Effects of obesity on lower extremity muscle function during walking at two speeds
Introduction
Obesity is a worldwide public health concern and obese adults and children are advised to engage in daily physical activity. Walking is a recommended form of physical activity for obese adults because it is convenient and suitable to elicit a moderate-vigorous metabolic response [1]. However, obese individuals have lower relative muscle strength compared to nonobese individuals [2]. Weakness and susceptibility to fatigue of certain key muscles (e.g. vasti (VAS) and gluteus medius (GMED)) can result in an abnormal gait pattern due to their critical role in locomotor tasks [3], predisposing individuals to musculoskeletal injury or pathology (e.g. large joint osteoarthritis (OA) and low back pain) [4], [5]. In addition, muscle force requirements increase with walking speed [6], so at the faster walking speeds used during exercise, certain muscles, including those responsible for forward progression (e.g. the gastrocnemius (GAST) and soleus (SOL)), may be unable to effectively perform their respective functions, resulting in gait deviations that may increase the risk of musculoskeletal injury/pathology.
Surprisingly, the degree to which obesity affects gait kinematics and kinetics is not clear. Some studies report that kinematics are similar in obese and nonobese groups [7], [8], while others report that obese individuals walk with a more extended leg and similar knee extensor moments during stance and greater step width compared to their nonobese counterparts [9], particularly at faster walking speeds. Unfortunately, there is limited information regarding how investigators did or did not account for the peripheral adiposity that obscures the motion of the underlying skeleton. Thus, differences in methodology may explain these equivocal kinematic results. In addition, studies that have reported lower extremity gait biomechanics in obese individuals [8], [9] have not provided a quantitative assessment of individual muscle function, which may help explain the observed gait patterns.
Musculoskeletal simulations can provide us with an improved understanding of the force requirements and roles that individual muscles play during locomotor tasks [10]. Recent studies have estimated the contributions of individual muscles to the ground reaction force (GRF) during walking in nonobese adults [11], [12]. These studies have shown that during early stance, VAS and GMED muscles are significant contributors to the vertical GRF (GRFV), and function to decelerate and support the body, while during mid-late stance, the gastrocnemius (GAST) and soleus (SOL) are the primary contributors to the GRFV and the anterior-posterior GRF (GRFAP). In the frontal plane, GMED acts to maintain mediolateral (ML) stability and balance, and has been shown to be the primary contributor to the ML GRF (GRFML) [13]. Unlike in the sagittal plane, where a more aligned skeleton would reduce knee extensor muscle requirements, support and stability of the body in the frontal plane is largely accomplished by the hip abductor muscles (e.g. GMED). The effect of GMED weakness may be altered frontal plane kinematics of the pelvis (e.g. increased pelvic obliquity, an increase in pelvic drop of the contralateral hip) resulting in pathological hip joint articulation [14]. For this study, we focused our investigation on the muscles that have large contributions to all three components of the GRF (VAS, GMED, GAST, and SOL) [12].
The purpose of this study was to quantify joint kinematics, estimate individual muscle forces (VAS, GMED, GAST, SOL), and the individual muscle contributions to the walking GRFs at two speeds (1.25 and 1.50 m s−1) in obese and nonobese adults. It has been reported that obese adults walking with a more erect posture and similar knee extensor joint torques compared to nonobese adults [9], suggesting reduced knee extensor muscle forces. We hypothesized that (1) peak knee flexion during stance would be less, while pelvis obliquity would be greater in the obese vs. nonobese group, and the differences between the obese and nonobese groups would be greater at the faster walking speed; (2) absolute and lean mass normalized forces for all muscles, except VAS, which we predict to be similar, would be greater in the obese vs. nonobese adults at both speeds; and (3) VAS contribution to the GRFV would be similar between the obese and nonobese individuals at a velocity of 1.25 m s−1 but would be reduced at a velocity of 1.50 m s−1 in the obese group.
Section snippets
Subjects
A convenience sample of nine obese (8 female) adults and 10 nonobese adults (5 female) participated in our study. Inclusion criteria included a BMI of <25 kg m−2 (nonobese) and 30–40 kg m−2 (obese), age 18–45, and sedentary to moderately active (< 2–3 bouts of exercise/week or participation in any sporting activities < 3 h/week), while exclusion criteria included orthopedic, metabolic, or neurologic impairments, other than obesity, that would hinder movement and prevent safe participation in the
Results
The kinematics of the lower extremity, specifically, pelvic obliquity and knee joint angle, were affected by obesity but not speed (Fig. 1). At the slower speed, there were no statistical differences in peak sagittal plane hip and knee joint angles between groups. At the faster speed, the obese group walked with a more extended knee during early stance compared to the nonobese group (p = 0.012). The peak knee flexion angle during early stance at the faster vs. slower speed in the nonobese group
Discussion
Obese individuals walk with similar sagittal plane (hip and knee), but altered frontal plane (pelvic obliquity) kinematics compared to non-obese individuals at 1.25 m s−1, which is close to the reported preferred walking speed for obese adults (1.29 m s−1) [9]. At a speed of 1.50 m s−1, obese individuals walk with both sagittal and frontal plane kinematic alterations (more extended knee, greater pelvic obliquity) vs. their nonobese counterparts. As hypothesized, compared to nonobese individuals,
Conflict of interest statement
The authors declare no conflict of interest.
Acknowledgments
Research reported in this publication was supported by the National Institute of Arthritis and Musculoskeletal and Skin Diseases of the National Institutes of Health under Award Number R03AR059264. The content is solely the responsibility of the authors and does not necessarily represent the official views of the National Institutes of Health.
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