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Hemorrhagic shock in obstetrics.

Acute postpartum hemorrhage is the leading worldwide cause of maternal mortality, such deaths being usually related to the development of hemorrhagic shock and its consequences, especially the multiple organ dysfunction syndrome. Obstetricians should be aware of the clinical manifestations and principles of management of hemorrhagic shock. Initial assessment of the bleeding patient requires monitoring blood pressure, pulse, capillary refill, mental status and urinary output. This allows estimation of the amount and the rate of blood loss and helps direct treatment. Hemorrhagic shock is a condition in which inadequate perfusion of organs results in insufficient availability of oxygen to satisfy the metabolic needs of the tissues. A catabolic state develops. The consequences of these changes are inflammation, endothelial dysfunction, and disruption of normal metabolic processes in vital organs. Once these events become established, the process of shock is often irreversible, even if volume and red cell deficits are corrected. The principal goals of management are controlling the source of the blood loss; restoring adequate oxygen carrying capacity; and maintaining adequate tissue perfusion. Patients with severe postpartum hemorrhage are at risk of developing hypothermia, an insidious complication that contributes substantially to morbidity and mortality. It must be prevented or treated promptly. Successful treatment of exsanguinating postpartum hemorrhage depends on efficient collaboration among all members of the patient care team, and a management plan based on an understanding of the pathophysiology of shock and tailored to the individual patient's situation.

Blood Transfusion↗

Erythropoiesis in pregnancy.

There is a dramatic increase in total blood volume during healthy pregnancy. The disproportionate expansion in plasma volume (50%) and red cell mass (18-25% depending on iron status) results in a decrease in haemoglobin concentration maximal at 32 weeks gestation. This should not fall below 11 g/dl at any time during pregnancy. Deficiency of essential haematinics arising from increased requirements and inadequate intake may have far reaching effects on mother, fetus and neonate which bear no relationship to the impaired oxygen carrying capacity of the reduced cell mass. Pathological anaemia of pregnancy is due to over 90% of cases to iron deficiency associated with depleted stores and deficient intake. The single largest demand for iron arises from the increased red cell mass under the influence of erythropoietin. Tissue enzyme malfunction occurs even in the very first stages of iron deficiency before significant anaemia develops. Increased blood loss at delivery and preterm birth are observed associated complications. Off-spring of iron deficient mothers have decreased iron stores and may develop anaemia in the first year of life. Studies have shown behavioural abnormalities in children with iron deficiency and poor performance in the Bayley Mental Developmental Index. The poor performance in mental and motor development can be improved to the level of iron-sufficient infants by treatment with ferrous sulphate. Folate deficiency often accompanies iron deficiency as they are both associated with a poor diet. The haematological effects of folate deficiency are usually masked by iron deficiency.(ABSTRACT TRUNCATED AT 250 WORDS)

Erythropoiesis↗

Erythropoietin--from gene structure to therapeutic applications.

All forms of oxygen deprivation act as a stimulus for the production of the hormone erythropoietin. The main sites of production are specialized renal fibroblasts in adult mammals and hepatic cells in mammalian fetuses and neonates. The hormone's name is a succint description of its main effect: erythropoietin stimulates red cell production from bone marrow precursors and hence controls the O2-carrying capacity of the blood. The peripheral red cell count is kept constant by a closely controlled feedback mechanism involving O2 supply, erythropoietin secretion and erythropoiesis; the system may become unbalanced in conditions such as chronic renal disease, chronic inflammation and prematurity. Recombinant human erythropoietin is used as hormonal replacement therapy to correct various types of anemia and replenish the red cell count following hemorrhage or blood donation for autologous transfusion.

Anemia↗

The use of haemoglobin glutamer-250 (HBOC-201) as an oxygen bridge in patients with acute anaemia associated with surgical blood loss.

For the treatment of substantial blood loss in surgery, allogeneic blood is transfused to maintain stability and organ perfusion and function. Continued concerns about the availability, safety, efficacy and storage-related problems of allogeneic blood products have led to an intense effort to find alternatives that can serve the same physiologic functions. Haemoglobin-based oxygen carriers (HBOCs) are compounds that can match the oxygen-carrying capacity of red blood cells (RBCs), and several HBOCs have reached advanced stages of development and clinical testing. Multi-centre, randomised, Phase III, controlled trials have demonstrated the safety and efficacy of haemoglobin glutamer-250 (bovine) (Hemopure), Biopure Corporation, Cambridge, MA, USA), also known as HBOC-201. HBOC-201 is bovine-derived, modified haemoglobin that has been ultrapurified to remove any plasma proteins, RBC stroma and potential pathogenic material. During the manufacturing process, crosslinking and polymerisation stabilise the haemoglobin molecule, which increases its vascular persistence as well as the efficiency of oxygen transport to tissue. Results from clinical trials indicate that HBOC-201 can be used as an oxygen 'bridge' for patients experiencing anaemia due to surgical blood loss, until their own red blood cells are replenished or have regenerated (haematinic effect). HBOC-201 is generally well-tolerated and is approved for use in South Africa, where it is indicated for use in adult surgical patients who are acutely anaemic, and is used to eliminate, delay or reduce the need for allogeneic RBCs. A Biologics License Application for HBOC-201 is currently under review by the US FDA.

Acute Disease↗

What have we learned about gonadotropin function from gonadotropin subunit and receptor knockout mice?

A number of biochemical and physiological studies elucidated the roles of pituitary and placental glycoprotein hormones. Advances in the past two decades in manipulating the mouse genome by random or site-specific mutagenesis have heralded a new dimension to our understanding of the biology of gonadotropins. It is now possible to model many human reproductive disorders involving gonadotropins/gonadotropin-signaling in the mouse. Mutant mice selectively lacking either FSH or LH or their cognate receptors have been generated. The gonadotropin ligand and the corresponding receptor knockout mice mostly phenocopy each other. Analyses with these genetic models confirmed earlier physiological studies; in addition they also revealed novel roles for gonadotropins previously unrecognized. While FSH action seems dispensable for male but not female fertility, absence of LH causes infertility in both the sexes. While Sertoli cell number and germ cell carrying capacity of the Sertoli cells in compromised in FSH mutants, both somatic and germ cell lineages are affected in the LH mutants resulting in complete male infertility. FSH mutant females demonstrate a preantral stage block in folliculogenesis and FSH alone is not sufficient to promote full folliculogenesis in the absence of LH. Pre-ovulatory stage follicles do not form and most of the follicles undergo apoptosis in the absence of LH. Many extra-gonadal phenotypes have been described for the receptor knockout mice and whether these bear any resemblances to those in patients with similar inactivating mutations in the receptors for FSH and LH remains an open question. Thus the in vivo models will continue to have a significant impact in understanding gonadotropin physiology and pathophysiology and serve as novel genetic tools to study signaling mechanisms in the gonads.

Animals↗

Trans-kingdom transposition of the maize dissociation element.

Transposons are very valuable tools for genetic manipulation. However, the number of transposable elements that have been suitably adapted for experimental use is insufficient and the spectrum of heterologous hosts in which they have been deployed is restricted. To date, only transposons from animal hosts have been utilized in heterologous animal species and transposons of plant origin have been used in plant genetics. There has been no experimental evidence that any of the known elements could transpose in hosts belonging to both kingdoms. Here we demonstrate that the maize Dissociation (Ds) element is capable of effective Activator (Ac) transposase-mediated transposition in the zebrafish Danio rerio, yielding remarkable germline transmission rates. In addition, mammalian cells were also found to be conducive to Ds transposition. Furthermore, we demonstrate that nuclear localization of Ac transposase is essential for genomic Ds transposition. Our results support the hypothesis that Ac/Ds elements do not rely on host-specific factors for transposition and that host factors involved in their mobility mechanism are widely conserved. Finally, even in vertebrate cells, the Ac/Ds system displays accurate transposition, large-fragment carrying capacity, high transposition frequencies, efficient germline transmission, and reporter gene expression, all of which are advantageous for various genetic applications and animal biotechnology.

Animals↗

The effects of myocardial perfusion with perfluorochemical substances.

The effects of coronary arterial perfusion with a perfluorochemical substance (perfluorotributylamine) on the segmental myocardium of the beating heart were studied in 12 open chest anesthetized dogs. Following 10 min of left anterior descending coronary artery occlusion, perfusion of the coronary artery with the perfluorochemical returned myocardial function and metabolism toward control states, although myocardial diastolic properties as well as coronary venous PCO2 and lactate were not restored completely within 7 min after reperfusion. Perfluorochemicals may be of clinical importance in protecting the ischemic myocardium because of their oxygen carrying capacity together with favorable physiochemical properties for protection of the microcirculation.

Adenosine Triphosphate↗

Water pollution and degradation in Pearl River Delta, South China.

The Pearl River Delta Economic Zone is the most dynamic economic area in South China. One of the major problems in the region is the sustainable utilization of the water resources. On the basis of analysis of the water environment status and pollution sources, it is suggested that domestic sewage is the primary cause of pollution. Two new concepts "degradation coefficient" and "degradation volume" of water resources, due to pollution, which may be used to assess macroscopically the carrying capacity of the water resources and sustainability of the water environment, are proposed by the authors. The results calculated indicate that the volumes of degraded water resources will be up to 204, 352, and 537 million m3 in 2002, 2010, and 2020. It is suggested that water for daily consumption and domestic sewage must be controlled more effectively and there should be cross-regional coordination in tackling problems of water environment.

China↗

Capybaras in an anthropogenic habitat in Southeastern Brazil.

Capybaras (Hydrochoerus hydrochaeris) are widely distributed in the Neotropics, living in both natural and anthropogenic habitats. In the present study, we monitored the fluctuating capybara population at the Campus "Luiz de Queiroz", University of São Paulo, in Piracicaba, Southeastern Brazil from 1998 to 2000. To assess population fluctuation and growth rates, we used an abundance index based on direct weekly daylight counts. Population monitoring was carried out in an anthropogenic wetland associated with an agroecosystem. The observers bias was established as directly related to their distance from the animals. The capybara population density and biomass in the anthropogenic wetland in question were found to be significantly higher than in pristine habitats. The species seems to present a seasonal pattern of fluctuation, with a peak in late spring (Oct to Dec). Unlike young capybaras, adults and juveniles present similar seasonal fluctuation patterns. In this anthropogenic wetland, the carrying capacity may be as high as 195 individuals/Km2. At a conservative exploitation rate (17%) in anthropogenic wetlands of Southeastern Brazil, capybara productivity may reach approximately 630 Kg/Km2/year.

Animals↗

Neonatal administration of FSH increases Sertoli cell numbers and spermatogenesis in gonadotropin-deficient (hpg) mice.

We previously demonstrated that androgens alone, in the complete absence of gonadotropins, initiated qualitatively complete spermatogenesis in hypogonadal (hpg) mice. Although germ cell to Sertoli cell ratios were normal in hpg mice with androgen-induced spermatogenesis, testicular size. Sertoli cell and germ cell numbers only reached 40% of those of non-hpg mice, and Sertoli cell numbers were unaffected by androgen treatment started at 21 days of age. We postulated that these observations were due to diminished gonadotropin-dependent. Sertoli cell proliferation during perinatal life while the Sertoli cells still exhibited normal carrying capacity for mature germ cells. In order to test this hypothesis, we examined the effects of administering androgens and gonadotropins to hpg mice during the first 2 weeks of postnatal life when Sertoli cells normally continue to proliferate. The study end-points were Sertoli and germ cell numbers in hpg mice following induction of spermatogenesis by 8 weeks treatment with 1 cm subdermal silastic testosterone implants. Newborn pups (postnatal day 0-1) were injected s.c. with recombinant human FSH (rhFSH) (0.5 IU/20 microliters) or saline once daily for 14 days, with or without a single dose of testosterone propionate (TP) (100 micrograms/20 microliters arachis oil) or human chorionic gonadotropin (hCG) (1 IU/20 microliters). Untreated hpg and phenotypically normal littermates were studied as concurrent controls. At 21 days of age, all treated weaning mice received a 1 cm silastic subdermal testosterone implant and, finally, 8 weeks after testosterone implantation, all mice were killed. As expected, qualitatively complete spermatogenesis was induced in all groups by testosterone despite undetectable circulating FSH levels. Exogenous rhFSH increased testis size by 43% (P < 0.002) but a single neonatal dose of either TP or hCG reduced the FSH effect although neither TP nor hCG had any effect alone. In contrast, a single neonatal dose of TP or hCG increased final seminal vesicle size whereas FSH had no effect. FSH and TP treatment significantly increased absolute numbers of testicular spermatids compared with saline treatment, whereas hCG and TP significantly increased testicular sperm when expressed relative to testis size. Stereological evaluation of Sertoli and germ cell numbers demonstrated a rise in the absolute numbers of Sertoli and all germ cell populations induced by neonatal administration of hormones. When expressed per Sertoli cells the numbers of germ cells in the treated mice were between 85 and 90% of non-hpg controls. We conclude that exogenous FSH treatment during the first 2 weeks of postnatal life, coinciding with the natural time of Sertoli cell proliferation, increases Sertoli cell numbers and thereby the ultimate size of the mature testis and its germ cell production. Thus neonatal gonadotropin secretion may be a critical determinant of the sperm-producing capacity of the mature testis. In addition, neonatal exposure to androgens could be important for the imprinting of sex accessory organs in hpg mice, with the long-term effects of altering the sensitivity of the accessory organs to exogenous testosterone later in life.

Animals↗

Application of an ecological framework linking scales based on self-thinning.

Barnes and Roderick developed a generic, theoretical framework for vegetation modeling across scales. Inclusion of a self-thinning mechanism connects the individual to the larger-scale population and, being based on the conservation of mass, all mass flux processes are integral to the formulation. Significantly, disturbance (both regular and stochastic) and its impact at larger scales are included in the formulation. The purpose of this paper is to illustrate how this model can be used to predict patch and ecosystem dry mass, and consequently system carbon. Examples from pine plantations and mixed forests are considered, with these applications requiring estimates of system carrying capacity and the growth rates of individual plants. The results indicate that the model is relatively simple and straightforward to apply, and its predictions compare well with the data. A significant feature of this approach is that the impact of local scale data on the dynamics of larger patch and ecosystem scales can be determined explicitly, as we show by example. Further, the general formulation has an analytic solution based on characteristics of the individual, facilitating practical and predictive application.

Adaptation, Physiological↗

Incorporating known sources of uncertainty to determine precautionary harvests of saltwater crocodiles.

It has been demonstrated repeatedly that the degree to which regulation operates and the magnitude of environmental variation in an exploited population will together dictate the type of sustainable harvest achievable. Yet typically, harvest models fail to incorporate uncertainty in the underlying dynamics of the target population by assuming a particular (unknown) form of endogenous control. We use a novel approach to estimate the sustainable yield of saltwater crocodile (Crocodylus porosus) populations from major river systems in the Northern Territory, Australia, as an example of a system with high uncertainty. We used multimodel inference to incorporate three levels of uncertainty in yield estimation: (1) uncertainty in the choice of the underlying model(s) used to describe population dynamics, (2) the error associated with the precision and bias of model parameter estimation, and (3) environmental fluctuation (process error). We demonstrate varying strength of evidence for density regulation (1.3-96.7%) for crocodiles among 19 river systems by applying a continuum of five dynamical models (density-independent with and without drift and three alternative density-dependent models) to time series of density estimates. Evidence for density dependence increased with the number of yearly transitions over which each river system was monitored. Deterministic proportional maximum sustainable yield (PMSY) models varied widely among river systems (0.042-0.611), and there was strong evidence for an increasing PMSY as support for density dependence rose. However, there was also a large discrepancy between PMSY values and those produced by the full stochastic simulation projection incorporating all forms of uncertainty, which can be explained by the contribution of process error to estimates of sustainable harvest. We also determined that a fixed-quota harvest strategy (up to 0.2K, where K is the carrying capacity) reduces population size much more rapidly than proportional harvest (the latter strategy requiring temporal monitoring of population size to adjust harvest quotas) and greatly inflates the risk of resource depletion. Using an iconic species recovering from recent extreme overexploitation to examine the potential for renewed sustainable harvest, we have demonstrated that incorporating major forms of uncertainty into a single quantitative framework provides a robust approach to modeling the dynamics of exploited populations.

Alligators and Crocodiles↗

Dispersal per recruit: an efficient method for assessing sustainability in marine reserve networks.

Marine reserves are an increasingly important tool for the management of marine ecosystems around the world. However, the effects of proposed marine reserve configurations on sustainability and yield of populations are typically not estimated because of the computational intensity of direct simulation and uncertainty in larval dispersal and density-dependent recruitment. Here we develop a method for efficiently assessing a marine reserve configuration for persistence and yield of a population with sedentary adults and dispersing larvae. The method extends the familiar sustainability criteria of individual replacement for single populations based on eggs-per-recruit (EPR) to spatially distributed populations with sedentary adults, a dispersing larval phase, and limited carrying capacity in the settlement-recruit relationship. We refer to this approach as dispersal-per-recruit (DPR). In some cases, a single DPR calculation, based on the assumption that post-settlement habitat is saturated (i.e., at maximum recruitment), is sufficient to determine population persistence, while in other cases further iterative calculations are required. These additional calculations reach an equilibrium more rapidly than a full simulation of age- or size-structured populations. From the DPR result, fishery yield can be computed from yield-per-recruit (YPR) at each point. We assess the utility of DPR calculations by applying them to single reserves, uniformly distributed systems of reserves, and randomly sized and spaced systems of reserves on a linear coastline. We find that for low levels of EPR in fished areas (e.g., 10% or less of the natural, unfished EPR when post-settlement habitats are saturated by 35% of natural settlement), a single DPR calculation is sufficient to determine persistence of the population. We also show that, in uniform systems of reserves with finite reserve size, maximal fisheries yield occurs when the density of reserves is such that all post-settlement habitat is nearly saturated with settlers. Finally, we demonstrate the application of this approach to a realistic proposed marine reserve configuration.

Animals↗

Effects of atrazine on embryos, larvae, and adults of anuran amphibians.

We examined the effects of atrazine (0-20 mg/L) on embryos, larvae, and adult anuran amphibian species in the laboratory. Atrazine treatments did not affect hatchability of embryos or 96-h posthatch mortality of larvae of Rana pipiens, Rana sylvatica, or Bufo americanus. Furthermore, atrazine had no effect on swimming speed (measured for R. pipiens only). However, there was a dose-dependent increase in deformed larvae of all three species with increasing atrazine concentration. In adult R. pipiens, atrazine increased buccal and thoracic ventilation, indicating respiratory distress. However, because atrazine had no affect on hemoglobin, this respiratory distress was probably not indicative of reduced oxygen-carrying capacity of the blood. Frogs exposed to the highest atrazine concentration stopped eating immediately after treatment began and did not eat during the 14-d experiment. However, no decreases in mass were measured even for frogs that were not eating, probably because of compensatory fluid gain from edema. Atrazine concentrations found to be deleterious to amphibian embryos and adults are considerably higher than concentrations currently found in surface waters in North America. Therefore, direct toxicity of atrazine is probably not a significant factor in recent amphibian declines.

Analysis of Variance↗

Predicting fracture through benign skeletal lesions with quantitative computed tomography.

BACKGROUND: There are no proven radiographic guidelines for predicting fracture risk in children and young adults with a benign skeletal lesion. An in vivo diagnostic study was conducted to determine whether a reduction in the load-carrying capacity of a bone measured with quantitative computed tomography was more accurate than current radiographic guidelines for predicting pathologic fracture in patients with a benign skeletal lesion. METHODS: Eighteen patients who presented with a fracture through a benign skeletal lesion were compared with eighteen patients who had a benign skeletal lesion that had been thought to be at increased risk for fracture on the basis of currently used radiographic criteria but had not fractured over a two-year period. Structural analysis was performed to calculate the resistance of the affected bones to compressive, bending, and torsional loads with use of serial transaxial quantitative computed tomography data obtained along the length of the bone containing the lesion and from homologous cross sections through the contralateral, normal bone. At each cross section, the ratio of the structural rigidity of the affected bone divided by that of the normal, contralateral bone was determined. The cross section with the greatest reduction in compressive, bending, and torsional rigidity was identified as that most likely to fracture. RESULTS: The mean age (and standard deviation) of the thirty-six patients was 12.5 +/- 3.6 years. Twenty lesions were located in the femur; eleven, in the tibia; three, in the humerus; one, in the ulna; and one, in the pelvis. A combination of the minimum bending and torsional rigidities calculated from the tomographic data provided optimal performance in differentiating between the fracture and non-fracture groups (100% sensitivity and 94% specificity). In contrast, plain radiographic criteria demonstrated 28% to 83% sensitivity and 6% to 78% specificity. CONCLUSIONS: The combination of bending and torsional rigidity measured noninvasively with quantitative computed tomography was more accurate (97%) for predicting pathologic fracture through benign bone lesions in children than were standard radiographic criteria (42% to 61% accuracy). We believe that this method can provide accurate objective criteria for planning treatment of benign bone lesions and monitoring treatment response.

Adolescent↗

Clinical pharmacokinetics in patients with liver disease.

From considerations of hepatic physiology and pathology coupled with pharmacokinetic principles, it appears that altered drug elimination in liver disease may result from the following mechanisms: reduction in absolute cell mass, in cellular enzyme content and/or activity, in portal vein perfusion due to extrahepatic/intrahepatic shunting, or of portal perfusion of hepatocyte mass due to decreased portal flow or sinusoidal perfusion; increase in arterial perfusion relative to portal perfusion; preferential perfusion of the sinusoidal midzone and terminal zones by arterioles; potential for direct mixing of arterial blood within the space of Disse; reduced exchange across the endothelial lining; and impaired diffusion within the space of Disse. In general, oxidative drug metabolism is impaired in liver disease and the degree of impairment of oxidisation differs between drugs but correlates best with the degree of sinusoidal capillarisation, i.e. the degree of access of the drug from the sinusoid to the hepatocyte. Drug conjugation appears to be relatively unaffected by liver disease, whereas elimination by biliary excretion correlates best with the degree of intrahepatic shunting and not with sinusoidal capillarisation. As the latter should impair hepatocyte access of all compounds similarly, a potentially important mechanism could be impaired access of oxygen to hepatocytes as oxidative metabolism is much more sensitive to oxygen supply than are conjugation or biliary excretion. This suggests a potentially important therapeutic role for agents which increase the hepatic oxygen supply. Useful adjunctive strategies may also derive from the oxygen limitation hypothesis. Anaemia should be targeted as a critically important variable, as should oxygen-carrying capacity, i.e. modification of the smoking habit. Additionally, enzyme inducers such as barbiturates may be used if overriding hypoxic constraints are removed by oxygen supplementation. Agents likely to seriously compromise arterial perfusion of the hepatic vascular bed should be avoided, e.g. those causing postural hypotension or vasospasm. Vasodilators can be used to actively promote arterial perfusion. While the effect of liver disease on drug handling is highly variable and difficult to predict, there are well recognised principles for modifying dosage. These include halving the dose of drugs given systemically (or of low clearance drugs given orally) and a 50 to 90% reduction in the dose of drugs with a high hepatic clearance given orally. Changes in the pharmacodynamic effects of drugs (either alone or in addition to pharmacokinetic changes) can also be profound, and awareness of this possibility should be increased.

Humans↗

Physiological differences between genders. Implications for sports conditioning.

It is commonly accepted that there are physiological and morphological gender differences. These differences become evident in the specific responses or magnitude of response to various training regimens. Very little difference is seen in the response to different modes of progressive resistance strength training. Men and women experience similar relative strength gains when training under the same programme. The evidence on body composition changes that occur with strength training is equivocal at this point. Researchers, however, suggest that there appears to be less muscle hypertrophy with strength improvement in women when compared to men. The data suggest that there are no differences between genders in central or peripheral cardiovascular adaptations to aerobic training. However, women in general have a reduced O2 carrying capacity. Another factor that may be responsible for the sex differences seen in the metabolic responses to exercise may be the greater, essential sex specific fat of women. Sparling and Cureton (1983) have shown that differences in similarly trained male and female distance runners are due largely to percentage body fat, less to cardiorespiratory fitness and least to running economy. Pate et al. (1985) determined that men and women who are capable of similar performances, in this case a 15 mile race, do not differ in body composition, cardiorespiratory response or metabolic response. There appear to be no differences in relative increases in VO2max for men and women when they are trained under the same intensity, frequency and duration. Mode of training also appears to elicit no sex difference. Hormonal factors lead to greater initial levels of high density lipoproteins in women. This appears to cause a smaller change in the total cholesterol-high density lipoprotein ratio than occurs with aerobic training in men. Generally, the menstrual cycle phase makes no difference to performance in women. The special cases of exercise in hot and cold environments present conflicting evidence. When men and women are matched for surface area:mass, VO2max and percentage body fat, the major disadvantages women have in the heat disappear. The question of gender differences in the cold has yet to be fully explored. When the general population is compared, men appear to have an advantage over women.

Adaptation, Physiological↗

Aerobic exercise during pregnancy. Special considerations.

Alterations in maternal physiology during pregnancy affect the physiological respect to aerobic exercise. Maternal resting oxygen consumption (VO2) and cardiac output increase during pregnancy. Heart rate (HR) becomes progressively elevated through gestation, whereas stroke volume (SV) increases until the third trimester and then declines until term, probably because of diminished venous return. Plasma volume increases earlier and to a greater magnitude than red cell volume, resulting in the 'haemodilutional anaemia' of pregnancy and a decline in the oxygen-carrying capacity. Ventilation is greater during pregnancy because of elevated tidal volume and unchanged rate of breathing. The acute and chronic (training) responses to aerobic exercise during pregnancy have not been thoroughly investigated. Specifically, the effect of gestational age, maternal activity status, and type, duration and intensity of exercise on maternal cardiovascular response have only recently begun to be explored. During pregnancy cardiac output during submaximal exertion increases above values in non-pregnant women, except perhaps late in gestation. Both heart rate and stroke volume contribute to the elevated cardiac output. Changes in submaximal exercise VO2 during pregnancy are dependent on the mode of exercise. At the same workload, VO2 increases during weight-bearing exercise, but usually does not differ from postpartum values during weight-supported exercise. One study found no change in VO2max during pregnancy compared to postpartum values. Some recent evidence indicates that the cardiac output vs VO2 relationship for pregnant women is within the range of average values reported for non-pregnant individuals. Exercise arterial-venous oxygen difference is lower during pregnancy, suggesting that the higher cardiac output is distributed to non-exercising vascular beds. The data are limited but suggest that the perfusion of exercising muscle is unchanged during pregnancy and that the major haemodynamic change is an augmented cardiac output so that blood flow to the uterus and fetus is not compromised. Only one study has measured blood flow during exercise in pregnant women. The reported 25% decrease in uterine blood flow during supine cycle exercise in women late in gestation must be interpreted cautiously because the uterus may obstruct the vena cava in the supine position. Studies of exercising pregnant animals usually indicate a decreased uterine blood flow but an enhanced oxygen extraction; the lower blood flow may be limited to non-placental areas. The applicability of these results to humans is unknown.(ABSTRACT TRUNCATED AT 400 WORDS)

Exercise↗