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