Systemic hypoxia produces microvascular inflammation in several tissues, including skeletal muscle. Exercise training (ET) has been shown to reduce the inflammatory component of several diseases. Alternatively, ET could influence hypoxia-induced inflammation by improving tissue oxygenation or increasing mechanical anti-adhesive forces at the leukocyteendothelial interface. The effect of 5 weeks of treadmill ET on hypoxia-induced microvascular inflammation was studied in the cremaster microcirculation of rats using intravital microscopy. In untrained (UT) rats, hypoxia (PaO₂ = 32.3 ± 2.1 Torr) increased leukocyte-endothelial adherence from 2.3 ± 0.4 to 10.2 ± 0.3 leukocytes per 100 µm of venule (P < 0.05), and was accompanied by extravasation of FITC-labelled albumin after 4 h of hypoxia (extra/intravascular fluorescence intensity = 0.50 ± 0.07). These responses were attenuated in ET, (leukocyte adherence was 1.5 ± 0.4 during normoxia and 1.8 ± 0.7 leukocytes per 100 µm venule after 10 min of hypoxia; extra/intravascular fluorescence intensity = 0.11 ± 0.02, P < 0.05 vs. untrained) in spite of similar reductions of arterial (PaO₂ = 32.4 ±1.8 Torr) and microvascular PO₂ (measured with an oxyphor quenching method) in both groups. Shear rate decreased during hypoxia to similar extents in ET and UT. In addition, circulating blood leukocyte count was similar in ET and UT. The effects of ET on hypoxia-induced leukocyte-endothelial adherence remained up to 4 weeks after discontinuing training. Thus, ET attenuated hypoxia-induced inflammation despite similar effects of hypoxia on tissue PO₂, venular shear rate and circulating leukocyte count.