Cardiovascular disease (CVD) is a leading cause of death in the United States. Specifically, heart disease and stroke rank first and third, respectively, as causes of death in the United States in 2007 (9). According to the 2007 mortality rate data, more than 2,200 Americans die each day of CVD (3). Football players represent a unique subset of the American population who may be at increased risk for CVD. Although they are a group whose training does involve varying frequency and intensity of physical activity, the increased size of the average football player, particularly in recent years, may put them at higher risk. A study of retired National Football League (NFL) linemen showed that football players were at an increased risk for death secondary to CVD (4).
Risk factors for CVD include gender, hypertension (HTN), obesity, hypercholesterolemia, diabetes, waist-to-hip circumference ratio, tobacco use, family history of CVD, and sedentary lifestyle. Although there has been a growth in the scientific literature in recent years in regards to the increased risk of football players for these risk factors, at this point, limited data have been published on football players' risk factors for CVD.
Additional potential CVD risk factors include C-reactive protein (CRP), homocysteine (HCY), insulin resistance, and sleep-disordered breathing (SDB). These have not been well studied in populations of football players but may have an independent or additive effect in helping to clarify those who are at increased CVD risk.
The development of CVD risk factors occurs over the course of a lifetime, and thus, an important factor in discussing these risks is not only the measurements during the athlete's playing career but also how these players fare later in their lives. Therefore, the focus of the present review includes studies of retired players who, although no longer active in football, may reflect lifelong changes in cardiovascular risk associated with having participated in the sport.
CVD Risk Factors
The Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation and Treatment of High Blood Pressure (JNC7) defines HTN as a systolic blood pressure (SBP) >140 mm Hg and diastolic blood pressure (DBP) >90 mm Hg "based on the average of two or more properly measured, seated BP readings on each of two or more office visits" (46).
Furthermore, JNC7 defined "prehypertension" as an SBP between 120 and 139 mm Hg and/or a DBP between 80 and 89 mm Hg. Prehypertensive patients are encouraged to pursue lifestyle modifications including weight reduction, the Dietary Approaches to Stop Hypertension (DASH) diet, physical activity, and moderation of alcohol consumption (46). Often in football players, weight reduction is not considered to be a viable option particularly at higher levels of participation because of perceived negative effects of lower weight on performance.
Factors that affect the measurement of BPs in football players include timing of BP measurement and cuff size. Frequently, preparticipation examinations and other medical evaluations of athletes are done in close proximity to athletic activity, and it is imperative to get true resting measurements with the athlete in a seated position. Also, given the larger arm circumference of many football players, a cuff bladder that encircles at least 80% of the arm should be used for an accurate BP reading.
There have been limited studies in regards to BP readings in football players. In 2009, Tucker et al. (47) reported on CVD risk factors in 504 NFL players in comparison to a sample of healthy young adult men and found an increased risk of HTN (13.8% vs 5.5%) and prehypertension (64.5% vs 24.2%). In this study, these values did not differ significantly according to position. An important limitation in their study was that the BP measurements in the professional football players were done on only one occasion. The study authors did set up procedures to ensure that the players were seated and resting for 5 min prior to the readings. In addition, biceps measurements were made to ensure proper cuff size. Interestingly, they found a decrease in other CVD risk factors as discussed below (47).
In a survey of 36 of 41 NFL players performed 35 years after Super Bowl 1969, 13 of 36 participants were noted to carry a diagnosis of HTN (30). In a study assessing metabolic syndrome, Wilkerson et al. (50) showed a mean SBP and DBP in the prehypertensive range in 62 collegiate football players.
Given the limited data on HTN in football players, further studies need to be performed. In particular, there may be an increased prevalence of prehypertension in the younger football athletes suggesting the possibility of increased rates of HTN as football players' age.
Dyslipidemia is also an important risk factor for CVD. The Adult Treatment Panel III (ATP III) lists guidelines for fasting blood cholesterol (Table). Risks for CVD events are determined by correlation with known presence of atherosclerotic disease in the individual, as well as major risk factors for CVD (13). Treatment options include dietary changes, weight management, increased physical activity, and, ultimately, medications if indicated.
Lynch et al. (25) compared lipid profiles of former professional football players with age-, body mass index (BMI)-, current activity level-, and race-matched never-athletic men and revealed that high-density lipoprotein cholesterol (HDL-C) was 37% higher and triglycerides were 31% lower in the former players, suggesting that previous participation may have conferred a long-lasting positive lipid effect. Garry and McShane (14) studied the lipid profiles and BMI of 70 NFL players and found lower HDL levels, higher triglyceride levels, and higher total cholesterol-to-HDL ratios with increasing BMI. An association between a lower BMI and a more desirable lipid profile was found in this population of athletes. In the largest study of football players and lipid levels to date, Tucker et al. (47) found no difference in the prevalence of abnormal cholesterol, low-density lipoprotein cholesterol, or HDL-C between NFL players and age- and race-matched controls. The study authors hypothesized that the higher level of physical activity of these football players helped to compensate for their increased size.
To our knowledge, no study has been performed on football players specifically using ATP III guidelines for risk assessment. Given the recognized association between dyslipidemia and CVD, an investigation of the lipid levels in football players in conjunction with other risk factors to determine the true incidence of dyslipidemia in this patient population would appear critical.
Obesity has been independently linked to chronic conditions including diabetes, HTN, hypercholesterolemia, heart disease, certain cancers, and arthritis (26). Obesity has been shown to be an independent risk factor of CVD (12,19). BMI, waist-to-hip circumference ratio, and body composition are three measures that can be used to assess obesity.
There is abundant evidence to support the use of BMI as a marker of obesity. Increased BMI has been shown to be a risk factor for CVD (5). Numerous studies have reported that the BMI of professional, collegiate, and high school football linemen is above the healthy range (14,16,20,22,24,32). Football position and BMI were found to correlate in a study of 70 NFL players. Linemen were found to have the highest average BMI (38.1 kg·m−2) and 100% of the linemen had a BMI >32 kg·m−2 (14). A study of 3,683 high school football linemen reported that, by BMI criteria, 45% were overweight compared to the 18.3% prevalence of overweight in boys aged 12 to 19 years reported in the National Health and Nutrition Examination Survey 2003 to 2004 (24). Finally, Harp and Hecht (17) reported on the BMI of 2,168 NFL players and found that 97% had a BMI of >25 kg·m−2.
While BMI might be easy to measure and calculate, it may not adequately reflect obesity in athletic populations. A study of BMI and body fat percentage in college athletes (including football players) suggested that a BMI cutpoint of 27.9 and 34.1 kg·m−2 for the classification of obesity, rather than the standard 30 kg·m−2 used for the general population, be used for male athletes and football linemen, respectively (32).
Body composition, rather than body weight, has been shown to be a risk factor for CVD in men (44). Multiple studies in football players, both collegiate and professional, have shown a discrepancy between mean BMI values, which typically fall in the obese range, and mean body fat percentages, which are typically within a healthy range (20,22,32).
Reports have shown that body fat in professional football players, especially in certain player positions, is increasing. This may be an important variable to measure when considering risk of CVD (21,45). Snow et al. (45) reported higher body fat percentages in professional football players, especially in linemen, studied in the mid to late 1990s compared to their counterparts studied in the 1970s with values ranging from 7% to 31%.
Body composition measured by dual-energy x-ray absorptiometry (DXA) allows for analysis of the body regions or segments in which the fat and muscle are being gained or lost, which may be an important factor due to the link between central obesity and CVD (8). A study of 16 former professional football players compared to never-athletic men matched for age, BMI, current physical activity, and race found, by DXA measurements, 13% higher muscle mass, 26% lower body fat mass, and 26% lower visceral fat tissue area in former players versus controls (25).
Waist-to-hip circumference ratio
The waist-to-hip circumference ratio is a measure of central obesity and has been shown to be the best anthropometric measurement to predict myocardial infarction across all ages, genders, and ethnic groups. This has also been shown to predict for multiple CVD risk factors (HTN, tobacco use, dyslipidemia, and diabetes) (54). This ratio has not been reported in collegiate or professional football players.
Poor cardiovascular fitness has been shown to be an independent risk factor for CVD and is as important a predictor of CVD as diabetes, HTN, obesity, and tobacco use (48). Cardiovascular fitness is measured by tests of aerobic capacity such as the maximal oxygen uptake test (V˙O2max). V˙O2 is defined as the maximum capacity of an individual's body to transport and utilize oxygen during incremental exercise. V˙O2max testing generally is felt to be the single best measure of cardiovascular fitness. Football tends to be an anaerobic sport, and studies of collegiate and professional football players have found cardiovascular fitness levels similar to age-matched controls (36). A study of former professional football players found, despite greater physical activity into middle age, that the football players and age-, BMI-, race-, and current physical activity-matched controls had similar CV fitness levels (25).
Other Potentially Important CVD Risk Factors
Results from both large cohort studies and clinical trials indicate that although 80% to 90% of those who experience coronary heart disease (CHD) events bear one or more of the main risk factors for the disease (HTN, hyperlipidemia, smoking, and diabetes), roughly 70% of those with one or more major risk factors never go on to develop CHD (15,21). Thus, the major CHD risk factors are quite sensitive (90%) but poorly specific (30%) (42). Accordingly, additional determinants of CHD risk have been sought. In particular, CRP, HCY, insulin resistance, and SDB may be specifically relevant to football players.
Significant advances in the understanding of the importance of atherothrombosis from plaque rupture in the pathogenesis of CHD events have led to a search for biomarkers of inflammation that may extend the predictive capabilities of the traditional major risk factors. CRP, an acute-phase reactant, is the best-studied biomarker for CHD-relevant inflammation and has been identified as the best available biomarker for this purpose (34).
The magnitude of risk imposed by elevated high-sensitivity CRP (hsCRP) values has been asserted to be similar to that imposed by high cholesterol or BP (39,40). CRP appears particularly useful in distinguishing those individuals with higher risk for CHD from among those previously labeled with intermediate risk by Framingham scoring (41).
Numerous studies have investigated the relationships between physical activity and hsCRP levels (37). Both long-term physical activity (2,36) and cardiorespiratory fitness (8,23) have been demonstrated to vary inversely with CRP levels. Further, CRP levels may decrease in response to exercise (37). The effects of elite-level training on CRP may be sport specific (11). Although we were unable to identify any studies of CRP among football players, this may be a potentially useful marker for future investigation.
HCY is a sulfur-containing amino acid generated from the essential amino acid methionine (49). Both case-control and prospective observational studies have identified an increased HCY level as an independent cardiac risk factor (10), with levels greater than 15 μmol·L−1 yielding a 2.4-fold increase in CHD (43). Physical activity results in increased HCY, either acutely or during prolonged exercise (18,33,51). Of great relevance to football athletes, a significantly higher percentage of athletes participating in winter sports bear elevated HCY levels when compared to nonathletic controls (6). A recent Italian study (7) identified 47% of athletes versus 15% of controls with elevated HCY levels even after controlling for BP, plasma folate or vitamin B12, cholesterol, lactate dehydrogenase, creatine kinase, or interleukin-6. Finally, users of anabolic steroids were demonstrated by a recent study to have higher HCY levels than weightlifting or sedentary controls, with differences not explained by serum levels of folate or vitamin B12. Of note, 3 of the 40 subjects in the study died suddenly from CVD, all of whom had elevated HCY levels (16). HCY offers another prospective area of study in assessing cardiovascular risk among football players.
It has been recognized for nearly 50 years that certain individuals respond to oral glucose challenge with higher levels of plasma immunoreactive insulin, and such individuals are defined as "insulin resistant" (52). The nature of the interrelationships among obesity, insulin resistance, type II diabetes, HTN, and increased CVD risk, collectively termed the "metabolic syndrome," has been addressed in a myriad of studies (38). Through such efforts, it has become clear that, of those with obesity, it is only the 30% with insulin resistance who likely are experiencing the associated set of abnormalities of the metabolic syndrome, including glucose intolerance, hyperinsulinemia, dyslipidemia, elevated CRP, and increased risk for CVD (38). Accordingly, insulin resistance has been identified as an independent risk factor for CVD, type 2 diabetes, and HTN (11,53,54).
The "gold standard" technique for assessing insulin resistance, the steady-state hyperinsulinemic clamp, is expensive, time-consuming, and invasive (27). One alternative method, the homeostasis model assessment, was generated through mathematic modeling of the normal physiologic relationship between fasting insulin and glucose, yielding the homeostatis model assessment-insulin resistance (HOMA-IR) (36). The logarithmic transformation of this value (logHOMA-IR) has been found to yield improved correlations with the values obtained from clamp assessments (25).
A recent cross-sectional prevalence study has identified dramatically higher rates of the metabolic syndrome and its component criteria among retired NFL linemen versus non-linemen. Specifically, BMI >30 kg·m−2 (85.4% vs 50.3%, P < 0.001), reduction in HDL-C (42.1% vs 32.7%, P = 0.04), and increase in fasting glucose (60.4% vs 37.6%) were each noted to be significantly more prevalent among former linemen. The syndrome itself, as defined by International Diabetes Federation criteria (2), also was significantly more frequent among the linemen than the nonlinemen (59.8% vs 30.1%, P < 0.001) (29). The authors conclude that these data may explain part of the increased risk for cardiovascular death, beyond that imposed by BMI alone, demonstrated for former NFL linemen versus non-linemen by the National Institute of Occupational Safety and Health Mortality Study (1).
Obstructive sleep apnea, which is a common diagnosis under the classification of SDB, has been linked to HTN; HTN is a well-known risk factor for the development of CVD. Even asymptomatic SDB has been found to be a risk factor for HTN (31,35). In a study of SDB among professional football players, the overall prevalence was 14%, which is increased compared to men of similar age, and furthermore, offensive and defensive linemen appeared to be the positions at the greatest risk (15). To our knowledge, there have not been other studies on SDB in football players, but SDB may represent an important risk factor for the development of HTN and future CVD.
In conclusion, several lines of evidence suggest that football players may have significantly increased cardiovascular risk. Paradoxically, there may be a cardioprotective effect associated with the higher levels of football. Future studies will help to elucidate the relationship between playing football and cardiovascular risk.
NFL Charities has provided a grant to authors Hecht and Concoff for a research study on cardiovascular risk factors in collegiate athletes.
1. Albert MA, Glynn RJ, Ridker PM. Effect of physical activity on serum C-reactive protein. Am. J. Cardiol.
2. Alberti KG, Zimmet P, Shaw J. Metabolic syndrome - a new world-wide definition. A consensus statement from the International Diabetes Federation. Diabet. Med.
3. American Heart Association. Executive summary: heart disease and stroke statistics - 2011 update: a report from the American Heart Association. Circulation
. 2011; 123:459-63.
4. Baron S, Rinsky R. NIOSH Mortality Study of NFL Football Players 1959-1988
. Cincinnati (OH): Center for Disease Control, National Institute of Occupational Safety and Health; 1994.
5. Bogers RP, Bemelmans WJ, Hoogenveen RT, et al
. Association of overweight with increased risk of coronary heart disease partly independent of blood pressure and cholesterol levels: a meta-analysis of 21 cohort studies including more than 300 000 persons. Arch. Intern. Med.
6. Borrione P, Pigozzi F, Massazza G, et al
. Hyperhomocysteinemia in winter elite athletes: a longitudinal study. J. Endocrinol. Invest.
7. Borrione P, Rizzo M, Spaccamiglio A, et al
. Sport-related hyperhomocysteinaemia: a putative marker for muscular demand to be noticed for cardiovascular risk. Br. J. Sports Med.
8. Brownbill RA, Ilich JZ. Measuring body composition in overweight individuals by dual energy x-ray absorptiometry. BMC Med. Imaging
. 2005; 5:1.
10. Chambers JC, Seddon MD, Shah S, Kooner JS. Homocysteine - a novel risk factor for vascular disease. J. R. Soc. Med.
11. Dufaux B, Order U, Geyer H, Hollmann W. C-reactive protein serum concentrations in well-trained athletes. Int. J. Sports Med.
12. Expert Panel on the Identification, Evaluation, and Treatment of Overweight and Obesity in Adults. Executive summary of clinical guidelines for identification, evaluation and treatment of overweight and obesity in adults. Arch. Intern. Med.
13. Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults. Executive summary of the Third Report of the National Cholesterol Education Program (NCEP) Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults (Adult Treatment Panel III). JAMA
. 2001; 285:2486-97.
14. Garry JP, McShane JJ. Analysis of lipoproteins and body mass index in professional football players. Prev. Cardiol.
15. George CF, Kab V, Levy AM. Increased prevalence of sleep-disordered breathing among professional football players. N. Engl. J. Med.
16. Graham MR, Grace FM, Boobier W, et al
. Homocysteine induced cardiovascular events: a consequence of long term anabolic-androgenic steroid (AAS) abuse. Br. J. Sports Med.
17. Harp JB, Hecht L. Obesity in the National Football League. JAMA
. 2005; 293:1061-2.
18. Hermann M, Schorr H, Obeid R, et al
. Homocysteine increases during endurance exercise. Clin. Chem. Lab. Med.
19. Hubert HB, Feinleib M, McNamara PM, Castelli WP. Obesity as an independent risk factor for cardiovascular disease: a 26-year follow-up of participants in the Framingham Heart Study. Circulation
. 1983; 67:968-77.
20. Kasier GE, Womack JW, Green JS, et al
. Morphological profiles for first-year National Collegiate Athletic Association Division I football players. J. Strength Cond. Res.
21. Khot UN, Khot MB, Baizer CT, et al
. Prevalence of conventional risk factors in patients with coronary heart disease. JAMA
. 2003; 290:898-904.
22. Kraemer WJ, Torine JC, Silvestre R, et al
. Body size and composition of National Football League players. J. Strength Cond. Res.
23. LaMonte MJ, Durstine JL, Yanowitz FG, et al
. Cardiorespiratory fitness and C-reactive protein among a tri-ethnic sample of women. Circulation
. 2002; 106:403-6.
24. Laurson KR, Eisenmann JC. Prevalence of overweight among high school football linemen. JAMA
. 2007; 297:363-4.
25. Lynch NA, Ryan AS, Evans J, et al
. Older elite football players have reduced cardiac and osteoporosis risk factors. Med. Sci. Sports Exerc.
26. Malnick SD, Knobler H. The medical complications of obesity. QJM
. 2006; 99:566-79.
27. Mather KJ, Hunt AE, Steinberg HO, et al
. Repeatability characteristics of simple indices of insulin resistance: implications for research applications. J. Clin. Endocrinol. Metab.
28. Matthews DR, Hosker JP, Rudenski AS, et al. Homeostasis model assessment: insulin resistance and beta-cell function from fasting plasma glucose and insulin concentrations in man. Diabetologia. 1985; 28:412-9.
29. Miller MA, Croft LB, Belanger AR, et al
. Prevalence of metabolic syndrome in retired National Football League players. Am. J. Cardiol.
30. Nicholas SJ, Nicholas JA, Nicholas C, et al
. The health status of retired American football players: Super Bowl III revisited. Am. J. Sports Med.
31. Nieto FJ, Young TB, Link BK, et al
. Association of sleep-disordered breathing, sleep apnea, and hypertension in a large community-based study. Sleep Heart Health Study. JAMA
. 2000; 283:1829-36.
32. Ode JJ, Pivarnik MJ, Reeves MJ, Knous JL. Body mass index as a predictor of percent fat in college athletes and nonathletes. Med. Sci. Sports Exerc.
33. Okura T, Rankinen T, Gagnon J. Effect of regular aerobic exercise on plasma homocysteine concentrations: the HERITAGE Family Study. Med. Sci. Sports Exerc.
34. Pearson TA, Mensah GA. Markers of inflammation and cardiovascular disease: application to clinical and public health practice: a statement for healthcare professionals from the Centers for Disease Control and Prevention and the American Heart Association. Circulation
. 2003; 107:499-511.
35. Peppard PE, Young T, Palta M, Skatrud J. Prospective study of the association between sleep-disordered breathing and hypertension. N. Engl. J. Med.
36. Pitsavos C, Chrysohoou C, Panagiotakos DB, et al
. Association of leisure-time physical activity on inflammation markers (C-reactive protein, white blood cell count, serum amyloid A, and fibrinogen) in healthy subjects (from the ATTICA study). Am. J. Cardiol.
37. Plaisance EP, Grandjean PW. Physical activity and high-sensitivity C-reactive protein. Sports Med.
38. Reaven G, Abbasi F, McLaughlin T. Obesity, insulin resistance, and cardiovascular disease. Recent Prog. Horm. Res.
39. Ridker PM, Cushman M, Stampfer MJ, et al
. Inflammation, aspirin, and the risk of cardiovascular disease in apparently healthy men. N. Engl. J. Med.
40. Ridker PM, Glynn RJ, Hennekens CH, et al
. C-reactive protein adds to the predictive value of total and HDL cholesterol in determining risk of first myocardial infarction. Circulation
. 1998; 97:2007-11.
41. Ridker PM, Rifai N, Rose L, et al
. Comparison of C-reactive protein and low-density lipoprotein cholesterol levels in the prediction of first cardiovascular events. N. Engl. J. Med.
42. Root M, Cobb F. Traditional risk factors for coronary heart disease. JAMA
. 2004; 291:299. Letter.
43. Sadeghian S, Fallahi F, Salarifar M, et al
. Homocysteine, vitamin B12
and folate levels in premature coronary artery disease. BMC Cardiovasc. Disord.
44. Segal KR, Dunaif A, Gutin B, et al
. Body composition, not body weight, is related to cardiovascular disease risk factors and sex hormone levels in men. J. Clin. Invest.
45. Snow TK, Millard-Stafford M, Rosskopf LB. Body composition profile of NFL football players. J. Strength Cond. Res.
46. The Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure: the JNC 7 report. JAMA
. 2003; 289:2560-72.
47. Tucker A, Vogel RA, Lincoln AE, et al
. Prevalence of cardiovascular disease risk factors among National Football League players JAMA
. 2009; 301:2111-9.
48. Wei M, Kampert JB, Barlow CE, et al
. Relationship between low cardiorespiratory fitness and mortality in normal-weight, overweight, and obese men. JAMA
. 1999; 282:1547-53.
49. Wierzbicki AS. Homocysteine and cardiovascular disease: a review of the evidence. Diab. Vasc. Dis. Res.
50. Wilkerson GB, Bullard JT, Bartal DW. Identification of cardiometabolic risk among collegiate football players. J. Athl. Train
. 2010; 45:67-74.
51. Wright M, Francis K, Cornwell P. Effect of acute exercise on plasma homocysteine. J. Sports Med. Phys. Fitness
. 1998; 38:262-5.
52. Yalow RS, Berson SA. Immunoassay of endogenous insulin in man. J. Clin. Invest
. 1960; 39:1157-75.
53. Yip J, Facchini FS, Reaven GM. Resistance to insulin-mediated glucose disposal as a predictor of cardiovascular disease. J. Clin. Endocrinol. Metab.
54. Yusuf S, Hawken S, Ounpuu S, et al
. Obesity and the risk of myocardial infarction in 27,000 participants from 52 countries: a case-control study. Lancet
. 2005; 366:1640-9.