Running is an activity loved by millions of people all over the world. It is estimated that there are more than 30 million runners in the United States alone (36). There are nearly 1,800 running clubs throughout the United States, with every state and the District of Columbia represented (32). More than 15.5 million runners completed running events in 2012, which is a steady increase from the 4.8 million in 1990 (Figure) (32).
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Figure: Number of running clubs in the United States. Figure based on information from
http://www.runningusa.org/statistics.
The rise in the popularity of running can be attributed in part to the many health benefits running produces.
Unfortunately, there is a common misconception that running can cause osteoarthritis (OA), which may deter many from the sport (14). But does science really support this assertion? OA affects millions of people and is a leading cause of disability in aging (8). Many risk factors are associated with OA, but there is no clear evidence that recreational running or running for exercise causes OA.
OSTEOARTHRITIS DEFINED
OA is a degenerative joint disease of the cartilage, underlying bone, and surrounding tendons and ligaments (1,6). OA results in a higher incidence of disability than any other chronic condition in adults older than 60 years (3) and is one of the most common reasons for total hip and knee replacements (16). OA occurs when tissues are unable to manage the mechanical stresses placed on joints as a result of conditions such as age, genetics, obesity, joint trauma, or repetitive movements (3,9,29). OA has been linked to metabolic and systemic conditions such as hypertension, hypercholesterolemia, and high blood glucose levels (9,15).
Physicians use symptomatology in combination with radiographic evidence to diagnose OA and determine the extent of the disease (1). On radiographs, OA presents as a progressive loss of hyaline cartilage, marginal outgrowths, osteophyte development, joint space narrowing, subchondral sclerosis, and subchondral cysts (3,5,16). However, many individuals with radiographic changes are asymptomatic. Often, it is only when symptoms such as joint line tenderness, motion restrictions, crepitus with motion, joint effusion, and deformity are present that people seek medical attention and a diagnosis is made (3,11).
INTRINSIC AND EXTRINSIC RISK FACTORS ASSOCIATED WITH OSTEOARTHRITIS
Many intrinsic and extrinsic risk factors are associated with the development of OA, including age, gender, genetics, injuries related to work and sport activities, and excess body weight (16) (Table 1).
TABLE 1: Intrinsic and Extrinsic Risk Factors for Osteoarthritis
Although OA is associated with age and gender, differences exist (16). Before the age of 45 years, the incidence of OA is higher in men, whereas, at ages more than 45 years, women have a higher incidence of OA (9,13). OA also appears to have a genetic component as evidenced by a study of twins that demonstrated a genetic predisposition accounted for 50% of cases of OA in hips and hands (34). Although age, gender, and genetics are not modifiable, some extrinsic risk factors such as activity level, injury, vocation, and obesity are modifiable and also are key risk factors in the development of OA (11).
Sports, particularly those requiring repetitive, high-impact, torsional joint loading, such as football or soccer, increase the risk of developing OA (5,19,20). Similarly, certain jobs requiring work activities such as persistent kneeling, low and repetitive squatting, or heavy lifting also can increase the risk of developing OA (16,19). In addition, prior injuries to joints, ligaments, tendons, or muscles can increase the risk of OA (13,28). Decreased muscle strength, malalignment, poor proprioception, knee laxity, and joint deformity all potentially alter joint mechanics and may increase the risk for cartilage degeneration as well (3,16).
Furthermore, as body mass index (BMI) increases, so too does the risk of OA (10,11,30). The Rotterdam study examined X-rays of 3,585 adults older than 55 years and determined that, as BMI increased, so did the risk of OA, specifically in the knee (30). Studies of radiographs demonstrated that the risk of disease progression also increased with increased weight (11). As weight increases, the biomechanics of movement change, as do the loading surfaces of the articular cartilage in weight-bearing joints (31). For example, in single-limb stance, for each 1-lb weight gain, the overall force across the knee increases 2 to 3 lbs (16,29).
Although we cannot modify the intrinsic factors that may lead to OA, diet and exercise can impact body composition and strength. In overweight individuals, body fat reduction through diet and exercise, rather than diet alone, has been shown to be effective in reducing osteoarthritic symptoms (3,26,41). These modifications may help mitigate some of the extrinsic factors that can lead to the development of OA across time.
RUNNING: BENEFITS AND RISKS
As noted earlier, running is a popular physical activity that is accessible widely (14). Many adults incorporate running into their daily routine for weight reduction and for the wide variety of positive health benefits that can be gained from running as a form of exercise (10) (Table 2).
TABLE 2: Benefits of Running as a Physical Activity
Numerous longitudinal studies comparing running group members with community-based controls (nonrunners) have noted a decrease in morbidity and mortality in the runners (7,8,12,22,23,39). A 21-year longitudinal study demonstrated improved health outcomes and decreased disability and mortality rates of runners. By year 19 of this study, 34% of subjects who were nonrunners (controls) had died compared with 15% of subjects who were runners (8).
A 12-year longitudinal study of subjects older than 50 years included 450 running club members and 300 community-dwelling nonrunners (12). Data collection included age, sex, BMI, smoking history, comorbid conditions, and radiographic evidence. The Health Assessment Questionnaire, a validated self-administered questionnaire assessing activities of daily living, also was used to determine the presence of disability in subjects (4). The rate of disability was 64% lower in subjects who were runners versus subjects who were nonrunners in both males and females. Mortality rates also were lower in subjects who were runners (1.5%) compared with subjects who were nonrunners (7%) (12).
Finally, similar results were found in a 13-year longitudinal prospective study of 464 individuals (39). Onset of disability, as defined by the Health Assessment Questionnaire, was delayed by 8.7 years, and the mortality rate was 3.3 times lower in the running group subjects compared with the nonrunning group controls (39). The author proposed that running might increase longevity by increasing muscle strength, cardiovascular reserve, bone mineral density, and glucose tolerance. In addition, it has been suggested that running may be a surrogate for other positive lifestyle factors, such as healthy eating and abstaining from cigarette smoking (39).
However, running is not without risk. The incidence of running injuries in general has been reported to be as high as 79.3% (37). Injuries most commonly reported are at the knee and ankle and are most often the result of overuse syndromes, such as patellofemoral pain syndrome, iliotibial band syndrome, and Achilles tendonitis (35). Certain variables have been linked to injury, such as increasing age, female gender, malalignment, training volume, muscle strength, and past injury (37). The question remains whether the injuries related to overuse syndromes in running lead to OA.
RUNNING AND OSTEOARTHRITIS
Several researchers using animal (2,18,29) and human subjects (8,12,19,21–23,25) examined the relationship between running and the development of OA. Running can load joints up to eight times that of walking and, when muscles are fatigued, stresses are reported to be even higher (17). Moderate joint loading is considered necessary for articular cartilage health (28). Animal studies have been used to simulate force production on joints and its relationship to changes in articular cartilage and bone, but studies are limited and results are contradictory. Changes in articular cartilage of rats were studied with a 6-week strenuous running program resulting in degradation of the collagen matrix and load-bearing joint surfaces. The author did indicate that differences in anatomy, structure, posture, and locomotion, along with body weight, should be considered in the development of OA (2). Conversely, beagle puppies running 4 km a day for 15 weeks demonstrated an increase in cartilage and proteoglycan production, leading to an increase in cartilage thickness (18), which, in fact, can be protective against OA (33).
Animal studies are helpful in controlling variables but limit the generalizability to humans. Many human studies related to OA and running examined health outcomes and reported conflicting evidence as well (7,12,17,18,21–23,25,40), leaving little evidence to support the assertion that recreational running causes OA.
Although running is repetitive in nature and does increase joint loading, it does not impose extreme torsional loads and risk for traumatic injuries to joints and ligaments, as do sports such as soccer and weightlifting (19). Radiographic evidence of OA is higher in soccer players (29%) and weightlifters (31%) compared with long-distance runners (14%). Professional soccer players have been shown to have a higher risk of knee and ankle OA compared with age-matched controls (20). This is explained in part by higher rates of torsional loads and injuries in soccer, such as ligamentous and meniscal tears, and higher BMI in weightlifters (19).
In longitudinal studies of recreational runners and runners older than 50 years, running was not associated with increased radiographic evidence of OA, increased severity of knee OA, or knee replacements during the period of observation (8). Similarly, an 8-year longitudinal study on running and the development of OA reported no acceleration in radiographic or clinical evidence of OA of the knee (12).
One study comparing runners and nonrunners examined bone mineral density of the spine, hip OA, and knee OA. This study reported increased bone mineral density present in the running group. No differences were noted between groups in joint space narrowing, crepitation, joint stability, or symptomatic OA (21). Furthermore, a 9-year longitudinal study comparing bone mineral density of the spine, hip OA, and knee OA reported no difference in progression of OA between groups. Lumbar bone mineral density remained higher in the running group but, across time, had similar changes with aging. The author concluded that running does not increase the development of OA across time (23).
Most recently, data from multiple cohorts in the National Runners and Walkers Health Study in 2013 were analyzed. This report included 89,377 individuals and stated that running, including participation in marathons, did not increase the risk of OA. These results are from self-reported surveys, which included questions addressing energy expenditure, volume of activity, and whether they had been diagnosed with OA by a physician or had a hip replacement. This study also concluded that running decreases the risk of OA and hip replacement because of the lower BMIs present in the running population (40).
More advanced imaging technologies such as magnetic resonance imaging (MRI) have been used to assess changes in cartilage before and after running as well. MRIs have been used to examine changes in cartilage volume, compression, and thickness under loads using images such as T1- and T2-weighted MRIs (27). T1-weighted images allow for viewing of the proteoglycan matrix of the cartilage and acute fluid changes. A decrease in this matrix is present at early stages of OA. T1 images may be helpful in determining long-term changes to the cartilage itself (24). Water and collagen content is best viewed using T2 mapping techniques, which may be helpful in determining short-term changes in water content and fluid balance (24). Cartilage appears to respond positively to moderate exercise but, again, there are conflicting results with high-volume (i.e., marathon) runners. One study compared 9 subjects who were female runners in a start-to-run program with 10 sedentary controls for 10 weeks using gadolinium-enhanced MRI to view cartilage changes. The results demonstrated that moderate running had a protective effect on cartilage in healthy subjects, which is consistent with previous animal models (18,38).
A study using MRIs of 10 healthy runner subjects (having run no more than 3 marathons in their lifetime) noted changes in T1 and T2 images immediately postmarathon. However, within 3 months, T2 images returned to baseline, whereas changes persisted in T1 images. This suggests the possibility of some negative long-term biomechanical changes to articular cartilage (24). However, another study using T1-weighted MRI of eight runners premarathon and postmarathon did not find any changes in bone marrow edema, joint effusion, or periosteal reactions and determined that long-distance running does not lead to increased internal stresses on bones and joints (17). Although there is great potential for MRI studies to improve our knowledge about running and OA, currently, given the small sample sizes and conflicting outcomes (17,18,24,38), there is no clear evidence that running leads to the development of OA nor is there clear evidence that running does not cause OA.
In summary, although high-intensity running, such as marathon running, possibly may have a negative impact on cartilage and the development of OA, there is little empirical evidence to suggest that recreational running can lead to OA. On the contrary, moderate running actually may have a protective effect on cartilage and, of equal if not greater importance, on health outcomes such as disease and disability.
LIMITATIONS IN THE LITERATURE
Many studies of OA and running compare radiographic evidence of OA in running and nonrunning subjects but do not consider clinical symptoms in their analyses. Lack of large-sample size prospective studies and low-level evidence hinder the ability to draw conclusions on OA and running (13,28). Many of these studies fail to stratify or differentiate based on mileage, history of injury, BMI, and vocation, which also may alter outcomes (8,10). Running mechanics, strength, and alignment are not accounted for in studies of running and OA. All of these factors place an individual at greater risk for the development of both running injuries and, potentially, OA.
RECOMMENDATIONS AND FUTURE STUDIES
Although the literature provides very little empirical evidence to suggest that recreational running leads to OA, it does suggest that injuries, repetitive strain, and faulty biomechanics do contribute to the development of OA. Similarly, there is no clear evidence to suggest that running does not lead to OA. Therefore, rather than completely eliminate running as a means of achieving health benefits, it is important to identify those individuals at risk for running injuries and increased potential for developing OA and those who could achieve health benefits from running with or without modification.
Running assessments enable health and fitness experts to differentiate between runners with faulty mechanics and those who should avoid running because of the potentially negative impact of abnormal loading on joints. A running evaluation minimally includes assessment of movement patterns as well as strength and flexibility assessments of the core and lower extremities. Slow-motion video camera analysis of a runner on a treadmill can provide both the fitness professional and runner visual feedback on stride asymmetries, slow cadence, and faulty mechanics. Recommendations should be individualized based on the specific limitations identified both on video analysis and functional assessment of strength and range of motion. For example, a runner who presents with low cadence on video analysis would benefit from a recommendation to increase cadence by 10% to decrease injury risk, whereas a runner who presents with an asymmetric pattern and weakness would benefit from a recommendation for specific muscle strengthening and stretching. For runners with faulty mechanics, which may lead to OA, health and fitness professionals can prescribe specific adaptive and corrective exercises for muscle groups including hip abductors, hip extensors, hip external rotators, hamstrings, and quadriceps to improve those mechanics and allow for continued healthy running.
For individuals who should avoid running, health and fitness experts can provide education on OA management as well as healthy alternatives such as swimming or biking. OA is a progressive disease that can worsen across time. Fitness professionals should encourage further evaluation when clients and patients become symptomatic. The symptoms can include pain at the joint line, edema, crepitus, decreased range of motion, and deformity.
Runners with OA may modify their running to minimize symptoms. Modifications can include reducing mileage, alternating running with cross training, running on an antigravity treadmill, and incorporating aqua jogging. Alternating running days with strength-training or cross-training days will allow the runner to maintain strength and cardiovascular fitness while reducing joint impact and loading.
Future studies by health and fitness experts could add to our understanding of the most appropriate dose-response for runners with and without OA. In addition, although the standard of care for diagnosing OA is the use of radiographs, MRIs can better detect bone marrow edema, periosteal reactions, and changes in cartilage. Future studies using MRIs would enhance our knowledge of cartilage response to mileage, speed, changes in BMI, and the development and diagnosis of OA.
CONCLUSIONS
Current evidence on the link between running and OA is inconclusive. Most studies suggesting a causal link between running and the development of OA have examined a limited number of elite runners. Although limitations exist in our current body of evidence, there is little to suggest that recreational running or running for exercise causes OA; alternatively, there is little evidence to indicate clearly that it does not cause OA.
The risk of developing OA should be identified individually, based on existing intrinsic and extrinsic factors, and weighed against the positive health benefits of running. Multiple strategies can be used to mitigate the risks and optimize the benefits of running, such as cross training, strengthening, biomechanical analysis, and training modifications. In an economy where health care costs are rising, the relatively inexpensive habit of running may provide significant positive health benefits and aid in disease prevention.
BRIDGING THE GAP
The etiology of osteoarthritis is multifactorial. No clear evidence exists to suggest recreational running or running for exercise does or does not cause osteoarthritis. The risk of developing osteoarthritis should be identified individually, based on existing intrinsic and extrinsic factors, and weighed against the positive health benefits of running. Multiple strategies can be used to mitigate the risks and optimize the benefits of running in disease prevention.
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