Stress Fractures and Bone Loss In Distance Running: Part I and II
This article was written for UltraRunning Magazine (ISSN 0744-3609) Volume 31, Issue 3, page 30-31, 2011
Stress Fractures and Bone Loss In Distance Running: Part I
Stress fractures and bone loss (osteoporosis) are two of the most common injury states associated with distance running. However, in theory and practice these unfortunate consequences are often preventable, provided a thorough understanding of how exercise and nutrition interactions influence the skeleton.
Bone is a dynamic connective tissue that is constantly undergoing change through a process known as remodeling or turnover. Two specialized cells known as osteoclasts and osteoblasts are responsible for the degradation (a.k.a. resorption) and formation of the skeleton, respectively. It is the combination of these two actions that are collectively termed remodeling. The main purposes of remodeling are: (1) to prevent the accumulation of abnormal or damaged bone, (2) to adapt bone in a manner that is most consistent with the maintenance of skeletal integrity, and (3) to assist in the maintenance of normal systemic calcium and pH levels.
In the adult skeleton, bone loss and gain are typically balanced and relatively steady state. When bone loss exceeds gain, skeletal strength is decreased and conversely, when formation exceeds resorption, the reverse is true. The manifestations of an unfavorable balance may include either a localized fracture or systemic bone loss (osteopenia or osteoporosis). The overall rate and ratio of remodeling is contingent upon numerous interactive factors that include mechanical, nutritional, and hormonal signals.
The primary mechanical signals that govern bone remodeling are muscle contractions, which act on bone through tendon insertions, and ground reaction or impact forces. Running involves both of these and they are described as stresses which in turn induce bone strain. Strain is defined as the deformation in bone that results from an applied stress. Under normal loading circumstances, bone is deformed on a very small scale and these micro deformations occur in a variety of directions including compression and bending. In a long bone, such as the tibia (shin) or metatarsal (foot), bending strain results in tension on one side and compression on the other. Because bone is capable of withstanding greater stress in response to compression than tension, stress fractures are more likely to occur in locations subjected to tensile strains.
Skeletal muscles serve a dual role as they both induce and reduce bone strain. Strong and fatigue resistant muscles reduce bone strains created by ground reaction and impact loads. For example, in a situation during which a runner lands on the heel and “rolls through” the forefoot the metatarsal bones are subjected to a bending strain that is countered by the eccentric or lengthening contractions of the muscles on the bottom of the foot. Accordingly, when muscles are inhibited, because of fatigue or dysfunction, injury risk is elevated as bone strain magnitudes are increased.
In addition to the very important role of muscles, both the shape and density of a bone are important determinants of its strength and resistance to injury. A long and narrow bone is subject to a greater degree of bending strain than a shorter and wider one and therefore will be more likely to fail under a given stress. Dense bones are stronger than those with less mineral mass and even slight reductions in density may result in a significantly increased fracture risk.
Consistent application of physical or mechanical stress is essential for skeletal health and the maintenance of normal remodeling balance. Periods of unloading, such as during bed rest or cast immobilization, result in accelerated rates of bone loss. Increases in physical loading, when combined with favorable nutritional and hormonal states, may induce elevated formation processes that result in increases in a bone’s density, cross sectional area or both.
It is important to realize however that bone can actually lose strength as a result of an increase in either the frequency or magnitude of loading. In the case of stress fractures, this weakness is presumed to be the result of fatigue damage that follows an increase in training mileage or faster running speeds. A progressive continuum of damage begins with the disruption of intermolecular bonds and may ultimately advance to the macroscopic level. Early stage damage results in both mechanical and chemical signals that serve to activate osteoclasts whose local resorbing actions further compromise bone strength. During the embryonic stages of damage, no overt symptoms are present to alert a runner of the impending injury. If the damage continues to accumulate and coalesce, the onset of pain begins. When pain is first experienced, it is generally described as an ache and may be limited to either the early stages of a run (then improve), the later stages of a long run, or following a run. This stage is often described as a stress reaction rather than an overt stress fracture. In addition to mild pain, palpation usually reveals subtle swelling and warmth. If these early symptoms and signs are ignored and training continues, pain generally worsens to the point that running (and even possibly
walking) becomes severely limited. At this stage, based on history and physical exam, a diagnosis of stress fracture is made. The provisional diagnosis may be supported or confirmed through the use of ancillary tests including x-ray, MRI, CT, ultrasound, or bone scan. The false negative rate for some of these tests is significant and therefore their results should be interpreted with caution.
As previously described, the remodeling process consists of both the resorption and formation of bone. The processes are linked together as bone resorption triggers the development of osteoblasts and thus the synthesis of new bone formation. Remodeling is typically described as being staged and characterized by several key events, including:
A region of bone surface is activated by a stimulus which may be mechanical, chemical, nutritional, or hormonal. Osteoclasts are called to action and attach themselves to a specific site and dissolve the underlying bone through a complex chemical enzymatic process. Approximately two weeks time lapses between the onset of resorption and the initiation of formation and this period is termed the reversal phase.
Osteoblasts then form new bone during the last stage which consists of synthesis and mineralization components. Final phase success is contingent upon the presence of both normal hormone levels as well as numerous nutritional factors. The stage of formation requires at least 6-12 weeks time to complete. Hence there is a significant window from which damaged bone will continue to be vulnerable to loading. It is important for runners to appreciate that bone damage that may have occurred during a single training session or race typically requires up to three months time before complete structural integrity is restored.
Research and empirical evidence has consistently defined multiple interactive factors that are responsible for the development of stress fractures and accelerated rates of bone loss. In the next installment, we will detail these findings and suggest practical countermeasures in hopes of reducing injury risk or facilitating recovery.
Stress Fractures and Bone Loss in Distance Running: Part II
Stress fractures and bone loss are common consequences of ultrarunning and result from an imbalance in skeletal remodeling. In last month's column we provided an overview of bone cell physiology and in this issue we will detail some of the key factors that are responsible for the development of these injury states. We hope that after you appreciate how the skeleton adapts and responds to the prevailing mechanical, nutritional, and hormonal factors your training and racing will be improved and likelihood of injury will be reduced.
Scientific studies and clinical observation reveal that there are multiple factors that create a perturbation in bone breakdown relative to formation that may result in either stress fractures or bone loss and oftentimes both. They include:
Vitamin D deficiency
Energy deficit is described as an imbalance in dietary caloric intake relative to exercise expenditure. In financial terms, you are spending more than you are earning. There is strong evidence that most endurance athletes are chronically operating in a deficit of approximately 25%. In these circumstances bone formation activity is reduced and resorption processes are increased relative to the magnitude of the deficit. Under this prevailing milieu, the skeleton is both less capable of developing increased strength and progressively more susceptible to fracture and osteoporosis.
The reasons for an energy deficit are variable and range from simple neglect to purposeful restriction. In the same way that thirst is not always an accurate indicator of hydration status, an athlete’s hunger is not necessarily in sync with energy requirements. This is especially true in endurance athletes that are exercising at high intensity levels or training in hot climates as both conditions are known to actually suppress appetite. Additionally, because many athletes consume foods that are high in volume and low in calories, including many starchy carbohydrates like cereals, grains, and potatoes, a feeling of fullness may develop well before energy balance is achieved.
Many runners attempt to improve performance by purposefully restricting calories. The drive for thinness combined with a high prevalence of various disordered eating states, including anorexia athletica, are often to blame. Although excess body fat may be a performance limiter for some it is interesting to note that successful ultra endurance athletes come in all different shapes and sizes. In a recent scientific analysis of participants in a 7-day mountain ultra-marathon race that covered 350 km with 11,000 m of altitude change, investigators reported that none of the anthropometric variables including body mass, body mass index, or percentage of body fat was correlated with performance (Knechtle and Colleagues, 2010).
If you are uncertain about how to know if your caloric intake is adequate to counterbalance your training expenditure, a consultation with a sports medicine professional or registered dietician is strongly recommended. If you are an athlete that has been operating in a deficit anticipate that when balance is restored both your recovery and performance will be significantly improved. One study reported an impressive 18% increase in running speed at 80% VO2 max (Horvath and Colleagues, 2000) when trained runners caloric intake was increased to achieve energy balance.
The unfavorable balance of bone cell remodeling that is related to energy deficit may be explained through many different pathways but chief among them is the perturbation of certain key hormone levels. From an evolutionary perspective, the survival of any species is dependent upon reproducing and bearing offspring only during times of ample food availability. Accordingly, during times of famine or exercise induced energy deficit, reproductive hormone levels are reduced. Both estrogen and testosterone play critical roles in the maintenance of normal skeletal remodeling by reducing the rate and magnitude of resorption and increasing formation. These hormones act directly on the specialized bone cells known as osteoclasts and osteoblasts as well as on many other physiologic systems that influence calcium homeostasis.
Dietary patterns that are deficient in total energy are also typically associated with inadequate levels key vitamins and minerals including calcium and vitamin D. Nutritional researchers have consistently reported positive correlations between calcium intake and bone health as well as inverse relationships with fracture. The currently recommended level of calcium intake stands at 1,000-1,200 mg/day yet many endurance athletes ingest only half this much. Interestingly enough, even the current level of recommended calcium intake may be low for the ultrarunner as calcium metabolism is accelerated during exercise and sweat studies reveal that dermal calcium losses alone may be in the order of 100-150 mg per hour. In a 2008 study by Lappe and Colleagues stress fractures were reduced by 21% in a population of 3,700 U.S. Navy recruits by supplementing their usual diets with 2,000 mg of calcium and 800 IU of vitamin D.
Vitamin D is a group of fat-soluble prohormones with various forms; the two major types are D2 (ergocalciferol) and D3 (cholecalciferol). Vitamin D regulates blood calcium levels by promoting absorption in the intestine and re-absorption in the kidneys and is necessary for the incorporation of calcium into bone. Adequate vitamin D levels may be achieved with a combination of whole foods and 10-15 minutes of sun exposure per day. However, because very few routinely consumed foods contain meaningful amounts of vitamin D and many climates do not lend themselves to adequate sunlight throughout the year, manufactured supplements may be necessary. The current recommendation for supplemental vitamin D intake is an area of intense debate as many believe that the standard of 600 IU per day (recently increased from 400 IU) is inadequate for the masses of people, including athletes, which are reportedly deficient. As such, many experts routinely suggest daily doses in the range of 2,000-4,000 IU. In some cases, a weekly dose of 50,000 IU may be prescribed by a physician in order to achieve a desirable level.
According to the National Institutes of Health (NIH), an acceptable serum level of 25-Hydroxyvitamin D for bone and overall health is >20 ng/mL. However, most orthopaedic professionals would appear to favor a higher standard (40-70 ng/mL) as a large military study found stress fracture risk to be increased in soldiers with levels < 30. Your primary care sports medicine physician may order a simple blood test in order to determine your current level of vitamin D.
Because sun exposure may be so variable throughout the year, we typically recommend testing for high risk populations twice per year. In the United States good times to test would include late winter (February/March) and late summer (August/September).
Historically there has been little attention paid to running technique with respect to stress fracture development. The prevailing thought was that an individual’s running form was predetermined, unique, and not amenable to modification with training. However, more recent studies have demonstrated that runners with a history of stress fracture have certain gait characteristics that are significantly different than their peers who have never sustained a fracture. And, perhaps more importantly, these differences are amenable to modification with proper instruction and exercise interventions. Key considerations for gait and exercise training that may reduce the likelihood of sustaining a running related fracture include:
Reduce over striding and a heavy, heel-first landing pattern
Increase the degree of knee flexion to better absorb energy during landing
Increase cadence and decrease time on support (stance phase)
Improve muscular strength and elasticity
The importance of muscle strength and elasticity as well as the development of muscular fatigue resistance cannot be overstated as muscles acting through tendons are the protectors of the skeleton. When muscles fatigue their capability of shielding the skeleton is significantly reduced and bone strains become elevated. In addition to improving gait characteristics through technical training, supplemental strength and elasticity (plyometric) exercises have the potential to protect the skeleton but also improve performance. In a recent study (Storen and Colleagues, 2008) trained male and female runners improved their time to exhaustion at maximal aerobic speed by 21.3% after participating in an 8 week program of strengthening. These results are especially impressive given the fact that this improvement was achieved without any additional running mileage.
Scientific studies have demonstrated there may be certain intrinsic reasons why some individuals are more likely to sustain stress fractures. These include but are not limited to leg length inequalities and abnormalities in lower extremity alignment or ranges of motion. In one study, 70% of the track and field athletes with a confirmed stress fracture were found to have a leg length discrepancy. Unfortunately, most of the scientific studies performed to date fail to detail whether these discrepancies in limb length are true or apparent. A true discrepancy is defined as an actual difference in lower extremity length measurement. This situation is generally related to asymmetrical femur (thigh) or tibia (shin) bone length but may also be due to alterations in bone or joint geometry. Apparent limb length inequalities often result from muscle length or strength imbalances or contractures of joints that give rise to the appearance of a shorter limb.
In order to determine if you have a true or apparent leg length inequality, a comprehensive evaluation by a sports medicine professional specializing in running biomechanics is indicated. This examination includes a variety of tests for active and passive joint mobility, muscle length and strength, as well as weight bearing radiographs. The use of heel lifts or foot orthotics should be considered only in cases of true inequalities as most of the apparent or adaptive cases respond well to a program of corrective exercise and rehabilitation.
In summary, stress fractures and bone loss exist on a continuum that is created by imbalances in bone remodeling activity. This imbalance results from a combination of multiple interactive factors that are largely preventable. In our next installment we will attempt to answer your particular questions pertaining to stress fractures and exercise induced bone loss. Please address your questions or requests for further details on this topic to the editorial staff of Ultrarunning magazine.