Information for Health and Exercise Professionals

Impact of Stroke

Stroke is the largest single cause of severe disability in Scotland. Around 2.5% of men and 2.8% of women in Scotland are stroke survivors (Scottish Health Survey 2008, section 8.3 The majority of stroke survivors are left with some degree of on-going disability. In addition to this, around one sixth of people who have had a stroke are likely to experience another stroke within 5 years.

These two areas:

  • on-going disability after stroke
  • and the high incidence of secondary strokes in stroke survivors
have enormous public health implications. Exercise interventions have potential to reduce this disease burden and improve quality of life for people after stroke. As suggested by Deplanque and Bordet 'the famous Latin sentence mens sana in corpore sano ... may be of greater neurological importance than previously expected'.

How does physical activity help prevent strokes?

There are a number of established risk factors for stroke that are modified by exercise
We know that increasing physical activity:

  • Reduces blood pressure
  • Increases high-density lipoprotein cholesterol concentration
  • Reduces plasma fibrinogen level and platelet aggregation
  • Facilitates weight loss and weight maintenance
  • Increases insulin sensitivity because of increased number and activity of glucose transporters, both in muscle and adipose tissue

Lee et al in their study of the impact of physical activity on stroke risk in male physicians found that the impact of physical activity was mediated through effects on body mass, blood pressure, serum cholesterol, and glucose tolerance. The reduction in risk was not completely explained by reduction in vascular risk factors however.  There are theories that exercise has direct effects that reduce stroke risk. A plausible molecular mechanism is via nitric oxide levels.  Exercise of small and large muscle groups improves NO-vasodilator function in humans and increases the expression of endothelial nitric oxide synthase (eNOS). Nitric oxide is a vasodilator and prevents platelet aggregation (anti-clotting effects). Endres et al found that mice exposed to voluntary or forced exercise had increased levels of eNOS, increased vasodilation and reduced infarct size after left middle cerebral artery occlusion than mice that did not have the opportunity to exercise.  Mice that have had the gene for eNOS removed (eNOS knockout mice) did not experience the same protective effects from exercise.

At present, there is no direct evidence that exercise reduces the risk of recurrent stroke and other vascular events in people who have had a stroke. There is strong evidence that exercise reduces the risk of first ever stroke and it seems highly plausible that the same mechanisms will be effective in preventing subsequent as well as first-ever strokes.

For more information on this subject, please read this paper...