In horses, the natural breeding season (without light treatment) is centred on the longest day of the year (20th June in the northern hemisphere). The breeding season begins in spring when duration of daylight, ambient temperature and food availability increase. Consequently, a peak of births occurs 11 months later, at the end of May. For wild mares, winter ovarian inactivity is an important adaptation to the environment. Due to regulations of horses' races and competitions, births early in the year gave benefits for races or sports [1, 2]. Furthermore, if mares can be mated early in the year, the number of cycles, and then the success of pregnancy at the end of the year, increases .
Several authors have suggested that nutrition, and particularly energy intake, has an effect on the onset of ovulatory activity [4–8]. A proportion of adult mares (> 5 years old) ovulated continuously throughout the year [9, 10]. However, mares that had nursed a foal during the previous summer, young mares (< 4 years old) and lean mares all showed winter ovulatory inactivity [11–13]. Conversely, mares that did not show winter ovulatory inactivity had a higher percentage of body fat than mares with inactivity . These data indicate that body weight, fat reserves and the availability of food are important factors affecting the pattern of seasonal ovulatory inactivity and suggest that nutrition may be one factor that interacts with photoperiod to determine the precise onset and duration of ovarian inactivity in the mare.
The main site of action of nutrition on the ovarian cycle in cows [15, 16], gilts  and mares [10, 18] appears to be the hypothalamus, and the mechanism probably has multiple components including insulin, leptin, growth hormone (GH) and insulin-like growth factors (IGFs). It has been shown that induced hypoglycaemia decreases secretion of gonadotrophins and results in anovulation in different species including mares [14, 19–22].
Leptin, an adipocytokine, regulator of food intake and satiety , informs the brain on body condition and adiposity, and probably interacts with photoperiod to impacts reproduction. In horses, the plasma concentration of leptin is strongly correlated with body condition score . In human blood, this protein binds to five 'serum leptin-interacting proteins' . In adult castrated rams, a specific receptor present at the blood brain barrier seasonally modulates the active transport of leptin from the blood to the brain . Injection into the ovine cerebrospinal fluid strongly affects GnRH, LH and GH secretion [27, 28].
The GH and IGF systems influence reproduction . GH affects the ovary by enhancing the gonadotrophin responsiveness of this organ . IGF-I is the key mediator of most of the actions of GH and exerts negative feedback on secretion . In horses, plasma IGF-I concentrations are not influenced by time of day or by exercise, but are dramatically increased by exogenous GH .
In sheep , goats , deer  and horses [36–38], the annual reproductive season is synchronized by photoperiod through melatonin secretion. In mares, the date of first ovulation can be advanced by about two months by exposure to an artificial photoperiod in winter [36, 37, 39]. In anovulatory mares during winter, treatment with exogenous melatonin suppresses the stimulatory effect of artificial long photoperiods [40, 41]. Conversely, the effect of photoperiod or exogenous melatonin on the time of the last ovulation in autumn is controversial. In adult mares, melatonin treatment fails to change the date of the last ovulation [41, 42]. In horses [12, 14, 39, 41, 43–48], as in ewes , different experimental approaches indicate that the annual reproductive rhythm has a strong endogenous component. The phase of this annual endogenous rhythm is regulated by photoperiod through mediator melatonin.
The hypotheses, tested in this experiment study are 1) body condition induced by feed intakes affects the occurrence and duration of seasonal anoestrus in mare, 2) a change in feed intake can modify the date of the first ovulation of the year, 3) this change affects daily patterns of plasma glucose, insulin, melatonin, GH, IGF-1 and leptin.