Exercise and Osteoarthritis Joint Pain

The first OA Clinical Studies forum highlights key international research.

By Jill Tyrer

Exercise is widely recommended for people who have osteoarthritis (OA). Research has shown exercise reduces OA pain and inflammation and it can improve sleep, mood and overall health and fitness. But a lot is still unknown: How does it work to reduce pain and inflammation? How does exercise help non-weight-bearing joints, like hands? Which patients are more likely to benefit? What types of exercise help which patients? How much exercise is best for what conditions or patients?

Researchers continue to investigate these and other questions about exercise and OA joint pain.  The topic was the focus of the July 16, 2021, Osteoarthritis Clinical Studies (OACS) Forum Series, presented by the Arthritis Foundation. More than 400 scientists, physicians, patients and other stakeholders registered for the virtual forum, “Exercise Is Medicine: Managing OA Joint Pain.”

The OACS series is an important part of the Foundation’s commitment to supporting the research and development of safe and effective OA treatments as well as to improving the lives of people living with OA. The Foundation has played a key role in bringing together international researchers with regulators, clinicians, patients and others in the OA arena for several influential conferences and presentations, most recently in June for a workshop with U.S. Food and Drug Administration representatives.

“With OACS, I strive to bring together the best clinical scientists from diverse areas of expertise and geography to discuss and advance research into therapies to improve the lives of OA sufferers,” says Jason Kim, the Arthritis Foundation’s vice president of osteoarthritis programs.

Pain Mechanisms in OA

Lisa Carlesso, PT, PhD, led the discussion with a presentation on pain mechanisms in OA and exercise. Carlesso, a physiotherapist and assistant professor in the School of Rehabilitation Sciences at McMaster University in Canada discussed some of the challenges in studying pain from OA.

OA pain is complex, involving not only the disease process and what’s happening in the joint, but also the central nervous system (CNS), genetics, emotions, thoughts and beliefs. In broad terms, she explained, when some pain-causing stimulus is introduced to the body, such as joints affected by OA, it creates a reaction in the CNS, and signals travel to the brain. There, they combine with other information the individual has from experience, including beliefs, expectations and culture. If the brain decides that the body needs to be protected from the initial stimulus, then pain occurs, and the individual changes behavior to relieve or defend against the pain, she said.

But it’s not always that straightforward, either. In addition to the CNS, which involves the brain and spinal cord, there’s the peripheral nervous system involving the nervous system outside the brain and spine. In some cases, the signals traveling through these two nervous systems go awry, leading to increased sensitivity to pain (hyperalgesia) or even pain where there wouldn’t normally be any, as from a light touch (allodynia).

Carlesso discussed the role of exercise in pain modulation. Exercise-induced hypoalgesia (EIH), meaning reduced sensitivity to a painful stimulus following exercise, and conditioned pain modulation (CPM), a measure of the body’s natural pain-defense system where a person has less pain after exposure to previous pain, are important phenomena in this area of pain research. EIH and CPM may help patients experiencing OA pain adapt, but also confound measurements of pain in some research studies. 

Existing research on reducing pain with exercise showed the best results to be in regular exercisers, and the greatest effects were in the body part being exercised. “And it's important to note that the effect is impacted by one’s expectation around exercise and pain as well as messaging that we might receive from others around that,” Dr. Carlesso said. Furthermore, while people with shoulder, back, hip or knee OA pain benefited from exercise, those with fibromyalgia or chronic, widespread pain responded to it with heightened sensitivity, or hyperalgesia.

Questions still remain about how much exercise will optimize EIH and result in less pain. Also unclear is the influence of psychosocial factors, such as beliefs, experience and culture on EIH. Resistance, aerobic or other types of exercise may affect the pain relief provided by EIH or CPM.   

Individualized Exercise

In the second presentation, Melanie Holden, PhD, of Keele University in the United Kingdom, and Jos Runhaar, PhD, of Erasmus University Medical Center in The Netherlands, focused on the challenges of identifying which hip and knee OA patients would benefit from which kinds and doses of exercise. Many individual factors are involved, ranging from age and gender to pain level and function to expectations and emotions. Furthermore, while exercise therapy leads to less pain and disability, it’s unclear which factors contribute to the benefits.

Dr. Runhaar believes exercise therapy “mediators” may contribute to reducing pain and disability. Potential mediators may be muscle strength, proprioception and range of motion for knee OA; and muscle strength for hip OA.

Through a meta-analysis of clinical trials using data from individual participants, they found that pain level and function moderate the effects of exercise and developed tools to help identify the level of pain and function at which patients would respond to exercise therapy. (They found no evidence that age, mental well-being, number of comorbidities, duration of symptoms, strength, physical activity, education, arthritis self-efficacy or radiographic OA severity had an effect on pain after three months from initiating therapy.)

They determined that exercise therapy helped strengthen the knee, which helped reduce pain and disability. But the strength gains were very small, so other factors are likely responsible for the pain and function improvements, but more research is needed.

Is Exercise Safe With OA?

Alessio Bricca, PhD, a researcher at the University of Southern Denmark, addressed the questions of whether exercise therapy is safe for people with OA and whether it would further damage a joint affected by OA.

The answer: Yes, it is safe and will not cause further damage, he said. Exercise therapy — meaning a prescribed regimen with specific therapeutic goals — should be offered to OA patients as a first-line treatment, he advised, ideally three times a week and under supervision. In an eight-week exercise program, pain increased at first by about 10%, but consistently declined as sessions continued.

The type of exercise — aquatic, cardio, strengthening or other — doesn’t seem to matter, he added. They all help reduce pain in hip and knee OA and they’re safe.

Pain should be tolerable for exercise, though, so the patient’s pain level should be monitored before and during exercise and 24 hours later. Generally, it will go up during exercise then back down afterward. If it persists 24 hours later or if the patient is flaring, he should reduce the intensity or duration of exercise, Dr. Bricca said.

Meta-analyses also have shown that exercise does not damage cartilage or trigger inflammation, he explained. And exercise has benefits beyond OA: It helps prevent at least 35 chronic diseases, including heart disease, type 2 diabetes and depression, and it improves pain, function and quality of life.

Coping With Pain

In “Exercise and Pain Coping,” presenter Francis Keefe, PhD, of the Pain Prevention and Treatment Research Program at Duke University Medical Center, talked about how our understanding of pain has evolved, largely as a result of brain imaging. Pain involves a complex matrix of many neural networks — including sensory, salience, stress, emotion, action and pain modulation networks — and when a pain stimulus is introduced, these networks in the brain are activated.

When pain persists, as in chronic pain, links between the networks strengthen, and signals move more quickly along them from one area of the brain to the next, he explained. And when pain persists, the person experiencing it uses coping strategies to control it, tolerate it or reduce it.

Avoidance, Dr. Keefe said, is the “workhorse coping strategy,” and if exercise causes pain, the way to cope is to avoid it. That may prevent immediate pain, but in the long term, the result is more pain, poorer fitness and overall health, and more depression and discouragement.

The challenge, he said, is to make patients and health care professionals aware of the effects of pain on exercise and give them tools for better coping strategies.

For example, when patients were asked to think through their pain experience, or become more mindful, they learned to cope in healthier ways, he said. Instead of anticipating the worst, or catastrophizing, those who were asked to self-report — record their thoughts, feelings, actions and beliefs about their pain experience — began to change their thinking and make them more optimistic and open to ways of adapting.

Additionally, Dr. Keefe recommended having a plan for dealing with a flare — for instance, activity modifications, anti-inflammatory medications, practicing more relaxation or meditation — and sharing it with family, caregivers and health care providers. Just having the plan gives patients more confidence that they’ll be able to manage the flare and get through it, Dr. Keefe says.

Another strategy is to teach patients relaxation or meditation techniques and integrate these into their exercise routine. This also makes patients more mindful of their actions and feelings and makes them more open to problem-solving. Other potentially helpful strategies: pacing their activity, working out with a buddy and setting values-based goals, Dr. Keefe added.

The forum ended with a Q&A session and panel discussion.

Learn more about the 2020 OACS series and sign up for future 2021 OACS forums: Physical Activity and Exercise Behavior Change on Sept. 22 and Cell Therapies in OA on Nov. 3.


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