Arthritis and exercise

Question 1

Do you think that exercise training is worthwhile for people with RA? Can you justify your view point?

Answer 1

o Yes
o Although there aren’t reversible effects for personnel with RA, there can be improvements made in other aspects of life (to increase quality of life)
o Most of the studies show improvement in muscle strength; Reduced muscle function in patients with RA may also present itself as loss of functional balance and coordination
o Results suggest that aerobic capacity and strength improved without negative effects on pain and disease activity. So there is no harm in doing it anyway

Question 2

Disease activity is generally unaffected or improved. What mechanisms may explain why and how exercise may bring about an improvement?

Answer 2

o Evidence to date supports the clinical usefulness of exercise in RA to improve both muscle function and fitness.
o We need more information regarding the physiologic, metabolic, mechanical, and behavioural avenues through which exercise improves function, as well as a greater knowledge of the mechanisms by which exercise reduces pain and joint effusion.
o The evidence will come from applied research that includes various types of exercise in the test environment and from clinical trials that ask questions and measure results at the cellular level as well as at levels of body function and activity.

Question 3

What is arthritis?

Answer 3

Arthritis is a chronic joint disorder characterised by degeneration of joint cartilage and adjacent bone that can cause joint pain and stiffness.

Question 4

What causes arthritis?

Answer 4

o Age
 Increased prevalence in older people
 Natural decline in glucosamine and chondroitin sulphate production (less and less durable cartilage made)
o Gender
 Men have more hip OA
 Women more hand / knee OA
 Women > men RA
 Oestrogen appears to be protective, with increased OA post menopause – unclear
o Inactivity
 Weakness of quadriceps is a risk factor for OA
o Obesity (OA)
 Top 20% for BM ↑ risk 7-10 times for hip and knee OA
 Modest weight loss reduces OA
o Overuse
 Inconclusive data on athletes
 But history of damage predisposes to OA
 Moderate levels of PA does not increase risk of OA
 Indeed movement is needed to “feed” cartilage
o Infection (OA + RA)
o Genetic predisposition (OA + RA)
 Genetics (~ 30-60% influence) (MacGregor et al., 2000)

Question 5

What are the symptoms?

Answer 5

o	Pain and crepitation on movement 
o	Joints become enlarged and deformed 
o	Inflammation 
o	Ligaments becomes stretched = unstable 
o	↓ ROM or complete freezing

Question 6

How does osteoarthritis happen?

Answer 6

o Cells that produce collagen and proteoglycans (provides cartilage durability) become abnormal
o Initially an increase in cartilage growth and bone density (osteosclerosis), reducing joint space
o Soon cartilage thins and cracks. Rough cartilage causes pain during movement.
o Bone starts to be worn down. Bone moves against bone increasing erosion and pain
o Spurs develop to compensate = deformation = joint moves incorrectly = pain
o Inflammation means synovium is thickened
o Increase in synovial fluid
o Joint swells
o Ligaments become lax and muscles crossing joint are overstretched causing weakness

Question 7

How is Rheumatoid Arthritis caused?

Answer 7

o	Genetic (60%) and environmental involvement 
o	Nongenetic factors: 
	Age 
	Hormonal factors 
	Infection 
	Smoking 
	Obesity

Question 8

What causes Arthritis?

Answer 8

o Age
 Increased prevalence in older people
 Natural decline in glucosamine and chondroitin sulphate production (less and less durable cartilage made)
o Gender
 Men have more hip OA
 Women more hand / knee OA
 Women > men RA
 Oestrogen appears to be protective, with increased OA post menopause – unclear
o Inactivity
 Weakness of quadriceps is a risk factor for OA What causes arthritis?
o Obesity (OA)
 Top 20% for BM ↑ risk 7-10 times for hip and knee OA
 Modest weight loss reduces OA
o Overuse
 Inconclusive data on athletes
 But history of damage predisposes to OA
 Moderate levels of PA does not increase risk of OA
 Indeed movement is needed to “feed” cartilage
o Infection (OA + RA)
o Genetic predisposition (OA + RA)
 Genetics (~ 30-60% influence) (MacGregor et al., 2000)