Obesity is not associated with increased knee joint torque and power during level walking

Abstract

While it is widely speculated that obesity causes increased loads on the knee leading to joint degeneration, this concept is untested. The purpose of the study was to identify the effects of obesity on lower extremity joint kinetics and energetics during walking. Twenty-one obese adults were tested at self-selected (1.29 m/s) and standard speeds (1.50 m/s) and 18 lean adults were tested at the standard speed. Motion analysis and force platform data were combined to calculate joint torques and powers during the stance phase of walking. Obese participants were more erect with 12% less knee flexion and 11% more ankle plantarflexion in self-selected compared to standard speeds (both p<0.02). Obese participants were still more erect than lean adults with ∼6° more extension at all joints (p<0.05, for each joint) at the standard speed. Knee and ankle torques were 17% and 11% higher (p<0.034 and p<0.041) and negative knee work and positive ankle work were 68% and 11% higher (p<0.000 and p<0.048) in obese participants at the standard speed compared to the slower speed. Joint torques and powers were statistically identical at the hip and knee but were 88% and 61% higher (both p<0.000) at the ankle in obese compared to lean participants at the standard speed. Obese participants used altered gait biomechanics and despite their greater weight, they had less knee torque and power at their self-selected walking speed and equal knee torque and power while walking at the same speed as lean individuals. We propose that the ability to reorganize neuromuscular function during gait may enable some obese individuals to maintain skeletal health of the knee joint and this ability may also be a more accurate risk indicator for knee osteoarthritis than body weight.

Introduction

The prevalence of obesity has increased from ∼13% to ∼23% of the US population between 1971 and 1994 (Flegal et al., 1998). Obesity is associated with numerous health risks including an increased risk for cardiovascular disease (Melanson et al., 2001), insulin resistance (Kohrt et al., 1993; MacLean et al., 2000), and, most relevant to the current work, knee osteoarthritis. Sturmer et al. (2000) reported a strong association between obesity and bilateral knee osteoarthritis but no association between obesity and hip osteoarthritis. Based on this difference in responses across joints, they hypothesized that obesity is associated with increased knee loads leading to joint degeneration. Anderson and Felson (1988) reported the same strong association between obesity and knee osteoarthritis and concluded that obesity causes knee osteoarthritis. Others have also suggested that increased weight associated with obesity directly increases knee loads that subsequently lead to knee osteoarthritis (Felson, 1988; Felson and Zhang, 1998; Hochberg et al., 1995; Korner and Eberle, 2001).

While the hypothesis that obesity is associated with increased loads on the knee and these larger loads lead to knee joint degeneration is attractive, it is also untested in dynamic movements. Gait analyses on obese individuals have identified only kinematic adaptations including slower velocity, shorter step length, increased double support time, and decreased knee range of motion and larger ground reaction forces in obese compared to lean individuals (McGraw et al., 2000; Messier, 1994; Messier et al (1992), Messier et al (1996); Spyropoulos et al., 1991). Knee kinetics during gait or other movements remain unreported at this time. Since muscle forces and not joint reaction forces provide the largest component to total joint loads (DeVita and Hortobagyi, 2001; Glitsch and Baumann, 1997; Pedersen et al., 1997), we interpret the kinematic findings as suggesting that obesity is associated with reduced knee kinetics. Slower speed, shorter steps, increased double support time, and decreased knee range of motion (i.e. knee flexion in early stance) are normally associated with reduced muscle forces. A result analogous to comparing gait biomechanics between obese and lean participants reported identical knee torques in women in late pregnancy while carrying 13 kg more mass and 1 year later (Foti et al., 2000) suggesting that humans compensate for additional body weight to reduce knee loads. Thus, these findings lead us to hypothesize that obesity is associated with neuromuscular adaptations leading to reduced loads at the knee joint during gait. The purpose of the study was to identify the effects of obesity on lower extremity joint kinetics and energetics during walking. We have chosen to measure people with obesity but no other known medical condition to remove possible confounding effects and we are therefore not directly addressing the issue of osteoarthritis.