BIOMECHANICAL AND MUSCULOSKELETAL CHANGES IN OBESE INDIVIDUALS

By: Edrick Purnomo Putra

When discussing obesity, the conversation typically revolves around the metabolic impact on the body. However, the mechanical strain on the musculoskeletal system, due to the extra weight, is often overlooked. Overweight and obesity are independently associated with an increased risk of developing musculoskeletal disorders.1 For instance, a study involving 150 severely obese participants, with body mass index (BMI) of 35 kg/m2 or higher, indicated a high prevalence of pain in the ankles and feet (68.7%), lower back (62.7%), knees (53.3%), and upper back (52.0%). The pain is predominantly severe. The study also discovered associations between specific conditions and pain in particular sites: type 2 diabetes correlates with hand/wrist pain; hip pain is associated with sedentary time; insomnia with hip and knee pain; edema in the lower limbs with lower back and ankle/foot pain; obesity degree with ankle/foot pain; and percentage of total fat with ankle/foot pain.2 Yet, the correlation between an increased BMI and various musculoskeletal disorders isn’t extensively described for all musculoskeletal issues._¹

From a physiological standpoint, the human physique interacts with various forces during daily activities, and these forces progressively shift with body weight. The ground reacts to the body’s weight by exerting a force back, known as the ground force reaction (GFR). For people of normal weight, the mechanical forces and GFR acting on the body are relatively lower compared to those with a higher BMI. Joint alignment is maintained and loading effect is minimized by adequate muscle strength and low systemic inflammation. However, as weight or mass progressively increases, mechanical stress also increases, especially in weight-bearing joints. With this, the GFR also amplifies, causing further stress on joints, while muscle strength decreases, failing to provide adequate compensation. Systemic inflammation, which tends to increase with obesity, may also induce biochemical reactions in the musculoskeletal system.³

The link between obesity and osteoarthritis (OA) has been well-established in numerous studies. Obesity exerts both mechanical and systemic effects on the development of OA. Chronic low-grade inflammation, typically induced by obesity, might trigger the onset and progression of OA, not only in weight-bearing joints but also in non-weight-bearing ones. Inflammation enhances the production of inflammatory cytokines and might induce macrophage infiltration into the joint synovium, causing local inflammation, pain, swelling, and stiffness in the joint.4 Recent studies have also linked inflammation in obesity to adipokines from adipose tissue. These adipokines, when in excess, can disrupt cartilage homeostasis, degrade the cartilage matrix, and hinder chondrocyte function.5 Obesi-ty-associated vascular disease has led to the hypothesis that microvascular changes in the subchondral bone might accelerate the OA process by creating an ischemic effect and altering the nutritional supply to the bone.5 Furthermore, in diabetes induced by obesity, the formation of advanced glycation end products (AGEs) in the articular cartilage may contribute to increased collagen stiffness.⁵

Excessive and abnormal loading on weight-bearing joints cause shear stress on the knee joint, leading to inflammation and breakdown of articular cartilage. Chondrocytes, the cells within cartilage, have mechanoreceptors sensitive to pressure. Their activation can lead to the expression of cytokines, growth factors, and metalloproteinases, producing mediators that eventually inhibit matrix synthesis and degrade cartilage.5 Elevated body weight may increase stress on the knee joint, causing malalignment and exacerbating underlying joint issues. Muscle weakness, often associated with obesity, can further impair a joint’s ability to absorb stress, given the crucial role muscles play as shock absorbers in joints.⁶ Gait mechanics also change in people with obesity. On the whole, people with a higher BMI typically display slower gait velocity, shorter stride length, slower cadence, and a longer stance period compared to those with a normal BMI. The higher the BMI, the more pronounced the influence on gait energetics and mechanics.⁷ A decreased daily activity level is often a result of these walking impairments, as demonstrated by a lower daily step count in obese individuals compared to those of healthy weight.³ One study found that obese women exhibited a significantly greater touchdown angle, a more extensive total eversion range of motion, and faster maximum eversion velocity, which suggests abnormal rearfoot movement.⁸ These differences in walking are associated with an increased risk of musculoskeletal injury and falls in people with obesity.⁹

Another study demonstrated a correlation between a higher BMI and greater peak internal ankle plantar flexion, a lower arch with greater peak ankle eversion and abduction, and knee adduction during walking. Adults with a higher BMI often have lower arches or flat feet, resulting in more flexibility during the propulsive phase of walking and, subsequently, excessive foot pronation. Overpronated feet can lead to lower limb malalignment with excessive loads and a greater toe-out angle during walking, possibly causing foot pain such as chronic plantar heel pain. The combination of walking differences and foot misalignment in obese individuals contributes to musculoskeletal injuries, including posterior tibial tendon dysfunction, ankle sprains, and plantar fasciitis.⁹

Knee adduction also occurs in individuals with obesity. An external knee adduction moment (KAM) during the stance phase of gait is considered indicative of tibiofemoral knee joint loading in the medial compartment and is strongly associated with excessive body mass. One study found a robust association between an increased KAM and the risk of OA progression. Obese individuals often have larger thigh circumferences, necessitating greater hip abduction, a circumferential swing phase, and varus alignment of the knee to prevent thigh touching while walking. This malalignment, particularly in conjunction with a high BMI, intensifies knee OA progression, especially in the medial part of the tibiofemoral joint.⁶

The accumulation of body fat around the waist and hips in individuals with obesity results in an anteriorly tilted pelvis and lumbar lordosis. This tilt is caused by the habitual concentric contraction of the hip flexor, which lengthens the hip extensor eccentrically. Concurrently, abdominal and gluteal muscles weaken and elongate, while paraspinal and flexor muscles shorten. The resulting muscle strain leads to lower back pain (LBP).10 A study of lumbosacral angles in individuals with obesity concluded that a higher BMI and waist-hip ratio are associated with larger lumbosacral angles, which may increase the incidence of LBP.¹

Obese individuals with increased abdominal girth experience a ventral shift of the body’s center of gravity (COG), which leads to a loss of neutral position and sagittal alignment. This COG shift considerably amplifies the forces experienced by the spine. The extra weight also increases axial loading on the spine. Repetitive and excessive loads on the spine, coupled with a loss of sagittal balance, may initiate degenerative changes in the spine of obese individuals.¹¹

The primary management of obesity involves a multidisciplinary approach to promoting a healthy lifestyle to reduce body weight. However, due to the potential for musculoskeletal pain, fear avoidance behavior, or kinesiophobia and functional decline in patients with obesity, encouraging physical activity can be challenging.3 Therefore, proper pain management is crucial to facilitate patient participation in physical activity. It is important to reassure patients that pain can be managed and to provide a supervised, tailor-made exercise program that accommodates the patients’ fitness levels while ensuring their safety.

References:

• Onwuasoigwe O. Impact of overweight and obesity on the musculoskeletal system using lumbosacral angles. Patient Prefer Adherence. 2016;10:291–6.
• Mendonça CR, Noll M, Silva A, Santos DC, Paula A, Silveira EA. High prevalence of musculoskeletal pain in individuals with severe obesity : sites, intensity, and associated factors. Korean J Pain. 2020;33(3):245–57.
• Vincent HK, Adams MCB, Vincent KR, Hurley RW. Musculoskeletal Pain, Fear Avoidance Behaviors, and Potential Interventions to Manage Pain and Maintain Function. Reg Anesth Pain Med. 2013;38(6):481–91.
• Rujia A, Udduttula A, Li J, Liu Y, Ren P. Cartilage tissue engineering for obesity-induced osteoarthritis : Physiology, challenges, and future prospects. J Orthop Transl [Internet]. 2021;26(July 2020):3–15.
• Pottie P, Presle N, Terlain B, Netter P, Mainard D, Berenbaum F. Obesity and osteoarthritis: more complex than predicted! Ann Rheum Dis. 2006;65:1403–5.
• Chen L, Jun J, Zheng Y, Li G, Yuan J, Ebert JR, et al. Pathogenesis and clinical management of obesity-related knee osteoarthritis : Impact of mechanical loading. J Orthop Transl [Internet]. 2020;24(November 2019):66–75.
• Primavesi J, Fern A, Hans D, Favre L, Roten FC Von, Malatesta D. The Effect of Obesity Class on the Energetics and Mechanics of Walking. Nutrients. 2021;13(4546):1–18.
• Messier SP, Davies A, Moore DT, Davis SE, Pack RJ, Kazmar SC. Severe Obesity: Effects on Foot Mechanics During Walking. Foot Ankle. 1994;15:29–34.
• Kim D, Lewis CL, Gill S V. Effects of obesity and foot arch height on gait mechanics : A cross-sectional study. PLoS One [Internet]. 2021;16:1–13. Available from: http://dx.doi.org/10.1371/journal.pone.0260398
• Paul Y, Ellapen TJ, Swanepoel M, Hammill H V, Barnard M, Qumbu BT. An Exercise Rehabilitative Solution to Work-Related Musculoskeletal Lower Back Pain among Nurses. Open J Orthop. 2018;8:322–30.
• White A, Panjabi M. Clinical Biomechanics of The Spine. 2nd ed. Philadelphia: JB Lippincott; 1990.