Mechanisms that have been proposed to account for (i) premature regression or (ii) subnormal secretory activity of corpora lutea (CL) in cows or in ewes are reviewed. Processes which occur prior to, at the time of, or following, ovulation are considered. Infrequent pulsatile release of LH, particularly during early lactation, may result in ovulation of an immature follicle with the resulting CL exhibiting normal secretory activity. Such incompetent follicles possess reduced numbers of LH receptors and they secrete lower levels of oestradiol-17β. The evidence involving deficiencies, in (i) the preovulatory LH surge (ii) luteotropin support of the CL or (iii) LH receptors within the CL, is equivocal. A premature release of prostaglandin F2α from the uterus apparently results in early demise of the first CL in cows and in ewes.