Scheepers et al.

, Fetal and maternal metabolism during labor

457

Review article

J. Perinat. Med.
29 (2001) 457464

Fetal and maternal energy metabolism during labor in

relation to the available caloric substrate
H. C. J. Scheepers1, P. A. de Jong1, G. G. M. Essed2, and H. H. H. Kanhai3
1

Deptartment of Gynecology and Obstetrics, Leyenburg Hospital, The Hague,

of Gynecology and Obstetrics University Hospital Maastricht, and
3Department of Gynecology and Obstetrics Leiden University Medical Center,
Leiden, The Netherlands
2Deptartment

1 Introduction
During delivery, it is not unusual for women to
have little or no nutrient intake in spite of the fact
that the demand for energy increases for skeletal
and smooth muscle contractions. The question remains as to what the optimal policy in nutritional
intake during labor should be. The major reason
for restricting oral intake is the possible risk or
aspiration of gastric contents leading to the Mendelson syndrome. In many countries, a totally restrictive policy is adhered to [14, 31] although in
recent years, there is a tendency towards a more
liberal policy. The American Society of Anesthesiologists, stated in 1999 that, during normal labor, parturients should be allowed to drink clear
liquids and in Great Britain an increasing number
of institutes allow eating or drinking during labor
[5, 50].
Mortality figures due to the Mendelson syndrome
in The Netherlands, where oral intake is left to
the decision of laboring women are, comparable
to that of countries where a restrictive policy is
adhered to [47, 50]. Although many authors of
review articles conclude that the restriction of
eating and drinking during labor should be reconsidered [5, 29, 33, 52, 55], little evidence is recorded on the actual effects of eating and drinking on the course of labor [22].
Maternal and fetal metabolism during labor has
been studied, but studies on the relationship to the
availability of energetic substrate and metabolic

parameters are rare. The influence of intravenous

glucose administration on maternal and fetal metabolism has been studied, but the role of oral
caloric intake on metabolites remains relatively
unstudied. In this paper we discuss maternal and
fetal metabolic events during labor, the effects of
intravenous glucose administration and the possible role of oral caloric intake.
2 Maternal energy metabolism and acid
base balance
Energy demands can be met by different pathways [19]. The first is the use of ATP and creatinine phosphate, and the second, is the oxidative
pathway. This latter pathway is used when sufficient oxygen is available and glucose, glycogen,
triglycerids and amino acids can be used as fuel.
The third pathway is the non-oxidative pathway,
which is active when insufficient oxygen is available and in which lactate is produced. The oxidative pathway is used in prolonged moderate exercise and the non-oxidative pathway is important
for giving extra power.
During normal labor, maternal blood glucose increases [17, 23, 25, 26, 39, 58] which can be explained by the increased gluconeogenesis due to
cortisol and adrenaline, produced as a stress reaction [19]. In prolonged labor, however, a decrease
in maternal glucose levels has been described
[17]. The glucose turnover during labor, is mark-

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Scheepers et al., Fetal and maternal metabolism during labor

edly elevated suggesting that glucose is probably

the major energy source for the myometrium during labor [30, 56].
Gluconeogenesis may be insufficient when deliveries are long of duration and glucose supply is
lacking. During normal labor, the concentration
of both free fatty acids [23, 26, 57] and ketobodies [15, 17, 26] rise. This suggests an increased
mobilization of substrates other than glucose and
indicates a relative shortage of carbohydrates.
Maternal lactate concentrations rise in the last
part of the first stage and during the second stage
[10, 17, 25, 26, 60] and indicate an increased
need for the non-oxidative pathway. The rise in
lactate is more pronounced when the second stage
lasts longer [24] or when uterine contractions are
more frequent [26]. In hypoactive labor, the
increase in lactate is not significant [17].
When comparing glycogen concentration in the
myometrium of pregnant women to non-pregnant
women, Wilmidsky and Gutman found 13 mg
glycogen per 1 g of myometrium opposed to
3 mg in non-pregnant women. The activities of
glycogen synthase phosphatase and phosphorylase were also significantly higher [59] this would
suggest a preparation for labor. During labor, a
significant decrease in glycogen in the myometrium is noticed, the glycogen store is almost depleted and the energetic load, calculated by the
adenylate energy charge (which is equal to the
Atkinsons quotient), being the relative ATP, ADP
and AMP concentrations, is decreased [27].
Fetal acid base balance during labor has been described extensively. The maternal acid base balance and its relation to the fetus have received
relatively less attention. Since fetal acid base
status is mostly determined by fetal oxygenation
and to a far lesser extent by maternal acid base
status, [6] this is understandable.
In humans, the acid base balance can be equated
in: CO2 H20 L H2CO3 L H HCO3. The
pH is defined by the concentrations of CO2 and
HCO3. A higher CO2 concentration results in a
lower pH and HCO3 acts as a buffer by binding
H ions. The base excess (or base deficit), is an
expression of the amount of buffer that is used in
order to maintain the acid base balance. In humans, the concentration of HCO3 can be

adapted by means of changes in the excretion in

the kidney, but this process is slow. A faster way
of reducing the pH is an increased excretion of
CO2 by means of breathing [4, 19]. In adults, under normal circumstances, the HCO3 concentration is 24 mmol/l, the pCO2 is 5.3 kPa (40 mm
Hg) and the pH is 7.4. The base excess/deficit
varies from 2 to 2 mmol/l.
During pregnancy, progesterone directly stimulates the maternal respiratory centre resulting in
a hyperventilation and a lower maternal pCO2
(mean 4.3 kPa). During labor, the maternal pCO2
further decreases due to the increased hyperventilation during contractions [4, 6, 39]. The fetomaternal CO2 gradient increases, which facilitates the
fetal transfer of CO2 to the maternal circulation.
The maternal pH increases during the first stage
of labor [10, 39]. Maternal base deficit, however,
increases [10, 39]. This indicates an increase in
the need for the buffer mechanism. Therefore,
during the first stage of labor in the mother, a
combination of a metabolic acidosis and a respiratory alkalosis is present, in which the respiratory component is more dominant. During the second stage, maternal pH decreases back to normal values and the base deficit further decreases
[10, 39]. This indicates an increasing metabolic
acidosis, which agrees with the findings of an
increase in lactate concentrations that are measured during the second stage. Table I summa-

Table I. Maternal energy metabolism and acid base

balance during labor
1) glucose most important fuel, but ketobodies suggest
shortage
2) increased concentration of glycogen in myometrium
of pregnant women
3) mainly oxidative pathway
4) non-oxidative pathway : formation of lactate
in: polysystolic contractions
second stage
5) first stage: metabolic acidosis/respiratory alkalosis
(hyperventilation)
A pH
A base deficit
6) second stage: due to increase of lactate: increase
metabolic acidosis
B pH ( to normal levels)
further A base deficit

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Scheepers et al., Fetal and maternal metabolism during labor

rizes maternal energy metabolism and acid base

balance during labor.
3 Fetal metabolism and its relation to
maternal metabolites
The fetus needs maternal supply of nutrients for
metabolic processes and growth [2]. The most important substrate for the fetal energy metabolism
is glucose. In neonates, the respiratory quotient
(RQ) approaches one, suggesting an almost exclusive use of carbohydrates for metabolic needs.
A premature infant has a RQ of 0.91.0 and an
infant at term has a RQ of 0.7 [7].
Hay has described the process of fetal carbohydrate and lipid metabolism [20]. The main source
of fetal glucose is the maternal circulation. The
glucose-transfer through the placenta is directly
related to the maternal glucose concentration. In
cases of low fetal glucose concentration, a
smaller portion of the delivered glucose is used
by the uterus and placenta resulting in a buffer
mechanism to maintain fetal glucose supply.
Furthermore, due to a higher fetal capacity to use
glucose because of higher levels of insulin and an
increase of insulin-sensitive tissue, the maternalfetal glucose gradient increases.
The relationship between maternal and fetal metabolites was studied in the late 1960s1970s.
Glucose was found to be higher in maternal than
in fetal blood [34, 42] and venous umbilical cord
blood glucose was higher than arterial umbilical
blood, suggesting fetal usage of glucose. Hay has
described the effects of changes in maternal
blood glucose concentrations [20] and concluded
that short term severe hypoglycemia resulted in
lower fetal glucose supply. This lead to a decrease
in fetal glucose utilisation, fetal hypoinsulinemia,
a decrease in placental lactate formation and a
decrease in fetal lactate uptake. However, during
most parturitions, maternal blood glucose levels
increased and in even in prolonged labor, in
which a decline was described, the glucose concentration did not reach hypoglycemic levels
[17].
Short-term maternal hyperglycemia resulted in an
increasing amount of glucose which is shunted
into the non-oxidative pathway, leading to an
increase in the lactate concentration. An increase

459

in glucose uptake and utilization occurred and an

increase in fetal insulin was observed. Furthermore, fetal oxygen consumption was increased
[20].
Free fatty acids have been reported to higher in
maternal than fetal blood [42, 53]. Free fatty acid
concentration was found to be higher in cases of
prolonged labor and fetal arterial concentration
higher than the fetal venous concentration, suggesting fetal mobilization of free fatty acids. In
studies where glucose was administered intravenously during labor, a decline in the concentrations of both maternal and fetal blood free fatty
acids was observed [18, 42]. This would suggest
that improved glucose availability results in a decline of both maternal and fetal mobilization of
free fatty acids. This is confirmed by the fact that
the difference between arterial umbilical cord and
venous umbilical cord concentrations declines
[42, 53].
A plasma ketone rise during normal labor has
been described which correlated to the duration
of labor [18, 34]. Maternal blood concentrations
have been found to be higher than those in fetal
blood with a gradient of 2:1 [34]. The concentration of ketones in venous umbilical blood was
found to be higher than in arterial blood; this
would suggest a transplacental uptake by the fetus. In well-nourished mothers, it was found that
oxidation of ketone bodies was low and glucose
provided the major part of the fetal energetic substrate [1]. However, when there has been of maternal fasting, ketobodies can become a fetal fuel
source [46]. These ketobodies were mainly derived from the maternal circulation and fetal ketogenesis was almost inactive [9].
Schneider et al have described the homeostasis of
fetal lactate metabolism during labor [48]. They
concluded that during labor there was a gradual
rise in both maternal and fetal lactate. In most
cases fetal lactate concentrations were higher
than the maternal concentrations. Furthermore,
fetal arterial umbilical cord concentration was
higher than the venous umbilical cord concentration. This would suggest that during normal delivery the fetus produced lactate. Since lactate is
transferred by means of facilitated diffusion, in
most cases transport from the fetal to the maternal
circulation takes place. Fetal metabolic acidosis is

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Scheepers et al., Fetal and maternal metabolism during labor

therefore mostly of fetal origin and high lactate

concentrations during delivery suggest fetal nonoxidative metabolism and a (relative) shortage of
oxygen. It may however be the case that when
maternal lactate concentrations are high, the ability of the fetus to transfer lactate to the maternal
circulation diminishes. Very high maternal lactate
concentrations may even lead to a transport of
lactate from the maternal to the fetal circulation,
but only in about 6 % of deliveries [38]. However,
high maternal lactate concentration may have a
negative effect on fetal metabolic acidemia. Figure 1 summarizes the relationship between glucose and lactate in a maternal normoglycemic and
hyperglycemic situation.

estrogen and cortisol. This induces a diabetic-like

state in which peripheral glucose uptake is lower
whereby maternal blood glucose can be reserved
for the fetus. Pregnancy exaggerates the response
of the body to fasting, which make pregnant
women more prone to ketosis [15, 13]. Women
who eat during parturition have lower ketobodies
than those who do not [44]. Winkler and Hebeler
stated that uterine activity was reduced by the ac-

Conclusion: In most deliveries maternal blood glucose increases. A decline in maternal blood glucose can occur in long lasting deliveries without
adequate glucose supply, but this does not result in
severe hypoglycemia. Furthermore, due to the capacity of the placenta to regulate fetal glucose supply and fetal glucose sensitivity, it is unlikely that
fetal glucose supply will be jeopardized.
Fetal lactate is mostly of fetal origin, suggesting
fetal non-oxidative metabolism (a lack of oxygen). Hyperglycemia, however, may lead to an
increased production of lactate either in the maternal circulation and/or in the fetus/placenta. A
high maternal lactate furthermore diminishes the
ability of the fetus to transfer lactate to the maternal circulation. Combined with the increase in fetal oxygen consumption this may lead to a higher
risk of fetal acidemia.
4 Effects of fasting during labor and the
parallel to exercise
Deprivation of fluid and food during labor, theoretically, may have a negative impact on the progress
and outcome of labor. In animals, maternal and fetal blood glucose levels decline in fasting [54]. The
fetus is dependent upon glucose as its major energy
source and fetal activity has been shown to be
greater in higher maternal blood glucose levels
[32]. A lack of glucose, results in a higher mobilization of free fatty acids resulting in ketosis.
In pregnancy, the carbohydrate metabolism is altered [21]. There is a higher resistance to insulin
due to the effects of human placental lactogen,

Figure 1. Glucose and lactate metabolism in maternal

normo- and hyperglycemia
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Scheepers et al., Fetal and maternal metabolism during labor

cumulation of ketone bodies, but the cause and

effect relationship between prolonged labor and
the concentration of ketones is uncertain [60].
Since glucose is the main energy source not only
for the fetus, but also for the myometrium, gluconeogenesis is important. Although maternal glucose concentration, in most parturitions do not
decline, the rise in ketobodies and the increase in
mobilization of free fatty acids would suggest a
relative shortage of glucose.
A similar relationship between energy supply and
availability and the occurrence of fatigue occurs
in skeletal muscles during exercise. In this situation, fasting or a declining carbohydrate supply
leads to accelerated fatigue, enhanced lipolysis
and increased protein catabolism [58]. Studies
during exercise have shown that in a fasting state,
the usage of free fatty acids is enhanced [49].
During both exercise and labor, a sympathetic activation exists, resulting in a redistribution of
blood. Despite the lower blood supply to the intestinal tract, it has been shown that oral carbohydrate feeding during exercise results in a slower
occurrence of fatigue [8, 12, 45, 58]. The American College of Sports Medicine advises athletes,
who exercise for longer than one hour to ingest
carbohydrate solutions during exercise [11].

461

hyperglycemia resulting in fetal hyperinsulinemia

and neonatal hypoglycemia [3, 35, 43].
Maternal hyperglycemia, which can be caused by
an infusion of a highly concentrated glucose solution, may lead to a rise in both maternal and fetal
lactate and therefore to a metabolic acidosis. Fetal
metabolic acidosis was observed after a rapid infusion of 100 g glucose per hour [28, 36]. When
using lower dosages, this does not seem to be the
case. It was suggested by Piquard et al, that an
infusion of 10 % glucose at a rate of 30 g glucose
per hour, did not result in acidosis. Should fetal
acidosis occur, however, this would be more
likely be as a result from hypoxia than of maternal glucose administration [37]. Recently it has
been shown that the use of a 5 % glucose infusion
reduces fetal cord acidemia compared to the use
of Ringers lactate without glucose [16].
Yancey and Harlass have reviewed fetal acid base
status in relation to glucose administration and
have concluded that results are conflicting [61].
They stated that infusions which result in maternal
and fetal hyperglycemia have been correlated to alterations in fetal metabolic and acid-base status.

5 Glucose administration

To our knowledge, the only randomized controlled study on oral intake and maternal metabolic parameters has been published by Scrutton
et al [51]. They did not find a rise in maternal
lactate, nor maternal hyperglycemia, in women
who ate versus those who were starved. The formation of ketones was prevented by eating. Due
to the physiologic increase in the insulin concentration, it seems unlikely that oral intake can lead
to hyperglycemia in non-diabetic pregnant
women. Given the fact that most women in labor
do not eat or drink large amounts, oral caloric
intake is likely to be safe with regard to possible
effects on the fetal acid-base balance.

In the past, parenteral glucose administration was

considered a reasonable way to combat ketosis.
Even hyperglycemia was induced to fortify patients and it was considered good treatment for
both maternal and fetal distress [41]. However,
later studies showed fetal deterioration and fetal

Conclusion: the infusion of hyperglycemic solutions may cause fetal acidemia. Using 510 %
glucose solutions would appear to be safe. Oral
supplementation of carbohydrates may be considered. It is unlikely that oral intake would cause
hyperglycemia, but relevant data is scarce.

Conclusion: it would appear that pregnant women

are more prone to ketosis. No data are available on
the effects of caloric intake on the course of labor.
In athletes, the use of oral carbohydrates has
proven to be effective in reducing fatigue, without
adverse effects upon the gastro-intestinal tract.

Abstract
Aim: To discuss maternal and fetal metabolic events
during labor and the possible role of glucose administration.

Results: The oxidative pathway covers the largest part

of the energy demand of labor, although in the second
stage or, in polysystolic labor, the non-oxidative path-

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Scheepers et al., Fetal and maternal metabolism during labor

way becomes important as well. Glucose is the main

maternal energy source, but the rise in ketobodies, even
during normal labor, suggests a relative shortage. In the
first stage of labor, a combination of a respiratory alkalosis, and to a lesser extent, a metabolic acidosis, result
in a rise in the maternal pH. In the second stage of labor,
the maternal pH decreases due to an increasing metabolic acidosis. Glucose is also the main fetal energetic
fuel. In fetal hypoxia, lactate is produced, which in most
cases is transferred to the maternal circulation. High

maternal lactate concentrations, however, may interfere

with this process. Furthermore, fetal hyperglycemia
may lead to an increased fetal lactate production.
Conclusions: Maternal hyperglycemia, may lead to an
increase in maternal and fetal lactate production resulting in metabolic acidosis. Unlike high dosage intravenous glucose administration, it is not likely that oral
intake of carbohydrates leads to maternal and fetal hyperglycemia and subsequently to metabolic acidosis, but
studies are rare.

Keywords: Acid-base balance, fetal, glucose, lactate, maternal, metabolism.

Acknowledgements: The authors gratefully acknowledge the assistance of M. C. J. Thans and Dr. G. E. Beverstock
for reviewing this manuscript.

References
[1] Adam PAJ, P Felig: Carbohydrate, fat and aminoacid metabolism in the pregnant women and fetus.
In: Falkner F, JM Tanner: Human Growth. Principles and Prenatal Growth. Bailliere Tindall London 1978, pp 461
[2] Aldoretta PW, WW Hay: Metabolic substrates for
fetal energy metabolism and growth. Clinics in
Perinatology 22 (1995) 15
[3] Anderson GG, L Cordero, EH Hon: Hypertonic
glucose infusion during labour. Effects on acidbase status, fetal heart rate and uterine contractions. Obstet Gyn 36 (1970) 405
[4] Berg vd PP, JG Aarnoudse: Het foetale zuur-base
evenwicht. In: Nijhuis JG, GGM Essed, HP van
Geijn, GHA Visser: Foetale bewaking. Elsevier/
Bunge, Maarssen 1998, pp 123
[5] Berry H: Feast or famine? Oral intake during labour: Current evidence and practice. Br J Nurse
Midw (1997) 413
[6] Blechner JN: Maternal Fetal Acid Base Physiology: Clin Obst Gyn 36 (1993) 3
[7] Boisieu de D, F Rocchiccioli, N Kalach, PF Bougneres: Ketone body turnover at term and in premature newborns in the first 2 weeks after birth. Biol
Neonate 67 (1995) 84
[8] Bosch AN, SM Weltan, SC Dennis, TD Noakes:
Fuel substrate turnover and oxidation and glycogen sparing with carbohydrate ingestion in noncarbohydrate loaded cyclist. Pflugers Arch 432
(1996) 1003
[9] Bougneres PF, C Lemmel, P Ferre, DM Bier: Ketone body transport in the human neonate and infant. J Clin Invest 77 (1986) 42
[10] Cohen AV, H Schulman, SL Romney: Maternal
acid-base metabolism in normal human parturation. Am J Obstet Gynaecol 107 (1970) 933
[11] Convertino VA, LE Armstrong, EF Coyle, GW
Mack, MN Sawka, LC Senay jr, WM Sherman:

[12]

[13]
[14]

[15]

[16]

[17]

[18]

[19]

[20]

[21]

American College of Sports Medicine position

stand. Exercise and fluid replacement. Med Sci
Sports Exerc 28 (1996) i-vii
Dennis SC, TD Noakes, JA Hawley: Nutritional
strategies to minimize fatigue during prolonged
exercise: fluid electrolyte and energy replacement.
J Sports Sci 15 (1997) 305
Dumoulin JG; JE Foulkes: Ketonuria during labor.
Br J Obstet Gyn 91 (1984) 97
Elkington KW: At the waters edge: where obstetrics and anaesthesia meet. Obstet Gynecol 77
(1991) 304
Felig P, V Lynch: Starvation in human pregnancy;
hypoglycemia, hypoinsulinemia and hyperketonemia. Science 170 (1970) 990
Fisher AJ, JF Huddleston: Intrapartum maternal
glucose infusion reduces umbilical cord acidemia.
Am J Obst Gyn (1997) 765
Friedberg V, RH Ackermann: Aspekte des endokrin-metabolischen Zusammenspiels unter der Geburt. Geburtshilfe Frauenheilk 43 (1983) 8
Gardmark S, G Gennser, L Jacobson, G Rooth, J
Thorell: Influence on fetal carbohydrate and fat
metabolism and on acid-base balance of glucose
administration to the mother during labour. Biol
Neonate 26 (1975) 129
Guyton AC. Lipid Metabolism In: Guyton AC:
Textbook of medical physiology. Seventh edition.
Philidelphia W. B. Saunders 1986, pp 822
Hay WW: Nutrition and development of the fetus:
carbohydrate and lipid "metabolism In: Nutrition
in pediatrics. Walker 24 (1997) 364
Helmerhorst FM, MJNC Keirse: De normale
zwangerschap. In: Treffers PE et al, Obstetrie en
Gynaecologie. De voortplanting van de mens. Utrecht: Wetenschappelijke uitgeverij Bunge 1993,
pp 116
J. Perinat. Med. 29 (2001)

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Scheepers et al., Fetal and maternal metabolism during labor

[22] Johnson CJ, MJNC Keirse, M Enkin, I Chalmers:

Nutrition and hydration in labour. In: Chalmers I,
Effective care in pregnancy and childbirth. Oxford
University Press Oxford 1989, pp 827
[23] Kashyap ML: Carbohydrate and lipid metabolism
during human labor: free fatty acids, glucose, insulin and lactic acid metabolism during normal and
oxytocin-induced labor for postmaturity. Metabolism 25 (1976) 865
[24] Katz M, E Lunenfeld, I Meizner, N Bashan, J
Gross: The effect of the duration of the second
stage of labour on the acid-base state of the fetus.
Br J Obst Gyn 94 (1987) 425
[25] Katz M, D Kroll, Y Shapiro, N Cristal, I Meizner:
Energy expenditure in normal labor. Isr J Med Sci
26 (1990) 254
[26] Krolikowska von M. T Laudanski, J Mikaszewska-Pietraszum, T Paprocka-Raba: Einfluss der
Wehentatigkeit auf Parameter des Kohlenhydratund Fettstoffwechsels im Blut. Zbl. Gynakol 101
(1979) 1151
[27] Laudanski T: Energetischer Metabolismus des
Myometriums wahrend der Schwangerschaft und
der Geburt. Zbl. Gynakol 107 (1985) 568
[28] Lawrence GF, VA Brown, RJ Parsons, ID Cooke:
Feto-maternal consequences of high-dose glucose
infusion during labour. Br J Obstet Gyn 89 (1982)
27
[29] Ludka LM, CC Roberts: Eating and drinking in
labor. A literature review. J Nurse-Midw 38(4)
(1993) 199
[30] Maheux PC, B Bonin, A Dizazo, P Guimond,
D Monier, J Bourque, JL Chiasson: Glucose homeostatis during spontaneous labour in normal human pregnancy. J Clin Endocrin Metab 81(1996)
209
[31] Michael S, CS Reilly, JA Caunt: Policies for oral
intake during labour. A survey of maternity units
in England and Wales. Anaesthesia. 46(12) (1991)
1071
[32] Miller FM, H Skiba, H Klapholz: The effect of
maternal blood sugar-levels on fetal activity. Obstet Gyn 52 (1978) 662
[33] OSullivan G: The stomach, fact and fantasy: eating and drinking during labor. Int Anesthesiol Clin
32(2) (1994) 31
[34] Paterson P, J Sheath, P Taft, C Wood: Maternal
and foetal ketone concentrations in plasma and
urine. Lancet i (7495) (1967) 862
[35] Pearson JF, R Shuttleworth: The metabolic effects
of a hypertonic fructose infusion on the mother
and fetus during labor. Am J Obst Gynec 15
(1971) 259
[36] Philipson EH, SC Kalhan, MM Riha, R Pimentel:
Effects of maternal glucose infusion on fetal"acidbase status in human pregnancy. Am J Obst Gyn
157 "(1987) 866

463

[37] Piquard F, R Hsiung, A Schaefer, P Haberey, P

Dellenbach: Does fetal acidosis develop with maternal glucose infusion during normal labor? Obstet Gyn 74 (1989) 909
[38] Piquard F, A Schaefer, P Dellenbach, P Haberey:
Is fetal acidosis in the human fetus maternogenic
during labor? A reanalysis. Am J Physiol 261
(1991) R1294
[39] Pontonnier G, F Puech, H Grandjean, M Rolland:
Some physical and biochemical parameters during
normal labour. Biol-Neonate 26 (1975) "159
[40] Practice guidelines for obsetrical anesthesia: A report by the American Society of Anesthesiologist
Task Force on Obstetrical Anesthesia. Anesthesiology 90 (1999) 600
[41] Romney SL, MS Gabel: Maternal glucose loading
in the management of fetal distess. Am J Obst Gyn
96 (1966) 698
[42] Roux JF, SL Romney: Plasma free fatty acids and
glucose concentrations in the human fetus and
newborn exposed to various environmental conditions. Am J Obst Gynec 97 (1967) 269
[43] Rutter N: Glucose during labor. Lancet 2 (1980)
155
[44] Sabata V, H Wolf, S Lausmann: The role of free
fatty acids, glycerol, ketone bodies and glucose in
the energy metabolism of the mother and fetus
during delivery. Biol Neonatol 13 (1968) 7
[45] Sayed el MS, D MacLaren, AJ Rattu: Exogeneous
carbohydrate utilisation: effects on metabolism
and exercise performance. Comp Biochem Physiol
A Physiol 118 (1997) 789
[46] Schambaugh GE: Ketone body metabolism in the
mother and fetus. FASEB J. 44 (1985) 2347
[47] Scheepers HCJ, GGM Essed, F Brouns: Food and
fluid intake during labour; policies on oral intake
during labour in The Netherlands: Eur J Obst Gyn
and Repr Biol 78 (1998) 37
[48] Schneider H, J Danko, R Huch, A Huck: Homeostasis of fetal lactate metabolism in late pregnancy
and the changes during labor and delivery. Eur J
Obst Gyn Repr Biol (1984) 183
[49] Schneiter P, Di-Vetta V, Jequier E, Tappy L. Effect
of physical exercise on glycogen turnover and net
substrate utilization according to the nutritional
state. Am J Physiol 269 (1995) E1031
[50] Schuitemaker N, J Roosmalen, G Dekker, P
Dongen van, H Geijn van, J Bennebroek Gravenhorst: Maternal mortality after cesarean section
in The Netherlands. Acta Obstet Gynecol Scand
76 (1997) 332
[51] Scrutton MJL, GA Metcalfe, C Lowy, PT Seed, G
OSullivan: Eating in labor. A randomized controlled trial assessing the risk and benefits. Anaesthesia 54 (1999) 329
[52] Sharp DA: Restriction of oral intake for women in
labour. Br J. Midwifery 5 (1997) 408

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464

Scheepers et al., Fetal and maternal metabolism during labor

[53] Sheath J, J Grimwade, K Waldron, M Bickley, P

Taft, C Wood: Arteriovenous nonesterified fatty
acids and glycerol differences in the umbilical
cord at term and their relationship to fetal metabolism. Am J Obstet Gynecol 113 (1972) 358
[54] Simmons M, G Meschia, E Makowski: Fetal metabolic response to maternal starvation. Pediatr Res
(1974) 830
[55] Sleutel M, SS Golden. Fasting in labor: relic or
requirement: J Obstet Gynecol Neonatal Nurs 28
(1999) 507
[56] Steingrimsdottir Th, G Ronquist, U Ulmsten, A
Waldenstrom: Different energy metabolite pattern
between uterine smooth muscle and striated rectus
muscle in term pregnant women. Eur J Obst Gyn
Reprod Med (1995) 241
[57] Wagemakers AJM, EJ Beckers, F Brouns, H Kuipers, PB Soeters, GJ van der Vusse, WHM Saris:
Carbohydrate supplementation, glycogen depletion, and amino acid metabolism during exercise.
Am J Physiol 1991 (1991) E883

[58] Whaley WH, FP Zuspan, GH Nelson, RP Ahlquist:

Alterations of plasma free fatty acids and glucose
during labor. Am J Obstet Gyn 67 (1967) 875
[59] Wilmidsky A, Guman A: Glycogen metabolism of
normal human myometrium and leiomyoma. Possible hormonal control. Gyn Obstet Invest 15
(1983) 147
[60] Winkler H, Hebeler F: Investigation of the acetone
and lactic acid concentrations in blood during
birth and their importance for uterine action. Archiv Gynekol 168 (1939) 64
[61] Yancey MK, Harlass FE: Extraneous factors and
their influences on fetal acid-base status. Clin Obst
Gyn 36 (1993) 60
H. C. J. Scheepers,
Leyenburg Hospital
Leyweg 275
2545 CH The Hague
The Netherlands
Fax:
31 70-3592204
e-mail: HCJ. Scheepers@hetnet.nl

J. Perinat. Med. 29 (2001)

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