Hd. Kvernmo et al., Enhanced endothelium-dependent vasodilatation in human skin vasculature induced by physical conditioning, EUR J A PHY, 79(1), 1998, pp. 30-36
Citations number
25
Categorie Soggetti
Physiology
Journal title
EUROPEAN JOURNAL OF APPLIED PHYSIOLOGY AND OCCUPATIONAL PHYSIOLOGY
Functional alterations to the endothelial cells of the vascular system may
contribute to the improved circulatory performance induced by physical cond
itioning. We evaluated microvascular reactivity to iontophoretic applicatio
n of acetylcholine (ACh) and sodium nitroprusside (SNP) through the skin an
d blood perfusion measurements in the same area using laser Doppler flowmet
ry. Whereas ACh acts on smooth muscle cells of the vascular system via the
production of vasodilator substances from the endothelium, SNP is an endoth
elium-independent vasodilator acting on vascular smooth muscle cells direct
ly. The study was performed using two groups of subjects with different lev
els of aerobic endurance, long distance runners competing at national level
(n = 9) and controls (n = 9). The subjects were tested for 40 min on a tre
admill before and after an exercise test at 80% of their maximal oxygen upt
ake. During stimulation by ACh cutaneous perfusion increased to a higher le
vel in the athletes than in the controls (overall P < 0.05), whereas an acu
te period of exercise abolished this difference (overall P > 0.6). There wa
s no significant difference between the athletes and the controls with resp
ect to the SNP-induced increase in cutaneous perfusion either before (P > 0
.9) or after(P > 0.9) exercise. The higher cutaneous perfusion responses to
stimulation with ACh in the athletes than in the controls may support the
hypothesis that regular exercise modifies the responsiveness of the cutaneo
us endothelium. The difference in ACh-induced perfusion and in unstimulated
forearm perfusion between the two groups was present only at rest. This fi
nding indicated that mechanisms were introduced during exercise, which comp
ensated for the lower endothelial sensitivity to stimulation in the control
s at rest.