Bone health and the masters runner
Abstract
Masters runners are often defined as those ages 35 years and older who train and compete in running events. These runners represent a growing population of the overall running community and experience running-related injuries including bone stress injuries (BSIs). Similar to younger runners, health considerations in masters runners include the goal to optimize bone health with focus on mitigating age-associated loss of bone strength and preventing BSIs through a combination of ensuring appropriate physical activity, optimizing nutrition, and correcting faulty biomechanics. Importantly, BSIs in masters runners may include characteristics of both overuse injury from insufficient recovery and failure of bone weakened by age-related loss of bone (insufficiency fractures). This narrative review covers the limited available research on strategies to optimize bone health in masters runners. Applying knowledge on masters athletes and extrapolating from other populations, we propose strategies on treatment and prevention of BSIs. Finally, the review highlights gaps in knowledge that require further age-specific discoveries to advance treatment and prevention.
INTRODUCTION
Overall participation in distance running events has been growing and this may be largely due to increased numbers of older runners engaging in the sport.1 This growth parallels increased competition of masters athletes in other sports.2 Although research on the masters athlete has grown over the past decade,3 limited work has focus specifically on the masters runner. The masters runner category commonly refers to age 35 years and older1 as classified by USA Track and Field.4 These runners are becoming more competitive, reflected by improved performance times.5 Unfortunately, running-related injuries are common in this population. In a survey study by McKean et al., 34% of the runners were older than 40 years old and experienced more soft tissue injuries and multiple concurrent injuries as compared to their younger counterparts.6 Age-related changes may contribute to development of running-related injuries in the masters runner including decline in muscle strength, flexibility, and bone density and degeneration of joints. Soft tissue injuries have been the primary musculoskeletal injury reported in the literature to affect the masters runner.6, 7 However, bone stress injuries (BSIs) occur in this population and represent an overuse injury to bone from cumulative load that exceeds ability to repair.8 This form of injury may occur in athletes with normal bone strength and in runners with lower bone density.
Age-related bone loss would be expected to elevate risk for future BSI, as lower bone mineral density (BMD) has been shown to be a risk factor for BSI in younger athletes.9-11 Due to limited research on the topic of bone health in the masters runner, BSI risk in this population has not been well characterized. A survey study of adult female runners average age 40 years revealed that approximately one quarter had experienced a stress fracture, an advanced form of BSI.12 Due to increasing prevalence of lower bone density with older age, BSIs in the masters runner are more likely to take on characteristics of both fatigue and insufficiency fractures, resulting in a unique distribution of injuries. Additional factors that contribute to the BSIs affecting masters runners include age-related changes in biomechanics and nutritional needs. The purpose of this review is to describe available research and clinical guidelines that can be applied to optimizing bone health in the masters runner and injury prevention. This includes identifying sex-specific considerations that may influence bone health and injury in the masters runner, such as menopause. This review concludes by identifying knowledge gaps that require further research to advance care of the masters runner.
Clinical cases
- A perimenopausal woman in her early 50s who presents with fatigue and undesired weight gain and describes persistent bilateral medial leg pain that has prevented her from maintaining her usual training to prepare for completing 10k races
- A male marathoner and lifelong runner in his early 60s who is healing from his first BSI with medical workup that has revealed osteopenia.
Methods
Authors performed literature searches from July through September 2023 of all available research. Relevant terms such as “masters runner,” “bone stress injury,” “bone mineral density,” and “osteoporosis treatment” were searched and identified articles were reviewed. Relevant articles from initial searches as well as relevant articles identified in their reference lists were included in this review.
Female and masters age athletes as well as those who identify as non-white or lower socioeconomic status are underrepresented in the current research limiting the available body of literature for review but also making this subject matter an area of interest given the research gap. Only articles available in English were included.
Defining the masters runner
The term “masters runner” typically refers to the physically active competitive runner aged 35 years and over,1 though there is no true consensus regarding “masters” age. Research studies on the masters runner population are heterogeneous with regards to age and have examined age groups of over 40, 50, and 70 years. Performance is estimated to naturally begin to decline over the age of 50 years,1 during which women are often perimenopausal, with more notable declines after age 70 years.5 Nutrition and physical activity can modify the rates of decline of both overall health and physical performance related to the aging processes.3
SPECIAL CONSIDERATIONS FOR BONE STRESS INJURIES IN THE MASTERS RUNNER
Limited reports describe the pattern of BSIs in the masters runner. In a female runner population with mean age of 40 years, 25.4% reported stress fractures and odds of experiencing a BSI increased with presence of osteopenia or osteoporosis (p < .01) and lower body mass index (BMI; p < .01).12 Extrapolating from what is known in younger running populations,9, 10, 13 low bone mineral density (BMD Z-scores < −1.0) may increase susceptibility of older runners to develop BSIs particularly in trabecular-rich anatomical sites of bone such as the femoral neck and pelvis. Furthermore, some less common sites of pelvic BSIs have been presented in case reports primarily in masters age runners including the acetabulum14 and ilium.15-17
Biomechanical risk factors for BSI have not been described in masters runners. In younger runners, risk factors may include higher ground reaction forces and poor alignment including greater femoral adduction and rearfoot eversion18-20; these studies have primarily characterized risk for tibial BSI in younger women. Biomechanical changes with older ages include decreased velocity, decreased stride length, decreased ground reactive forces, and decreased ankle power.21 Masters runners also experience decreased tendon stiffness and decreased leg stiffness.1 These age-related changes make interpreting running biomechanics within a masters runner with BSI difficult. Until further research guides risk factor assessment of biomechanics with BSIs, practical applications may include ensuring masters runners have any significant deviations in asymmetries for gait mechanics or strength deficits corrected to address overall injury risk.
EVALUATION OF A MASTERS RUNNER WITH BONE STRESS INJURY
Similar to younger runners, masters runners presenting with current or history of BSI should be screened for health factors that contribute to injury including skeletal health.
Medical evaluation
Similar to younger runners, factors such as training errors, changes in footwear, and any other factors creating change in skeletal load should be identified through a detailed history. Nutrition factors in endurance athletes across age include evaluating for risk factors for low energy availability, which can contribute to risk for BSI and lower BMD.22-24 Endurance runners are at elevated risk for low energy availability described as the difference of energy intake with exercise energy expenditure standardized to fat-free mass.25 Threshold for low energy availability has been described in exercising women at less than 30 kcal/fat-free mass per day and may be lower in male athletes.24 However, optimal energy availability in masters runners has not been described. If the athlete does have signs and/or symptoms concerning for low energy availability, there are several lab tests that can help delineate low energy availability from other causes of hormonal imbalance including perimenopause and menopause in women (Table 1). In addition to energy availability, other key nutrients include calcium and vitamin D, with increased needs at older ages.26
| General | |
|---|---|
| CBC | TSH |
| CMP | Free T4 |
| Vitamin D | Total T3 |
| Iron studies including ferritin | Free T3 |
| Female athletes | Male athletes |
| Estradiol | Total and free testosterone |
| FSH | Possible: FSH |
| LH | Possible: LH |
| Prolactin | Possible: Prolactin |
| hCG | Possible: CRP/ESR |
| Possible: Total and free testosterone | |
| Possible: Early AM progesterone | |
- Abbreviations: CBC, complete blood count; CMP, comprehensive metabolic panel; CRP/ESR, C-reactive protein/erythrocyte sedimentation rate; FSH, follicle-stimulating hormone; hCG, human chorionic gonadotropin; LH, luteinizing hormone; TSH, thyroid-stimulating hormone.
In contrast to younger athletes, there are additional medical conditions which are more common with age to consider as risk factors for BSI (Table 2). The diagnostic test to measure BMD is dual energy x-ray absorptiometry (DXA). The International Society for Clinical Densitometry has published guidelines for DXA screening.27 DXA is also suggested if the athlete has one or more “high-risk” risk factors or two or more “moderate-risk” risk factors according to the Female28 or Male29 Athlete Triad Cumulative Risk Assessment Tools. In older populations, a T-score (comparing BMD with a young adult of the same sex) from −1.1 to −2.4 designates osteopenia, and a score of −2.5 and lower provides the diagnosis of osteoporosis.27, 30 A Z-score (BMD matched to same age, race, and sex) < −1.0 indicates low BMD for age in an athlete involved in weight bearing sports.31 Although BMD is the most widely used proxy of bone strength, especially in the clinical setting, there are several other variables used in the research setting to evaluate bone quality. These include bone geometry and structural qualities, cortical density, trabecular and cortical bone mineral content, and stress–strain index. Peripheral quantitative computed tomography is able to evaluate these additional measurements as well as differentiate between trabecular and cortical bone.32, 33
| Pathologic fractures | Inflammatory bowel disease |
| Hyperthyroidism | Insulin dependent diabetes |
| Hyperparathyroidism | Hyperprolactinemia |
| Renal failure | Polycystic ovarian syndrome |
| Hypophosphatasia | Multiple sclerosis |
| Malignancies | Cushing's syndrome |
SEX-SPECIFIC DIFFERENCES IN BONE HEALTH
Sex-specific differences in evaluation and management of bone health should be considered. The terminology of sex is being used for those primarily with high estradiol as female and high testosterone levels as male. Limited research has defined hormonal changes to bone health of athletes who identify as gender nonbinary or are intersex. Females reach peak bone mass at younger ages due to average earlier age of puberty than males. Due to higher levels of circulating androgens during adolescence and early adulthood, males tend to have higher BMDs than females; this includes peak bone mass, which is achieved in an athlete's early 20s.34 Between the ages of 30 and 50 years, both sexes experience declines in BMD, but this decline is accelerated in females during perimenopause and menopause due to a decrease in estrogen production.35 Thus, females present with osteoporotic fractures about 10 years earlier than males.36 After age 60, the rate of bone loss is relatively similar between sexes and may actually be more pronounced in males.37
Because peak bone mass is established in early adulthood, the focus is on maintaining bone health and reducing bone loss in masters runners. Low energy availability, or lack of calories to support energy expenditure, can play a role and can lead to changes in bone turnover within 5 days of entering a low energy availability state.38 To avoid a negative balance of bone resorption versus bone formation, training volume should be increased before training intensity and both should never be increased simultaneously. For a 10% increase in running loads, there is a 100% decrease in load to failure for bone.39 It is well known that loading stimulates bone remodeling and bone formation, but after 100 loading cycles in run gait, bone may no longer continue to respond positively.40 Similar to proposed in younger athletes41, 42 participation in multiple sports, sports with multidirectional loading, and/or strength training may help preserve BMD in masters runners by stressing bone in a variety of ways and stimulating maintenance of BMD.
Pregnancy and lactation
Running is considered safe during pregnancy and lactation and allows pregnant women to continue to meet recommended activity guidelines. Females during pregnancy and lactation experience many physiological changes to support growth of the fetus and baby. Changes in hormones and body composition may affect the risk for general running-related injuries. In an observational study that surveyed 110 competitive female distance runners, training volumes generally decreased during the pregnancy and postpartum periods; self-reported injury rates were 3.9% in pregnant women and 10% in lactating women.43 Although running during pregnancy can be safe and beneficial, these changes do affect overall energy44 and calcium requirements45 and can also affect bone remodeling.46 Pregnancy is a time of high bone turnover when serum calcium decreases. And in the final trimester, bone resorption peaks. Significant decreases in BMD occur in trabecular-rich bone specifically, such as the lumbar spine and greater trochanter,47 which is of particular interest with regards to BSIs in the runner. Overall, BMD may decrease by up to 5% during pregnancy at the lumbar spine.48 During lactation, persistent estrogen and progesterone elevations along with the secretion of prolactin can affect bone health by suppressing the bone remodeling process.49
The bone remodeling increases during pregnancy and lactation highlight the importance of optimizing nutrition. Women should increase caloric intake by 200 to 300 kcal/day during pregnancy50 and 500 kcal/day during lactation.51 During the second and third trimesters of pregnancy, recommended protein intake increases to 1.1 g of protein/kg/day, in contrast to 0.8 g of protein/kg/day at baseline.52 Recommended carbohydrate intake of 46% to 64% of daily calories and total fat intake of 22% to 35% of daily calories are similar to that of nonpregnant women.53 Recommended weight gain during pregnancy varies based on prepregnancy weight. From what is known about low energy availability, masters runners who are pregnant or lactating who do not meet increased nutritional demands may develop overuse injuries including BSIs.
Perimenopause and menopause
BMD may more rapidly decline in women during perimenopause and menopause.54 This occurs due to hormonal changes, primarily related to decrease in estrogen.55 Estrogen promotes bone formation, decreases bone resorption, and inhibits osteoclasts56; therefore, when estrogen levels decline in menopause, so do the protective effects on bone. This results in accelerated bone loss as well as increased risk for osteoporosis and bone fractures.57 Women with a lower body weight also experience a quicker decline in BMD through menopause.58 These physiological changes that result in a precipitous drop in BMD in women may explain why the prevalence of BSIs is higher in women than in men of older ages.59
Andropause
“Andropause” is defined as a syndrome of decreased sexual satisfaction and declining well-being in the setting of low testosterone in older men.60 With aging, testosterone declines at 1% per year, though the rate of decline varies.61 Emotional stress may contribute to decline of testosterone and suggests efforts to support mental health through physical activity including running could be protective. In addition to the decline of testosterone in aging, prolonged participation in endurance running may contribute to significantly lower serum testosterone levels than sedentary males.62-65 This has been termed the exercise-hypogonadal male condition.66 Endurance runners training at higher volume and intensity may be at greater risk for development of low testosterone.64, 67, 68 Low testosterone, along with low energy availability, places runners at increased risk of BSIs; nevertheless, given the heterogeneity of age in published data, the specific effects in masters runners are unknown.69-71
MITIGATING BONE LOSS AND PROMOTING SKELETAL HEALTH
Screening for low energy availability
Masters runners, similar to any endurance athlete, are at risk for low energy availability state and should have nutrition assessed if presenting with BSI or other running-related injury to support health. There are numerous screening tools available, such as the Female or Male Athlete Triad Cumulative Risk Assessment Tools, the Relative Energy Deficiency in Sport Clinical Assessment tool (RED-S CAT),72 and Androgen Deficiency in the Aging Male.73 Any indication of hormonal imbalance in the setting of low energy availability needs to be further investigated, and if present, comprehensively addressed. Amenorrheic athletes in their 20s have been found to have lower BMD compared to eumenorrheic athletes, especially at trabecular bone including up to 25% lower BMD at the lumbar spine.74, 75 Exercise cannot mitigate decreases in bone mass that result from amenorrhea.74
Lifestyle changes and supplements
In the absence of hormonal imbalances and/or low energy availability, there are other interventions that can be considered to maximize peak bone mass. A higher peak bone mass can decrease risk of osteoporosis, and it has been found that up to 60% of osteoporosis risk can be related to early adulthood BMD.76 General recommendations include smoking cessation/avoidance, a well-rounded diet with adequate caloric and protein intake (Table 3), regular weight-bearing physical activity, and appropriate vitamin D and calcium levels via diet and/or supplementation.
| Age | Sex | Protein RDA (g/day) |
|---|---|---|
| 9–13 years | Females/males | 34 |
| 14–18 years | Females | 46 |
| Males | 52 | |
| >18 years | Females | 46 |
| Males | 56 | |
| Pregnancy and lactation | 71 |
- Note: *based on 0.8g protein/kg body weight for reference body weight.
- Abbreviation: RDA, recommended dietary allowance.
Literature on calcium and vitamin D supplementation is mixed. Calcium supplementation has been found to increase BMD in prepubertal children but not in peripubertal or postpubertal children.74 There is also an incongruent effect of age on calcium supplementation in adults with bone loss, as there does not appear to be protection during early menopause, but there is slowing of bone loss with calcium supplementation in women 6 years postmenopausal.74 Overall, the National Osteoporosis Foundation does recommend calcium supplementation in children and adolescents with level of evidence A grading based on the finding of a statistically significant positive effect on BMD and/or BMC accrual in 16 randomized controlled trials.77 Although a recent Cochrane review did not show a positive effect of calcium and/or vitamin D supplements in healthy premenopausal women,78 there are multiple studies suggesting supplementation could benefit young adult athletes at higher risk of BSIs. Lappe et al. found a 20% lower risk of stress fracture if taking 2000 mg calcium and 800 IU vitamin D in female Navy recruits aged 17 to 35 years.79 Similarly, Nieves et al. found low-fat dairy products and higher daily intakes of calcium, vitamin D, and protein were associated with lower risk of BSIs as well as increased BMD in female runners aged 18–26.80 Overall, data are inconsistent and heterogenous and therefore not strong enough to support a vitamin D supplementation dose or target 25(OH)D serum level.81 However, adults can tolerate a higher dose of daily vitamin D in regard to safety.81 If the athlete is at a high risk of stress fracture, supplementation of at least 800 to 2000 IU of daily dietary vitamin D can be considered.82
Physical activity
Most studies looking at the effect of exercise on BMD development in children and adolescents are observational in nature. Regular physical activity in children is an important factor in the development of normal adult BMD.83 A 15-year longitudinal study of males and females found that reaching the highest lumbar peak BMD at age 27 years is mostly dependent upon weight-bearing exercise and normal body weight as opposed to daily calcium intake.84 Sport involvement involving multidirectional loading as a young athlete can play a more beneficial role in bone health later in life compared to repetitive low-impact sports.41 Notable to masters runners are recommendations to continue weight-bearing exercise and promote strength training to maintain bone mass. An optimal program has not been established for adult ages; however, physical activities involving weight bearing and resistance training could be incorporated to maintain bone health.
MEDICAL MANAGEMENT OF LOW BONE MINERAL DENSITY
Hormone replacement therapy
Estrogen is the most influential hormone regulating bone health in women. Low estrogen, both in the setting of hypothalamic oligomenorrhea or amenorrhea as well as during peri-/postmenopause, permits greater osteoclastic activity and subsequent bone resorption. Hormone replacement therapy for women can be delivered using oral, transdermal, or transvaginal delivery. Nearly all studies investigating the use of hormone replacement therapy (HRT) using estrogen monotherapy or combined estrogen with progesterone have measured gains in BMD and reduced incident osteoporotic fractures when used in postmenopausal women,74, 85-88 perimenopausal women,89 and women with functional oligomenorrhea or amenorrhea89, 90 but not in healthy women or women with anorexia nervosa.89 Enthusiasm for HRT was reduced due to adverse events in women receiving treatment that included myocardial infarctions, stroke, invasive breast cancer, and pulmonary embolism; and, in one study, both the estrogen-only and the estrogen plus progestin intervention arms were prematurely discontinued.91 In a randomized clinical trial where transdermal estradiol was compared to ethinyl estradiol-containing oral contraceptive pills to increase BMD in oligo-amenorrheic endurance athletes aged 14 to 25 years, transdermal estradiol was found to be superior, but it is unknown if these findings can be extrapolated to the masters runner population.92 Additionally, a dose-related effect of BMD increase with vaginal estradiol administration was observed in a postmenopausal population younger than 65 years old.93
In the masters runner population, the etiology of hormonal imbalance and determination of menopausal status as well as contraindications are important for consideration of use of HRT. In otherwise healthy postmenopausal women under the age of 60 years with low BMD or risk factors for low BMD, HRT may be considered a first-line therapy for both prevention and treatment of low BMD94; however, research specifically in use of HRT in masters runners is limited. One study of masters female runners found that HRT was not protective of hip BMD in the postmenopausal group95 and a later study from the same lab showed no changes in BMD in postmenopausal runners with or without HRT over the course of 5 years.96 A history of thromboembolic disorder, breast cancer, migraine disorder, or current pregnancy precludes use of HRT. A meta-analysis from prospective studies of menopausal hormone therapy showed an increase in breast cancer risk with all menopausal hormone therapy types except for vaginal estrogens. The risk of developing breast cancer was higher with combination therapy of estrogen plus progesterone compared to estrogen only.97
In the setting of exercise-hypogonadal male condition in males, low testosterone can be addressed pharmacologically with either testosterone stimulating agents such as gonadotropin-releasing hormone (GnRH), or exogenous testosterone. However, both testosterone and GnRH are prohibited by the World Anti-Doping Agency and are limited in use due to being an ergogenic aid. Evidence supports the use of testosterone replacement to benefit bone health98, 99 and is, therefore, suggested by multiple clinical guidelines from the Endocrine Society.100, 101 Similar to HRT in female athletes, male masters runners should consider hormone therapy under the guidance of an endocrinologist or other providers with expertise in this topic and optimize nonpharmacological therapies given concern for increased risk of cardiovascular disease and stroke using testosterone replacement.22, 23
Bisphosphonates
Bisphosphonates (oral or intravenous) are commonly used to treat osteoporosis in men and postmenopausal women. The World Health Organization Fracture Risk Assessment Tool (FRAX) algorithm, which applies to men and women aged 40 to 90, predicts the 10-year absolute risk for hip and major osteoporotic fractures. If the FRAX risk is determined to be greater than or equal to 3% for hip fracture or greater than or equal to 20% for major osteoporotic fracture, bisphosphonates could be considered for treatment.30 In the premenopausal population, the Food and Drug Administration (FDA) has approved bisphosphonates only for those who are receiving glucocorticoids.102 The most commonly used oral bisphosphonates are alendronate, ibandronate, and risedronate.103 Treatment with bisphosphonates can be considered in patients with known ongoing bone loss or with a history of fragility fractures. Bisphosphonates are designated Category C by the FDA for use in pregnant women due to risk of teratogenic effects and therefore would not be recommended in that population.102 Bisphosphonate-associated osteonecrosis of the jaw is a rare but potentially significant adverse effect seen with bisphosphonate use.104, 105 Further, due to the possibly excessive mineralization induced by bisphosphonates, there is concern for brittleness and risk of atypical femoral fractures. However, a study of almost 200,000 women found the absolute risk of atypical femur fractures was very low compared with reduction of risk of hip and other fractures from treatment with bisphosphonates.106 Of note, the risk of atypical femur fractures increased with longer treatment duration and promptly decreased after completion of bisphosphonate therapy.106
Other medications
Recombinant human parathyroid hormone, or teriparatide (subcutaneous injection), is FDA approved for use in men with primary or hypogonadal osteoporosis at high risk for fracture, postmenopausal women with osteoporosis at high risk for fracture, and glucocorticoid-induced osteoporosis. Teriparatide induces more bone formation rather than resorption, and this is shown to increase BMD, improve bone microarchitecture resulting in higher strength and bone quality, and decrease risk of fractures at the lumbar spine and hip.107 Teriparatide has been favorably compared to bisphosphonate therapy showing lower total occurrence of vertebral fractures108-110 and nonvertebral fractures108 as well as improved BMD at the lumbar spine,108, 109 total hip,109, 111 and femoral neck.108, 110, 111 A recent systematic review showed mixed but mostly positive results on fracture healing in adults from a collection of prospective studies, retrospective studies, and case series.112 However, most of the data are from studies involving postmenopausal women and therefore extrapolation to other populations is unclear.113-118
Raloxifene (oral tablet) is a selective estrogen receptor modulator with FDA approval to prevent and treat postmenopausal osteoporosis. Because of its specific pharmacology, it is applicable only to female patients and is a Category X drug, meaning that pregnancy and lactation are contraindications. Development of clotting conditions, such as deep vein thrombosis, pulmonary embolism, or cerebrovascular accident, are the main risks of raloxifene.
Denosumab is a total human IgG2 monoclonal antibody (subcutaneous injection) that decreases bone resorption by blocking osteoclast formation. Denosumab is FDA approved for men and postmenopausal women with osteoporosis at high risk for fracture, glucocorticoid-induced osteoporosis with high risk of fracture, and bone loss from androgen deprivation or aromatase inhibitor. This class of medication has not been adequately studied in athlete populations.
BACK TO CLINICAL CASES
Each masters runner deserves additional workup to optimize treatment of known or suspected BSI and optimize skeletal health.
With regard to case 1, perimenopausal athletes deserve special consideration for symptoms related to sex hormone changes including weight gain and loss of BMD that occurs rapidly during early menopause. Medial leg pain can be the result of soft tissue or presentation of BSI and requires imaging to clarify diagnosis. There should be a low threshold to consider DXA and perform additional workup including lab work, particularly in those meeting criteria for osteopenia or osteoporosis, dietician evaluation, and exploration of symptomatic treatment and/or hormonal support with an appropriate provider.
When considering case 2, trabecular-rich BSIs in a masters athlete may be a presenting feature of runners with impaired skeletal health. Though this type of injury is arguably more commonly described in females, these conditions also affect male runners. Though BMD declines earlier and more rapidly in postmenopausal females, males are also expected to experience declining BMD that can affect development of BSIs.
Any active BSI requires treatment with appropriate relative rest according to the anatomical location, grade of injury, and pain with weight bearing.8 However, relative rest does not address the entire picture and puts an athlete at risk of recurrent injury without treating the whole athlete. During this time, additional treatments may also consist of optimization of overall energy balance and calcium/vitamin D intake under the guidance of a sports dietician, possible hormone replacement therapy counseling with a qualified provider, referral to appropriate providers (such as gynecology, endocrinology, or rheumatology) if history or lab values bring up concern for other underlying diagnoses, assessment of training loads and progressions and, when safe to do so, physical therapy and run gait retraining.
CONCLUSIONS AND FUTURE DIRECTIONS
Ultimately, primary prevention is the ideal form of care for maintenance of bone health and avoidance of BSIs in the masters runner. If optimal bone density can be achieved during adolescence and into young adulthood and maintained as the runner ages, there is greater likelihood of preventing low BMD and BSIs into the masters years. Modifiable risk factors for BSIs in runners include physical activity levels, nutritional needs, and biomechanics, all of which evolve as a runner ages. Early bone health education and optimization in the runner is key to ensure development of optimal peak bone mass going into young adulthood. Ongoing education throughout the lifespan of the runner is also important, especially as runners are continuing to run into later years during which time they may face unique challenges such as pregnancy, lactation, menopause, and development of low testosterone. Although prevention is ideal, in masters runners who develop low BMD and BSIs, there are pharmacological treatments that can be considered. The literature investigating treatments for low BMD is tailored for a more generalized population rather than the masters runner; future studies involving this particular population could shed light on optimal treatment strategies.
DISCLOSURES
Adam Tenforde serves as senior editor for PM&R Journal. He gives professional talks such as grand rounds and medical conference plenary lectures and receives honoraria from conference organizers. He has participated in research funded by Arnold P. Gold Foundation (physician and patient care disparities), Football Player Health Study at Harvard (health in American-style football players), American Medical Society for Sports Medicine (bone density research), Uniform Health Service and Enovis (Achilles tendinopathy), and MTEC/Department of Defense (bone stress injuries with shockwave). He is a paid consultant for State Farm Insurance and Strava. No other authors have disclosures.
REFERENCES
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