Uterine contractility issues, such as preterm or dysfunctional labours, remain major obstacles to female reproductive and neonatal health. The mechanisms of uterine contraction and its dysfunction, need to be better clarified. During labour, contractions produce transient ischemia, consequently, glucose supply to the myometrium becomes limited. A direct cause-and-effect relationship between the exhaustion of glucose and impairment of muscle function is still to be established in the myometrium. We explore this and compare effects under hypoxic conditions. Myometrial strips were taken from labouring and non-labouring pregnant women undergoing emergency and elective caesarean sections at Liverpool Women Hospital. Samples were equilibrated in oxygenated physiological saline (pH7.4) at 37°C.Contractile activity was isometrically measured. The effects of zero-glucose, combined zero-glucose and hypoxia (N2) were tested. N is number of women. The amplitude of spontaneous contractions declined significantly (t-test) to 87±2% (n=5) of control in labouring women and 82±6% (n=12) in non-labouring. Studied so far in non-labouring samples, this inhibition was significantly greater with hypoxia and zero-glucose 48±6% (n=7).Our results reveal that zero-glucose significantly inhibits uterine contractions. The results suggest that glucose depletion in vivo will contribute to the pathway underlying uterine contractility related disorders. The mechanism of its effect needs to be better elucidated