Stress at foaling has been demonstrated to delay birth. In this study, we followed the hypothesis that even a short delay of foaling increases catecholamine and cortisol release in foals, induces acidosis and impairs neonatal adaptation. Foaling was prolonged for 5鈥痬in by transferring mares to an unfamiliar environment at rupture of the allantochorion (group delay, n鈥?鈥?) while control mares (n鈥?鈥?) were left undisturbed. In their foals, times from birth to first standing and first suckling, heart rate, heart rate variability (HRV) and salivary cortisol concentration were analysed. Blood for analysis of epinephrine, norepinephrine, hematology and blood gases was collected directly and 30鈥痬in after birth. Statistical comparisons were made by repeated measures ANOVA. Times to first standing and suckling did not differ between groups. Fetal heart rate remained unchanged during birth and increased within 15鈥痬in postnatum (p鈥?鈥?.001) while HRV decreased during the first hour of life in foals of both groups (p鈥?鈥?.05). Immediately after birth, actual base excess was lower in foals with delayed birth than in control foals (p鈥?鈥?.05). Epinephrine concentration immediately after birth was higher in group delay foals and increased from 0 to 30鈥痬in after birth in control foals (time p鈥?鈥?.001, time x group p鈥?鈥?.001). Cortisol concentration peaked at 1鈥痟 after birth in both groups (p鈥?鈥?.001). Leukocyte and PMN count decreased from 0 to 30鈥痬in after birth (p鈥?鈥?.001). In conclusion, a 5-min delay at foaling affected epinephrine release and acid base balance, but was without further effect on neonatal adaptation.