Article Text

Regular pace training increases endothelium-dependent vasodilatation in untrained women
  1. D Reihmane,
  2. P Tretjakovs,
  3. A Jurka
  1. O Vaciesa street 4, LV-1004 Riga, Latvia


Almost all scientific research that investigates how exercise training affects the circulatory system estimates main arteries, like brachial artery and few focus on the cutaneous microvascular function. The aim of this study was to estimate the impact of 25 Programmed Aerobic/Anaerobic/Accommodating Circuit Exercise (PACE) training sessions on changes in vasomotor reactions (microvascular beds of the skin) in healthy untrained women. PACE training is a short duration (∼30 min), intense physical activity that includes both aerobic and anaerobic states, that changes after every 30 s. 20 women participated in this study (age 35±10 years; body mass index 26.7±4.2). The laser Doppler flow technique (MoorLDI2) was used to estimate the regional blood flow changes on the upper part of the palm induced by local acetylcholine (1% Ach) and sodium nitroprusside (1% SNP) iontophoresis; assessment of concentrations of C reactive protein and cortisol were made with the Immulite 2500. There was an increase in endothelium-dependent vasodilatation after 25 PACE training sessions, that was estimated by laser dopplerography test with 1% Ach iontophoresis (292±80 PU vs 335±88 PU, p<0.01). 25 PACE training sessions did not cause any significant changes in endothelium-independent vasodilatation (1% SNP iontophoresis). There was a negative correlation between 1% Ach-induced vasodilatation and C reactive protein (p<0.05; r=−0.38), but there was a positive correlation between 1% SNP-induced vasodilatation and cortisol (p<0.01; r=0.53), when data from pre and post 25 PACE training sessions are taken together (n=40). In conclusion, 25 PACE training sessions improve endothelium-dependent vasodilatation, but have no effect on endothelium-independent vasodilatation. Inflammatory processes (higher C reactive protein level) reduce the capacity of endothelium-dependent vasodilatation.

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