3.9 Article

Effects of exercise training on forearm and calf vasodilation and proinflammatory markers in recent heart transplant recipients: a pilot study

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SAGE PUBLICATIONS LTD
DOI: 10.1097/HJR.0b013e3282f0b63b

Keywords

endothelial-dependent vasodilation; exercise; heart transplantation; inflammation

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Background Aerobic exercise training improves vasodilatory capacity of peripheral resistance vasculature and modifies plasma proinflammatory markers in chronic heart failure patients. It is, however, currently unknown whether aerobic exercise has a similar effect in heart transplant recipients (HTR). Design and Methods Eight weeks after transplantation, 14 HTR were randomly assigned to 12 weeks of supervised aerobic exercise training (TRAINED; n = 8) or attention-time control (CONTROL; n = 6) in addition to posttransplantation medical care. Peak forearm blood flow and calf blood flow (CBF) during reactive hyperemia after 5 min of limb ischemia was used as a measure of endothelium-dependent vasodilation of limb resistance arteries. Plasma C-reactive protein, interleukin-6 (IL-6), tumor necrosis factor-alpha (TNF-alpha), soluble intercellular adhesion molecule-1 (sICAM-1), and exercise capacity were measured at baseline and again after 12 weeks in both groups. Results Peak CBF increased 22% in the TRAINED (25.9 +/- 5.8-31.6 +/- 7.9 ml/min/100ml, P<0.05), but there was no change in peak CBF after 12 weeks in CONTROL. Plasma C-reactive protein, IL-6, TNF-alpha, sICAM-1 did not change in TRAINED, but there was a significant increase in TNF-alpha (1.66 +/- 1.02 vs. 3.07 +/- 1.10 pg/ml, P<0.05), and sICAM-1 (205.9 +/- 59.1 vs. 245.0 +/- 47.9 ng/ml, P<0.01) in CONTROL after 12 weeks. Furthermore, exercise test duration improved 51.7% (P<0.01) and there was a trend toward an increase in peak VO2 (P=0.05) in TRAINED after 12 weeks but neither changed in CONTROL. Conclusion A program of supervised aerobic exercise improves endothelium-dependent vasodilation of the calf, but not forearm resistance arteries, and may attenuate a progressive increase in selected proinflammatory markers in HTR.

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