Number 26, 2005
Cardiovascular effects of exercise

Risks and benefits of exercise in cardiac disease

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Neil Smart, Thomas H. Marwick
University of Queensland, Brisbane, Australia
Correspondence: Mr Neil Smart, University of Queensland Department of Medicine, Princess Alexandra Hospital, Brisbane, Qld 4102, Australia.
Tel: +61 732405346, fax: +61 732405399, e-mail: nsmart@soms.uq.edu.au

Background
Exercise training became a component of cardiac rehabilitation 30 years ago. Subsequent data have shown that exercise is considered beneficial for cardiac patients in terms of improved mortality, morbidity, quality of life, functional capacity, and cardiac and vascular function [1]. Nevertheless, some health professionals remain skeptical about inherent risks of training, despite higher levels of fitness being associated with lower risk of all-cause and cardiac mortality in healthy, hypertensive, normotensive, and diabetic [2] cohorts.
We sought evidence of the relative merits and hazards of exercise training for cardiac patients (Table I). MEDLINE, Medscape, and the Cochrane Controlled Trials Registry were searched for meta-analyses, systematic reviews and individual studies of exercise training in cardiac patients. Data relating to training procedures and outcomes were reviewed.

Table I. Commonly reported benefits and risk of exercise in cardiac patients.

Exercise therapy after myocardial infarction

Mortality and morbidity benefits
Two recent meta-analyses of cardiac rehabilitation programs reported the findings summarized in Table II [3,4]. The reduction in overall and cardiac mortality ranges from 20% to 30%, with little difference between comprehensive rehabilitation and exercise training only. In a meta-analysis of patients undergoing cardiac rehabilitation, quality-of-life assessment was unequivocal in demonstrating benefit, which was shown by 18 different instruments used in 11 studies [4]. The effect of rehabilitation on rates of revascularization could not be determined by meta-analysis because of the small number of studies and heterogeneity between trials [3].

Table II. Findings from two recent meta-analyses of cardiac rehabilitation.

Exercise training compared with lifestyle guidance
A recent analysis [4] showed that comprehensive cardiac rehabilitation was not clearly superior to exercise only. To an extent, this is surprising, as cessation of smoking may reduce all-cause mortality by 36% in coronary artery disease [5], although this appears substantial compared with therapies such as decreasing cholesterol. Perhaps the explanation for similar effects of exercise training and control of risk factors is that the former may effect the latter. Indeed, a 12-month German study of coronary artery disease showed exercise training to provide superior event-free survival and exercise capacity at lower cost (from reduced rates of admission to hospital and repeat revascularizations) compared with angioplasty [6].

Patients with heart failure

Mortality
Table III summarizes findings from two recent reviews of exercise training in patients with heart failure [7,8].

Table III. Findings from two meta-analyses of exercise training in patients with heart failure.

Functional capacity
Peak oxygen consumption (VO₂) remains a strong independent predictor of cardiac mortality in men and women: values greater than 13–14mL/kg per min may confer a 50% reduction in cardiac mortality, whereas a 1mL/kg per min increase may be associated with a 10% lower cardiac mortality [9]. Both resistance and aerobic exercise promote 15–17% increments in peak VO₂ in patients with heart failure [10]. In patients undergoing cardiac rehabilitation, increments of 35–50% in peak VO₂ are possible in compliant patients with initial peak metabolic equivalent of task units (METS) less than 5 [11].

Quality of life
A recent review of changes in quality of life after exercise training in patients with heart failure reported significant increments in 11 of 16 studies [10].

Exercise for preclinical disease

Effects of aging
Current evidence supports a 10% per decade decline in functional capacity of men and women, regardless of activity level. The decline may be due to reductions in maximal heart rate and lean body mass. Exercise training does not influence declines in maximal heart rate, but lean body mass can be maintained [12].

Diabetes
The STENO-2 study (Multifactorial Intervention and Cardiovascular Disease in Patients with Type 2 Diabetes) [13] showed a significant (50%) reduction in relative risk in those who underwent lifestyle modification including exercise training. Stratified analyses indicate that both physical inactivity and adiposity are important determinants of the risk of mortality in diabetic men, and this association was independent of body mass index [14]. Exercise training in patients with type 2 (non insulin-dependent) diabetes mellitus improves baroreflex sensitivity, exercise capacity, muscle strength and glucose control. These beneficial effects in refractory autonomic regulation and glucose control may be associated with the improved prognosis in type 2 diabetes [15].

Obesity
Generally, exercise training does not expend many calories, suggesting that modification of risk factors may be effectively achieved by a combination of dietary and exercise interventions. However, in the short term, body weight reduction has been shown to be able to modify the autonomic profile favorably in a population of normotensive, severely obese individuals. The reduction in heart rate and increased parasympathetic activity may contribute consistently to reducing the risk of cardiovascular morbidity and sudden cardiac death in this group of patients [16].

Hypertension
Exercise training of patients with hypertension may help to control their hypertension and regress left ventricular hypertrophy [17].

Risks

Strategies to minimize exercise-induced events
Exercise training, 4 weeks after myocardial infarction, has been performed without complication [18]. After an uncomplicated recovery period, 4–6 weeks after an event (myocardial infarction or an episode of heart failure) may be the optimum time to begin exercise.
Supervised outpatient trials may produce better rates of adherence than home exercise, possibly because of poor motivation and concerns about safety [19]. Strategies improving compliance with home exercise require regular contact with the patient and methods of verifying the patient's adherence to the regimen. Nevertheless, it is possible to sustain peak VO₂ and quality of life in a ‘home’ exercise program 12 months after discharge from cardiac rehabilitation [20]. A tailored exercise program may optimize health benefits while minimizing the risk of exertional events. Periodic measurement of functional capacity, either directly or indirectly, may protect against under- or overestimation of the optimal training intensity.

Risks of cardiac events or death
The additional risk of cardiac arrest from exercise has been estimated subjectively at 100-fold during or after vigorous exertion [21]. Table IV summarizes the findings of large analyses in three groups of patients.

Table IV. Risk of sudden death in exercise training of cardiac patients.

Mechanisms of risk
A high-intensity (90% peak VO₂) exercise-induced platelet hypercoagulable state may increase the risk of acute and fatal cardiac events [22]. However, evidence exists that low-intensity (55% peak VO₂) exercise does not present a risk of thrombosis.
After cardiac rehabilitation, statistically significant reductions in QT and JT dispersion have been reported. These may reduce the subsequent risks of malignant ventricular arrhythmias and sudden cardiac death [23].

Conclusions
Exercise training is safe and effective in reducing cardiac deaths and admissions to hospital, improving functional capacity, quality of life and cardiac risk factors in cardiac patients. However, the populations studied have been predominantly male and middle aged, and the ethnic origin of participants has seldom been reported. Nonetheless, the failure of many cardiac patients to be referred for exercise rehabilitation represents a lack of application of evidence-based medicine. ?

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REFERENCES

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