain ethnic groups. Based upon the current evidence, the following exercise prescription is recommended for those with high BP:
Frequency: on most, preferably all, days of the week
Intensity: moderate-intensity (40-<60% of V̇O2R)
Time: ≥ 30 min of continuous or accumulated physical activity per day
Type: primarily endurance physical activity supplemented by resistance exercise
Habitual physical activity reduces coronary heart disease events, but vigorous activity can also acutely and transiently increase the risk of sudden cardiac death and acute myocardial infarction in susceptible persons. This scientific statement discusses the potential cardiovascular complications of exercise, their pathological substrate, and their incidence and suggests strategies to reduce these complications. Exercise-associated acute cardiac events generally occur in individuals with structural cardiac disease. Hereditary or congenital cardiovascular abnormalities are predominantly responsible for cardiac events among young individuals, whereas atherosclerotic disease is primarily responsible for these events in adults. The absolute rate of exercise-related sudden cardiac death varies with the prevalence of disease in the study population. The incidence of both acute myocardial infarction and sudden death is greatest in the habitually least physically active individuals. No strategies have been adequately studied to evaluate their ability to reduce exercise-related acute cardiovascular events. Maintaining physical fitness through regular physical activity may help to reduce events because a disproportionate number of events occur in least physically active subjects performing unaccustomed physical activity. Other strategies, such as screening patients before participation in exercise, excluding high-risk patients from certain activities, promptly evaluating possible prodromal symptoms, training fitness personnel for emergencies, and encouraging patients to avoid high-risk activities, appear prudent but have not been systematically evaluated.
Regular physical activity is widely advocated by the medical community in part because substantial epidemiological, clinical, and basic science evidence suggests that physical activity and exercise training delay the development of atherosclerosis and reduce the incidence of coronary heart disease (CHD) events (1-4). Nevertheless, vigorous physical activity can also acutely and transiently increase the risk of acute myocardial infarction (AMI) and sudden cardiac death (SCD) in susceptible individuals (5-7). This scientific statement presents the cardiovascular complications of vigorous exercise, their pathophysiological substrate, and their incidence in specific patient groups and evaluates strategies directed at reducing these complications. The goal is to provide healthcare professionals with the information they need to advise patients more accurately about the benefits and risks of physical activity.
Most studies of exercise-related cardiovascular events have examined events associated with sports participation in young subjects and with vigorous exercise in adults. Vigorous exercise is usually defined as an absolute exercise work rate of at least 6 metabolic equivalents (METs), which is historically assumed to equal an oxygen uptake (V˙O2) of 21 mL·kg-1·min-1. Six METs approximates the energy requirements of activities such as jogging. Six METs is an arbitrary threshold and does not account for the fact that the myocardial oxygen demands of any physical activity are more closely related to the V˙O2requirements relative to maximal exercise capacity than to the absolute work rate per se. Consequently, exercise work rates < 6 METs may still place considerable stress on the cardiovascular systems of unfit and older individuals.