Existing data suggest bariatric surgery-induced weight loss can lead to rapid improvements in gait and physical function. The surgery may also help to address factors associated with knee osteoarthritis, which itself can affect mobility and function in obese patients.
By Andrew W. Froehle, PhD, Neal Dollin, MS, Richard T. Laughlin, MD, Donovan D. Teel II, MD, Richard J. Sherwood, PhD, and Dana L. Duren, PhD
Obesity is a major public health issue, with worldwide rates that have doubled since 1980.1 Defined as body mass index (BMI, weight/height2 in kg/m2) greater than 30, obesity affects about 36% of US adults older than 20 years and about 18% of children older than 6 years.2 Obesity is associated with three of the top 10 leading causes of death in the US and worldwide, including heart disease, stroke, and type 2 diabetes.3,4 Risk for these comorbidities increases with greater obesity. (Class I obesity is defined as BMI 30–34.99 kg/m2, and has moderate risk; Class II, BMI 35−39.99 kg/m2, severe risk; Class III, BMI ≥ 40 kg/m2, very severe risk.)5
Obesity is also a risk factor for functional impairment, including altered walking gait, which limits mobility and the ability to perform activities of daily living.6,7 Unlike metabolic and cardiovascular disease, in which excess body fat and fat distribution are thought to underlie increased risk, the simple fact of having substantial excess body weight (EBW, defined as actual weight minus ideal body weight8) is a key factor in obesity-related gait impairment. High EBW poses a challenge to balance and stability,9,10 resulting in slower and stiffer gait. Obese gait is thus characterized by reduced walking speed, cadence, and stride length; wider base of support; more time spent in the stance phase of the gait cycle; and reduced flexion at hip, knee, and ankle joints.11-14
Changes in gait not only limit mobility, concomitant altered biomechanics and increased joint loading also cause irreversible degeneration of cartilage in lower limb joints and development of pathologic lower limb alignment. As such, obese gait is a key factor in the etiology of lower limb joint osteoarthritis (OA), particularly in the knee OA.15,16 Gait abnormalities specific to obesity are also characteristic of knee OA, and are exacerbated with the additional disease burden.17 The pairing of obesity and knee OA gait abnormalities creates a feedback loop hastening the pace of knee OA progression and functional limitation (Figure 1). Reduced mobility imposes greater limits on activity in already highly sedentary obese individuals, generating greater positive energy balance, additional weight gain, and further risk for comorbidities.18 Thus, obesity and knee OA-related functional impairments are leading causes of general disability among adults.19
There is no cure for knee OA and treatment options are limited.20 The eventual solution is total knee arthroplasty (TKA), which has many benefits and a relatively low complication rate. Still, there is a 25% patient dissatisfaction rate for TKA, and 15% to 17% of patients will likely require at least one revision surgery.21 Revision rates are higher when the surgery is performed in younger people, and complication rates and operative times are greater in obese patients.22 Thus, as obesity and its related functional effects become more common, especially in younger people, the public health burden of TKA will likely rise.21 (See “Active Stance: Developing the sustainable knee in an age of early TKA.”)
Solutions to the functional complications of obesity and obesity-related OA therefore need to focus on weight loss and sustained long-term restoration of gait to increase mobility and slow the pace of OA disease progression. Such solutions are of great potential benefit to public health and to individuals affected by obesity and OA.
Weight loss is the major goal in treating obesity and limiting its impact on gait, mobility, pain, and other issues associated with knee OA.23,24 There is a strong and growing body of evidence that weight loss of any type is associated with functional gains and improvement in biomechanical risk factors for OA. Even modest weight loss (2.6% of body weight) as a result of medium-term (18 months) diet and exercise interventions produces significant improvements in compressive and resultant forces at the knee, as well as in knee abduction moments, which, when abnormal as with excess weight, likely contribute to knee cartilage damage and knee OA.24 Although diet and physical activity are the first-line methods for weight loss, they are effective only over an extended period and often result in noncompliance, especially when patients have functional limitations and joint pain due to obesity and knee OA.
An effective and increasingly common alternative treatment is weight loss through bariatric surgery.25 Historically, the most common procedure has been the Roux-en-Y gastric bypass (RYGB), which creates a 15- to 30-ml gastric pouch, a gastrojejunostomy, and a jejunojejunostomy and induces weight loss through restriction of food volume and reduced hunger that result in a significant reduction of caloric intake.26,27 The RYGB procedure typically leads to a 55% to 75% loss of EBW,28-30 far greater and more rapid weight loss than is typically achieved with diet and exercise interventions alone.
In terms of the effects of bariatric surgery and subsequent weight loss on functional recovery, there are four major questions:
1) Does rapid weight loss due to bariatric surgery restore gait and function to a level considered normal for postsurgical weight?
2) If not, or if incompletely, what characteristics of obese gait are retained postsurgically?
3) What effects does weight-loss surgery have on biomechanical risk factors for lower limb joint OA and disease progression?
4) Does surgery-induced weight loss have a greater positive effect on functional outcomes than other less invasive and less risky weight-loss strategies?
Two studies examined functional improvement using questionnaires and timed movement tests, mostly in women, in the year following their RYGB surgery. Miller and colleagues31 found significant improvements in balance, walking time, chair rise time, lateral mobility, quadriceps strength, and self-reported function as assessed by the Fitness Arthritis and Seniors Trial Disability Questionnaire (FAST). Improved performance was evident shortly after surgery and continued up to six months, after which values tended to plateau despite further weight loss to a final total weight loss value of 34.2%. Gains in quadriceps strength and muscle quality, however, did not manifest until six to 12 months after surgery.
Our research group32 investigated post-RYGB functional improvement using the Timed Get-Up-and-Go Test (TGUG), the Short-Form Health Survey-36 (SF-36) and the Short Musculoskeletal Function Assessment questionnaire (SMFA). As in other studies, we observed significant functional gains within six months of surgery. Little to no additional improvement occurred between six and 12 months, despite continued weight loss to a final weight loss value of 36.4%.
Short-term changes in gait
We are aware of three studies using quantitative gait analysis to investigate changes in gait biomechanics between preoperative tests and three-month to one-year follow-up tests (Table 1).33-35 Vincent and colleagues33 assessed spatiotemporal gait variables three months after surgery, comparing the surgical sample with nonsurgical obese controls. Vartiainen and colleagues34 observed changes in spatiotemporal, kinematic, and kinetic variables with a slightly longer follow-up period of 8.8 months, with no control or comparison group. Finally, Hortobágyi and colleagues35 examined changes in spatiotemporal, kinematic, and kinetic variables with two follow-up measurements in obese individuals at seven and 12.8 months that they compared with healthy nonobese controls.
Surgical patients exhibited significant weight loss, ranging from 19.4% at three months33 up to 33.6% at one year.35 Both Vincent et al and Hortobágyi et al found significant changes in spatiotemporal variables, including increased self-selected walking speed, cadence, and stride length; decreased time spent in stance phase; and narrower base of support, which affects knee alignment.33,35 With the exception of cadence, the degree of change in these variables was proportional to weight loss, and continued to change between follow-up time points as weight loss continued.35 Vartiainen et al also found a narrower base of support, but did not observe changes in support times or stride length.34 This may be a product of Vartiainen et al using standardized walking speeds rather than self-selected walking speed used in the two other studies.
It is noteworthy that, while changes in many functional measures appear to plateau by six months after surgery, Hortobágyi et al showed continued gait improvement with ongoing weight loss between seven and 12.8 months. This may in part reflect the psychological component of function questionnaires, in that self-perception of functional capabilities may respond more rapidly to weight loss than do gait biomechanics.
As for functional tests, such as the TGUG, that focus on speedy completion of a task and may not reflect common daily experience, there may be a weight-loss threshold past which any further gains are marginal. Indeed, our sample’s TGUG times had improved by six months after surgery to within the normal range for healthy nonobese individuals aged 19 to 29 years,36 suggesting little room for further improvement. Gait, on the other hand, may continue to change over a longer period as walking is a common daily experience to which obesity generally causes significant biomechanical adaptations. These adaptations may require substantial gait retraining that proceeds on a longer time scale and with continued weight loss.
Several kinematic and kinetic variables were also altered following bariatric surgery. Hip flexion angle; peak knee extensor torque; and peak knee abductor, knee flexor, and hip extensor moments all decreased significantly.34,35 In addition, by 12.8 months Hortobágyi et al observed significant changes in weight-specific vertical ground reaction and braking forces, as well as in hip range of motion.35 Finally, whereas Vartiainen and colleagues found no postsurgical adjustments in knee joint angles,34 Hortobágyi et al showed a significant increase in maximal knee flexion angle, indicating reduced gait stiffness.35
Long-term functional improvements
The above studies provide evidence of short-term functional gains with weight loss after bariatric surgery. It is also important to assess whether gains are sustained over longer periods. Our research group followed a subset of women from our previous study32 to assess changes in weight, functional status, and gait almost five years after surgery.37 Nine women participated, with an average follow-up time of 4.7 years. They had maintained weight loss, with current weight averaging 68.2% of presurgical weight.
Longitudinal data for TGUG times and SMFA function scores showed sustained improvement over preoperative conditions, and were similar to values measured at one-year follow-up.32 We did not collect gait data in the earlier study, so we compared cross-sectional gait data from the five-year follow-up to a healthy age- and BMI-matched reference sample that had not undergone surgery. This allowed us to determine if gait in the bariatric surgery sample was typical of current weight, or if they instead still exhibited aspects of severely obese gait.
In the reference sample, self-selected walking speed, cadence, base of support, and time spent in stance phase were significantly related to EBW. The bariatric surgery sample’s values for these relationships fell entirely within the reference sample’s 95% confidence limits. Support times were also significantly related to EBW loss in the bariatric surgery sample, with greater weight loss associated with less time in stance phase. This result suggests a dose-response relationship between weight loss and gait patterns five years after surgery. Interestingly, however, seven bariatric patients fell below the reference sample regression lines for walking speed and cadence, suggesting that some aspects of gait after surgical weight loss remained below average. We did not control for activity level, which can affect gait;38,39 thus, if the bariatric sample was less active than the reference sample it could explain the former’s below-average values for gait parameters.
A wide range of data types from varying follow-up times overwhelmingly show sustained functional recovery is a key outcome of weight loss due to bariatric surgery. Although current data are somewhat limited by variation in study design and a paucity of data on men (partly a byproduct of sex-biased rates of bariatric surgery,40,41 existing evidence provides preliminary answers to the most important questions in functional recovery after bariatric surgery. As to whether postsurgical weight loss is associated with regained function, the answer is clearly yes. Expanding on that answer, however, is the observed dose-response relationship between weight loss and functional recovery across a variety of domains: with greater weight loss comes better function. The reverse is also likely true, in that weight regain after surgery may lead to renewed loss of function; thus maintenance of weight loss is critical. Continued research should focus on strategies to sustain surgical weight loss, since up to 20% of patients are expected to experience significant weight regain.42
There are few data that speak to the second question on retention of presurgical gait and functional traits. Our finding that bariatric patients tended to remain below average for walking speed and cadence may indicate retained characteristics reflecting presurgical weight status.37 The third question of effects on OA risk factors remains largely unanswered, though some of the biomechanical changes reported above34,35 may lessen forces that lead to destruction of knee cartilage. Continued work in our bariatric surgery sample will focus on kinematic and kinetic variables related to knee OA.
Finally, more data from larger studies are needed to answer the central question of whether bariatric surgery has a greater positive effect on functional outcomes than other weight-loss strategies. Current data suggest rapid weight loss may provide the most immediate functional gains through dose-response relationships, whereas slower weight loss with diet and exercise may take longer to induce functional change. This is particularly important when considering the effects of prolonged exposure to excess weight on OA risk. Exercise does, however, provide functional benefits related to strength and balance that surgical weight loss alone likely does not. As such, even if exercise does not form the basis for rapid weight loss, it should form part of any postsurgical maintenance plan aimed at functional recovery.
Existing data are promising with regard to the potential for bariatric surgery-induced weight loss to lead to rapid improvements in function, as well as to possible reductions in factors that lead to or exacerbate OA, a major challenge to function and mobility. Bariatric surgery thus offers a compelling option for weight loss and functional restoration when noninvasive interventions have been unsuccessful.
Andrew W. Froehle, PhD, is assistant professor in the Department of Community Health and the Department of Orthopaedic Surgery, Sports Medicine and Rehabilitation at Wright State University Boonshoft School of Medicine in Dayton, OH. Neal Dollin, MS, is an MD candidate and Richard T. Laughlin, MD, is professor and chair of the Department of Orthopaedic Surgery, Sports Medicine and Rehabilitation at Wright Sate University. Donovan D. Teel II, MD, is a surgeon with Premier Metabolic and Bariatric Associates, and voluntary faculty in the Department of Surgery at Wright State University. Richard J. Sherwood, PhD, is professor and director of the Division of Morphological Sciences and Biostatistics in the Department of Community Health and professor in the Department of Pediatrics and Dana L. Duren, PhD, is associate professor in the Department of Community Health and the Department of Orthopaedic Surgery, Sports Medicine and Rehabilitation, and director of Orthopaedic Research at Wright State University.
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