Saanichton Physical Therapy Blog

Running and Osteoarthritis! Good news

Williams, P.T. OSTEOARTHRITIS IN RUNNERS AND WALKERS Medicine & Science in Sports & Exercise


The number of runners studied here is larger than any

previous study of physical activity and OA and hip replacement

and exceeds by more than 10 times the number of

runners previously studied in all previous cross-sectional

studies combined. Included among these were 863 runners

who reported running 60 miles/wk. Contrary to many

previous reports (2,3,6,16,23,31,32,37), we find no evidence

than running increases the risk of OA, including participation

in marathon races, and, in fact, subjects that ran

12.9 km/wk were at significantly

lower risk for both OA and hip replacement. The reduction

in risk for running

more than compensates

for the 1.6% per year risk increase for hip replacement

during the first 21 yr. Moreover, there was no particular

advantage to walking rather than running in reducing OA

and hip replacement risk. In fact, runners were more likely to

benefit from less OA and fewer hip replacements because a

greater proportion exceeded

(89.5% vs 52.8%).

Previous studies suggesting a protective role for physical

activity are much fewer than those showing a risk increase or

no effect. In one, joint space loss was observed in nonrunners

but not runners, suggesting that running preserved cartilage

thickness (18). In another, knee replacements decreased with

increasing cumulative hours of recreational physical activity

(24). Our data even showed that marathon frequency, marathon

intensity, and 10-km intensity did not predict any risk

increase for OA or hip replacement, in contrast to the report

of Michaelsson et al. (26) that skiers who repeatedly participated

in a 90-km ski race increased OA risk in proportion

to the number of races run and performance (speed).

The OA-protective effects of running or walking appeared

have already occurred by suggesting the

association may be due primarily to increased OA in the

least active individuals. Articular cartilage thickness is reduced

in animals subject to prolonged immobilization (36).

Cartilage is also thinned in the absence of normal joint

loading in spinal cord injury patients (35). In children, articular

cartilage volume is increased in association with

vigorous physical activity and muscle strength cross sectionally

(13), and those who engaged in more intense sport

gained more cartilage over time (12). Triathletes have

thicker patellae cartilage than inactive subjects, albeit thinner

medial femoral condyle cartilage (28). Some (4), but not

all (8), studies suggest that physical activity may enlarge the

knee joint surface area in adults. Glycosaminoglycans are

used in the synthesis of proteoglycans, which provide

cartilage_s viscoelastic properties (22). Early OA consists of

a focal loss of proteoglycans (5). Running increases the

glycosaminoglycan content of human knee cartilage (34).

Roos and Dahlberg_s (30) randomized trial showed that

exercise produced a healthier distribution of proteoglycans

in cartilage vis-a-vis nonexercising control. Animal studies

also suggest that the patellar cartilage of sedentary hamsters

have a lower proteoglycan content than those that are active

(29). Moderate exercise has also been shown to inhibit the

development of surgically induced OA in the rat (7). In

dogs, however, shifting from moderate to strenuous running

eliminated increases in cartilage thickness and proteoglycan

content produced with moderate running (14).

Our analyses showed that in contrast to running, other

(nonrunning) exercise increased the risks for both OA and

hip replacement. This result is consistent with more than

twofold greater prevalence of tibiofemoral or patellofemoral

OA in soccer players (29%) and weight lifters (31%) than

runners (14%) reported by Kujala et al. (15). Research on

occupational activity shows that OA is more common in

jobs requiring knee bends, kneeling, or squats (25), which

may be more characteristic of exercise performed in gyms,

circuit training, and aerobic classes than running or walking.

Work-related knee bending exposure increases the odds for

knee OA by up to sixfold (21).

Our analyses confirmed the well-established association

between BMI and incident risk of OA and hip replacement

even within the purported healthy weight range, and attributed

45% and 28% of the running associated decrease in OA

and hip replacement to BMI, respectively. In addition to

promoting weight loss directly (39), running attenuates

middle-age weight gain (38), such that higher mileage runners

gain only half as much as low mileage runners. The prevention

of weight gain is an additional mechanism for limiting

risk OA and hip replacement risk. Body weight has a much

weaker association with other exercise than with running

(40), which may explain in part their different associations

with OA and hip replacement, particularly given that adjustment

for BMI did not affect the concordance between baseline

other exercise and both OA and hip replacement.

There are important limitations to these analyses that

warrant acknowledgment. The results are based on self reported

physician-diagnosed OA and hip replacement

rather than medical chart review or imaging. However, reviews

suggest stronger associations have been reported for

clinically assessed hip OA than its radiographic assessment

(20). Patient self-report of physician-diagnosed arthritis has

been found by others to be the best predictor of radiologically

ascertained OA, showing 64% specificity, a 57%

positive predictive value, and 71% negative predictive value

(33). We do not believe that the declining incidence of OA

and hip replacement with greater MET-hour per day walked

or run was due to fewer opportunities for diagnosis in the

more athletic men. The Health Professional Study reported

that their more vigorously active participants had more

routine medical checkups than less active men (19). It is

possible that there is a higher pain threshold in longer distance

runners, but it is unclear why this would not also be

true for other exercise as well. It is unclear whether the exclusion

of preexisting injury would be warranted in

assessing the OA risk in runners, if such injuries were the

consequence of the exercise per se. Finally, we acknowledge

that the analyses would have benefited from the complete

follow-up of NRHS-II and NWHS. Heretofore, we have

been unable to secure funding for their follow-up, and there

is no evidence that the NRHS-I (80% follow-up) and NRHSII

(51.7% follow-up) show different relationships between

MET-hour per day run and the risks for OA (P = 0.45 for

difference) or hip replacement (P = 0.89 for difference). The

lower follow-up of the walkers (33.2%) than NRHS-II

(51.7) reflected our recruitment priorities rather than differences

in the responsiveness of the walkers and runners;

however, we do not believe that this affected the comparison

of walkers and runners given that comparable results were

obtained when the analyses were restricted to the initial

33.2% of the NRHS-II runners recruited.

In conclusion, these results may not apply to truly elite

athletes, but for recreational runners who even substantially

exceed current guideline activity levels and participate in

multiple marathons annually, running does not appear to

increase OA and hip replacement risk and may, in fact, be

preferable to other exercise.