In our musculoskeletal model, the quadriceps, hamstrings, and gastrocnemius muscle forces account for a major portion of the knee compressive and shear forcesas in other studies (19
). Hence, any change in compressive or shear forces will be due, in large part, to changes in one of more of these muscle forces. Although quadriceps forces increased between 9 and 18% across the groups, the high weight loss group maintained peak knee compressive forces at baseline values, in part by reducing hamstring forces by 11%. This did not occur in the low and no weight loss groups, resulting in greater peak knee compressive forces relative to the high weight loss group. We presume the reduction in hamstring and knee compressive forces in the high weight loss group were caused by the reduced total body weight, thereby decreasing the amount of muscle force required to support and propel the subjects. Since walk speed can also influence knee joint forces and moments, we adjusted for group differences in our analyses. We do note however, the beneficial effect weight loss seemed to have on self-selected walking speed; i.e. the low and high weight loss groups increased walking speed ~7%. Himann et al.(22
) noted that walk speed declined 1–2% per decade of life until age 63 yrs., when the decline per decade increased to 12.4% for females and 16.1% for males. Hence, the increase
in walking speed in our older adult cohort suggests a slowing in the decline in mobility associated with aging and knee osteoarthritis consequent to long-term weight loss and/or exercise interventions.
Intuitively, a reduction in body weight would lower the vertical ground reaction forces. A mean weight loss exceeding 10% in the high weight loss group significantly reduced peak vertical ground reaction loads. Interestingly, these changes did not exactly coincide with the changes observed in the knee compressive forces. Most notably, the vertical ground reaction force was reduced after 18 months in the low weight loss group, but the knee joint compressive force was actually increased from baseline to 18-month follow-up. We suggest, therefore, that while the external ground reaction force provides an approximation of joint loads, observed changes over time may not be indicative of the actual changes occurring within the joint.
shows the timing of peak compressive, quadriceps, hamstring, and gastrocnemius forces during gait. The period of greatest challenge for an older adult with knee OA occurs shortly after heel strike during weight acceptance (23
). As shown through electromyographic data, the quadriceps and the hamstrings contract simultaneously (i.e. co-contract) to help stabilize the knee during this challenging load bearing period, and this co-contraction is increased in knee OA patients (24
). The hamstrings also lessen the anterior shear force caused by the quadriceps, and control hip extension throughout stance. The more co-contraction, however, the greater the compressive forces exerted on the knee. Within the limitations of our muscle force predictions (see appendix
below), our data enable us to uniquely estimate co-contraction through the relationship of actual muscle forces instead of muscle activation patterns. These data suggest that with greater weight loss, osteoarthritic patients were able to reduce the level of co-contraction by reducing hamstrings but not quadriceps force, thereby limiting the compressive load exerted on the knee. Indeed, there was a significant dose response to weight loss, with the high weight loss group having significantly lower peak knee compressive forces relative to the low and no weight loss groups at 18-month follow-up.
(A) Knee compressive, and (B) Hamstring, (C) Quadriceps, and (D) Gastrocnemius muscle forces of a complete stance phase of a typical participant. Note: 1 body weight = 923.1N (94.1kg).
The gastrocnemius, as part of the triceps surae complex, acts primarily to stabilize the ankle, restrain the rate of tibial advancement throughout stance, and provide force at push off to support and propel body mass (23
). Gastrocnemius forces peak during terminal stance (20
) and, therefore, have more influence on the magnitude of the second peak knee compressive force (see ). Taken together, the lower peak forces in the knee flexors and, to a lesser extent, the ankle plantar flexors among the high weight loss participants suggests that the greater weight loss resulted in less co-contraction for knee stabilization and reduced force requirements for ankle stabilization, tibial advancement, and push off.
The high weight loss group had significantly lower knee compressive forces and was the only cohort that reduced the internal knee abduction moment, a surrogate measure of knee joint loading, from baseline to follow-up. Reduced knee joint loading through intense weight loss may play a role in slowing disease progression by eliciting positive changes in the mechanical pathway to knee OA. These mechanical improvements, however, did not result in concomitant changes in disease progression. Radiography is relatively insensitive to change and does not evaluate disease in soft tissue structures. A larger sample size, the use of a more sensitive measure of progression, such as MRI, or a longer intervention period (i.e., the effect that weight loss has on progression may be evident sometime later) may have enhanced our ability to detect differences in progression among the groups.
Our previous study of dietary therapy and its effect on gait in people afflicted with knee OA was limited to moderate weight loss (12
). We expanded the boundaries of weight loss to larger, potentially more clinically meaningful amounts and found that higher weight loss than previously studied elicited beneficial effects. Specifically, high weight loss (mean = 10.2%) reduced knee joint compressive loads, primarily by reducing hamstring co-contraction during the initial portion of the stance phase.
The importance of the aggressive use of non-pharmacologic co-therapies such as intensive weight loss for improving symptoms associated with OA, slowing disease progression, and impacting the underlying mechanisms of OA is under appreciated. Our study provides evidence that intensive long-term weight loss affords biomechanical improvements in knee joint loads not seen in low or no weight loss groups. Future study of long term high intensity weight loss as a possible osteoarthritis disease modifying intervention is needed using more sensitive measures of disease progression. The potential benefits of intensive weight loss for co-morbidities common to obese, knee OA patients such as heart disease, stroke, and type II diabetes enhance further the import of this non-pharmacologic intervention.