Evidence-based risk assessment and recommendations for exercise testing and physical activity clearance in apparently healthy individuals
Publication: Applied Physiology, Nutrition, and Metabolism
29 July 2011
Abstract
Increased physical activity (PA) is associated with improved health and quality of life in the general population. A dose–response effect is evident between increasing levels of PA participation and a lower relative risk for cardiovascular disease and all-cause mortality. However, there is also clear evidence that PA acutely increases the risk of an adverse cardiovascular (CV) event and sudden cardiac death (SCD) significantly above levels expected at rest. Adverse CV events during PA may be triggered acutely by the physiological stress of exercise. This investigation will review the available literature describing the CV risks of exercise testing and PA participation in apparently healthy individuals. A systematic review of the literature was performed using electronic databases, including Medline, CINAHL, SPORT discus, EMBASE, Cochrane DSR, ACP Journal Club, and DARE; additional relevant articles were hand-picked and the final grouping was used for the review using the AGREE process to assess the impact and quality of the selected articles. Six hundred and sixteen relevant articles were reviewed with 51 being identified as describing adverse CV events during exercise and PA. Data suggests the risks of fatal and nonfatal events during maximal exercise testing in apparently healthy individuals rarely occur (approximately <0.8 per 10 000 tests or 1 per 10 000 h of testing). The incidence of adverse CV events is extremely low during PA of varying types and intensities, with data limited almost exclusively to fatal CV events, as nonfatal events are rarely reported. However, this risk is reduced by 25%–50% in those individuals who have prior experience with increased levels of PA, particularly vigorous PA. Throughout a wide age range, the risk of SCD and nonfatal events during PA remain extremely low (well below 0.01 per 10 000 participant hours), but both increasing age and PA intensity are associated with greater risk. In most cases of exercise-related SCD, undetected pre-existing disease is present and SCD is typically the first clinical event. The risks of an adverse CV event during exercise testing and PA are rare and are outweighed by the health benefits. Given this risk-benefit relationship, the PAR-Q is an appropriate method to identify those at higher risk across a wide age span and should be used in conjunction with appropriate clinical guidelines for guiding individuals towards graduated PA. There are not adequate data to describe the risks of PA in those individuals considered to be at higher risk but without cardiovascular disease.
Résumé
L’augmentation de la pratique de l’activité physique (PA) est associée à une meilleure santé et à une meilleure qualité de vie chez les gens en général. On observe une relation dose–réponse entre l’augmentation de la pratique de la PA et la diminution du risque relatif de maladie cardiovasculaire et de mortalité, toutes causes confondues. En revanche, les études démontrent que la PA augmente significativement dans l’immédiat le risque de trouble cardiovasculaire (CV) et de mort subite d’origine cardiaque (SCD) comparativement à ce qu’on prévoit au repos. Les troubles CV associés à la pratique de l’activité physique sont probablement déclenchés par le stress physiologique associé à l’effort. Cet article présente le bilan des études sur les risques CV des tests d’effort et de la pratique de l’activité physique chez des personnes asymptomatiques. L’analyse documentaire systématique est réalisée dans les bases de données suivantes : Medline, CINAHL, SPORT discus, EMBASE, Cochrane DSR, ACP Journal Club et DARE. D’autres articles localisés manuellement sont ajoutés à l’ensemble. Afin d’évaluer l’impact et la qualité des articles, on en fait l’analyse au moyen de la grille AGREE. Des 616 articles pertinents analysés, 51 présentent des troubles CV associés à l’effort physique. D’après les données obtenues, le risque d’accident fatal ou non au cours d’une épreuve d’effort maximal chez des personnes asymptomatiques est minime; il est inférieur à environ 0,8/10 000 tests, soit 1/10 000 h d’évaluation. L’incidence des troubles CV au cours de la pratique de divers types d’activité physique d’intensités variées est très faible; en fait, on ne rapporte essentiellement que les événements CV fatals, car les incidents non fatals sont très peu rapportés. Néanmoins, le risque diminue de 25 % à 50 % chez les personnes ayant un vécu en matière de PA d’intensité élevée, activité physique particulièrement vigoureuse. Même sur une tranche d’âge élargie, le risque de SCD et d’incidents non fatals au cours d’une activité physique est extrêmement faible (bien inférieur à 0,01/10 000 heures de participation); le risque augmente néanmoins avec l’âge et l’intensité de l’activité physique. Dans la plupart des cas de SCD associée à l’exercice physique, on note la présence d’une maladie présente avant l’incident, mais qui n’était pas diagnostiquée; la SCD est dès lors le premier accident clinique. Le risque de troubles CV au cours d’un test à l’effort et au cours de la pratique d’une activité physique est rare et les bénéfices sur le plan de la santé sont nettement supérieurs. Du fait de cette relation entre le risque et les bénéfices, on devrait se servir du Q-AAP pour dépister les individus à haut risque sur une large tranche d’âge; de plus, on devrait l’utiliser de concert avec les recommandations pour la pratique clinique à l’intention des individus augmentant graduellement leur effort physique. Il n’y a pas de données appropriées pour décrire les risques associés à l’activité physique chez les personnes considérées à haut risque, mais sans présence d’une maladie cardiovasculaire.
Lay synopsis
Increased participation levels of physical activity (PA) are known to reduce the risk of developing cardiovascular disease (CVD) and lower all-cause mortality rates. There appears to be a dose–response relationship in this regard, as vigorous PA is associated with the greatest reduction in risks and general improvements in health. However, the risk of having a fatal or nonfatal cardiovascular (CV) event is briefly increased during and immediately following PA and maximal exercise testing. The acute risk of an adverse event is significantly lower in those with long-standing PA experience. There is insufficient evidence to restrict the use of the PAR-Q to any specific age group; however, more precise questions are required that probe an individual’s history for assessing for CVD risk. A process should be developed to allow a qualified exercise professional to assess risk based upon positive responses to the PAR-Q and allow for unrestricted or restricted PA using an appropriate risk algorithm.
Introduction and background
The transient risk of adverse CV events during or following acute PA–exercise is extremely low. When adverse CV events precipitated by exercise do occur, they often attract considerable media attention and health professionals are called upon to provide insights regarding the safety of exercise for the general population. It is estimated that 4%–17% of myocardial infarctions (MIs) in men are linked to physical exertion, with much lower rates observed for women (Tofler et al. 1990; Wang et al. 1994). Not withstanding, the long-term benefits of regular participation in PA, particularly at a vigorous level, is thought to greatly outweigh these risks in healthy individuals. This is also true for a wide spectrum of pathologies addressed in this series of articles, including CV (Thomas et al. 2011), respiratory (Eves et al. 2011), metabolic (Riddell and Burr 2011), musculoskeletal (Chilibeck et al. 2011), cancer (Rhodes et al. 2011) cognitive–psychological (Rhodes et al. 2011), and spinal cord and neurovascular (Zehr 2011) conditions. Although this particular paper addresses the risks of CV events occurring during PA in the apparently healthy population, it is part of a larger objective to provide evidence-based recommendations for screening prior to PA participation in apparently health individuals and those with chronic disease states. Consequently, to ensure a uniform approach in methodology given the global objectives, the following section was written by the consensus panel that guided the overall revision of the PA clearance process. This information is reprinted in each of the systematic review papers so that these reviews can stand alone from the paper describing the overall consensus process (Jamnik et al. 2011).
PA participation is recommended and beneficial for all asymptomatic persons and for persons with chronic diseases (Warburton et al. 2006, 2007). However, the PA participation of persons with certain chronic disease conditions or constraints may need to be restricted. The Physical Activity Readiness Questionnaire (PAR-Q) is a screening tool completed by persons who plan to undergo a fitness assessment or to become much more physically active; for example, when initiating PA participation that is beyond a person’s habitual daily activity level or when beginning a structured PA–exercise program. Screening is also recommended when a person is joining a health club, commencing a training program with a fitness professional, or joining a sports team. If a person provides a positive response to any question on the PAR-Q, then he or she is directed to consult with his or her physician for clearance to engage in either unrestricted or restricted PA.
The Physical Activity Readiness Medical Evaluation (PARmed-X) is a screening tool developed for use by physicians to assist them in addressing medical concerns regarding PA participation that were identified by the PAR-Q. Recent feedback from PA participants, fitness professionals, and physicians has brought to light substantial limitations to the utility and effectiveness of PA participation screening by the PAR-Q and PARmed-X. In short, the exercise clearance process is not working as intended and at times is a barrier to PA participation for those persons who may be most in need of increased PA. The aim of the present project is for experts in each chronic disease, together with an expert panel, to revise and increase the effectiveness of the PAR-Q and PARmed-X screening process using an evidence-based consensus approach that adheres to the established Appraisal of Guidelines for Research and Evaluation (AGREE) (AGREE Collaboration 2001, 2003).
An important objective of this project is to provide evidence-based support for the direct role of university-educated and qualified exercise professionals in the exercise clearance process. An example of a qualified exercise professional is the Canadian Society for Exercise Physiology Certified Exercise Physiologist (CSEP-CEP). The CSEP-CEP is the highest nationally recognized certification in the health and fitness industry. It recognizes the qualifications of those persons who possess advanced formal academic preparation and practical experience in health-related and performance-related PA–exercise science fitness applications for both nonclinical and clinical populations.
The AGREE instrument was developed by a group of researchers from 13 countries to provide a systematic framework for assessing the quality and impact on medical care of clinical practice guidelines (CPGs) (AGREE Collaboration 2003). The AGREE collaboration published the rigorous development process and associated reliability and validity data of the AGREE instrument based on a large-scale study focusing primarily on CPGs (AGREE Collaboration 2003). The AGREE instrument is now a commonly used tool for assessing CPGs and other health management guidelines (Lau 2007). The AGREE guidelines were applied in the present project to assess the formulation of risk stratification and PA participation clearance recommendations for each of the critical chronic diseases. One of the authors of this project (J.M.) is an AGREE instrument expert, and she was responsible for evaluating the compliance of the overall process to the AGREE guidelines.
In addition to adhering to the AGREE process, the Level of Evidence (1 = randomized control trials (RCTs); 2 = RCTs with limitations or observational trials with overwhelming evidence; 3 = observational studies; 4 = anecdotal evidence) supporting each PA participation clearance recommendation and the Grade (A = strong; B = intermediate; C = weak) of the PA participation clearance recommendation was assigned by applying the standardized Level and Grade of Evidence detailed in the consensus document (Warburton et al. 2011).
In this series of articles, each chronic disease condition was considered in reference to a continuum of risk from lower risk to intermediate (moderate) and higher risk categories. Particular attention was paid to the short-term (acute) risks of PA–exercise vs. the long-term (chronic) benefits on the chronic disease. PA participation may transiently increase the risk acutely while leading to physiological and psychological adaptations that markedly reduce the long-term risk. Adverse events were considered as any adverse change in health status or a “side effect” that resulted in relation to PA–exercise participation.
The risk–benefit paradox of vigorous PA
The benefits of PA
The CV health benefits conferred by increased habitual PA have been well documented in the scientific literature (Powell et al. 1987; Paffenbarger et al. 1993) and through knowledge translation to the community (Pace et al. 2001; CSEP 2011). Growing evidence indicates a wide range of PA confers some benefit in a dose–response pattern, demonstrating a continuum of increasing benefit and risk reduction as one progresses from low-intensity to more vigorous levels of PA intensity (Paffenbarger et al. 1986; Lee and Paffenbarger 2000; Lee and Skerrett 2001; Kohl 2001). In healthy individuals, low-intensity exercise performed regularly (3–5 times per week) can elicit significant improvements in measures of quality of life, body composition, and triglycerides (Kannel and Sorlie 1979; Morris and Froelicher 1991; Lee 1993; Pace et al. 2001; Warburton et al. 2006; Myers 2008). More vigorous PA has been associated with pronounced risk reductions and all mortality rates in individuals with various chronic diseases (Blair et al. 1989; Oguma et al. 2002; Katzmarzyk et al. 2004). Data obtained from self-reported inventories of PA from both leisure time (Paffenbarger et al. 1986, 1993; Lee et al. 1995; Lee and Skerrett 2001) and occupational settings (Paffenbarger and Hale 1975; Paffenbarger et al. 1978) have demonstrated consistent reductions in relative risk between 10% and 40% for CVD (Paffenbarger et al. 1986; Berlin and Colditz 1990; Blair et al. 1995; Lee et al. 1995; Kohl 2001), metabolic diseases (Katzmarzyk et al. 2004), various forms of cancer, and all-cause mortality (Lee and Paffenbarger 2001). Energy expenditure through vigorous PA of at least 4187 J·week–1 (1000 kcal·week–1), but optimally closer to 8374 J·week–1 (2000 kcal·week–1) has yielded the greatest risk reductions for CVD (Paffenbarger et al. 1978; Paffenbarger and Lee 1998).
PA as a trigger of CV events
Despite the evidence supporting long-term participation in vigorous PA as a means to reduce long-term morbidity and mortality, there is also evidence that each exercise session acutely and paradoxically increases the risk of both nonfatal CV adverse events and sudden cardiac death (SCD). The notion of the “risk paradox” of exercise dates back to the early 1990s (Friedewald and Spence 1990), with reviews relating to this topic occurring earlier (McManus et al. 1981) and more recently (Franklin 2005) that confirm that long-term risk reduction through vigorous PA is also linked to transient risk elevation.
A significant concern amongst health practitioners is that exercise itself may precipitate an adverse CV event in apparently healthy individuals who embark on a program of vigorous PA, or in those with long-standing experience with such activity. This concern has been amplified due to widespread reports of apparently healthy children, adolescents, and adults dying suddenly during or immediately after PA, regardless of their long-standing participation history (Waller and Roberts 1980; Corrado et al. 2003, 2006; Maron and Pelliccia 2006; American College of Sports Medicine (ACSM) and American Heart Association (AHA) 2007). Given these concerns, a clear understanding of the risks of exercise and exercise testing is required such that appropriate recommendations and screening procedures can reduce the likelihood of adverse events without unduly restricting individuals from the benefits PA can provide.
Underlying causes of adverse CV events triggered by PA
The physiological stress of exercise is normally met with ample reserve of coronary blood flow and normal cardiac electrical activity. However, in the presence of CVD, exercise may act as a “trigger”, initiating a cascade of physiological events and malignant substrates that may interact to precipitate serious, if not a fatal adverse event (Franklin 2005) (Fig. 1). Significant coronary occlusion and vascular dysfunction compromises coronary reserve, and the increase in myocardial oxygen demand and reduced diastolic perfusion time induced by vigorous PA can lead to myocardial ischemia and increased vulnerability to ventricular arrhythmias (Franklin 2005). A similar sequence of events may occur immediately following exercise, particularly if there is a rapid reduction in arterial blood pressure that compromises coronary perfusion pressure (Franklin 2005).
Fig. 1.
Numerous reports have described the pathophysiology contributing to exercise-induced SCD (Corrado et al. 2006; Kapetanopoulos et al. 2006; ACSM and AHA 2007; Maron 2007; Möhlenkamp et al. 2008). Although beyond the scope of this review, the consensus is that the vast majority of SCD cases in those above 30–35 years of age are secondary to acute complications of atherosclerosis (Maron et al. 2004, 2009; Maron and Pelliccia 2006; Chevalier et al. 2009; de Noronha et al. 2009), whereas cases less than 30–35 years of age are most often ascribed to disorders of myocardial structural and (or) conduction (Maron et al. 2004; Maron and Pelliccia 2006; de Noronha et al. 2009). These include inherited genetic diseases that account for the majority of pathological findings in cases of SCD (including hypertrophic cardiomyopathy, arrhythmogenic right-ventricular cardiomyopathy, long QT syndrome, Brugada’s disease, Marfan’s syndrome), and less common congenital conditions, including anomalous coronary arteries. Disturbances in electrical conduction may be a “concealed” cause of death in young athletes despite normal histology, because the conduction systems are rarely examined thoroughly or have gross abnormalities upon inspection (Corrado et al. 2006, 2008).
Atherosclerotic disease is associated with over 80% of exercise-related SCD in those over 35 years of age, and over 95% of cases when the age exceeds 40 years. Autopsy findings generally indicate prior or acute MI, but evidence of coronary thrombosis is not always identified. Notwithstanding the limited data available, exercise is considered to be a risk factor for acute and vulnerable atherosclerotic plaque (Hammoudeh and Haft 1996; Burke et al. 1999; Giri et al. 1999; Chevalier et al. 2009). The fissuring of fragile, non-occlusive plaque may induce acute coronary artery occlusion and (or) malignant arrhythmia; however, it is not clear what mechanisms unique to exercise are involved. Exercise may alter the geometric and hemodynamic state of the coronary arteries by elevated shear stress or change the shape of epicardial arteries, which may in turn lead to plaque disruption. Plaque rupture may also be spontaneously induced through increased fibrinolytic activity triggered by vigorous PA since acute exercise is associated with a prothrombotic state (increased fibrinolysis and platelet activation) (Weiss et al. 1998; Lee and Lip 2003). Limited data suggest that low- to moderate-intensity exercise may have little effect on platelet adhesiveness and reactivity, whereas a higher intensity and prolonged exercise may induce a prothrombotic state (Wang et al. 1994; Weiss et al. 1998; Hilberg et al. 2008). Collectively, this evidence offers a plausible mechanism of action for exercise-induced acute coronary events; however, the identification of disease remains the limiting factor given that in most cases of SCD, no prior symptoms are reported and screening has not been performed prior to activity (de Noronha, Sharma et al. 2009).
The occult nature of coronary disease remains a primary challenge of screening procedures. It is likely that SCD involves an acute and rapid progression in the disease state without warning in the moment immediately preceding death (Thompson et al. 2007). Consequently, ascertaining the overall risk profile may help to minimize the risk of adverse events during vigorous exercise (Fletcher et al. 2001; de Noronha et al. 2009).
Questionnaires as a screening tool for determining CV risk of exercise
Various questionnaires have been developed to identify elevated risk of CV events during exercise. The modified AHA–ACSM Facility Pre-participation Screening Questionnaire (ACSM and AHA 1998; Balady et al. 1998) provides a basis of risk stratification and addresses a broader range of diseases that may complicate the response to exercise (ACSM 2006). The PAR-Q questionnaire was designed to be a simple, self-administered questionnaire that directs individuals who are potentially at greater risk towards medical clearance prior to PA.
Exercise testing as a screening tool for CVD: current approaches and limitations
Current guidelines from the ACSM and AHA call for preparticipation exercise testing in individuals considered “moderate risk” (ACSM 2006); these guidelines are based largely on the knowledge of increasing CVD prevalence in the population. Specifically, exercise testing is not necessary for men and women less than 45 and 55 years old, respectively, if they are without coronary risk factors (ACSM 2010). However, consideration should be given for those over these age thresholds when 1 risk factor is present, and should be strongly considered when 2 or more risk factors have been identified (Fletcher et al. 2001; ACSM 2006). Medical supervision of maximal exercise testing is recommended for those considered to be “high risk” (Gibbons et al. 2002; ACSM 2006), but a wide range of practice exists in both the scope of exercise programs and the clinical profile of participants. A systematic review examining exercise testing and detection of coronary disease recommended against clinical exercise testing in low-risk patients (Fowler-Brown et al. 2004). This was due to the lower likelihood of coronary artery disease and in many cases, the inability of an individual to reach maximal effort during exercise testing. Collectively, these factors lead to a lower sensitivity for detecting changes in the ST segment (Ashley et al. 2000), thereby limiting the efficacy of stress testing in low-risk patients. In addition, the greater likelihood of false-positive test results may lead to labelling of the individual as “higher risk”, which in turn may prompt unnecessary invasive diagnostic procedures, anxiety, and possibly poorer future health (US Preventive Services Task Force 2004).
A major limitation of clinical exercise testing with standard electrocardiographic monitoring is the wide range of specificity and sensitivity across cohorts and diagnostic techniques. This is dependent on the extent of disease or inherent predisposition for false positives, such as those seen in women (Fletcher et al. 2001). Even when performed in conjunction with cardiac imaging modalities (perfusion scanning or stress echocardiography), a positive test result remains dependent on the presence of well-established flow-mediated lesion or a spontaneous disruption in plaque that elicits ischemia (Thompson et al. 2007). Since plaque fissuring and lethal arrhythmia may not occur during stress testing but rather during subsequent vigorous PA (Waller and Roberts 1980; Albert et al. 2000; Eckart et al. 2004), exercise testing at a given time may fail to detect evidence of an unstable coronary lesion that may subsequently induce an exercise-induced coronary event.
Methods
Methodological approach
Continuum of risk
In this review, “apparently healthy” was considered in reference to a continuum of risk from lower risk to intermediate (moderate) risk, the latter considered when risk factors but no primary disease condition may be identified (Fig. 2). Those deemed at higher risk were excluded from discussion because of the presence of disease and are considered in detail (Thomas et al. 2011).
Fig. 2.
Operational definitions: health, health-related physical fitness, PA, and exercise
Throughout each review in this series, the effects of habitual PA and (or) exercise training on health status are considered extensively. The classic definition of physical activity refers to all leisure and nonleisure body movements resulting in an increased energy output from rest (Bouchard et al. 1994). However, it is important to note that there are 4 broad PA domains, including domestic (house work, yard work, child care, chores), transportation (bicycling or walking), occupational (work-related), and leisure-time (discretionary or recreational time for PA, sports, exercise, and hobbies) (Warburton et al. 2011).
Exercise refers to structured and repetitive leisure-time PA whose main objective is to maintain or improve physical fitness, work performance, quality of life, exercise performance, and (or) health status (Warburton et al. 2011).
PA–exercise classifications
Objective physiological markers (such as heart rate) are commonly used to classify and monitor exercise interventions in patients with chronic disease. Both percent heart rate reserve (%HRR) and percent of maximum heart rate (%HRmax) are utilized routinely in clinical exercise prescription and intensity of effort was based upon the classifications described in Table 1 (Jamnik et al. 2011).
Table 1.
Note: Adapted from Warburton et al. (2006). %HHR, percent heart rate reserve; %HRmax, percent maximum heart rate; RPE, rating of perceived exertion; MET, metabolic unit relative to resting metabolism.
*
3 METs × 30 min × 5 days = 450 MET min·week–1.
†
6 METs × 30 min × 5 days = 900 MET min·week–1.
‡
10 METs × 30 min × 5 days = 1500 MET min·week–1.
Systematic review search strategy
This review article was based upon a systematic review of the evidence describing the CV risks of exercise testing and participation in PA in apparently healthy individuals. A comprehensive, computer-assisted literature search of existing evidence was performed using the following electronic databases: Medline, CINAHL, SPORT discus, EMBASE, Cochrane DSR, ACP Journal Club, and DARE. Preference was given to randomized controlled trials, but all literature, including previous systematic reviews, meta-analysis, simple reviews, and nonrandomized studies, were captured and screened for applicability as well as additional references. The main search was further supplemented with articles identified by subject matter experts, who were aware of publications that may not have been captured.
We sought English language articles on human subjects that were indexed before the second week of June 2008 and searched both keywords and MeSH headings to keep the search intentionally broad. The keywords were developed using the originally published PARmed-X terms identified as contraindications to exercise and attempted to exclude subject matter devoted exclusively to CVD states. Terms were included in the search that covered cardiac sudden death, myocardial infarction, syncope, and exercise syncope.
One author (J.B.) reviewed titles and abstracts of the identified articles, removed duplicates and retrieved all potentially relevant literature. When there were uncertainties, full text copies of the articles were obtained. Two other authors (J.M.G. and S.G.T.) further reviewed the selected articles to ensure agreement on article relevance and significance. Specific attention was given to articles that examined the risks of exercise as well as reports of adverse events, excluding articles that examined subjects with CVD only.
The quality of evidence of identified articles was first assessed by a team of researchers that considered each article as a stand-alone study. Referenced articles were further re-evaluated by the authors with consideration of the article in and of itself and also in the context of the current project. This distinction was felt to be an important step because although a study may have met the criteria for Grade 1 evidence as a stand-alone, often times the outcome measure was not specifically designed to address the issue of the risk of participating in exercise, and thus the evidence for or against this point was of a lower grade. Articles that contained data regarding both healthy and CVD subjects were retained and relevant data and conclusions were made about the healthy cohort accordingly.
Results
More than 190 000 articles were initially identified by electronic searches. Of these, 616 papers were identified as being related to PA and adverse events; 527 were obtained through electronic searching and 89 were physically hand-picked by the authors. Of these, 51 papers reported directly on adverse events during exercise or exercise testing (Fig. 3). A summary of the key findings is provided below.
Fig. 3.
Risks of exercise testing triggering adverse CV events
Graded exercise testing is used as a clinical diagnostic probe to rule out CVD, assess disease severity and to monitor the efficacy of treatment. However, it also routinely used to more precisely prescribe exercise and to monitor progress during an exercise training intervention. A limited number of observational studies have described risks of exercise testing in the healthy population. The lack of prospective randomized controlled trials has limited our ability to draw conclusions about risk because most data are derived from a wide range of fitness testing facilities or referral-based clinical exercise testing laboratories. This makes interpretation problematic given the disparate pre-test likelihood of CV risk that existed from cohorts of widely-differing designs and inclusion criteria. In addition, it is possible that when most data were acquired (late 1960s to early 1980s), routine referrals to clinical exercise laboratories were more likely to confirm or reject a physician’s clinical suspicion of disease and the risks to the general population attributed from these studies may be overstated compared with more recent investigations. A further limitation is the manner in which risk is determined. All studies of this type report incidents per test rather than attribute per person hour, the latter method more commonly used in studies examining risk of PA or exercise training (Foster and Porcari 2001). There are no data that specifically describe risks of submaximal exercise testing, which is more common in the fitness industry. Although such testing would likely incur lower risks, there are no data available to confirm this.
The classic study of Rochmis and Blackburn (1971) reported data from 130 stress testing facilities in the United States, totalling 170 000 tests. They reported 16 deaths per 170 000 tests (1 per 10 000 or 0.01%). However, 4 of the deaths occurred at least 2 days after exercise testing, and all subjects were either screened (11 subjects) or had suspected (2 subjects) or confirmed CVD (3 subjects). In fact, 34% of the tests were symptomatic. The risk stated in this study remains the most commonly cited for exercise testing in healthy individuals; however, given that the majority of subjects in their study had established CVD, the risks for the healthy population is likely to be considerably lower. In fact, the authors themselves indicated that the incidence of 0.01% overestimates the risk in normal individuals; if one excludes deaths occurring beyond 24 h following the test, the actual risk would be 0.005%.
McHenry (1977) examined 650 male state police (aged 25–54 years) that were undergoing a periodic physical evaluation, and reported the incidence of arrhythmias during graded treadmill testing. The incidence of premature ventricular contractions was surprisingly high in normal subjects (occasional, 70%; frequent, 30%). The incidence of paired or multifocal premature ventricular contracations was only 2.2% and 1.1%, respectively, and ventricular tachycardia was only observed once (0.4%). These data indicate that arrhythmias during exercise testing are relatively common. Results from early European studies that employed cycle ergometry stress testing produced similar trends, although they reported higher mortality rates than Rochmis and Blackburn (1971). Data from 50 000 tests yielded complication rates equal to 18.4, a morbidity rate of 5.2, and mortality rates of 0.4 per 10 000 tests (Atterhög et al. 1979). This large prospective study included a greater proportion of high risk patients (Atterhög et al. 1979).
A large retrospective study surveyed 518 448 stress tests across 1375 centres (Stuart and Ellestad 1980). Data from cycle ergometry, step-testing, and treadmill testing from clinical centers that responded to questionnaires in Canada, the United States, and Puerto Rico were compiled (the majority of tests using the Bruce protocol). They reported a complication rate MIs) of 3.58 per 10 000 tests and 4.78 per 10 000 tests for complex and dangerous arrhythmias. The total complication rate was 8.9 per 10 000 tests. They also reported 0.5 deaths per 10 000 tests. The authors suggested that their significantly lower adverse response rate (compared with Rochmis and Blackburn (1971)) may have been due to the enhanced screening and knowledge of exercise testing accrued over many years (Stuart and Ellestad 1980). Consequently, it is possible that their screening procedures created a cohort more closely resembling an “apparently healthy” population with a lower pre-test likelihood of disease vs. an “at risk” group (despite the fact they were referred for exercise testing).
Knight et al. (1995) found risks comparable to other studies (Rochmis and Blackburn 1971; Stuart and Ellestad 1980) when retrospectively examining 28 133 stress tests performed by nonphysicians (exercise physiologists), with zero deaths and 1.42 myocardial infarctions and 1.77 ventricular fibrillation per 10 000 tests. The complication rates were similar to those reported in centres using direct physician supervision, suggesting that nonphysicians with training can safely oversee stress testing in healthy and diseased populations. Myers et al. (2000) surveyed 72 of the largest Veterans Affairs Medical centres in the United States and reported that 75 828 exercise tests performed within one year had a 1.2 per 10 000 event rate.
A rarely cited large European study (Wendt et al. 1984) reported no life-threatening complications during exercise testing when using cycle ergometry in 384 938 athletes. In more than 1 000 000 clinical exercise tests that involved patients with CVD, the complication rate was 1 per 12 000; the evidence of reducing risk was with less vigorous, submaximal protocols such as step testing. Similar observations from a German study were also reported, using cycle ergometry (Scherer and Kaltenbach 1979), with no serious complications observed in 353 638 athletic individuals, but an incidence of 1 per 7500 for nonfatal events in patients with heart disease. The latter studies share common limitations (Gibbons et al. 1989): the testing modalities (cycle erometry vs. treadmill) and criteria for terminating the tests varied, a mix of maximal and submaximal tests were reported and incompletely described, and finally, the risk profile of those tested varied considerably.
The most relevant data for determining exercise testing-risk in a relatively healthy cohort was a comprehensive study by Gibbons et al. (1989) who surveyed 26 471 men and 7824 women who underwent maximal exercise testing (modified Balke and Ware protocol) at the Cooper Clinic (Dallas, Tex., USA) over a 16-year period. A key distinction of this study from those reporting clinical exercise test data is that only 4% of the men and 2% of the women in this study had a clear history of coronary artery disease (CAD). However, of the total cohort, 15% had high blood pressure, 20% had a history of chest pain, and 6% reported a vague diagnosis of “heart trouble”; these figures are likely to be expected during screening based upon existing disease prevalence rates. Based upon the first exercise test performed (some received a second follow-up test upon an initial abnormal result), 88% of the tests in men and women were normal. In total, 6 complications occurred, and of these, 5 had a prior history of CAD. The 95% confidence interval of complications was 0.3–1.8 per 10 000 tests, yielding an overall rate of 0.8 per 10 000 tests, 20% less than reported in clinical exercise testing facilities according to Rochmis and Blackburn (1971). A mandatory cool-down procedure was introduced midway through the study, and no complications were reported in over 45 000 tests since the procedure was routine. These lower complication rates reflect a healthier cohort undergoing testing in a preventative medicine clinic and may well offer a more accurate assessment of the risks of maximal exercise testing in an apparently healthy population. Based upon these data, the risk of death from exercise testing is well below the commonly stated value of 1 per 10 000 tests and ranges from less than 0.2 to 0.8 per 10 000 tests.
The number of submaximal exercise tests (e.g., “fitness tests”) performed each year is unknown, but it is likely the vast majority of them are not supervised by a physician. Notwithstanding, it appears the adverse response rate is not influenced by nature of the supervision during exercise testing in either healthy individuals or those with CAD (Knight et al. 1995).
Foster and Porcari (2001) reported the risk nonfatal events during exercise testing was 1.59 per 10 000 h for clinically indicated tests, and 1.06 per 10 000 h for screening tests. The risk of death would be considerably less than this. This assumed that each test included risk period of 0.75 h, including both the testing (0.25 h) and recovery (0.50 h) time periods.
In conclusion, the mean rate of adverse events during exercise testing, including individuals referred for clinical exercise testing, based on our review of the literature is less than 0.3 fatal events per 10 000 tests and 2.9 nonfatal events per 10 000 tests. Higher rates are observed for nonfatal events, although the adverse event reported in this context varies from mild arrhythmias that are not considered to be life-threatening, to serious ventricular arrhythmias associated with increased risk of sudden death. A summary of these studies is presented in Table 2. Where possible, common units of risk (per 10 000 h) have been calculated.
Table 2.
Note: CAD, coronary artery disease; MI, myocardial infarction; VF, ventricular fibrillation.
*
Calculated from original data; exercise tests converted to per person hours assuming 45 min (testing and recovery period included (Foster and Porcari 2001).
Risks of PA and exercise training triggering CV events
Methodological limitations
Similar to the evaluation of risk during exercise testing, a number of issues limit the study of risk during PA. First, in the healthy population most studies report only deaths (Foster and Porcari 2001), with little data reported for nonfatal adverse events. Second, few studies have data specific to exercise intensity and given the dose-response relationship that may exist between exercise intensity and risk of adverse CV events, it is difficult to offer exercise intensity-specific conclusions. Finally, there is a variation in the units of risk (per person hour, per session, etc.) in which adverse events are reported, making the interpretation of studies more challenging. We have attempted to summarize these data and where possible, have calculated common endpoints (Table 3).
Table 3.
Supporting evidence
One of the first reports of CV events during exercise was that of Jokl et al. (Jokl and Melzer 1940; Jokl 1971) who reported data obtained in the 1920s and 1930s. The most common cause of death from the 64 cases described were secondary to what were considered to be congenital conditions, suggesting the majority of cases were of a young age (Maron 2003; Corrado et al. 2006), yet neither age nor a specific exercise intensity were reported.
More recent retrospective studies have provided most of the data regarding risk of exercise. They have relied on either hospital or institutional records to link adverse CV responses to exercise. The early and frequently cited study of Ragosta et al. (1984) examined records of 81 deaths during or immediately after recreational exercise, with the majority of deaths occurring during golf (23%), jogging (20%), and swimming (11%). Of these deaths, 88% were attributed to atherosclerotic disease and the presence of symptoms, risk factors, or prior history of heart disease. Using census data from Rhode Island (USA), they determined the population incidence of death from recreational activity was 0.36 per 100 000 for men that were less than 29 years of age. The incidence of death for men and women over 30 years of age was 4.46 and 0.05 per 100 000, respectively. The overwhelming cause of death (81%) in the older group (averaging 53 years of age) was attributed to atherosclerotic disease, and 37% of these had a prior history or symptoms of coronary heart disease. In the follow-up study (1975–1980) of Rhode Island joggers, Thompson et al. (1982) reported 1 death per 396 000 person-hours of jogging. These data, based upon 1 death report from 7620 regular joggers, suggests that acute exercise increased the risk of an acute coronary event expected in a nonexercising state by 7 times. Although not categorically stated, it is likely that the exercise intensity was within the vigorous to very hard categories using our criteria (Table 1). These data are in agreement with Siscovick et al. (1984a), who reported a gradient of risk according to the amount of PA performed in the Seattle, Washington, United States area. Those with the highest reports of habitual PA (≥140 min·week–1) had a 5-fold increase in the risk of cardiac arrest during vigorous PA, and those with the least (1–19 min·week–1) had a 56-fold greater relative risk during exercise. Although the study may be limited by the method of determining habitual activity patterns (through interviews of spouses), this was the first study to report an inverse relationship between a history of habitual activity and the risk of an adverse CV event during exercise. A later German study involving 1194 individuals (Willich et al. 1993) observed a similar trend for participants of vigorous PA (defined as >6 METs, corresponding to “vigorous effort” (Table 1); however, a relative risk of only 2.1 was reported, increasing to 6.3 for those exercising less than 4 times per week and as low as 1.3 for those exercising more than 4 times per week. While prior PA appears to lessen the acute risk of exercise (Level of Evidence 3), the time period devoted to vigorous PA for each session or extent of history (months or years of participation history) that is required to significantly lower risk is unknown.
In a large retrospective analysis of 48 fitness facilities (Vander et al. 1982), individuals responded to questionnaires (response rate, 48%) to amass data on fatal and nonfatal CV events. The 5-year analysis period represented a total of 22 726 000 participant hours of PA. The incident rate for nonfatal and fatal events was 1 per 1 124 200 h and 887 526 h of participation, respectively (0.13 and 0.16 complications per year). Although exercise intensity was not documented, the activities linked to events included racquetball, handball, squash, and jogging; these were also the most commonly performed activities, thus making conclusions regarding higher risk activities unreliable, yet suggestive of a dose–response effect between exercise intensity and the risk of adverse events. Malinow et al. (1984) performed a 10-year retrospective study of events at undisclosed YMCA facilities, representing a cumulative exposure to exercise of 82 227 600 h. They reported only a single fatal CV event for every 2 897 057 person-hours of PA, which is less than 50% the rate reported by Vander et al. (1982). The nonfatal event rate was 1 per 1 267 462, and assumed that the age-range in the group was 25–44 years. Apart from concluding that the risk of adverse cardiac events was extremely low, the authors also suggested that routine exercise testing as a screening procedure in apparently healthy individuals is unwarranted (Malinow et al. 1984).
Gibbons et al. (1980) followed 2935 screened (including exercise testing with ECG, risk factor assessment) adults with a mean age of 37 years over a period of 65 months in a highly supervised exercise program. From a total of 374 798 person-hours of exercise (2 726 272 km of running and walking), they reported 2 cardiac events with no deaths. This yielded a fatal event rate of 0.3 to 2.7 events per 10 000 person-hours of exercise (across all age groups) for men and 0.6 to 6.0 events per 10 000 person-hours for women. This is in contrast with most literature describing SCD in Europe or the United States, since the incidence of exercise-induced SCD in women is typically 5%–10% the rate seen in men (de Noronha et al. 2009; Maron et al. 2009). Although Gibbons et al. (1980) attributed the higher rate in women to a lower sample size, gender bias in referrals to their program at that time may have produced a female cohort self-selected for CVD. More recently, Albert et al. (2000) examined acute risks of vigorous exercise during a 12-year follow-up of 21 248 physicians using self-reported habitual exercise levels at baseline. During this time-period, 122 cases of sudden death were reported, yielding a relative risk (during and up to 30 min after vigorous exertion) of 16.9 (95% confidence interval, 10.5 to 27.0). This equaled an absolute risk of 1 sudden death per 1.51 million episodes of exertion. These values are higher than most reports, possibly reflecting an older cohort (aged 40 to 84 years), the exclusion of women, and the lack of classification for exercise duration.
Further insights into the incidence of sudden cardiac death during vigorous exercise come from a 25-year retrospective study of military training (Eckart et al. 2004). A death rate of 13 per 100 000 was reported in a cohort of 6.3 million screened military recruits aged 18–35 years, with 86% of the cases related to exercise. As with other reports of exercise-related cardiac sudden death in young individuals (aged <35 years) (Corrado et al. 2006; Maron and Pelliccia 2006; Maron 2007), the pathology was most commonly hypertrophic cardiomyopathy, with a smaller percentage having anomalous coronary arteries and over 30% of cases failing to have any identifiable pathology.
In a recent prospective study in the French population, Chevalier et al. (2009) examined the incidence of sport-related acute cardiovascular events (ACVE) in 1 954 382 patients registered in 4 hospital emergency departments. The mean age of the participants was 45.5 years. The global incidence of sports-related ACVEs was 6.5 out of 100 000 participants per year (81.1% in males), with an incidence rate of SCD reported to be 1.9 per 100 000 participants. These rates are considerably higher than reported by Gibbons et al. (1980) or by Ragosta et al. (1984); however, the etiology of death was not confirmed by autopsy, nor was the specific nature of the activity (e.g., duration or intensity) recorded. Finally, the reporting of CV events through emergency admissions may yield a higher incidence rate than previously reported data that was obtained retrospectively.
Non-endurance activity
There are few data that described specific adverse responses to alternate forms of PA (other than endurance activity). The CV risks of resistance training (RT) appear to be relatively low (Williams et al. 2007); however, data from relatively small studies were insufficient to provide accurate estimates of risk across the population (McCartney 1999). The use of appropriate techniques, including the avoidance of the Valsalva manoeuvre, has been shown to elicit blood pressure responses similar to aerobic exercise, providing the effort is within a range of 80%–100% of 1-repetition maximum (McCartney 1999). Indeed, a study examining the safety of maximal strength testing failed to observe any clinically significant CV events in 6 653 men and women (Gordon et al. 1995). All underwent stringent pretesting medical exams to rule out CVD; therefore, it remains unknown if a less vigorous screening process would have yielded a similar result.
Limited data from a small study involving circuit training (Harris and Holly 1987) also yielded no adverse responses and concluded that circuit training appears to be appropriate and safe for apparently healthy, sedentary individuals. At this stage there are insufficient data to make conclusions about this form of exercise.
CV risk during mild (<3 METs) to vigorous (>6 METs) mountain activity was reported in Ponchia et al. (2006). Activities included mountaineering, downhill skiing, cross-country skiing, and mountain biking, representing 7 742 120 person-days of participation, and was interviewed by telephone or in person. This provided 12 449 877 person-days of exposure, yielding an incident rate of 1 CV event per 319 000 person-days of PA in the mountains, and 1 SCD per 980 000 person-days of PA in the mountains, with most occurring in those over 40 years of age. In a similar study, 1 death per 5 000 000 hiking hours and 1 per 630 000 downhill skiing hours was reported earlier in men over the age of 34 years (Burtscher et al. 1993). Despite the limitations of sampling and description of PA, these studies suggest a low incidence rate for fatal and nonfatal events for activities related to winter alpine sports.
There have been a number of retrospective reports that describe the risk of individual endurance activities, particularly marathon running and cross-country ski racing in Europe. This is of particular interest given the trend of increasing participation rates in marathons (rising more than 12-fold since 1976) and, more importantly, the shifting of the age group: the fastest growing cohort of these events are those older than 40 years of age, with 40% of all runners over 40 years of age, compared with 23% in 1980 (Road Running Information Center 2008). This trend is expected to continue as the population ages and the “baby boom” age group continues to engage in this form of activity (Möhlenkamp et al. 2006). Media reports of fatal cardiac events at various marathons in Canada and the United States have heightened the concern and have led to a number of retrospective analyses of risk (Maron et al. 1996; Roberts and Maron 2005; Redelmeier and Greenwald 2007; Tunstall Pedoe 2007). Earlier reports from the United States indicated that the risks of a fatal CV event during marathon running were 1 per 50 000 (Maron et al. 1996), but more recent data suggest that the risk may be as low as 1 per 200 000 (Roberts and Maron 2005). In the retrospective study by Maron et al. (1996), 4 exercise-related sudden deaths amongst 215 413 runners who completed marathons were reported; 3 deaths occurred during and 1 following the race. This incident rate (0.002%) was considered to be 1/100th the risk of sudden death during a typical day without exercise. A recent report summarizing over 500 000 participants in the London Marathon indicates that the incidence of cardiac sudden death is 1 per 80 000 participants (Tunstall Pedoe 2007).
The incidence rates for CV events were reported for 698 102 starters of ski races in Sweden, amounting to 581 person-years of cross-country skiing (Farahmand et al. 2007). Overall, 13 deaths (12 secondary to CVD) were reported, whereas 1.68 were predicted from population norms during the same time period of skiing, resulting in a mortality ratio of 7.7. This ratio is similar in some studies (Thompson et al. 1982; Ragosta et al. 1984; Siscovick et al. 1984a; Willich et al. 1993), but lower than others where screening was not performed (Albert et al. 2000).
Gender and CV risks of PA
Women have a considerably reduced incident rate of fatal CV events that are related to exercise, likely due to the delay seen in coronary heart disease and lower participation rates in vigorous PA (Thompson et al. 2007). In one of the few prospective studies examining PA in women, the ongoing Nurses’ Health Study (Whang et al. 2006) examined 84 888 women who responded to the questionnaire in 1980 (which recorded type and intensity of PA), and only 3.1% of the cohort died during moderate or vigorous activity, which included yard work (n = 3), housework (n = 2), physical therapy (n = 1), snow shovelling (n = 1), and swimming (n = 2). This yielded a risk of cardiac sudden death in women associated with moderate or vigorous exercise of 1 per 36.5 million hours. These rates are much less than those reported by Gibbons et al. (1980) (0.6 to 6.0 events per 10 000 person-hours for women); as stated earlier, they attributed a higher incidence to a small sample of women in the study and it is likely their referral to exercise testing was based upon a higher likelihood of coronary heart disease.
Young adults and children
Although the cause of adverse CV events that occur during or following exercise in young adults and adolescents has been well documented (Corrado et al. 2003, 2006; Maron et al. 2004, 2007; de Noronha et al. 2009), there are few data that describe the incidence rate of this cohort in the general population. The lack of survey studies that document adverse events for children is largely due to their limited PA within fitness facilities or the failure to record such data from organized recreational activities, including municipal leagues, etc. This lack has limited our knowledge and ability to report data on adolescents involved in competitive sports.
Van Camp et al. (1995) reported an SCD incidence rate of adolescents and young college athletes (7.47 per 1 million participants for men, and 1.33 per 1 million participants for women), and reported very low incident rates for men (0.4 per 100 000) and women (0.13 per 796 000) for men and women, respectively. A significantly higher incidence rate was observed for college students compared with high school students. CVD was the underlying pathology in 75% of the cases, with the majority being secondary to hypertrophic cardiomyopathy. A large Italian study (Corrado et al. 2003) was based on 2 368 590 athlete-years of observation (1 904 490 males and 464 100 females), with a mean age of 23 years (range 12–35 years). As per Italian law, all had undergone comprehensive screening and the incidence of SCD by all causes was 2.3 per 100 000 (2.6 per 100 000 in males and 1.1 per 100 000 in females, and 2.1 per 100 000 from CVD). This higher rate, when compared with data from Van Camp et al. (1995), has been attributed to an older cohort and possibly to higher levels of exercise intensity (Thompson et al. 2007).
The presence of exercise-induced ventricular arrhythmias in athletes or the sedentary population during exercise testing has uncertain prognostic value, but likely elevates risk (Kwok et al. 1999; Nishime et al. 2000). Abnormal repolarization patterns are seen in 1%–4% of athletes aged 18–35 years (Sharma et al. 1999; Pelliccia et al. 2000, 2008). In older individuals, increasing frequency of ectopic beats is associated with poor clinical outcomes and increased risk of atherosclerosis (Marieb et al. 1990), although the short-term prognosis is not necessarily worsened (Fleg and Lakatta 1984). The increased presence of ECG abnormalities in young, trained athletes are more likely secondary to increased vagal tone and training-induced morphological changes (Maron and Pelliccia 2006). Most anomalies of this type are a reflection of increased vagal tone and do not warrant follow-up (Estes et al. 2001), yet their presence poses additional challenges in ruling out an increased risk of CV events. A very small number of athletes have highly disturbed ECG patterns that may indicate pathology, including hypertrophic cardiomyopathy and arrhythmogenic right ventricular cardiomyopathy (Pelliccia et al. 2008). Clearly, the presence of any cardiac arrhythmia and (or) symptoms, particularly syncope at rest, during, and (or) following exercise increases risk and should be investigated aggressively. Other cardiac arrhythmias may not carry immediate risk but remain a concern. For example, the prevalence of atrial fibrillation and (or) flutter appears to be higher in long-standing, middle-aged endurance athletes (Campion 2006; Farrar et al. 2006; Baggish et al. 2008; Mont et al. 2009), yet the mechanisms responsible for its manifestation and its clinical significance remains unclear and requires further investigation (Swanson 2006; D’Andrea et al. 2008; Lampert 2008; Mont et al. 2009).
Screening of young individuals prior to sport participation, particularly ECG screening, remains controversial. Such screening is mandatory in Italy and has been strongly advocated by some to be adopted on a world-wide basis (Corrado et al. 2008). Despite strong support in some countries, this has not been widely accepted in North America (Maron 2007). In fact, a recent study (Maron et al. 2009) compared SCD data from Italy and the United States (which does not perform ECG screening) and failed to show lower SCD rates when ECG was included in the screening process. The economic and ethical considerations related to mandatory screening have also argued against their use in the general community (Warburton et al. 2007). The correct identification of occult disease remains a primary challenge, since 80% of SCD cases are clinically silent and are rarely associated with prodromal symptoms. Recent data suggests that screening for inherited cardiac pathologies is more effective if family history and questionnaires are combined with ECG (Wilson et al. 2008). However, positive responses to questionnaires regarding symptoms and family history are more frequent in school children compared with young athletes. Unfortunately, they also have a high false-positive rate, and therefore may be poor predictors of CV pathology (Wilson et al. 2008). Notwithstanding these limitations, the inclusion of relevant questions in a screening questionnaire may help to identify elevated risk and offer a basis of further investigation.
Prior PA reduces the acute risk of vigorous PA
The acutely increased risk of CV events during exercise is significantly lower if the individual regularly participates in routine exercise, particularly when it is vigorous in nature. Siscovick et al. (1984b) reported that the transient risk of vigorous activity doubled for those who had no prior experience with vigorous exercise. Similar observations were reported from the Physicians’ Health Study (Albert et al. 2000), and the Triggers and Mechanisms of Myocardial Infarction study, the latter showing a risk reduction of 5-fold or more if an individual exercised more than 4 days per week. A more profound risk reduction in those with increased participation rates was reported in the OSLO study (Mittleman et al. 1993); exercising at least 5 times per week reduced risk of a myocardial infarction by 50-fold, with significant reductions in risk observed for modest participation rates (1–2 times per week). Similar overall reductions for CVD risk have been reported for “weekend warriors” who only exercise 1–2 times per week (Lee et al. 2004). Recently, data from the Nurses’ Health study (Whang et al. 2006) indicated that the transient increased risk was virtually eliminated in those reporting more than 2 h of moderate to vigorous PA per week. In either case, as with other studies, the long-term risk was lower with increasing rates of PA, particularly at vigorous intensities. As with men, increasing fitness level may attenuate the risk of SCD in women. For example, in a prospective study of 5721 asymptomatic women (aged 52.4 ± 10.8 years at baseline), exercise capacity was shown to be an independent and more powerful predictor of death in asymptomatic women compared with men (Gulati et al. 2003). A 17% reduction in mortality rate was observed per MET increase in exercise capacity, adjusted for the Framingham Risk Score, compared with a 12% risk reduction for a similar increase in exercise capacity in men (Myers 2008). These data suggest that higher fitness levels and, in particular, ongoing participation in PA, reduces the risk of CV events during exercise.
Low-intensity exercise and CV risk
There are fewer data describing risk of lower intensity exercise (less than moderate intensity). Goodrich et al. (2007) evaluated 13 274 participants on a diet and lifestyle intervention who were at risk for or had documented CVD by having them perform light exercise. Only 1 serious complication (atrial fibrillation) was reported (1.4%), with minor to moderate adverse events related to CV symptoms comprising 2.6% of the population. This low rate of events (mostly musculoskeletal) occurred despite the cohort being considered high risk with at least 1 major risk factor (mean number of comorbidities = 5.2).
Summary and overall implications for the PAR-Q
Conclusions
1.
Vigorous exercise transiently increases the relative risk of a CV event above that which is expected at rest by chance alone. Based upon the available evidence, the adjusted risk of a CV event for adults is approximately 0.01 per 10 000 to 0.03 per 10 000 participant hours. (Level 2–3). Fewer data are available for children and adolescents; however, the adjusted risk of a fatal CV event is considerably lower (Level 3).
2.
The routine use of maximal exercise testing in apparently healthy individuals is relatively safe and the risks of testing have been overstated by 20%–25% based upon limited data from individuals with and without cardiac disease. The estimated risk for a fatal event during maximal exercise testing ranges from 0.2–0.8 per 10 000 tests (rather than 1 per 10 000 tests), and approximately 1.4 per 10 000 tests for nonfatal events (Level 3).
3.
The majority of events in individuals aged over 35–40 years are secondary to coronary heart disease, with the vast majority of cases aged under 30–35 years linked to undetected congenital and heritable heart conditions. In both cases, adverse events are likely triggered by various malignant substrates related to the physiological stress of exercise in the presence of disease. (Evidence Level 3).
4.
Risk factors that have been identified that increase the risk for adverse responses, and in particular SCD, include
a.
Increasingly vigorous intensity (6 METS and above, Table 1) (Level 2–3);
b.
Male sex (Level 2);
c.
The absence of or limited previous PA history (Level 2–3); and
d.
Increased age (Level 3).
Given this evidence, the health benefits conferred by PA participation appear to outweigh the associated risks.
Should the PAR-Q be modified to reflect our understanding of adverse CV events? When considering this question, it is important to distinguish between the risk of an adverse CV response and the likelihood of detecting CVD, per se (e.g., determining the “pre-test likelihood” of detecting CVD). The latter is determined through a process of risk stratification, as summarized in Fig. 4; this process aids the qualified exercise physiologist (QEP) in determining an appropriate PA prescription. As the likelihood of disease increases, the nature of the PA prescription may be modified accordingly. However, even when examining risks of PA in patients with CVD, the risk of having an adverse CV event during exercise is low (Thomas et al. 2011).
Fig. 4.
However, it is now apparent that individuals at “intermediate risk” (i.e., those with CV risk factors) may be unduly restricted in their PA participation because of overly stated concerns of risk from either exercise testing or participation in PA. While the presence of certain chronic diseases (and some acute conditions) may trigger adverse events more readily, these risks remain extremely low and can be managed by qualified professionals and, where appropriate, contraindications. Consequently, those with intermediate risk can participate in less vigorous PA without medical screening. If more vigorous PA is desired, medical screening may be warranted. These issues can be further resolved through the development of clinical practice guidelines across the health spectrum.
There are no data available that describes the efficacy of the PAR-Q (or any other questionnaire) as a screening device. More sophisticated screening tools, including ECGs, may not reduce SCD incidence in adolescent participants (Maron et al. 2009) despite the fact that it may aid in the detection of occult disease when a comprehensive questionnaire is administered (Wilson et al. 2008). Therefore, any changes in the PAR-Q should be focused at increasing the precision of certain questions that may reveal elevated risk of occult CV, particularly symptoms during or following exercise that are closely associated with SCD, including dizziness, syncope, shortness of breath, and chest discomfort. In addition, a process of risk stratification would allow those with intermediate risk to participate in less vigorous and potentially unsupervised PA without further medical screening unless more vigorous PA is desired.
Recommendations specific to the exercise screening process
1.
There are insufficient data to indicate that the PAR-Q should be restricted according to a particular age. Age is highly related to the etiological basis of SCD and it is likely that exercise-related adverse CV events increases with age. Therefore, it recommended that the PAR-Q be used without an age limitation to ensure the scope of screening is maintained over a broad range of the population (Level 3, Grade A).
2.
Symptoms of dizziness and (or) syncope, chest discomfort, and unexplained shortness of breath during or following PA are associated with nonfatal CV events or SCD; however, in most cases SCD is the first clinical event. Despite the limitations of screening questionnaires alone (without ECG) for the detection of cardiac disease, efforts to identify those at high risk by this approach is warranted given the low risk of adverse events. Positive responses to such questionnaires should be used in conjunction with an accepted risk profile algorithm to clarify symptoms or to expand the screening process which may include ECG; the QEP may re-enter the persons into an appropriate level of PA once intermediate or high risk is ruled out, or guide them to further investigation (Level 3, Grade B).
3.
Maximal exercise testing in the apparently healthy population is used extensively in clinical settings for screening for CVD, determination of aerobic fitness in high performance athletics, and in research settings. Given that the risks of maximal exercise testing have been overstated by 20%–25%, the stated risks for fatal events should be 0.2–0.8 per 10 000 tests (rather than 1 per 10 000 tests) and approximately 1.4 per 10 000 tests for nonfatal events (Level 3, Grade B). There is insufficient evidence to attribute an adjusted risk for submaximal exercise testing; however, given that PA risk is related to the intensity of effort, it is likely that the risk is considerably lower than maximal exercise testing.
Areas of research for which information is lacking
1.
Despite the literature describing the benefits of PA on health and physiological function, few prospective exercise training studies have reported adverse events during PA in healthy or diseased populations. This has greatly limited our ability to evaluate the risk of exercise. Future prospective studies should report adverse events, including musculoskeletal and related comorbidities. This would allow for the documentation of actual risks of PA; future reviews and meta analyses can be conducted on the range of adverse events related to PA participation.
2.
The modification of existing standards for exercise testing and risk stratification (Balady et al. 1998; Fletcher et al. 2001; ACSM 2006), along with our current understanding of the risks of PA, should be considered in developing clinical exercise guidelines. The development of evidence-based clinical practice guidelines will aid in determining appropriate PA for those determined to have CV risk factors without detectable disease.
3.
Given the lack of coordinated documentation of exercise-related adverse CV events, the creation of a common registry to systematically document all exertion-related CV events is recommended. This would provide an important database to allow the study of the various factors that increase the risk of adverse CV events during PA.
Acknowledgements
Funded by the Public Health Agency of Canada, administrative support from the CSEP Health and Fitness Program. Special thanks are extended to Dr. Sarah Charlesworth for her technical assistance in the development of this project.
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Applied Physiology, Nutrition, and Metabolism
Volume 36 • Number S1 • July 2011
Pages: S14 - S32
History
Received: 18 September 2010
Accepted: 11 February 2011
Version of record online: 29 July 2011
Notes
This paper is one of a selection of papers published in this Special Issue, entitled Evidence-based risk assessment and recommendations for physical activity clearance, and has undergone the Journal’s usual peer review process.
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© 2011.
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GoodmanJack M., ThomasScott G., and BurrJamie. 2011. Evidence-based risk assessment and recommendations for exercise testing and physical activity clearance in apparently healthy individuals. Applied Physiology, Nutrition, and Metabolism. 36(S1): S14-S32. https://doi.org/10.1139/h11-048