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Exercise and Osteoarthritis: Cause and Effects

Kim Bennell, Rana S. Hinman, Tim V. Wrigley, Mark W. Creaby, Paul Hodges

10.1002/cphy.c100057

Source: Volume 1, Issue 4, October 2011

Published online: October 2011

Full Article on Wiley Online Library



Abstract

Osteoarthritis (OA) is a common chronic joint condition predominantly affecting the knee, hip, and hand joints. Exercise plays a role in the development and treatment of OA but most of the literature in this area relates to knee OA. While studies indicate that exercise and physical activity have a generally positive effect on healthy cartilage metrics, depending upon the type of the activity and its intensity, the risk of OA development does appear to be moderately increased with sporting participation. In particular, joint injury associated with sports participation may be largely responsible for this increased risk of OA with sport. Various repetitive occupational tasks are also linked to greater likelihood of OA development. There are a number of physical impairments associated with OA including pain, muscle weakness and altered muscle function, reduced proprioception and postural control, joint instability, restricted range of motion, and lower aerobic fitness. These can result directly from the OA pathological process and/or indirectly as a result of factors such as pain, effusion, and reduced activity levels. These impairments and their underlying physiology are often targeted by exercise interventions and evidence generally shows that many of these can be modified by specific exercise. There is currently little clinical trial evidence to show that exercise can alter mechanical load and structural disease progression in those with established OA, although a number of impairments, that are amenable to change with exercise, appears to be associated with increased mechanical load and/or disease progression in longitudinal studies. © 2011 American Physiological Society. Compr Physiol 1:1943‐2008, 2011.

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Figure 1. Figure 1.

Etiopathogenesis of osteoarthritis 473.

Reprinted by permission from Macmillan Publishers Ltd: Nature Reviews Drug Discovery volume 4 issue 4, Wieland HA, Michaelis M, Kirschbaum BJ, Rudolphi KA – Osteoarthritis: an untreatable disease? 331‐344, copyright April 2005.
Figure 2. Figure 2.

Pathological features of osteoarthritis 202.

Reproduced from BMJ, Hunter DJ and Felson DT, Osteoarthritis, 332:639‐642, copyright notice 2006 with permission from BMJ Publishing Group Ltd.
Figure 3. Figure 3.

T1 relaxation times for femoral weightbearing cartilage in men (○) and women (▾) participating in different levels of physical activity 433. Longer relaxation times were observed in the moderately active and elite sportsmen compared with sedentary individuals. This indicates higher glycosaminoglycan (GAG) content in the knees of the active groups.

Reprinted from Magnetic Resonance Medicine 51(2):286‐290, Tiderius CJ, Svensson J, Leander P, Ola T, Dahlberg L. dGEMRIC (delayed gadolinium‐enhanced MRI of cartilage) indicates adaptive capacity of human knee cartilage, copyright notice 2004 with permission from John Wiley & Sons Inc.
Figure 4. Figure 4.

Inter‐relationships between pathological features and impairments in osteoarthritis with particular applicability to knee osteoarthritis.
Figure 5. Figure 5.

Inter‐relationships between obesity, physical inactivity, and reduced muscle mass and strength 486.

Reprinted from Nutrition, Metabolism and Cardiovascular Diseases vol 18, Zamboni M, Mazzali G, Fantin F, Rossi A, Di Francesco V, Sarcopenic obesity: a new category of obesity in the elderly, pp388‐395, copyright 2008 with permission from Elsevier.
Figure 6. Figure 6.

Comparison of effect of land‐based exercise on pain and function in knee osteoarthritis according to mode of exercise delivery 141.
Figure 7. Figure 7.

Long‐term effect of exercise in people with hip and knee OA 447,449. NSAIDs, nonsteroidal anti‐inflammatory drugs.
Figure 8. Figure 8.

Comparison of effect sizes for exercise on pain relative to common oral drug therapies in people with hip and/or knee osteoarthritis 490. NSAIDS, nonsteroidal anti‐inflammatory drugs; GS, glucosamine sulphate; CS, chondroitin sulphate.
Figure 9. Figure 9.

Change in muscle cross‐sectional area following isokinetic training in people with knee osteoarthritis 161.
Figure 10. Figure 10.

Mean change in voluntary quadriceps activation following home‐based quadriceps strengthening exercise 318.
Figure 11. Figure 11.

Weakness of the hip abductor muscles can lead to a drop of the contralateral pelvis during stance 32. This can increase the length of the frontal plane knee lever arm (perpendicular distance from the centre of the knee joint to the ground reaction force vector shown as the thick arrow) thereby increasing the external knee adduction moment and the load on the medial knee joint compartment.

Reprinted, with permission, from Bennell et al. (32).


Figure 1.

Etiopathogenesis of osteoarthritis 473.

Reprinted by permission from Macmillan Publishers Ltd: Nature Reviews Drug Discovery volume 4 issue 4, Wieland HA, Michaelis M, Kirschbaum BJ, Rudolphi KA – Osteoarthritis: an untreatable disease? 331‐344, copyright April 2005.


Figure 2.

Pathological features of osteoarthritis 202.

Reproduced from BMJ, Hunter DJ and Felson DT, Osteoarthritis, 332:639‐642, copyright notice 2006 with permission from BMJ Publishing Group Ltd.


Figure 3.

T1 relaxation times for femoral weightbearing cartilage in men (○) and women (▾) participating in different levels of physical activity 433. Longer relaxation times were observed in the moderately active and elite sportsmen compared with sedentary individuals. This indicates higher glycosaminoglycan (GAG) content in the knees of the active groups.

Reprinted from Magnetic Resonance Medicine 51(2):286‐290, Tiderius CJ, Svensson J, Leander P, Ola T, Dahlberg L. dGEMRIC (delayed gadolinium‐enhanced MRI of cartilage) indicates adaptive capacity of human knee cartilage, copyright notice 2004 with permission from John Wiley & Sons Inc.


Figure 4.

Inter‐relationships between pathological features and impairments in osteoarthritis with particular applicability to knee osteoarthritis.



Figure 5.

Inter‐relationships between obesity, physical inactivity, and reduced muscle mass and strength 486.

Reprinted from Nutrition, Metabolism and Cardiovascular Diseases vol 18, Zamboni M, Mazzali G, Fantin F, Rossi A, Di Francesco V, Sarcopenic obesity: a new category of obesity in the elderly, pp388‐395, copyright 2008 with permission from Elsevier.


Figure 6.

Comparison of effect of land‐based exercise on pain and function in knee osteoarthritis according to mode of exercise delivery 141.



Figure 7.

Long‐term effect of exercise in people with hip and knee OA 447,449. NSAIDs, nonsteroidal anti‐inflammatory drugs.



Figure 8.

Comparison of effect sizes for exercise on pain relative to common oral drug therapies in people with hip and/or knee osteoarthritis 490. NSAIDS, nonsteroidal anti‐inflammatory drugs; GS, glucosamine sulphate; CS, chondroitin sulphate.



Figure 9.

Change in muscle cross‐sectional area following isokinetic training in people with knee osteoarthritis 161.



Figure 10.

Mean change in voluntary quadriceps activation following home‐based quadriceps strengthening exercise 318.



Figure 11.

Weakness of the hip abductor muscles can lead to a drop of the contralateral pelvis during stance 32. This can increase the length of the frontal plane knee lever arm (perpendicular distance from the centre of the knee joint to the ground reaction force vector shown as the thick arrow) thereby increasing the external knee adduction moment and the load on the medial knee joint compartment.

Reprinted, with permission, from Bennell et al. (32).
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Article Title: Exercise and Osteoarthritis: Cause and Effects
 

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Kim Bennell, Rana S. Hinman, Tim V. Wrigley, Mark W. Creaby, Paul Hodges. Exercise and Osteoarthritis: Cause and Effects. Compr Physiol 2011, 1: 1943-2008. doi: 10.1002/cphy.c100057