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At the time of the study, Dr. Atwal was a resident in the Department of Family Medicine, Dalhousie University, Halifax, NS. Dr. Porter is with the Department of Human Kinetics, University College of Cape Breton, Sydney, NS. Dr. MacDonald is with the Department of Cardiology, Cape Breton Regional Hospital, Sydney, NS.
Correspondence to: Dr. Paul MacDonald, Cape Breton Regional Hospital, 1482 George St., Sydney NS B1P 1P3; fax 902 567-8009; paulmdcb@ns.sympatico.ca; www.hockeyheart.com
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Abstract |
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Methods: We assessed baseline cardiac risk factors in 113 male volunteers recruited from a recreational hockey league. Each subject underwent holter electrocardiographic monitoring before, during and after at least one hockey game (maximum of 115 holter data sets). We used the data to assess exercise heart rate, arrhythmias and ST-segment changes and for correlation with symptoms and other predictors of fitness.
Results: For all participants, maximum heart rate (HRmax) (mean 184 [standard deviation 11] beats/min) was greater than target exercise heart rate (calculated as 55% to 85% of age-predicted HRmax), and in 87 (75.6%) of the 115 holter data sets, the heart rate exceeded the age-predicted HRmax. The mean period for which heart rate exceeded 85% of the age-predicted HRmax was 30 (SD 13) min. For 80 (70.1%) of 114 data sets, heart rate recovery was poor. Nonsustained ventricular tachycardia was seen in data from 2 holter monitoring sessions and ST-segment depression in data from 15 sessions.
Interpretation: The physical activity pattern that occurred during recreational hockey caused cardiac responses that might be dangerous to players' health. More specifically, the players exceeded target and maximum heart rates, had poor heart rate recovery after exercise, and had episodes of nonsustained ventricular tachycardia and ST-segment depression of uncertain clinical significance.
The benefits of exercise have been well studied. Mild to moderate exercise at an intensity level of as low as 40% to 50% of maximum oxygen uptake reserve or 55% to 65% of age-predicted maximum heart rate (HRmax) is associated with better fitness and fewer cardiac events.7,8,11,12,13 Maximum oxygen uptake can be measured in specialized cardiac rehabilitation clinics but is either not available or not widely accessible to the general public. Predicted HRmax can be easily calculated from age (HRmax = 220 – age in years).14 Concerns have been raised about risk for cardiac events, as well as musculoskeletal injuries, with higher-intensity exercise.7
We hypothesized that some participants in adult recreational hockey may not have adequate conditioning for intense competitive exertion, and we therefore sought to analyze their cardiac risk factors as well as measuring heart rates, arrhythmias and unrecognized ischemia.
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Two participants per hockey game were outfitted with a Marquette holter electrocardiographic monitor (General Electric, Milwaukee) placed on the hip under the person's hockey pads. Leads were attached with Medi-Trace (Kendall-LTP, Chicopee, Mass.) or BioTac (Kendall-LTP) connectors in a standard 7-lead fashion.15 Monitoring was conducted throughout the hockey game (60 to 90 minutes) and for a 20-minute cool-down period after the game. Body mass index (BMI) and waist to hip ratio,16 a 12-lead electrocardiographic tracing, and fasting sugar and cholesterol levels were also obtained.
Data from leads V1 and V5 of the 7-lead holter monitors were analyzed by Schiller Scanner software (model NP147, version 3.1, Century Advanced, Ottawa, Ont.) and reviewed by a cardiologist (P.M.) to determine observed HRmax, number of beats by which observed HRmax exceeded the target heart rate (THR), the period for which heart rate exceeded THR, heart rate 1 minute after exercise, and presence of ectopic beats, sustained arrhythmias and ST-segment depression. Age-predicted HRmax was calculated as 220 – age,14 and THR was defined as 55% to 85% HRmax.17,18
ST segment changes were classified as either suspicious (flat ST segment or 1- to 2-mm ST-segment depression in one lead) or highly suspicious (ST-segment depression of more than 2 mm in one lead). ST-segment depression of less than 1 mm or upsloping ST segment was considered normal. Participants with suspicious ST-segment changes were investigated with standard exercise stress testing according to the Bruce protocol.12 If the findings were suspicious, the participant underwent further evaluation with a 2-day nuclear sestamibi stress test.
Means and standard deviations were calculated for baseline parameters and cardiac risk factors.
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Symptoms reported while playing hockey included one report each of shortness of breath, palpitations, and chest pain or heaviness.
A total of 115 sets of monitoring data were available for analysis (see Table 1). Observed HRmax exceeded THR in all participants (Fig. 1) for a mean of 30 minutes. Observed HRmax exceeded age-predicted HRmax in 87 (75.6%) of the 115 data sets.
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In 80 (70.1%) of 114 data sets, heart rate had slowed by less than 12 beats/min at 1 minute after cessation of exercise.
Holter monitoring revealed isolated supraventricular and ventricular ectopic beats, as well as short runs of supraventricular tachycardia. Atrial fibrillation occurred in one subject and nonsustained ventricular tachycardia (runs of more than 3 beats lasting less than 30 seconds) in 2 patients. Of the 2 patients with nonsustained ventricular tachycardia, one had a significant amount of arrhythmia, especially in the cool-down period. The results of subsequent sestamibi stress testing (during which he attained a heart rate of 170 beats/min with no ventricular arrhythmia) and cardiac ultrasonography were normal. The second patient had many fewer episodes of ventricular tachycardia (short runs). Exercise stress testing yielded negative results (13 metabolic equivalents [METs; 1 MET = 3.5 mL O2/kg/min]) with no ectopy, and sestamibi study yielded positive results; however, the latter was considered a false positive because of normal wall motion.
Flat or downsloping ST-segment depression was identified. Exercise stress tests were performed for 17 other subjects, of whom 15 exhibited ST-segment depression on holter monitoring; in addition, 1 had atypical chest pain, and 1 had supraventricular arrhythmia. For 10 of the subjects with ST-segment depression, the results of exercise stress testing were normal. For the other 5, the results of exercise stress testing were abnormal, but the results of subsequent sestamibi stress testing were normal. These subjects had no significant cardiac disease.
There was a trend toward higher resting heart rates for older participants compared with younger participants (95% confidence interval [CI] –6.6 to 0.2, p = 0.06). Older participants had significantly lower maximum heart rates (95% CI 0.1 to 8.3, p < 0.05) but a greater number of beats (95% CI –249 to –8, p < 0.05) and they exercised a greater percentage of time above 85% of their maximum heart rate (95% CI –11 to –0.3, p < 0.05). Heavier hockey players tended to have fewer heart beats above the target (95% CI –9 to –233, p = 0.07), higher cholesterol levels ( 95% CI –0.8 to –0.4, p = 0.03) and higher triglyceride levels (95% CI –1.1 to –0.3, p < 0.001). Players who exercised 3 or more times per week had a slower heart rate recovery 1 minute after exercise (95% CI –13.8 to –0.2, p < 0.05).
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The American College of Sports Medicine7 recommends an intensity of training from 55% or 65% to 90% of age-predicted HRmax. The college further cautions that "Higher-intensity exercise is associated with greater cardiovascular risk and orthopaedic injury."7 Although the benefits of exercise are widely recognized,8,9,10 there have also been reports of an increase in frequency of cardiac events and sudden death triggered by vigorous exercise.3,4,6 Regular exercise seems to diminish this risk.6,20
It is important to emphasize that no adverse events occurred during our study. Franklin and colleagues21 reported that moderate to vigorous exercise was associated with a mortality rate of 1 per 50 000 among people who exercised infrequently, a rate above that in the general population.
Willich and collaborators,4 in a retrospective analysis, found that 7.1% of patients who presented with myocardial infarction but only 3.9% of the control group were engaged in physical exertion at the time of the myocardial infarction (relative risk 2.1). Those who exercised fewer than 4 times per week had a relative risk of 6.9, whereas the relative risk was just 1.3 for those who exercised 4 times or more per week (p < 0.01). Mittleman and associates3 found that 4.4% of patients who had experienced myocardial infarction had been involved in heavy exertion. The relative risk (compared with little or no exertion) was 5.9. Again, regular exercise was shown to greatly attenuate the risk.
The subset of 19 participants (16.8%) who underwent exercise stress testing in this study all reached or exceeded 85% of age-predicted HRmax at a workload of 7 to 17.2 METs (mean >> 10 METs). Although the sample was small, this finding indicates the relatively high intensity of recreational hockey. In addition, there is generally little or no warm-up before recreational games, nor are substitutes, interruptions or rest periods available to allow players to cool down.
The limitations of this study include the small sample size and a lack of a control group. Some subjective features were observed that were not prespecified or objectively measured, such as limited warm-up and rest periods. Finally, sestamibi stress testing is not the gold standard for coronary artery disease, and subclinical obstructions may have been missed. Cardiac catheterization was not available in our community, and in any case the potential risks associated with this procedure would have made it ethically impractical to use for asymptomatic volunteers.
It is important to maintain a balanced perspective on risks. Although the relative risk may be significantly increased during strenuous exercise, the absolute risk of sudden death is just 1 per 1.5 million episodes of vigorous exercise.6 If 500 000 Canadian men each play hockey 30 times a year, this would account for 10 deaths.
In conclusion, the participants in our study, men playing recreational hockey, were generally healthy. No adverse events were observed, but all participants experienced high heart rates for prolonged periods of time. Arrhythmias and ST-segment changes of uncertain clinical significance were also noted.
ß See related article page 331
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Footnotes |
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Contributors: Dr. Atwal was involved in study design and background research, recruitment of subjects, attachment of holter monitors and collection of data, as well as data analysis and writing of the manuscript. Dr. Porter was involved in study design, recruitment of subjects and manuscript preparation. Dr. MacDonald was involved in study design and background research, data analysis (including data from holter monitors, exercise stress testing, sestamibi stress testing and electrocardiography) and manuscript preparation.
Acknowledgements: We thank Dr. Frank Renwick, University College of Cape Breton, for statistical assistance with this manuscript. We also thank Cathy Smith for her work on the manuscript and Georgette Sparks, Cathy Butler and Rose Flood for technical assistance. This research was supported by the Cape Breton Regional Hospital.
Competing interests: None declared.
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This article has been cited by other articles:
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  M. Shulman The good old hockey game Can. Med. Assoc. J., April 1, 2002; 166(9): 1131 - 1131. [Full Text] [PDF]
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E. A. Cohen The good old hockey game Can. Med. Assoc. J., April 1, 2002; 166(9): 1131 - 1131. [Full Text] [PDF]
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M. A. Mittleman The double-edged blade of recreational hockey Can. Med. Assoc. J., February 1, 2002; 166(3): 331 - 332. [Full Text]
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