EXERCISE TRAINING FOR INTERMITTENT CLAUDICATION - DOES IT ADVERSELY AFFECT BIOCHEMICAL MARKERS OF THE EXERCISE-INDUCED INFLAMMATORY RESPONSE

Objectives: To identify a stable biochemical marker of disease severit y in patients with intermittent claudication and to use these findings to assess the effect of therapeutic exercise training. Design: Case-c ontrol study: prospective randomised-controlled trial of exercise trai ning. Materials and methods: Plasma fibrinogen, serum amyloid A protei n (SAA), C-reactive protein (CRP) and urinary albumin-creatinine ratio (ACR) were measured in 67 claudicants and 15 controls. Twenty-two pat ients were randomised to supervised exercise training and 17 randomise d to observation. Subjects were reviewed at 3, 6 and 12 months. Result s: The median (interquartile range) baseline fibrinogen was 3.7 g/l (3 .3-4.25) in claudicants and 3.5 g/l (2.9-3.95) in controls (p = 0.045) ; CRP was 4.7 mg/l (2.2-9.0) and 2.1 mg/l (1.0-2.8), respectively (p < 0.0001); SAA was 72 mg/l (35-132) and 30 mg/l (20-89) (p = 0.0009). C laudicants showed an increased urinary ACR following treadmill exercis e (Wilcoxon, p < 0.0001) with no change in controls. Exercise training reduced SAA at 6 months, CRP at 3 months and progressively attenuated the post-exercise increase in ACR. No similar changes were found in c ontrols. Conclusions: Repetitive low-grade inflammatory events in clau dicants lead to elevation of serum acute-phase proteins. Exercise trai ning is associated with symptomatic improvement and reduction in infla mmatory markers. The concern that exercise has adverse systemic effect s therefore seems to be unjustified.