The effects of exercise on biochemical markers of vascular inflammation and walking distance for patients with peripheral arterial occlusive disease (PAOD)

University of Cambridge (2004) J Physiol 555P, PC81

Communications: The effects of exercise on biochemical markers of vascular inflammation and walking distance for patients with peripheral arterial occlusive disease (PAOD)

S. McIntosh*, D. Cotterrell† and P. Edwards*

* Countess of Chester Hospital and †University College Chester, Chester, UK

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Cramping pain and walking impairment results from muscular ischaemia in PAOD patients (Hiatt et al. 1990). Increases in C-reactive protein (CRP) and urinary microalbumin (quantified by an albumin creatinine ratio (ACR)) suggest endothelial damage from inflammation (Yudkin 1988), and may be involved in the progression of atherogenesis and PAOD (Kuller, et al. 1996). This study aimed to investigate the effect of a 12-week home exercise regimen (HER) on CRP, ACR, patient claudication walking distance (CWD) and maximum walking distances (MWD).

Ethical consent for all testing procedures was obtained by the South Cheshire Ethical Committee alongside approval from University College Chester’s Ethical Board. Twelve PAOD patients (EG) and 12 age and sex match controls (CG) exercised for 1 h a day, five times per week for 12 weeks. Twelve age and sex matched healthy controls (CG) maintained normal activity. CWD was assessed as the distance (m) at which ‘cramping’ pain was first identified. MWD was recorded as the distance achieved upon cessation of the exercise test using a Gardner grade stage walking test. Venous CRP and urinary ACR were taken at T1 = baseline, pre HER, T2 = post treadmill test pre HER,T3 = baseline post HER and T4 = post treadmill test post HER.

CWD and MWD increased significantly in the EG (CWD 124m-258m) and (MWD 291m-543m) from pre-therapy distances. ACR levels in the EG increased from T1 (4 mg/mmol)-T2 (7.25 mg/mmol) (P < 0.05) and T3 (2.3 mg/mmol)-T4 (5.5 mg/mmol) (P < 0.05). ACR levels were significantly lower at post HER at T4 (5.5 mg/mmol) compared to pre-HER T2 (7.25 mg/mmol)(P < 0.05), suggesting an attenuation of the acute phase response to persistent reperfusion injury. EG subjects’ ACR levels were not significantly different to the CG at T3 and T4 indicating the possible normalisation of ACR levels post treatment. Analysis of CRP levels in the EG showed T4 (6 mg/l) being significantly higher than T2 (4 mg/l) levels indicating no lowering of any acute inflammatory response. T3 (EG 5 mg/l, CG 2 mg/l) and T4 (EG 6 mg/l, CG 2 mg/l) CRP levels were significantly higher in the EG than the CG). Results were analysed using Wilcoxon signed ranks test. Although the EG subjects increased both their CWD and MWD, it is not possible to suggest this is a result of a reduction in the acute phase response or an attenuation of inflammatory markers. Mechanisms into the benefits of improved exercise tolerance have yet to be fully elucidated. The continued use of exercise therapy may be an effective tool in the treatment of PAOD.



Where applicable, experiments conform with Society ethical requirements.

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