Running and other strenuous sports activities are purported to increase osteoarthritis (OA) risk, more so than walking and less-strenuous activities. Analyses were therefore performed to test whether running, walking, and other exercise affect OA and hip replacement risk and to assess the role of body mass index (BMI) in mediating these relationships.
In this article, we studied the proportional hazards analyses of patients’ report of having physician-diagnosed OA and hip replacement versus exercise energy expenditure (METs).
Of the 74,752 runners, 2004 reported OA and 259 reported hip replacements during the 7.1-yr follow-up; whereas of the 14,625 walkers, 696 reported OA and 114 reported hip replacements during the 5.7-yr follow-up. Compared with running <1.8 MET·h·d−1, the risks for OA and hip replacement decreased as follows: 1) 18.1% (P = 0.01) and 35.1% (P = 0.03) for the 1.8- and 3.6-MET·h·d−1 run, respectively; 2) 16.1% (P = 0.03) and 50.4% (P = 0.002) for the 3.6- and 5.4-MET·h·d−1 run, respectively; and 3) 15.6% (P = 0.02) and 38.5% (P = 0.01) for the ≥5.4-MET·h·d−1 run, suggesting that the risk reduction mostly occurred by 1.8 MET·h·d−1. Baseline BMI was strongly associated with both OA (5.0% increase per kilogram per square meter, P = 2 × 10−8) and hip replacement risks (9.8% increase per kilogram per square meter, P = 4.8 × 10−5), and adjustment for BMI substantially diminished the risk reduction from running ≥1.8 MET·h·d−1 for OA (from 16.5%, P = 0.01, to 8.6%, P = 0.21) and hip replacement (from 40.4%, P = 0.005, to 28.5%, P = 0.07). The reductions in OA and hip replacement risk by exceeding 1.8 MET·h·d−1 did not differ significantly between runners and walkers. Other (nonrunning) exercise increased the risk of OA by 2.4% (P = 0.009) and hip replacement by 5.0% per MET·h·d−1 (P = 0.02), independent of BMI.
Running significantly reduced OA and hip replacement risk due to, in part, running’s association with lower BMI, whereas other exercise increased OA and hip replacement risk.
Life Sciences Division, Lawrence Berkeley National Laboratory, Berkeley, CA
Address for correspondence: Paul T. Williams, Ph.D., Life Sciences Division, Lawrence Berkeley National Laboratory, Donner 464, Berkeley, CA; E-mail: email@example.com.
Submitted for publication October 2012.
Accepted for publication January 2013.