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Metabolic Control of Anaerobic Glycolysis (Overexpression of Lactate Dehydrogenase in Transgenic Tomato Roots Supports the Davies-Roberts Hypothesis and Points to a Critical Role for Lactate Secretion.

Roots of all plants examined so far have the potential for both ethanol and lactate fermentation. A short burst of lactate fermentation usually occurs when plant tissues are transferred from normoxic to anoxic conditions. According to the Davies-Roberts hypothesis, the consequent pH drop both initiates ethanol fermentation and blocks further production of lactate by inhibiting lactate dehydrogenase (LDH). However, the role of LDH in this pH control mechanism is still a matter of debate. To perturb the control system in a defined way, a barley LDH cDNA under the control of the cauliflower mosaic virus 35S promoter was introduced into tomato (Lycopersicon esculentum Mill. cv VFMT) using Agrobacterium rhizogenes. The transgenic root clones expressed up to 50 times the LDH activity of controls. The fermentative metabolism of these clones was compared using roots grown previously in normoxic conditions or roots given a 3-d hypoxic pretreatment. During the transition from normoxia to anoxia, lactate accumulation was no faster and no more extensive in transgenic roots than in controls. Similarly, during prolonged anoxia the flux of 14C from [U-14C] glucose to lactate and ethanol was not modified by the expression of the transgene. However, in both transgenic and control roots, hypoxic pretreatment increased the flux to lactate and promoted lactate export to the medium. These results show that LDH has a very low flux control coefficient for lactate fermentation, consistent with the Davies-Roberts hypothesis. Moreover, they suggest that lactate secretion exerts major control over long-term lactate glycolysis in vivo.

Journal Article↗

Hyperoxia decreases muscle glycogenolysis, lactate production, and lactate efflux during steady-state exercise.

The aim of this study was to determine whether the decreased muscle and blood lactate during exercise with hyperoxia (60% inspired O2) vs. room air is due to decreased muscle glycogenolysis, leading to decreased pyruvate and lactate production and efflux. We measured pyruvate oxidation via PDH, muscle pyruvate and lactate accumulation, and lactate and pyruvate efflux to estimate total pyruvate and lactate production during exercise. We hypothesized that 60% O2 would decrease muscle glycogenolysis, resulting in decreased pyruvate and lactate contents, leading to decreased muscle pyruvate and lactate release with no change in PDH activity. Seven active male subjects cycled for 40 min at 70% VO2 peak on two occasions when breathing 21 or 60% O2. Arterial and femoral venous blood samples and blood flow measurements were obtained throughout exercise, and muscle biopsies were taken at rest and after 10, 20, and 40 min of exercise. Hyperoxia had no effect on leg O2 delivery, O2 uptake, or RQ during exercise. Muscle glycogenolysis was reduced by 16% with hyperoxia (267 +/- 19 vs. 317 +/- 21 mmol/kg dry wt), translating into a significant, 15% reduction in total pyruvate production over the 40-min exercise period. Decreased pyruvate production during hyperoxia had no effect on PDH activity (pyruvate oxidation) but significantly decreased lactate accumulation (60%: 22.6 +/- 6.4 vs. 21%: 31.3 +/- 8.7 mmol/kg dry wt), lactate efflux, and total lactate production over 40 min of cycling. Decreased glycogenolysis in hyperoxia was related to an approximately 44% lower epinephrine concentration and an attenuated accumulation of potent phosphorylase activators ADPf and AMPf during exercise. Greater phosphorylation potential during hyperoxia was related to a significantly diminished rate of PCr utilization. The tighter metabolic match between pyruvate production and oxidation resulted in a decrease in total lactate production and efflux over 40 min of exercise during hyperoxia.

Adult↗

Lactate in fetal tissue during hypoxia; correlation to lactate, pH and base deficit in the fetal blood.

It was the aim of this study to investigate the relationship between the tissue concentrations of lactate in different organs, the blood lactate concentrations, and pH and base deficit in the extracellular fluid (BDecf) during fetal hypoxia. With regard to fetal blood analysis during labour the question is of major importance to what extent blood measurements can provide information concerning intracellular lactate concentrations, especially in the cerebral tissue. In 15 guinea-pig fetuses acute hypoxia was induced by anaesthesia, operative stress and abruption of the placenta. After puncture of the umbilical artery for blood analysis, tissue specimens were taken from the cerebral tissue, heart, liver, lung, muscle and fascia of the abdominal wall, bowel and kidney within 1 to 2 minutes and analyzed for lactate. The lactate concentrations were corrected according to the time interval from blood sampling to collection of tissue specimen. In acute hypoxia the lactate concentrations of the heart and the cerebral tissue were closely correlated to lactate, pH and base deficit measured in arterial blood. The tissue concentration of lactate in the heart and in the cerebrum exceeded the blood level approximately by 70 and 30-50%, respectively. At a pH greater than 7.10 and BDecf less than 8 mumol/ml, the lactate concentration in the cerebrum was about half the lactate concentrations leading to cerebral edema and cell necrosis in the hypoxic monkey fetus (Myers RE. In: Gluck L, ed. Intra-uterine asphyxia and the developing fetal brain. 1977, 37-97).

Acid-Base Equilibrium↗

Comparison of the D-lactate stereospecific dehydrogenase of Limulus polyphemus with active-site regions of L-lactate dehydrogenases.

Lactate dehydrogenase (D-lactate:NAD+ oxidoreductase, EC 1.1.1.28) from the horseshoe crab, Limulus polyphemus, a dimeric enzyme stereospecific for D-lactate, has been purified by affinity chromatography. Maleyl tryptic peptides containing arginine residues isolated from the Limulus enzyme have been characterized and sequenced. The small peptides obtained from similarly treated L-lactate-specific enzyme homologs define major portions of the substrate and coenzyme binding regions and are virtually identical among L-lactate-specific enzymes. Although the six small peptides and free arginine isolated from the Limulus enzyme indicate that the small number of arginine tryptic peptides are located in a few discrete consecutive clusters similarly to the L-lactate dehydrogenases, the peptides nevertheless show no obvious sequence homology to the corresponding peptides from L-lactate dehydrogenases. These results indicate that this lactate dehydrogenase of altered substrate specificity either evolved with major rearrangements of the active site if it evolved from an L-lactate dehydrogenase, or that D-lactate dehydrogenases have evolved from a different protein. The results contradict proposed models which suggest that minor changes in the spatial orientation of pyruvate resulting from minimal rearrangement of the active site could accommodate the change in substrate specificity.

Amino Acid Sequence↗

LH and IGF-1 release during oestrus and early luteal phase in lactating and non-lactating horse mares.

The aim of the present study was to determine effects of lactation on basal LH and IGF-1 concentrations and on the LH response to a GnRH-analogue at different stages of the oestrous cycle in mares. A total of 17 cyclic Haflinger mares were included in the study. Experiments were performed on lactating mares in first postpartum oestrus, the subsequent early luteal phase, and second postpartum oestrus. Non-lactating mares were used in oestrus and early luteal phase. Blood samples were taken for 1 h at 15 min intervals. Mares were then injected with the GnRH-analogue buserelin (GnRHa; 5 microg i.v.) and blood samples were drawn every 15 min for further 2 h. LH in all samples and basal IGF-1-concentrations were determined by RIA. In lactating mares, basal LH concentrations during the early luteal phase tended to be lower (p = 0.07) and the LH response to GnRHa, calculated as area under the curve, was significantly less pronounced compared to non-lactating mares (p < 0.01). As well in lactating mares, the basal LH concentration between first early luteal phase and second oestrus differed significantly (p < 0.05) and the net response to GnRHa was significantly lower between first oestrus as well as second oestrus and first early luteal phase (p < 0.05) but not between first and second oestrous postpartum. Within the group of non-lactating mares, the LH response to GnRHa was as well significantly lower during oestrus than during early luteal phase (p < 0.01). IGF-1 concentrations differed neither between groups nor stages of the cycle within groups. In conclusion, basal and GnRHa-stimulated LH release in lactating mares is lower than in non-lactating mares. This difference, however, occurs only in the early luteal phase. In lactating mares, concentrations of LH appear adequate to allow ovulation to occur.

Animals↗

Relationship between milk somatic-cell counts in the first lactation and clinical mastitis occurrence in the second lactation of French Holstein cows.

The relationship between 10 cell-level descriptors in the first lactation and the risk of clinical mastitis in the second lactation was studied in 10205 Holstein cows from 1254 commercial herds using logistic regression. These 10 cell descriptors were based on the mean cell level over the whole first lactation, on the cell level at the beginning or at the end of the first lactation or on the proportion of cell counts below or above given thresholds. Separate analyses were also performed for subsets of herds defined according to their clinical mastitis incidence risk and their lactation mean somatic-cell count (SCC). Odds of clinical mastitis in second lactation was highest (lowest) for high- (low-) yielding cows. All cell descriptors provided consistent results. Lower (higher) mean cell level, higher (lower) proportion of low SCC values, and lower (higher) proportion of high SCC values in the first lactation were associated with a lower (higher) risk of clinical mastitis in the second lactation. The same trends were observed in all subgroups of herds. Cows with the lowest mean SCC in the first lactation had the lowest risk for clinical mastitis in the second lactation. This suggests that selection for decreased SCC may effectively reduce clinical mastitis incidence and that the breeding goal should favor cows with the lowest observed SCC.

Animals↗

Postpartum body composition changes in lactating and non-lactating primiparas.

The objective of this study is to evaluate the postpartum body composition changes in lactating versus non-lactating or formula-feeding primiparas during the first 12 wk. Twenty primiparous females (age range 17-35 y) who decided to nurse or formula feed their infant were studied. The non-lactating mothers (n = 6) were younger (21 versus 29 y) and had a lower prepregnancy weight (55 kg versus 63 kg) than the lactating mothers (n = 14). Body weight, height, waist and hip measurements, 3-d dietary and activity records, skin-fold thickness from triceps, suprailiac, midthigh, and midupper arm circumference, and total body composition were evaluated at three time periods (at delivery, at 6 wk, and at 12 wk postpartum). Total body composition for bone mineral, lean, and fat mass was measured by dual energy x-ray absorptiometry. At delivery and 6 wk postpartum, the weights and heights were similar between the two groups. By 12 wk postpartum, the formula-feeding group had a weight loss that was different from delivery, 66 +/- 10 kg to 59 +/- 8 kg, P < 0.03. There was no significant weight change in the lactating group during the study. The weight loss consisted of more lean mass than fat mass. The total body bone mineral content did not differ between the two groups during the study. Both groups had reduction in their waist size from delivery to 12 wk postpartum. But only the non-lactating mothers had reductions in their hip and midthigh measurements. There were no changes between the two groups in the skin-fold measurements. Lactating mothers had a higher total daily calories (1974 +/- 318 versus 1464 +/- 178 calories, P < 0.002) and fat intake (63 +/- 14 versus 47 +/- 9 g, P < 0.02) than the non-lactating mothers. The energy expenditure was similar between both groups. In conclusion, during the first 12 wk postpartum, non-lactating mothers who were younger and weighed less prepregnancy lost body weight and had more waist, hip, and midthigh size reductions compared to lactating mothers.

Adolescent↗

Oxytocin and prolactin suppress cortisol responses to acute stress in both lactating and non-lactating sheep.

Cortisol response to stress appears to differ between lactating and non-lactating animals. Lactating (14 d post partum) and non-lactating sheep were fitted with probes so that drugs and hormones could be infused directly into the posterior pituitary and paraventricular nucleus of the hypothalamus. The animals were also fitted with instruments to allow monitoring of heart rate, body temperature and blood cortisol levels. Their reactions to a source of acute stress (a barking dog) were then followed, with or without drug and hormone manipulation. Results in both lactating and non-lactating animals indicated shortcomings in the use of cortisol as a stress indicator. Infusing prolactin and oxytocin into either the posterior pituitary or the paraventricular nucleus of the hypothalamus suppressed cortisol responsiveness to stress in both lactating and non-lactating animals (the latter to a greater extent). In the absence of drugs, lactating animals had a slightly higher basal level of cortisol and a lower cortisol response to stress than their non-lactating counterparts. Despite suppression of cortisol responses, with or without drugs, other indicators of stress still changed with the presence of a barking dog, suggesting the complexity of control involved in stress responses.

Animals↗

Lactate dehydrogenase has no control on lactate production but has a strong negative control on formate production in Lactococcus lactis.

A series of mutant strains of Lactococcus lactis were constructed with lactate dehydrogenase (LDH) activities ranging from below 1% to 133% of the wild-type activity level. The mutants with 59% to 133% of lactate dehydrogenase activity had growth rates similar to the wild-type and showed a homolactic pattern of fermentation. Only after lactate dehydrogenase activity was reduced ninefold compared to the wild-type was the growth rate significantly affected, and the ldh mutants started to produce mixed-acid products (formate, acetate, and ethanol in addition to lactate). Flux control coefficients were determined and it was found that lactate dehydrogenase exerted virtually no control on the glycolytic flux at the wild-type enzyme level and also not on the flux catalyzed by the enzyme itself, i.e. on the lactate production. As expected, the flux towards the mixed-acid products was strongly enhanced in the strain deleted for lactate dehydrogenase. What is more surprising is that the enzyme had a strong negative control ( CLDHJF1 =-1.3) on the flux to formate at the wild-type level of lactate dehydrogenase. Furthermore, we showed that L. lactis has limited excess of capacity of lactate dehydrogenase, only 70% more than needed to catalyze the lactate flux in the wild-type cells.

Fermentation↗

Effects of the resuscitation fluid and the hemoglobin based oxygen carrier (HBOC) excipient on the toxicity of the HBOC: Ringer's D,L-lactate, Ringer's L-lactate, and Ringer's ketone solutions.

Hemoglobin based oxygen carriers (HBOC) are resuspended in "excipients" consisting of Ringer's D,L-lactate containing antioxidants to prevent methemoglobin formation during storage. Investigators have reported cardiac arrhythmias following infusion of Ringer's D,L-lactate solution. Studies have shown that D-lactate stimulates human granulocytes to generate oxygen free radicals and L-lactate inhibits glycolysis. Patients receiving HBOC in Ringer's D,L-lactate excipient are also resuscitated or hemodiluted with Ringer's lactate solution. Oxygen-free radicals generated by Ringer's D,L-lactate and HBOC may oxidize nitric oxide in endothelial cells, causing the vasoconstrictor effects reported following HBOC infusion, and activate NF-kappab and the apoptotic cascade. The combination of Ringer's D,L-lactate and HBOC in Ringer's D,L-lactate excipient may be responsible for the severe adverse events observed in clinical studies of HBOC.Veech has recommended replacing the 27 mM of lactate in Ringer's with 27 mM D-betahydroxybutyrate (BHB). BHB reduces the generation of oxygen free radicals by mitochondria and human granulocytes.

Animals↗

Intracellular pH recovery and lactate efflux in mouse soleus muscles stimulated in vitro: the involvement of sodium/proton exchange and a lactate carrier.

The intracellular pH recovery after stimulation of mouse soleus muscles in vitro was studied by means of intracellular pH-sensitive microelectrodes. The lactate efflux and the total lactate content were measured by means of an enzymic method. During electrical stimulation for 2 min in a CO2/HCO3- -buffered Ringer's solution, pHi decreased by 0.5 units. The rate of pHi-recovery was independent of external bicarbonate, but dependent on the buffer concentration. The rate of intracellular pH recovery was reduced by the lactate transport inhibitors PCMBS and cinnamate, whereas the inhibitors of inorganic anion-exchange SITS and DIDS had no effect. The Na+/H+ exchange inhibitor amiloride reduced the rate of pHi recovery. The pHi recovery was faster than the lactate efflux, which could be accounted for by an Na+/H+ exchange. A number of inhibitor compounds were used in order to discriminate between the three possible lactate efflux pathways: the monocarboxylate carrier mechanism, the inorganic anion exchange, and the molecular (non-ionic) diffusion of lactic acid. The lactate efflux was partly inhibited by cinnamate, PCMBS and phloretin, but was unaffected by DIDS and tetrathionate. These experiments demonstrate the existence of a lactate carrier in mammalian skeletal muscles. The lactate carrier is responsible for more than half of the lactate efflux after muscle activity. Both the pHi recovery studies and the lactate efflux measurements showed that, under the given conditions, the inorganic anion-exchange mechanism is not essentially involved in the recovery processes after muscle activity.

Amiloride↗

Endurance training affects lactate clearance, not lactate production.

Primed-continuous infusion of [2-3H]- and [U-14C]lactate was used to study the effects of endurance training (running 2 h/day at 29.4 m/min up a 15% gradient) on lactate metabolism in rats. Measurements were made under three metabolic conditions: rest (Re), easy exercise (EE, 13.4 m/min, 1% gradient) and hard exercise (HE, 26.8 m/min, 1% gradient). Blood lactate levels in trained animals increased from 1.0 +/- 0.09 mM in Re to 1.64 +/- 0.21 in EE and 2.66 +/- 0.38 in HE. Control animals also demonstrated an increase in blood lactate with increasing work rate, but values were 1.93 +/- 0.21 and 4.62 +/- 0.57 mM at EE and HE, respectively. Lactate turnover rates (RtLA) measured with [U-14C]lactate increased from 214.0 +/- 17.0 mumol.kg-1.min-1 in Re to 390.3 +/- 31.6 in EE and 518.1 +/- 56.4 in HE. No significant differences in RtLA were observed between controls and trained animals under any condition. Identical relationships between RtLA and exercise or training were obtained with [2-3H]lactate; however, the values obtained were consistently 90% higher than those observed with [U-14C]lactate. Metabolic clearance rate (MCR) for 14C was not significantly different in Re between controls and trained animals (180.6 +/- 27.7 ml.kg-1.min-1). Metabolic clearance of lactate in trained animals was 37 and 107% greater than in controls during EE and HE, respectively. Results indicate that the effect of endurance training is not on production of lactate but on its clearance from the blood.

Animals↗

Myocardial lactate metabolism: evidence of lactate release during net chemical extraction in man.

Myocardial blood flow has been recognized to be heterogeneous in patients with coronary artery disease. Traditional arterial-coronary sinus sampling methods cannot demonstrate comparable heterogeneity of myocardial metabolism. In this study we used a tracer technique to investigate possible heterogeneity of myocardial lactate metabolism. Twenty-one patients with symptoms of ischemic heart disease were studied. We injected 14C-1-lactate intravenously as a constant infusion after a priming dose. Coronary sinus and arterial samples were obtained for chemical and radioisotopic analyses. At rest, myocardial lactate extraction by chemical analysis was 24.6 +/- 8.5% (mean +/- SD). By radioisotopic analysis, the lactate extraction was 41.0 +/- 10.2% (p less than 0.001). Thus, certain areas of the myocardium were releasing lactate despite global net extraction of lactate. In the 12 patients with significant left main or both left anterior descending (LAD) and left circumflex (LCX) lesions, the calculated amount of lactate released at rest was 0.136 +/- 0.045 mumol/ml of blood (mean +/- SD). In contrast, the amount released in the six patients with a significant lesion in only the LAD or LCX was 0.076 +/- 0.019 mumol/ml, and in the three patients without left coronary arterial lesions it was 0.039 +/- 0.004 mumol/ml. Using a tracer method, myocardial lactate metabolism was demonstrated to be heterogeneous at rest in patients with ischemic heart disease. A significant amount of lactate can be released by the myocardium at a time when chemical arterial-coronary sinus analysis indicates global myocardial extraction. The amount of lactate released appears to be related to the severity of the coronary artery disease.

Adult↗

Effects of sodium lactate infusion on cisternal lactate and carbon dioxide levels in nonhuman primates.

OBJECTIVE: To further the understanding of lactate-induced panic in patients with panic disorder, the authors examined cisternal lactate and carbon dioxide levels in nonhuman primates after infusions of sodium lactate comparable to those used in studies of human beings. METHOD: CSF and venous blood lactate, pH, PCO2, PO2, and bicarbonate were measured in five ketamine-anesthetized nonhuman primates, without mechanical ventilation, before and after they underwent infusions of sodium lactate. In addition, the same measurements were made for three of the five subjects who were given saline infusions. RESULTS: Despite the development of the characteristic peripheral biochemical effects of infused sodium lactate--increased lactate and bicarbonate levels and metabolic alkalosis--no increases in central lactate or carbon dioxide levels were observed. Saline infusions produced no biochemical effects on venous and cisternal measures. CONCLUSIONS: The results of this study are in keeping with previous findings of nonpermeability of the blood-brain barrier to anionic compounds such as lactate. They therefore support theories of lactate panic based on cognitive and/or brainstem misevaluation of peripheral somatic sensations.

Animals↗

Effects of lactation and season on plasma prolactin concentrations and response to bromocriptine during lactation in the Bennett's wallaby (Macropus rufogriseus rufogriseus).

Prolactin concentration was measured in plasma collected each week for 13 months from lactating and non-lactating Bennett's wallabies (Macropus rufogriseus rufogriseus). In non-lactating animals, prolactin concentrations decreased towards the end of the study but such changes did not appear to fit a seasonal pattern. Prolactin concentrations were low during early lactation and at a similar level to non-lactating animals, increased significantly during late pouch life (February-May), and then returned to non-lactating levels at a time coincident with permanent exit of the joey from the pouch. Temporary removal of joeys from their mothers in April was followed by a rapid decline in prolactin concentrations which remained low for 24 h until the joey was returned to its mother, whereupon prolactin concentrations increased significantly within 2 h. The effect of a single injection of bromocriptine (5 mg/kg) on lactation, embryonic diapause and plasma prolactin concentrations was examined at two stages of lactation. In November (lactational diapause), bromocriptine had no effect on prolactin concentrations but two out of four suckling joeys died on days 13 and 14 after treatment, and three out of four females gave birth on days 27, 27 and 28. Bromocriptine treatment in April (seasonal diapause) was followed by a significant reduction in prolactin concentrations and reduced growth rate of joeys belonging to treated females. New births were not observed. In view of the effect of bromocriptine on plasma prolactin concentrations in late lactation and the demonstration that domperidone (a dopamine antagonist) significantly increases plasma prolactin concentrations, it would seem that dopamine can act as a prolactin inhibitory hormone in this as in other mammalian species.

Animals↗

Ovarian structures and circulating steroids in heifers and lactating cows in summer and lactating and dry cows in winter.

Two experiments compared follicular and luteal development and circulating steroid concentrations from induced luteolysis to ovulation in lactating Holstein cows (n = 27; 40.0 +/- 1.5 kg milk/day) vs. nulliparous heifers (n = 28; 11 to 17 mo-old) during summer (Experiment 1), and in lactating (n = 27; 45.9 +/- 1.4 kg milk/d) vs. dry cows (n = 26) during winter (experiment 2). All females received PGF2,, 6 d after ovulation and were monitored until next ovulation by daily ultrasound and assay of serum progesterone (P4) and estradiol (E2). Every female was used two or three times. In Experiment 1, lactating cows had high incidence of multiple ovulation (63.5%) compared with heifers (1.3%). Among single ovulators, there was no difference in maximal size of ovulatory follicles between lactating cows and heifers (15.8 vs. 16.5 mm, respectively). However, lactating cows had lower peak serum E2 (8.6 vs. 12.1 pg/ml), took longer to ovulate after luteolysis (4.6 vs. 3.8 d), developed more luteal tissue volume (7,293.6 vs. 5,515.2 mm3), and had lower serum P4 on d 6 after ovulation (2.0 vs. 3.0 ng/ml) than heifers (data included multiple ovulators). In experiment 2, multiple ovulations were similar between lactating and dry cows (17.9 vs. 17.2%, respectively). Peak serum E2 was also similar between lactating and dry cows (7.6 vs. 8.5 pg/ml) although lactating cows had larger ovulatory follicles (18.6 vs. 16.2 +/- 0.4 mm). Lactating cows took longer to ovulate (4.8 vs. 4.2 d), developed more luteal tissue (7,599 vs. 5,139 +/- 468 mm3), but had similar serum P4 (2.2 vs. 1.9 ng/ ml) compared with dry cows. Therefore, lactating cows had similar or lower circulating steroid concentrations than dry cows or heifers, respectively, despite having larger ovarian structures.

Animals↗

Three or two times daily milking of older cows and first lactation cows for entire lactations.

Thirty-eight older (second and greater lactation) and 15 Holstein cows in first lactation were in a full lactation (44 wk) study to evaluate the effect of either twice or three times daily milking on yield of milk and milk components, milk composition, feed intake, and body weight change. All cows were managed alike and were fed diets of high, medium, and low energy concentration as lactation progressed from calving to 44 wk. First lactation cows were switched from diets of high energy to lower energy at the same milk production as lactation advanced. Dietary changes for older cows milked twice and three times (A) were at similar production, whereas three times (B) cows were switched to lower energy at higher milk production. Older cows milked three times daily (A and B) produced 17 and 13% more milk over the entire lactation than cows milked twice daily. Dry matter and energy intakes were not affected by three times milking, but gain of body weight was reduced. Cows milked three times daily during their first lactation produced 6% more milk than their twice counterparts, although this increase was not significant. Dry matter and energy intakes were not affected by three times daily milking, but three times milking of first lactation cows reduced weight gain over the lactation. Reproductive performance of cows milked three times daily was not significantly different from cows milked twice daily. Herds milking three times will require high management of nutrition and reproduction.

Animals↗

Relationship of yield during early lactation and days open during current lactation with 305-day yield.

To measure and to partition the effect of pregnancy on yield, the relationships among milk, fat, and protein yields during early lactation, current days open, and 305-d yields were investigated using sample day records of 247,310 Holstein cows. The model included fixed effects of calving herd-year-season, calving age, and days open; the continuous variable of early cumulative yield to 80, 100, 120, or 140 d; and a random residual effect. As days open during first lactation increased from 30 to 100 d, 305-d milk yield increased by 876 kg; as days open increased from 100 to 200 d, milk yield increased by only 172 kg. The impact of current days open was greater on second lactation than on first; the difference in 305-d milk yield between cows open 40 and 290 d was 1199 kg for first lactation and 1613 kg for second lactation. If early yield to 120 d was included in the model, the corresponding difference was reduced to 860 kg for first lactation and 1001 kg for second lactation. Inclusion of early yield in the model reduced regression coefficients for days open during first lactation by 22% for 80-d yield, 24% for 100-d yield, 27% for 120-d yield, and 30% for 140-d yield and by 31, 35, 38, and 41%, respectively, for second lactation. Statistical models to derive adjustment factors should account for early lactation yield so that those factors can remove effects of pregnancy but not correlations between yield and fertility caused by early yield.

Animals↗