Hypobaric live high-train low does not improve aerobic performance more than live low-train low in cross-country skiers.

Live high-train low (LHTL) using hypobaric hypoxia was previously found to improve sea-level endurance performance in well-trained individuals; however, confirmatory controlled data in athletes are lacking. Here, we test the hypothesis that natural-altitude LHTL improves aerobic performance in cross-country skiers, in conjunction with expansion of total hemoglobin mass (Hbmass , carbon monoxide rebreathing technique) promoted by accelerated erythropoiesis. Following duplicate baseline measurements at sea level over the course of 2 weeks, nineteen Norwegian cross-country skiers (three women, sixteen men, age 20 ± 2 year, maximal oxygen uptake (VO2 max) 69 ± 5 mL/min/kg) were assigned to 26 consecutive nights spent at either low (1035 m, control, n = 8) or moderate altitude (2207 m, daily exposure 16.7 ± 0.5 hours, LHTL, n = 11). All athletes trained together daily at a common location ranging from 550 to 1500 m (21.2% of training time at 550 m, 44.2% at 550-800 m, 16.6% at 800-1100 m, 18.0% at 1100-1500 m). Three test sessions at sea level were performed over the first 3 weeks after intervention. Despite the demonstration of nocturnal hypoxemia at moderate altitude (pulse oximetry), LHTL had no specific effect on serum erythropoietin, reticulocytes, Hbmass , VO2 max, or 3000-m running performance. Also, LHTL had no specific effect on (a) running economy (VO2 assessed during steady-state submaximal exercise), (b) respiratory capacities or efficiency of the skeletal muscle (biopsy), and (c) diffusing capacity of the lung. This study, showing similar physiological responses and performance improvements in the two groups following intervention, suggests that in young cross-country skiers, improvements in sea-level aerobic performance associated with LHTL may not be due to moderate-altitude acclimatization.

Effect of alterations in blood volume with bed rest on glucose tolerance.

Bed rest leads to rapid impairments in glucose tolerance. Plasma volume and thus dilution space for glucose are also reduced with bed rest, but the potential influence on glucose tolerance has not been investigated. Accordingly, the aim was to investigate whether bed rest-induced impairments in glucose tolerance are related to a concomitant reduction in plasma volume. This hypothesis was tested mechanistically by restoring plasma volume with albumin infusion after bed rest and parallel determination of glucose tolerance. Fifteen healthy volunteers (age 24 ± 3 yr, body mass index 23 ± 2 kg/m2, maximal oxygen uptake 44 ± 8 ml·min-1·kg-1; means ± SD) completed 4 days of strict bed rest. Glucose tolerance [oral glucose tolerance test (OGTT)] and plasma and blood volumes (carbon monoxide rebreathing) were assessed before and after 3 days of bed rest. On the fourth day of bed rest, plasma volume was restored by means of an albumin infusion prior to an OGTT. Plasma volume was reduced by 9.9 ± 3.0% on bed rest day 3 and area under the curve for OGTT was augmented by 55 ± 67%. However, no association (R2 = 0.09, P = 0.33) between these simultaneously occurring responses was found. While normalization of plasma volume by matched albumin administration (408 ± 104 ml) transiently decreased (P < 0.05) resting plasma glucose concentration (5.0 ± 0.4 to 4.8 ± 0.3 mmol/l), this did not restore glucose tolerance. Bed rest-induced alterations in dilution space may influence resting glucose values but do not affect area under the curve for OGTT.

Restoring heat stress-associated reduction in middle cerebral artery velocity does not reduce fatigue in the heat.

Heat-induced hyperventilation may reduce PaCO2 and thereby cerebral perfusion and oxygenation and in turn exercise performance. To test this hypothesis, eight volunteers completed three incremental exercise tests to exhaustion: (a) 18 °C ambient temperature (CON); (b) 38 °C (HEAT); and (c) 38 °C with addition of CO2 to inspiration to prevent the hyperventilation-induced reduction in PaCO2 (HEAT + CO2 ). In HEAT and HEAT + CO2 , rectal temperature was elevated prior to the exercise tests by means of hot water submersion and was higher (P < 0.05) than in CON. Compared with CON, ventilation was elevated (P < 0.01), and hence, PaCO2 reduced in HEAT. This caused a reduction (P < 0.05) in mean cerebral artery velocity (MCAvmean ) from 68.6 ± 15.5 to 53.9 ± 10.0 cm/s, which was completely restored in HEAT + CO2 (68.8 ± 5.8 cm/s). Cerebral oxygenation followed a similar pattern. V ˙ O 2   m a x was 4.6 ± 0.1 L/min in CON and decreased (P < 0.05) to 4.1 ± 0.2 L/min in HEAT and remained reduced in HEAT + CO2 (4.1 ± 0.2 L/min). Despite normalization of MCAvmean and cerebral oxygenation in HEAT + CO2 , this did not improve exercise performance, and thus, the reduced MCAvmean in HEAT does not seem to limit exercise performance.

Hemoglobin mass and intravascular volume kinetics during and after exposure to 3,454-m altitude.

High altitude (HA) exposure facilitates a rapid contraction of plasma volume (PV) and a slower occurring expansion of hemoglobin mass (Hbmass). The kinetics of the Hbmass expansion has never been examined by multiple repeated measurements, and this was our primary study aim. The second aim was to investigate the mechanisms mediating the PV contraction. Nine healthy, normally trained sea-level (SL) residents (8 males, 1 female) sojourned for 28 days at 3,454 m. Hbmass was measured and PV was estimated by carbon monoxide rebreathing at SL, on every 4th day at HA, and 1 and 2 wk upon return to SL. Four weeks at HA increased Hbmass by 5.26% (range 2.5-11.1%; P < 0.001). The individual Hbmass increases commenced with up to 12 days of delay and reached a maximal rate of 4.04 ± 1.02 g/day after 14.9 ± 5.2 days. The probability for Hbmass to plateau increased steeply after 20-24 days. Upon return to SL Hbmass decayed by -2.46 ± 2.3 g/day, reaching values similar to baseline after 2 wk. PV, aldosterone concentration, and renin activity were reduced at HA (P < 0.001) while the total circulating protein mass remained unaffected. In summary, the Hbmass response to HA exposure followed a sigmoidal pattern with a delayed onset and a plateau after ∼3 wk. The decay rate of Hbmass upon descent to SL did not indicate major changes in the rate of erythrolysis. Moreover, our data support that PV contraction at HA is regulated by the renin-angiotensin-aldosterone axis and not by changes in oncotic pressure.

OS011. Management of late preterm pregnancy complicated by mildpreeclampsia: A prospective randomized trial.

INTRODUCTION: In the absence of properly undertaken prospective randomized clinical trials, the optimal management of late preterm mild preeclampsia for best maternal and perinatal outcomes remains unclear for obstetricians worldwide. OBJECTIVES: We desired to determine if immediate or expectant management of the late preterm mother presenting with mild preeclampsia was more beneficial to her without compromise to her newborn. METHODS: This prospective randomized clinical trial of immediate versus expectant delivery for patients presenting with mild preeclampsia between the late preterm period of 34-0/7 to 36-6/7weeks gestation was undertaken using CONSORT guidelines. Patients were randomized to immediate delivery via induction of labor or cesarean delivery or inpatient expectant management with delivery at 37-0/7weeks gestation or earlier at onset of labor or progression to severe preeclampsia. The primary outcome was progression to severe preeclampsia; secondary outcomes were neonatal morbidity and mortality. Data were analyzed by appropriate tests for continuous or categorical outcomes with differences considered significant if p<0.05. RESULTS: One hundred and sixty nine patients during 2002-2008 satisfied and sustained protocol criteria in the immediate delivery (n=94) or inpatient expectant management (n=75) arms of the study. A third (33%) of expectantly managed patients developed severe preeclampsia during significantly longer hospitalization versus 3% in the immediately delivered patients (p=0.001). Cesarean delivery rates were similar. No significant neonatal morbidity differences were observed between groups; there were no maternal or neonatal deaths. The study was stopped in 2008 at 74% of the enrollment target when hospital policy changed to discourage inpatient hospitalization for uncomplicated mild preterm preeclampsia and in view of growing national concern for increased late preterm/early term neonatal morbidity and cost of care. CONCLUSION: Proceeding to delivery of the late preterm (⩾34weeks gestation) patient with mild preeclampsia lessens maternal risk without significantly increasing neonatal risk.

Antepartum eclampsia <34 weeks case series: advisable to postpone delivery to administer corticosteroids for fetal pulmonary benefit?

OBJECTIVE: To determine if postponement of delivery to administer fetal lung maturation corticosteroids (PDACs) in mothers with antepartum eclampsia <34 weeks gestation benefits the fetus without compromising the mother. STUDY DESIGN: A case series of 37 maternal-perinatal pairs over a 9-year period with antepartum eclampsia between 24 and 34 weeks gestation from a single tertiary center were reviewed retrospectively. Duration of PDAC, clinical course and maternal-fetal outcomes, including impact of duration of PDAC on neonatal pulmonary function, were recorded for each case. Group assignment was based on length of corticosteroid treatment course before delivery: Group A, 0 to ≤ 24 h, n=28; B, 24 to <48 h, n=5; C, ≥ 48 h, n=4. Data were collected and analyzed by one-way analysis of variance (ANOVA), ANOVA on ranks, χ(2)-test and Fisher's exact tests where appropriate; statistical significance was determined by a P-value <0.05. RESULT: Overall, 37 of 68 eclampsia patients in 1999 to 2007 met inclusion criteria. No adverse maternal or fetal event occurred while delivery was postponed. Immediate neonatal intubation or continuous positive airway pressure was required for 23/28 in A, 4/5 in B and 2/4 in C; room air was sufficient at birth for 5/28 in A, 1/5 in B and 2/4 in C. No newborn >33 weeks gestation required INI. Prolonged (that is, >1 day) mechanical ventilation was not required for any infant with a gestational age ≥ 32 weeks or PDAC ≥ 48 h. Two of three neonatal deaths in group A were attributed to pulmonary insufficiency. CONCLUSION: PDAC for antepartum preterm eclampsia, especially ≤ 32 weeks gestation, appears to offer notable fetal pulmonary benefit without significantly increasing maternal or fetal risk.

The LD label for relatively well-functioning students: a critical analysis.

The number of students identified since the mid-1970s as having learning disabilities has produced a corresponding increase in the population of such individuals in postsecondary programs. The Americans with Disabilities Act, along with Section 504 of the Vocational Rehabilitation Act of 1973, provide the basis for civil rights for students in higher education. These laws protect individuals who have a substantial limitation in a major life activity when compared with the general population. A disparity between the legal definition and the clinical definition of learning disabilities, which can encompass those identified on the basis of academic underachievement relative to intellectual potential, has stimulated debate about the fairest, most appropriate standard for declaring a student functionally impaired. Extending services to individuals without significant academic impairment may tax or even deplete scarce resources for others in greater needs, distort the normal processes by which individuals select careers, and diminish the credibility of the diagnosis itself.