Association between arterial elasticity, C-reactive protein and maximal oxygen consumption in well-trained cadets during three days extreme physical load: a pilot study.

Regular aerobic training has beneficial effects on inflammatory pathways and on arterial elasticity, which are both important cardiovascular risk factors. The aim of the present study was to evaluate the effect of extreme physical load on arterial elasticity and inflammatory markers in well-trained healthy men who participated in a high-ranking combat course. Seven well-trained male cadets were examined during an international military combat course of 3.5 days duration. Small (C2) and large (C1) artery elasticity was assessed using diastolic pulse wave analysis. Inflammatory markers and arterial elasticity measurement were performed before and after the competition. The extreme prolonged physical load caused individually different responses in arterial elasticity, C-reactive protein (CRP) and creatine kinase in individual cadets. Maximal oxygen consumption (VO(2) max kg(-1)) correlated significantly with the change (Delta-difference between baseline and 24 h recovery period) of creatine kinase (r= -0.78; p=0.04) and DeltaC2 (r=0.78; p=0.04) and DeltaC1 (r=0.82; p=0.02). In multivariate analysis (R(2)=0.89, p=0.01) the DeltaC2 correlated strongly with VO(2) max kg(-1) (p=0.005) and with the DeltaCRP (p=0.03), whereas the DeltaC1 correlated only with VO(2) max kg(-1) and did not correlate significantly with the DeltaCRP. Changes in small arterial elasticity induced by extreme physical load were significantly related to VO(2) max kg(-1) and DeltaCRP, whereas the change of large artery elasticity was only associated with VO(2) max kg(-1). Our preliminary results indicate that acute exercise-induced inflammation may affect small artery elasticity. However, further, more extensive studies are needed in this area.