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The lactate shuttle during exercise and recovery.

Most (75%+) of the lactate formed during sustained, steady-rate exercise is removed by oxidation during exercise, and only a minor fraction (approximately 20%) is converted to glucose. Significant lactate extraction occurs during net lactate release from active skeletal muscle; the total lactate extraction approximates half the net chemical release. Of the lactate which appears in blood, most of this will be removed and combusted by oxidative (muscle) fibers in the active bed and the heart. The "shuttling" of oxidizable substrate in the form of lactate from areas of high glycogenolytic rate to areas of high cellular respiration through the interstitium and vasculature appears to represent an important means by which substrate is distributed, metabolic "waste" is removed, and the functions of various tissues are coordinated during exercise. During recovery from sustained exhausting exercise, most of the lactate accumulated during exercise will continue to be removed by direct oxidation. However, as the muscle respiratory rate declines in recovery, lactate becomes the preferred substrate for hepatic gluconeogenesis. Practically all of the newly formed liver glucose will be released into the circulation to serve as a precursor for cardiac and skeletal muscle glycogen repletion. Liver glycogen depots will not be restored, and muscle glycogen will not be completely restored until refeeding. This is because the diversion of lactate carbon to oxidation during exercise and recovery represents an irreversible loss of gluconeogenic precursor and because the processes of protein proteolysis and gluconeogenesis from amino acids are insufficient to achieve complete glycogen restitution after exhausting exercise.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

Effects of season, lactation and plane of nutrition on the reproductive performance and associated plasma LH and progesterone profiles in hormonally treated ewes.

Two experiments were designed to determine the effects of duration of lactation and plane of nutrition on the reproductive performance of Finn x Dorset Horn ewes mated at a hormonally induced oestrus 9 weeks after lambing. In Exp. 1, ewes were mated on 4 December or 19 March and lactation was terminated at 35 or 15 days before mating or 7 or 35 days after mating. The fertility of ewes lactating at the time of mating was reduced, particularly in ewes mated in March. This was not attributable to differences between lactating and non-lactating ewes for the incidence of oestrus, ovulation rate, litter size or the pattern of LH production. Indirect evidence based on progesterone profiles and returns to service suggest that reproductive failure was due to failure of fertilization and to embryonic death. In Exp. 2 ewes were mated on 1 July or 15 October. Lactation was terminated 15 days before or 7 days after mating and the ewes in each group were subjected to a high or low plane nutrition. Lactation depressed fertility in ewes mated in July but not in those mated in October. While the fertility of non-lactating ewes was independent of nutritional treatment, lactating ewes on a low plane and mated in July had a higher lambing rate than those on a high plane of nutrition. Nutritional effects on fertility appeared to be mediated through changes in milk production and reproductive failures were attributed to failure of fertilization and embryonic death. Seasonal and treatment effects on the incidence of oestrus and on ovulation rates, litter sizes and LH production were small and of little importance.

Animal Nutritional Physiological Phenomena↗

Seasonal and circadian patterns of circulating prolactin during lactation and seasonal quiescence in the tammar, Macropus eugenii.

Prolactin was measured in peripheral plasma of female tammars once a week for 14 months and every 2 months it was measured in a subgroup of 7 tammars at hourly intervals for 28 h to determine short-term changes in concentration. During the course of the study 6 females gave birth in January/February and reared their young to weaning in October-November, while another 4 gave birth 1.5-3.0 months later and weaned their young in November-December. Concentrations of prolactin were less than 40 ng/ml in a non-lactating animal and for the first 140 days of lactation in the others. Between 140 and 180 days of lactation the concentrations of prolactin fluctuated between 10 and greater than 100 ng/ml and thereafter remained high until the young vacated the pouch for the last time at about 250 days. After pouch exit the concentrations declined to about 40 ng/ml even though lactation continued for a further 21-35 days. Although the short-term patterns of prolactin concentrations showed no consistent relationship between light-dark phases there was an increase in the magnitude and duration of peaks of plasma prolactin which correlated with the stage of lactation. Removal of pouch young aged between 203 and 242 days for 24 h resulted in a rapid decrease in plasma prolactin concentration which was reversed when the young was returned to the pouch, indicating that the high levels of prolactin in the second half of lactation may be maintained by the sucking stimulus of the pouch young. This period of lactation, therefore, may be equated with lactation in eutherians, but there appears to be no eutherian equivalent to early lactation in the tammar.

Animals↗

Embryo implantation during the short luteal phase of the corn mouse, Calomys musculinus, and the apparent lack of a lactational diapause in South American murid rodents.

As the corn mouse, Calomys musculinus, has a short luteal phase (2-3 days) that is not prolonged after copulation, it was hypothesized that (i) implantation would occur at the end of this phase, that is, earlier than it occurs in most murid species that have been studied, and (ii) a lactational embryonic diapause would not occur during the luteal phase. These hypotheses were tested in females that had copulated during postpartum oestrus and were either lactating or not lactating. Data were recorded from day 3 to day 5 of pregnancy (day 1 = day after coitus), at both 03:00-05:00 h and 17:00-19:00 h. Evidence of implantation in both non-lactating and lactating animals was apparent at 03:00-05:00 h on day 4 (endometrial 'blue reaction' in all cases and failure to recover free uterine embryos in some cases) and implantation swellings appeared within 24 h in both groups. In another experiment, the increase in duration of interbirth intervals in continuously mated females and their correlation with the number of suckling young were compared among C. musculinus, C. laucha, Akodon molinae (South American murid species) and Peromyscus maniculatus (a North American murid in which a lactational embryonic diapause has been shown). The results were indicative of a lactational embryonic diapause in the North American species, but not in the South American species. It was concluded that in C. musculinus (i) implantation occurs at the end of the spontaneous luteal phase, and (ii) that a lactational embryonic diapause does not occur: the absence of a lactational embryonic diapause may be common to other South American murid rodents.

Animals↗

Fat and energy contents of expressed human breast milk in prolonged lactation.

OBJECTIVE: To estimate fat and energy contents of human milk during prolonged lactation. METHODS: Thirty-four mothers, of term, healthy, growing children, who had been lactating for >1 year (12-39 months) were recruited. Control subjects were 27 mothers, of term infants, who had been lactating for 2 to 6 months. Fat contents of the milk samples were estimated as creamatocrit (CMT) levels. Energy contents of the milk were measured with a bomb calorimeter. RESULTS: The groups did not differ in terms of maternal height and diet, infant birth weight, gestational age, or breastfeeding frequency. They differed significantly in terms of maternal age, maternal weight, and BMI. The mean CMT levels were 7.36 +/- 2.65% in the short-duration group and 10.65 +/- 5.07% in the long-lactation group. The mean energy contents were 3103.7 +/- 863.2 kJ/L in the short-duration group and 3683.2 +/- 1032.2 kJ/L in the long-duration group. The mean CMT levels and mean energy contents were correlated significantly with the duration of lactation (R2 = 0.22 and R2 = 0.23, respectively). In multivariate regression analysis, CMT levels (or energy contents) were not influenced by maternal age, diet, BMI, or number of daily feedings but remained significantly influenced by the duration of lactation. CONCLUSIONS: Human milk expressed by mothers who have been lactating for >1 year has significantly increased fat and energy contents, compared with milk expressed by women who have been lactating for shorter periods. During prolonged lactation, the fat energy contribution of breast milk to the infant diet might be significant.

Breast Feeding↗

Mammary nucleic acids and pituitary prolactin secretion during prolonged lactation in mice.

Lactation was prolonged until 61 days by repeated renewal of litters every week after day 12 in primiparous C3H/He strain mice. On days 12, 19, 40, and 61 of lactation, litters were removed for 5 h and after 1 h of resuckling the synthesis of DNA and RNA in the mammary gland was estimated by the incorporation of (3H)thymidine and (14C)uridine into mammary DNA and RNA in vitro respectively. Mammary nucleic acid content and pituitary and plasma levels of prolactin were also assayed. Nulliparous mice were similarly treated on day 19 of pregnancy. The percentage gain in litter weight per week was highest between days 5 and 12 of lactation, declined until days 26-33 and became steady thereafter. Mammary DNA synthesis was extremely high on day 19 of pregnancy, decreased on day 12 of lactation to less than one-fifteenth of that on day 19 of pregnancy and increased linearly therafter. Changes in mammary DNA content were not so marked, but DNA content was high on days 12 and 19 of lactation. RNA synthesis was highest on day 19 of pregnancy, abruptly decreased on days 12 and 19 of lactation and increased again with the advance of lactation. Mammary RNA content, RNA:DNA and 14C:3H ratios increased from day 19 of pregnancy to days 12-19 of lactation and decreased on days 40 and 61. While the pituitary levels of prolactin were almost constant during lactation, they were significantly higher than those on day 19 of pregnancy. There were only slight differences in plasma prolactin levels at any stage.

Animals↗

Secretion rate and metabolic clearance rate of prolactin in the rat during mid- and late lactation.

The prolactin concentration in the plasma of lactating rats rose less rapidly and attained a significantly lower plateau level in response to suckling on day 20--21 of lactation than it did on day 13--14 of lactation. Neither differences in suckling stimulation of the older pups nor a higher metabolic clearance rate (MCR) of prolactin were implicated in the reduced prolactin concentration seen in the late-lactating rats. The MCR was, in fact, slightly reduced in both conscious and late-lactating rats anaesthetized with urethane when compared with those in mid-lactation. The MCR of prolactin was not significantly altered by urethane anaesthesia in rats on either day of lactation. However, the secretion rate of prolactin, computed from the MCR multiplied by the equilibrium concentration of prolactin during suckling, was considerably reduced (665 to 392 ng/min) from mid- to late lactation. We conclude from these data that the reduced plasma concentration of prolactin in response to suckling in late lactation is the result of an impairment within the prolactin secretory mechanism.

Anesthesia, General↗

Reduced oxytocin response to osmotic stimulus and immobilization stress in lactating rats.

The release of oxytocin in response to an osmotic stimulus and immobilization stress was compared in lactating rats 8-12 days after delivery and in non-lactating rats. Intravenous injection of hypertonic saline or immobilization stress induced an increase in blood oxytocin levels in both lactating and non-lactating rats, but the increment in the former was significantly lower than that in the latter. The lower responsiveness of oxytocin release to stress in lactating rats was not altered by ovariectomy 2 days after parturition. Oxytocin release induced by electrical stimulation of the anteroventral third ventricle (an osmoreceptive area), paraventricular nucleus and neurohypophysis was significantly lower, to a similar extent, in lactating rats compared with non-lactating rats. These findings indicate that the structural reorganization reported in the hypothalamo-neurohypophysial system may not function to facilitate release of oxytocin in response to stress and osmotic stimulus in lactating rats. The reduced responsiveness of the release of oxytocin is independent of the influence of ovarian hormones, and may be due to the low ability of the oxytocin neurone itself to release oxytocin, and/or due to the activated inhibitory influence on the oxytocin neurone in the lactating rat.

Animals↗

Reduced responses of prolactin and catecholamine to stress in the lactating rat.

Prolactin, GH, TSH, adrenaline and noradrenaline responses to the stress of immobilization were compared between lactating and non-lactating dioestrous rats. The concentrations of GH in plasma were reduced to a similar degree by the immobilization of lactating and non-lactating rats, and TSH levels were unchanged in both groups. The increases in plasma concentrations of adrenaline and noradrenaline induced by stress were significantly smaller in lactating than in non-lactating rats. Immobilization caused a marked increase in prolactin levels in the plasma of non-lactating rats but no increase in lactating rats. These changes may help to save energy and maintain milk production during the period of lactation.

Animals↗

Suppression of LH secretion in food-restricted lactating females: effects of ovariectomy and bromocryptine treatment.

It has been shown that restricting food in lactating rats for the first 2 weeks postpartum at a level of 60% of the ad-libitum daily ration increases the length of lactational dioestrus by about 7 days but little is known about correlated changes in hormone levels. In the first experiment we report changes in LH, prolactin (PRL) and ACTH secretion in food-restricted and ad-libitum fed lactating rats at various stages of lactation. Our results demonstrate that food restriction during the first 2 weeks of lactation did not affect PRL or ACTH secretion, but decreased plasma LH levels despite comparable GnRH receptor density between food-restricted and ad-libitum fed females. In the second experiments we investigated a possible causal relationship between the increased secretion of progesterone seen in food-restricted females and the suppression of plasma LH levels, by determining the effects of bromocryptine treatment and ovariectomy on LH secretion in both ad-libitum fed and food-restricted lactating females. LH suppression in food-restricted lactating females was not affected by ovariectomy or bromocryptine treatment, although the latter treatment significantly increased GnRH receptor number. These data suggest that factors other than ovarian steroids, PRL or increased adrenocortical activity modulate LH secretion and the length of lactational dioestrus in food-restricted lactating females.

Adrenocorticotropic Hormone↗

Regulation of serum leptin and its role in the hyperphagia of lactation in the rat.

The factors regulating serum leptin concentration and its relationship to the hyperphagia of lactation have been investigated in rats. Lactation results in hypoleptinaemia and loss, or at least marked attenuation, of the nocturnal rise in serum leptin. Litter removal resulted in a fall in food intake and restoration of the nocturnal rise in serum leptin. Returning the litter to the mother after a 48-h absence increased food intake and began to reinitiate milk production, but the nocturnal serum leptin levels were still increased at 48 h after litter restoration. Adjusting litter size to four, eight, ten or fourteen pups at parturition resulted in different rates of litter growth and food intake during the subsequent lactation, but had no effect on the degree of hypoleptinaemia. Reducing litter size from ten to four pups at mid-lactation resulted in a transient increase in both serum leptin and pup growth rate, while food intake fell to a level found in rats suckling four pups throughout lactation. Reducing milk production by injection of bromocriptine increased serum leptin, but did not restore the nocturnal rise in serum leptin; food intake decreased, but remained much higher than in non-lactating rats. Feeding a varied, high-energy diet resulted in a decrease in the weight of food ingested, but no change in calorie intake, and had no effect on the hypoleptinaemia. These studies suggested that the hypoleptinaemia of lactating rats is due to negative energy balance, but the loss of the nocturnal rise in serum leptin is due to the suckling stimulus. The negative energy balance of lactation does not appear to be caused by a physical constraint on food intake. While the hypoleptinaemia should facilitate the hyperphagia of lactation, other orexigenic signals must also be involved.

Animals↗

Diurnal changes in hypothalamic neuropeptide and SOCS-3 expression: effects of lactation and relationship with serum leptin and food intake.

Rats normally eat about 85% of their food at night. Lactation increases food intake 3- to 4-fold, but the diurnal pattern of food intake persists. The mechanisms responsible for the diurnal and lactation-induced changes in food intake are still unresolved, hence we have further investigated the possible roles of serum leptin and hypothalamic expression of neuropeptide Y (NPY), agouti-related peptide (AgRP) and pro-opiomelanocortin (POMC) in rats. Suppressor of cytokine signalling-3 (SOCS-3) acts as a feedback inhibitor of leptin signalling in the hypothalamus, hence changes in expression of SOCS-3 were also investigated. Changes in expression of NPY, AgRP or POMC alone could not account for the diurnal changes in intake and their alteration by lactation. However, there were increased AgRP mRNA:POMC mRNA ratios at night and also during lactation, which were very similar to estimated changes in food intake. Such changes in expression may result in dominance of the orexigenic AgRP peptide over the appetite-suppressing POMC-derived peptides, and so could contribute to the hyperphagia in these states. Diurnal and lactation-related changes in the AgRP mRNA:POMC mRNA ratio and food intake are not due to changes in leptin alone. However, hypoleptinaemia, possibly through increased expression of NPY, may contribute to the hyperphagia of lactation. In the dark, expression of SOCS-3 was decreased in non-lactating rats; lactation decreased SOCS-3 expression in both light and dark phases. However, such changes are likely to enhance the ability of leptin-responsive neurones to transmit the leptin signal, and so are unlikely to contribute to either the nocturnal increase in appetite or the hyperphagia of lactation.

Agouti-Related Protein↗

Determination of the lactate breakpoint during incremental exercise in horses adapted to dietary corn oil.

OBJECTIVE: To determine lactate breakpoint of horses and test for effects of training and dietary supplementation with corn oil on that breakpoint. ANIMALS: 7 healthy Arabian horses. PROCEDURES: Horses received a control diet (n = 4) or a diet supplemented with 10% corn oil (4). A training program, which comprised two 5-week conditioning periods with 1 week of rest, was initiated. Submaximal incremental exercise tests (IET) were conducted before the first and after both conditioning periods. Blood samples for determination of blood lactate and plasma glucose concentrations were collected 1 minute before IET and during the 15 seconds immediately preceding each speed change. Data collected were fit to one- and two-slope broken-line models and an exponential model. RESULTS: Good fits were obtained by application of the broken-line models (adjusted R2 > 0.92) to blood lactate concentration versus speed curves. Lactate breakpoints increased 41% after training. After training, slope 2 and peak blood lactate concentrations were greater in the corn oil group, compared with controls. Mean blood lactate concentration at the breakpoint was not affected by training or diet. Plasma glucose concentration versus speed curves also fit the broken-line models, and glucose breakpoints preceded lactate breakpoints by approximately 1 m/s in the second and third IET. CONCLUSIONS AND CLINICAL RELEVANCE: Lactate breakpoints can be determined for horses, using blood lactate concentration versus speed curves generated during submaximal IET and may be useful for assessing fitness and monitoring training programs in equine athletes.

Animal Feed↗

Effect of feeding thyrotropin-releasing hormone to lactating sows.

Two experiments were conducted to assess the effects of feeding thyrotropin-releasing hormone (TRH) during lactation on sows. In Exp. 1, sows were fed 0, 1, 10, 100 or 1,000 mg TRH on d 10.8 +/- .4 (mean +/- SE) after parturition. Blood samples were taken from sows every 30 min from -2 h to 8 h and at 10, 12 and 18 h from feeding. Consumption of 100 or 1,000 mg TRH increased mean serum concentrations of thyroxine (T4; P less than .001), 1,000 mg TRH increased growth hormone (GH; P less than .06) and 100 or 1,000 mg TRH increased prolactin (PRL; P less than .01), but insulin (INS; P greater than .10) was unaffected by TRH. Serum concentrations of T4 were elevated within 2 to 4 h after feeding TRH and remained elevated for 12 to 18 h. Concentrations of GH and PRL began to increase immediately after feeding 100 or 1,000 mg TRH and remained elevated for 6 and 8 h, respectively. In Exp. 2, sows were fed 0 or 200 mg TRH from d 111 of gestation to weaning at 27.1 +/- .3 d of lactation. Consumption of TRH elevated concentrations of T4 at all stages of lactation and increased respiration rate on d 10 and d 20, heart rate on d 20, and milk production on d 20 of lactation. Consumption of TRH did not influence number of pigs born, number born alive, survival rate during lactation, sow body weight, heartgirth, backfat depth, feed disappearance, or milk production on d 10 of lactation. Piglets nursing sows fed TRH were similar in weight to piglets nursing sows not fed TRH on d 0 and 5 of lactation, but they were heavier on d 10 (P less than .07), 15 (P less than .001), 20 (P less than .001) and 27 (P less than .0001). Sows fed TRH took longer (P less than .001) to return to estrus after weaning than control sows. Results indicated that feeding TRH elevated T4, GH and PRL and that feeding TRH for the duration of lactation increased milk production on d 20 of lactation and increased weaning weights, but it delayed estrus after weaning.

Administration, Oral↗

Postpartum hypophagia in primiparous sows: I. Effects of gestation feeding level on feed intake, feeding behavior, and plasma metabolite concentrations during lactation.

To investigate the relationship between feeding level during gestation and voluntary feed intake, feeding behavior, and plasma metabolite levels during lactation, 18 crossbred, primiparous sows were assigned to two dietary treatments. From d 60 of gestation until farrowing, sows were fed either a standard level of feed (SL; 1.85 kg/d) or were allowed ad libitum (AL) access to feed. During a 28-d lactation all sows were allowed ad libitum access to feed. Eight SL and seven AL sows completed the experiment. Feed intake was measured daily during the final 40 d of gestation and throughout lactation. On d 105 of gestation and d 1, 7, 14, and 21 of lactation, feeding behavior was observed and blood samples were collected via indwelling catheters. Plasma was analyzed for nonesterified fatty acids (NEFA), insulin, glucose, and alpha-amino N. During gestation AL sows ate more feed than did SL sows. This increased intake was balanced by reduced feed intake during lactation, when AL sows ate less than SL sows (P < .001). The AL sows gained more weight during gestation (P < .001) and lost more weight during lactation (P < .005) than did the SL sows. Feed intake and weight change during gestation and lactation combined were not different between treatments (P = .85). During lactation, the AL sows ate fewer meals (P < .05) of a similar size than did the SL sows. During lactation, the area under the curve formed by plasma NEFA concentration was greater (P = .06) and that for insulin was less (P < .01) in AL than in SL sows.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

Body composition at farrowing and nutrition during lactation affect the performance of primiparous sows: II. Milk composition, milk yield, and pig growth.

Sows that were either fat or lean at farrowing (340 or 280 g of body fat/kg BW, respectively) were offered either a low-protein (LP; 7.9% CP and 15.5 MJ DE/kg as fed) or a high-protein (HP; 19.0% CP and 15.6 MJ DE/kg as fed) diet on an ad libitum basis throughout a 4-wk lactation to test the hypothesis that the amount of milk and its composition are responsive to the supply of endogenous (body reserves) and exogenous (diet) substrates. Pigs were weighed at birth and weekly during lactation, milk yield was estimated using deuterium oxide in early (d 4 to 8) and late lactation (d 24 to 28), and milk samples were collected to determine composition in early (d 4 to 6) and late lactation (d 25 to 27). Throughout lactation, milk yield and composition were mainly associated with differences in litter size. Milk yield was about 15% higher in lean than in fat sows and in sows fed HP rather than LP, but large CV (17 to 32%) prevented these differences from attaining significance (P > .273). The responses in milk yield were reflected in pig growth. Differences in milk composition between treatment groups were not significant; however, during early lactation there was a tendency for fat sows to produce milk with a fat content 21% higher, and a protein content 12% lower, than that of lean sows. Changes in the protein:energy ratio of milk during the course of lactation and small changes in milk yield composition collectively suggested that in early lactation, sow body composition affected milk production but, as lactation progressed, the dietary supply of precursors for milk synthesis became more important.

Analysis of Variance↗

Changes in tissue composition associated with mammary gland growth during lactation in sows.

Twenty-four primiparous sows were used to determine the extent of mammary gland growth during lactation. Litter size was set to nine or 10 pigs immediately after birth. Sows were slaughtered in groups representing d 0 (within 12 h after farrowing), 5, 10, 14, 21, and 28 of lactation. Sows were provided 17.5 Mcal ME and 65 g of lysine per day during lactation. Mammary glands were collected at slaughter and trimmed of skin and extraneous fat pad. Each gland was weighed, cut in half to measure cross-sectional area, and ground for chemical analysis. Dry matter content, dry fat-free tissue (DFFT) content, protein content, amino acids composition, ash content, and DNA content were measured. Only glands known to have been suckled were included in these data. Wet and dry tissue weight; cross-sectional area; and the amount of DFFT, tissue protein, and amino acids in each suckled mammary gland increased (P < .05) during lactation to a peak on d 21. Fat percentage of each suckled gland declined (P < .05) and the percentage of protein and DFFT increased (P < .05) as lactation progressed. These results suggest that hypertrophy occurred in the tissue during lactation. There was a linear increase in the amount and percentage of DNA during lactation (P < .05), suggesting hyperplasia of the mammary tissue. Mammary tissue growth continues in suckled glands during lactation in sows, with gland wet weight increased by 55% and total gland DNA increased by 100% between d 5 and 21 of lactation.

Adipose Tissue↗

Dietary energy source at two feeding levels during lactation of primiparous sows: I. Effects on glucose, insulin, and luteinizing hormone and on follicle development, weaning-to-estrus interval, and ovulation rate.

Our objective was to study the effects of dietary-induced insulin enhancement during and after lactation on the reproductive performance of primiparous sows. During a 21-d lactation period, 48 sows were allotted to a 2x2 factorial experiment. Treatments were feeding level (high or low; 44 MJ or 33 MJ NE/d) and dietary energy source (fat or starch). After weaning, all sows received the same amount of feed (31 MJ NE/d from weaning to estrus and 17.5 MJ NE/d from breeding until slaughter) of the same energy source as fed during lactation. On d 7, 14, and 21 of lactation and d 22 (weaning), blood samples were taken every 12 min for 12 h and analyzed for plasma glucose, insulin, and LH. Sows were slaughtered on d 35 of the subsequent pregnancy, and ovulation rate was assessed. During lactation, postprandial plasma glucose and insulin concentrations were higher for sows fed the starch diet than for those fed the fat diet (P<.001), whereas feeding level had no effect. Basal and mean LH concentrations were not affected by treatments. The LH pulse frequency on d 7 of lactation was greater for sows fed the starch diet than for those fed the fat diet (.52 vs .17 pulses/12 h; P = .03). The high compared with the low feeding level resulted in a greater LH pulse frequency on d 21 of lactation (.89 vs .47 pulses/12 h; P = .05) and on d 22 (8.63 vs 5.77 pulses/12 h; P = .02), in a higher percentage of sows that exhibited estrus within 10 d after weaning (96 vs. 63%; P = .01), and a tendency for a higher ovulation rate (18.0 vs. 16.2; P = .09). Plasma glucose and insulin concentrations were not related to any of the LH traits. The LH pulse frequency after weaning was related to the weaning-to-estrus interval (WEI) and was best explained by a linear-plateau model. In sows fed the low feeding level, follicle size after weaning was correlated with LH pulse frequency after weaning and with the WEI, whereas in sows fed the high feeding level these correlations were not significant. Our results indicate that an improved dietary-induced insulin status during and after lactation does not overcome the inhibitory effects of lactation on subsequent reproduction at any of the feeding levels.

Animal Feed↗