The principal result from the current study is that in a cohort of mid-to-older age adults, slower walking speeds (in increments that have been previously demonstrated to be clinically significant between individuals, i.e., 0.10 m/sec as described above) are associated with higher incidence of radiographic and symptomatic knee OA, while faster walking speeds appear to be associated with lower incidence. Estimates in a smaller subsample designed to eliminate possible preclinical disease supported this result. There were no significant findings of walking speed related to hip OA-related outcomes.
A number of studies suggest that faster walking speeds might alter the overall biomechanics of walking. Biomechanical studies have shown increased angular excursions at the knee during the swing phase of faster versus slower walking, at least partly due to higher passive coriolis and centrifugal forces [31
], possibly resulting in altered alignment at heel strike (i.e., decreased knee extension) for slower versus faster walking. The relative contributions of different muscles and muscle activation patterns also appear to play a functional role in the known altered biomechanics of faster versus slower walking [31
]. Faster walking results in a decrease in the percentage of the walking cycle spent in stance phase (62.6% at self-selected normal speed versus 60.6% at faster speed) [32
], which would decrease the total duration of weight bearing load on a joint over time [33
]. Studies of children and young adults have demonstrated that joint moments and powers in the lower extremity are increased with faster walking speeds [34
], although patterns of joint loading and muscle activation differ among older adults [36
]. Finally, there is a relatively greater magnitude of lower extremity musculotendinous activity and coactivation at the knee and ankle observed among older adults during faster versus slower walking speed [36
] which may increase joint loading or may provide more stability to the joints to help attenuate overall joint moments (e.g., cushioning) [31
Interestingly, our results -- that slower walking is associated with higher incidence of knee OA are not consistent with a hypothesis that the mechanical effects of faster walking may have contributed to the development of knee or hip OA in this study and also are counter to recent hypotheses that reduced walking speed and/or “mindfulness walking” may help to reduce peak adduction moments and joint loads at the knee [39
],and also help reduce knee joint symptoms [41
]. Most of these studies are cross-sectional, with some investigators supporting, but others more neutral, on slower walking as an appropriate intervention to decrease knee joint loads.
Our findings may have important implications for prevention and treatment because pharmaceutical and exercise interventions have documented impact on walking speed [42
]. During fast walking, the rate of joint loading increases, as well as the rate of energy absorption, particularly at the knee [43
]. A healthy knee joint (one that does not have OA) would theoretically be able to tolerate a greater rate of joint loading. In a knee joint with damaged or weakened articular cartilage, faster walking may not be tolerated because the cartilage is less able to dissipate forces [44
]. Potentially, individuals without radiographic or symptomatic OA at baseline in this study may have had early joint changes that were not detectable. If so, such individuals may have slower self-selected walking speeds, as observed at baseline, to reduce the rate of joint loading, and possibly later developed detectable OA. The individuals who could walk more quickly at baseline may have also maintained better joint health during the study, contributing to decreased OA at follow-up. In an attempt to adjust for potential confounder effects, we controlled for lower extremity joint limitations and self-reported pain during walking test, and examined progressively more restricted (i.e., healthier) cohorts to reduce prevalent OA as a possible explanation for our findings.
One novel result of this study was the discrepancy in effects at the knee and hip. Incidence of hip OA is estimated to be approximately 88 per 100,000 person-years, compared to 240 per 100,000 person-years at the knee [45
]. The lower outcome incidence rates of the hip compared to the knee would reduce the power of this study to detect significantly significant associations, but not the magnitude of the association Neither the magnitude nor the direction of our hip ORs suggest the potential presence of a real effect at the hip. Possibly, the knee is more susceptible than the hip to joint load variations that occur with slower and faster walking speeds, as previously suggested by studies that report an association between obesity (resulting in a greater joint load) and knee OA [20
], but inconsistently with hip OA [46
]. Our results suggest that slower walking speed is likely a better marker for identifying those at risk of developing OA-related outcome for the knee but not for the hip.
General strengths of this study include the large, community cohort, the prospective study design, adequate representation of Caucasians and African Americans, and the fact that case ascertainment at baseline and follow-up was confirmed by clinical and radiographic assessment. In addition, in Sub-sample III, we were able to create a cohort more likely to be free of possible subclinical disease and report for the first time the simultaneous incidence of radiographic and symptomatic OA as well as the onset of isolated rOA and isolated symptoms.
There are several limitations as well. First, we do not have data on OA at other important lower extremity locations (ankles/feet) that could potentially impact our findings, and there were no lower extremity muscular strength, kinematic, or kinetic data collected that would allow us to further explore our findings. Anterior-posterior films of the knee were available, but other views, such as patellofemoral joint films, were not included in this analysis; alternate views may have provided additional evidence of radiographic disease of the knee. Second, the definition of OA (K-L grade ≥ 2) is primarily driven by the presence of an osteophyte, although osteophyte formation may not be the first feature that develops in all individuals. Assessments of individual radiographic features (i.e., separate examination of osteophyte formation or joint space narrowing) and their location (medial or lateral compartment) were not available for this cohort during the study period. Third, we assume that a clinically important difference in walking speed for individuals (0.10 m/sec) is also an important difference in walking speed when comparing populations. Previous work in the geriatrics literature has shown that differences between individuals in walking speed in increments as small as 0.10 m/sec are clinically significant for survival and functional mobility [3
]. There is little in the literature assessing important differences in walking speeds when comparing populations, but in a study of older veterans hospitalized for geriatric evaluation and management, each positive difference in walking speed at hospital admission of 0.10 m/s between people was associated with improved physical function as indicated by a 4.5 point higher standardized Short Form-36 score, 2.1 point higher standardized Physical Functioning subscale score on the Short Form-36, and 0.63 fewer total activities of daily living (ADL) disabilities [3
]. Fourth, approximately 40% of participants did not return for follow-up. Participants who did not return tended to be slightly older, African-American, and male compared to those who completed the follow-up visit. Analysis was limited to participants who were more likely to be younger and healthier at baseline, possibly biasing the association.
Although our analyses controlled for a variety of potential confounders, residual confounding is always possible in observational research. A randomized clinical trial design of a walking speed intervention and incident OA-related outcomes might more clearly describe the nature of the associations we observed and perhaps suggest additional avenues for future intervention development, although this type of study would require many years of observation.
Given the consistency of our findings across the different subsamples, walking speed may be a marker of knee joint health. We recommend further research to confirm these findings and consideration of walking speed assessment during clinic visits as a means to help identify patients at greatest risk of developing OA, especially at the knee, and who may benefit from pharmaceutical and/or preventive interventions. Other performance-based measures and self-report physical function measures should be explored in future research to determine their utility alone and in combination with walking speed for identifying those at risk of developing lower extremity OA.