Physical activity during growth increases peak bone mass (14,15,19,21,25,26), and 50% of the variance in bone mineral density (BMD) after age 65 yr is estimated to be predicted by peak bone mass (11). BMD is also considered a risk factor for osteoporosis and related fractures (5,22). Several prospective studies of mature age individuals have provided evidence of an inverse association between physical activity and hip fractures (5,12,18,24,30). However, the evidence of any long-term skeletal benefits after exercise at young adulthood is weak; reports of former athletes have both supported remaining residual benefits (16,27) whereas others have not (15,36). Two recent studies reported remaining benefits in BMD, one after 14 yr of follow-up with 10 yr of reduced training volume (9), the other after 39 yr of follow-up with 29 yr of reduced training volume (32). Still, most prospective studies that follow athletes into retirement suggest that only half of the exercise-induced BMD is maintained after a decade’s retirement from sports (10,27,34) and cross-sectional studies that most BMD benefits are lost with long-term retirement from sport (6,15,17). However, exercise also influences bone size (19,21,26), a trait that contributes to bone strength and fracture risk independently of BMD (1,2,6,8,35) and a trait that may be retained with long-term retirement from sports (6). Superior neuromuscular function (28,31) has also been shown to associate with a reduced fracture risk, partly due to a decreased risk of falling (5,24,29,30). Therefore, the clinically relevant end point variable when investigating the long-term fracture-preventive effects of physical activity should be fracture and not only surrogate end points such as BMD, bone structure, neuromuscular function, or fall frequency.
With these considerations in mind, we designed a retrospective matched controlled cohort study with the aim of investigating if former male elite athletes had a lower incidence of fractures than expected with age. We hypothesized, based on published data in the literature, that this would not be the case after long-term retirement from sports.
In a retrospective cohort design, lifetime fracture epidemiology was collected through a mailed questionnaire in 709 former internationally or nationally ranked male athletes collected from a review book of former Swedish elite athletes, the archives of the Swedish Olympic Committee, and from previously published cohort study of male elite athletes (25). The athletes had a mean age of 69 yr (range = 50–93 yr) and had retired from competitive sports a mean of 34 yr (range = 1–63) earlier (Table 1). There were 397 former soccer players, 147 handball players (also known as team handball or European handball), 69 ice hockey players, 43 canoeists, 20 long-distance runners, 9 weight lifters, 8 gymnasts, 8 swimmers, 6 biathletes, and 2 racing cyclists.
From the Swedish national computerized population records, two male controls were matched to each athlete, by sex and date of birth, and with their names standing closest to the former athlete in the register, giving unrelated individuals. The primary response rate was 74% for the former athletes and 64% for the controls. As our aim was to include two controls for every athlete, we invited the second closest individual in the register in those athletes missing one control and the control cohort from the cited study above (25). This rendered 1368 control participants, with a mean age of 70 yr (range = 51–93 yr), of whom 619 stated they had participated in some sort of athletic training during youth.
The mailed questionnaire, previously used in similar studies (15,27,33), included the evaluation of lifestyle characteristics such as nutrition, alcohol, smoking, occupational load, weekly hours of prior athletic training and competing, and current leisure-time physical activity. Also, data on anthropometrics (weight and height) and fracture incidences were self-reported. Fractures before an active career were defined as fractures sustained before age 15 yr, fractures during an active career were defined as fractures sustained between age 15 and 35 yr, and fractures after an active career were defined as fractures sustained at an age older than 35 yr. The limits chosen were the mean ages for initiation and end of competitive career (Table 1, Fig. 1). Fragility fractures were defined as factures due to a light trauma and after age 50 yr in proximal humerus, distal radius, vertebra, pelvis, hip, and tibial condyles (Table 2). For individuals living in Malmo (n = 439), the fracture ascertainment method was validated against the hospital radiographic archives where all radiographs have been saved for a century (13). All reported fractures after age 50 yr were found in the archives.
Informed written consent was obtained before study start. The study was reviewed and approved by a human research ethics committee and performed in accordance with the Declaration of Helsinki. Statistical calculations were performed using Statistica® (Version 7.1; StatSoft®, Tulsa, OK) and IBM® SPSS® Statistics (Version 20; IBM Corporation, Armonk, NY). Age wise, both of the cohorts were normally distributed (Shapiro–Wilk test). Data are presented as means with 95% confidence interval (CI) or as numbers with proportions (%). Group differences in anthropometrics and lifestyle factors were evaluated using the Student t-test and the chi-square test. Estimates of differences between athletes and controls in time to first fracture were analyzed using Poisson regression and presented as rate ratios (RR) with Kaplan–Meier survival plots. Cox proportional hazards regression was used for calculations of lifestyle-adjusted hazard ratios (HR) for fracture to occur. A P <0.05 was considered a statistically significant difference.
Anthropometry, current lifestyle, and fracture distribution in former athletes and controls are reported in Tables 1 and 2. There was no difference in fracture risk between athletes and controls before athletic career (RR = 0.77, 95% CI = 0.51–1.12). During an active career, athletes had a higher fracture risk (RR = 2.04, 95% CI = 1.57–2.63) than controls. After an active career, former athletes had a lower fracture risk than controls (RR = 0.70, 95% CI = 0.52–0.93) (Table 3, Fig. 1). The former athletes also had a lower risk of sustaining any fragility fracture after age 50 yr (RR = 0.50, 95% CI = 0.27–0.89). Regarding the site-specific risk of sustaining fragility fractures, former athletes had a significant lower risk of sustaining distal radius fractures (RR = 0.29, 95% CI = 0.09–0.74) but not hip fractures (RR = 0.79, 95% CI = 0.28–2.00) (Table 3, Fig. 1).
When using the same model but only comparing the former athletes with those controls reported sedentary during adolescence, the RR of any fragility fracture after age 50 yr was 0.44 (95% CI = 0.23–0.82). When only comparing the former athletes with those controls who reported some athletic training during adolescence, the corresponding RR was 0.61 (95% CI = 0.29–1.24).
When adjusting for group differences in lifestyle factors (occupational workload, smoking, alcohol, disease, and medication) in a Cox proportional hazards regression model, the hazard ratio (HR) of any fracture after an active career became 0.73 (95% CI = 0.54–0.99) and the HR of any fragility fracture after age 50 yr became 0.63 (95% CI = 0.35–1.16). In addition to being a former male elite athlete, also blue-collar work turned out as an independent determinant for any fracture after an active career (HR = 1.58, 95% CI = 1.14–2.18), whereas smoking turned out as an independent determinant for any fragility fracture after age 50 yr (HR = 1.83, 95% CI = 1.01–3.29).
Using the same Cox model with adjustment for covariates reported above and comparing athletes with controls who were sedentary as adolescents and controls who had some degree of athletic participation, the HR of any fragility fracture after age 50 yr became 0.56 (95% CI = 0.28–1.10) and 0.72 (95% CI = 0.36–1.41), respectively.
This study, currently the largest retrospective matched controlled cohort study published, with the aim at estimate any fracture and fragility fracture incidence in old former athletes, shows a 50% lower risk of sustaining fragility fractures in athletes after career end than would be expected with age. It seems as if lifestyle factors in the former athletes may have influenced the fracture risk because the adjusted group differences in fracture risk became slightly attenuated. However, when adjusting for covariates, the group difference for any fracture after an active career remained, although the difference was a significant borderline for any fragility fracture after age 50 yr. Nevertheless, these data indicate that the group differences shown in lifestyle may have influenced the outcome.
Joakimsen et al. (12) have shown that the relevant covariates for hip fracture in association with physical activity are age and sex. Our findings provide further evidence to the hypothesis of physical activity during growth being a preventive strategy against fragility fractures in old age. The hypothesis seems true when investigating mature age individuals prospectively (5,12,18,24,30). Although in the literature there is less evidence of any long-term effects of high-level exercise at youth when using fracture as an end point variable, some reports on former athletes suggesting a lower fracture risk (16,27) whereas others do not (15,36). The discrepancy could be explained by different study designs and examined individuals regarding factors such as sex, age when starting training, level of training, duration of active career, time since career end, and age at the evaluation of the fracture risk. Most studies also include fewer individuals than the current report, inducing a greater risk of making a type II error.
If physical activity was to be recommended as a fracture-prevention instrument, the lifetime risk of sustaining a fracture should also be reduced, which is not evident in this study (Table 3, Fig. 1). The findings of a higher fracture risk in physically active than that in sedentary individuals have also been reported in the literature (3,15). There is evidence of training modalities that do not increase the fracture risk but still produce musculoskeletal benefits (19), and if using similar training modalities (19), structured physical training during younger years may be used to reduce the lifetime burden of fractures.
The causality behind the low fracture risk found in former male athletes is debated. A recent study has reported BMD z-scores around 1.0 in retired athletes (32), which hypothetically would halve the fracture risk (1,5,22). On the contrary, most prospective controlled studies which have followed athletes from active career into retirement indicate a higher rate of BMD loss during the first decade after retirement than would be expected with age (10,27,34). Whether this high rate is temporary or persists with long-term retirement has not been clarified, although cross-sectional studies in elderly former athletes infer that all benefits in BMD will be lost after decades of retirement (6,15,17). Because exercise is also reported to produce larger bone size (19,21), and if the benefits remained long term (1,6), this would modulate fracture risk as bone size contributes to bone strength and fracture risk independently of BMD (1,2,6,8,35). Residual benefits in neuromuscular function may influence fracture risk too as it influences the risk of sustaining falls (5,24,29,30). To complicate the issue even further, exercise on a high level has shown to be associated with an increased incidence of soft tissue hip (7) and knee (20,33) injuries and prevalence of hip and knee OA (23,33), conditions that may lead to a less active lifestyle that is accompanied by low BMD (5) and a higher fracture risk (1,5,22). The low level of physical activity may also lead to less exposure to trauma and thereby, hypothetically, a lower fracture risk (3,15).
The advantages of this study include the large sample size, the controlled study design, and the lifetime inclusion of fracture risk. Limitations include the risk of selection bias with the nonrandomized and retrospective design, making statements about causal relationships between physical activity and fracture risk impossible. Inherited stronger bone and more suitable neuromuscular setup present before the start of training; thus, individuals prone to exercise cannot be ruled out. The recreational level of exercise in the control group may also have influenced the results. However, if all control subjects had been totally sedentary, the group difference in fracture risk ought to have been even more obvious. It would also have been advantageous to have included women and individuals on a more moderate level of physical activity suitable for the general population. The inclusion of a larger athlete cohort, in particular with older former sportsmen in ages when hip fractures occurs (4), had reduced the risk of making a type II error, a possible explanation to why the finding of 30% lower risk of hip fracture among the former sportsmen in our study did not reach statistical significance.
Despite reported limitations, we could conclude that former male elite athletes seem to live a healthier lifestyle, be in better health, and have a lower fracture risk than expected with age, a finding that accounts for all types of fractures as well as fragility fractures.
Financial support was obtained from the Swedish Medical Research Council, the Centre for Sports Medical Research (CIF), the Swedish Society of Medicine, and the Swedish Society of Medical Research. The results of the present study do not constitute endorsement by the American College of Sports Medicine.
The authors declare no conflict of interest.
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