Adult bone mineral density (BMD) is dependent on many variables. The greatest determinant of adult BMD is peak bone mass achieved during the adolescent years. Moderate- to high-impact exercise during growth has been shown to significantly increase peak bone mass (3,9,17,22). Studies have demonstrated that young athletes have higher bone density than their nonathlete counterparts (2,31). After the third decade of life, peak bone mass typically has been achieved. It is at this point that weight-bearing exercise becomes important in the maintenance of one's total BMD (30).
But is all exercise created equal? Research studies in endurance athletes, including adult male cyclists, have shown that not all forms of exercise have the same beneficial effects on BMD (6,12,13,21,24,27,30). The exact reasons for this have not yet been fully elucidated in the literature. Many studies have been conducted in an attempt to identify the causative factors, but data are mixed and additional, focused research is needed. Training-related suppression of sex hormones, energy imbalances, training volume, exertional calcium losses and inadequate intake, and mechanical loading stressors all have been evaluated in relationship to BMD (2,20,23,36,37). These variables alone and in concert can affect the relationship that weight-bearing exercise has on BMD.
BONE METABOLISM AND ADAPTATION
Direct evaluation of BMD is done by using dual x-ray absorptiometry (DEXA). Various sites can be used for assessment. Clinically significant sites include the lumbar spine, total hip, and femoral neck. The World Health Organization's definition of osteoporosis is a T-score at or below −2.5 standard deviations below peak young adult BMD, and osteopenia is a T-score between −1 and −2.5 standard deviations. Indirect evaluation of bone remodeling can be performed by measuring serum hormones and bone turnover markers. Hormones involved in bone remodeling include testosterone, estradiol, dehydroepiandrosterone (DHEA), cortisol, and free triiodothyronine (fT3). Alkaline phosphatase (bone-AP) and osteocalcin (OC) are secreted by osteoblasts and are markers of bone formation. C terminal telopeptide of type I collagen (CTX) is released when bone collagen is broken down and is a marker of bone resorption (23).
Animal studies have demonstrated the processes by which bone adapts to different external mechanical stimuli, allowing for a better understanding of how different sports may exhibit various different effects on BMD (25,33). Muscle tension at the site of its attachment during the contraction process produces the force that stimulates new bone formation (23). Sports that produce unevenly distributed, high-magnitude forces at high frequencies generate the greatest osteogenic stimuli (22). Bone response to mechanical loading is proportional to ground reaction forces and is site-specific (4,5,26,30). Cross-sectional studies of BMD in athletes who participate in high-impact sports, such as gymnastics, running, weight-lifting, and other running and jumping sports support these claims (1,7,18). Low-impact and nonweight-bearing sports, such as swimming and road cycling, do not have the same positive effects on BMD (30,32).
In a cross-sectional study, Warner et al. compared total and regional BMD in two different disciplines of cycling, road and mountain, both to each other and with age-matched, recreationally active controls. When BMD was adjusted for body weight and controlled for age differences, the mountain cyclists had significantly higher BMD at all sites measured when compared with both the road cyclists and the recreationally active controls (35). The authors propose that this may be caused by inherent differences in the two types of cycling, including the larger ground-surface-induced loads experienced in mountain cycling from terrain differences (8) as well as the greater loading at the legs through the pedals resulting from the increased time spent with two points of contact (hands and feet) in mountain cycling versus the three points of contact (hands, seat, and feet) more typical of road cycling (34).
Cycling is a high-intensity, low-impact, aerobic endurance activity that is performed in a relatively fixed body position (35). The biomechanics inherent to cycling produce a relatively low magnitude, evenly distributed muscular strain pattern. The combination of these factors may explain why cycling creates a weak osteogenic stimulus (20). But is that the whole story? The literature says that endurance exercise can lead to hormonally mediated suppression of bone turnover, both directly and indirectly. Hormone synthesis and secretion can be altered directly by exercise itself. In addition, hormonal homeostasis also can be altered indirectly through energy deficits created by exercising (10,14,27,37).
In a cross-sectional study, Nichols et al. compared the BMD of a group of master cyclists, aged 40 to 60 yr old, riding at least 150 miles or 10 h·wk-1 for a minimum of 10 yr with a group of young cyclists and an otherwise healthy group of sedentary controls. These younger cyclists ranged in age from 25 to 35 yr old, with a similar cycling profile to the masters except for a minimum duration of 5 yr. The group found that, when compared with the healthy men, matched for age and body weight, the master cyclists had lower BMD at the hip and spine. Of the master cyclists, 67% had low BMD at either or both the hip and the spine, 52% were osteopenic, and 15% were osteoporotic. Of the sedentary control subjects, 42% had low BMD classified as osteopenic, and none were osteoporotic. Of the young cyclists, 25% had osteopenia of the lumbar spine (20). The authors claim that these findings confirm previously reported studies that detail that long-term participation in cycling alone, with little or no exposure to impact or resistance activities, may negatively affect BMD in both early and especially later years of one's life (20).
Nichols then followed BMD in male master cyclists and nonathletes over a 7-yr period. At initial and 7-yr assessments, there was a consistent pattern of lower BMD in cyclists compared with nonathletes at all bone sites measured. There also was a statistically significant decrease in BMD in cyclists compared with nonathletes. Among all study participants, those who reported participating in weight training or impact exercise since the baseline assessment lost significantly less BMD at the spine and femoral neck compared with participants who reported no weight-training/impact exercise since baseline. A significantly greater percentage of cyclists than nonathletes met criteria for osteopenia or osteoporosis at baseline (84.2% vs 50.0%) and at follow-up (89.5% vs 61.1%). Further, 6 of the 19 (31.6%) cyclists who had osteopenia at baseline became osteoporotic, compared with one (5.6%) of the nonathletes (21).
Stewart et al. compared the BMD of a group of cyclists with the BMD of a group of runners, a group of runners/cyclists, and a group of healthy nonexercising controls. Subjects with a family history of osteoporosis or those who engaged in manual work were excluded. Significant differences among all four groups included a lower body fat percent in all athletes compared with controls. All athletes participated in their chosen form of training for, on average, 9 h·wk-1. The runners/cyclists had a higher body mass index than the runners and cyclists and also reported additional training with upper body activities that the other athletes did not. The authors found that compared with controls, cyclists had significantly lower lumbar spine BMD, while runners and runner/cyclists had significantly higher total and leg BMD. Compared with both the runners and the runners/cyclists, cyclists had significantly lower total, leg, and spine BMD. The authors postulated that this could be because of the increased forces imposed onto the skeleton during running that are absent from cycling (19,30). Compared with the runners, runners/cyclists had higher arm BMD but lower leg BMD. They proposed that this may have been because of their higher body weight and the additional upper body activities that these athletes performed (30).
Rector et al. in 2007 found that the BMD of male cyclists compared with the bone health of runners. Comparisons of rates of bone turnover, as well as serum hormone concentrations, also were made between the athletes in each of these two groups. Subjects in this study were, on average, the same age, height, weight, body mass index, and body composition, and they reported equivalent nutrient intake and physical activity levels when quantified as h·wk-1 or as daily energy expenditure during training. Lifetime, adolescent, and childhood bone-loading exposures were assessed by a comprehensive questionnaire, and they were equivalent in each group. These researchers found that the cyclists in this study had significantly lower whole body and lumbar spine BMD when compared with the runners. The results between the two groups were decreases in BMD of 4% and 10%, respectively. Based on the World Health Organization's definition, about 60% of the cyclists had osteopenia of the spine compared with 19% of the runners. Using a regression equation, and adjusting for age, body weight, and bone-loading history, the cyclists were found to be 7.4 times more likely to have osteopenia of the spine than the runners (23). The authors of this study could not attribute this large discrepancy in BMD between cyclists and runners to differences in age, body weight, body composition, diet, hormonal status, overall activity level, or bone-loading history. They concluded that cycling alone does not adequately provide the sustained skeletal loading required throughout adulthood to maintain the vital gains of bone mass acquired during adolescence (23).
Another proposed mechanism by which vigorous exercise, such as cycling, may lead to decreased BMD is through the increased release of parathyroid hormone (PTH), a potent stimulator of bone resorption. It is postulated that the dermal losses of calcium during exercise trigger this homeostatic mechanism of bone demineralization to maintain serum calcium concentrations (15). This theory is supported by one study in which calcium ingestion during bouts of cycling lead to a blunted rise in serum levels of PTH and CTX, an additional marker of bone resorption (11). There is added support for this theory and it is demonstrated by Klesges et al., who found that previously observed decreases in BMD in collegiate basketball players over the course of one season were not reproduced when calcium was supplemented during practices.
A study of competitive male cyclists conflicted with that study and did not demonstrate a positive relationship between calcium supplementation and BMD. In this study, Barry et al. found that all cyclists sustained significant decreases in BMD over the course of one full competitive season. The decreases in BMD in the cyclists who received high-dose calcium supplementation were not significantly different from those observed in the cyclists who received low-dose calcium supplementation. The authors suggest that these findings may be related to the timing of the calcium ingestion, as previous studies reporting a positive correlation between calcium supplementation and BMD were designed such that the calcium was ingested during exercise (2,29).
The study by Smathers et al. examined the BMD in a cohort of 32 cyclists compared with the BMD of 30 age- and weight-matched controls. Overall, the cyclists had a lower body fat percentage than the controls, as well as a significantly larger calcium-supplemented diet. They found that the cyclists had a significantly lower BMD in the spine than in the controls. However, all three hip measurements showed no differences between the two groups. Of note, cyclists who had weight lifted as a part of their training regimen did not have significantly higher BMD of the spine or any of the three hip sites measured. Finally, total testosterone was measured in both groups and was not significantly different in either group (28).
The increased risk of low impact fracture inherent in individuals and athletes with low BMD, combined with the increased risk of fracture inherent in high-velocity crashes, not uncommon in competitive cycling, is concerning. It therefore is reasonable to recommend that cyclists should be screened with DEXA to establish a BMD baseline or as a part of ongoing surveillance in the treatment of any identified low BMD. Accordingly, cyclists should be counseled to incorporate impact or resistance activities into training regimens as a preventative measure or as a part of a comprehensive treatment plan, as appropriate (20). Cyclists also should be encouraged to consume a balanced diet or supplement their diet to ensure adequate daily intake of calcium and vitamin D, currently recommended at 1200-1500 mg and 800-1000 IU, respectively (19). Those cyclists at high risk for fractures, based on other additional risk factors and/or BMD in the osteoporotic range, should consider adjunctive pharmacological treatment (20).
The majority of the data reported to date suggest that road cycling is a risk factor for the development of osteopenia or osteoporosis (20,23,30,35). The data presented have been mixed on potential etiologies of this finding; however, they are strongly suggestive that cycling lacks a significant weight-bearing component, which may be contributive. Additional factors also have been implicated, including dermal calcium losses, inadequate calcium supplementation, hormone-mediated bone turnover. Further research will be helpful in determining causes of bone loss and effectiveness of preventive measures in road cyclists.
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