No abstract

This study addresses the question of variability of immunoreactive human growth hormone (IRHGH) response to the following types of muscular exercise. 1) One hour of submaximal exercise with restarting for 30 min after 20 min of recovery. Three types of responses were observed: a rise of [IRHGH] occurred in response to muscular activity; [IRHGH] was maintained at rest level during the first bout and then rose in the second bout; or [IRHGH] rose during the first bout and was no longer modified by the restarting. 2) Thirty minutes of heavy exercise. In some subjects [IRHGH] change was almost linear with time, reaching very high values and dropping as soon as exercise had stopped, whereas in others peak values were similar to those of submaximal exercise but, in contrast, plateaued during recovery. 3) One hour of exercise performed either continuously or with alternate sequences of 30-s exercise and 30-s pause. In intermittent exercise, some subjects displayed a similar time course of [IRHGH] as in continuous exercise and others displayed markedly high values. 4) One hour of submaximal exercise at three different intensities carried out at ambient temperatures of 24 and 33 degrees C. At 33 degrees C, in some subjects, [IRHGH] time course at the three intensities was unchanged at 33 degrees C compared with that at 24 degrees C, whereas the maximal value increased in another subject up to 150 ng X ml-1. A significant intrasubject consistency to a given type of exercise was evident over several months. The study emphasizes that caution should be used in drawing definite conclusions from averaged results with high variability.

Hand blood flow was measured at rest, with local warming, and with local cooling. Three methods were simultaneously used: water plethysmography (WP), mercury-in-rubber strain gauge plethysmography (SG), and pulsed Döppler flowmetry (D). Of these, water plethysmography is the most sensitive and accurate; strain gauge plethysmography is simpler but less accurate; and pulsed Döppler flowmetry precisely measures instantaneous arterial blood flow without venous occlusion.

Nineteen women (mean +/- SD: 28 +/- 5 years) with small fetuses relative to gestational age (mean +/- SD: 32 +/- 2.2 weeks of gestation) were referred to our unit for cordocentesis for the determination of fetal karyotyping. Four of these 19 patients had small-for-gestational-age ultrasound-derived measurements under the third centile for gestational age. Fetal blood gases were measured in the umbilical vein. Umbilical artery and fetal internal carotid artery Doppler examinations were performed 15 min before cordocentesis. The results showed a progressive and proportional increase in umbilical artery resistance index with hypoxia (p < 0.001), hypercapnia (p < 0.025) and acidosis (p < 0.005). Moreover, the results showed a progressive and proportional decrease in fetal internal carotid artery resistance index with hypoxia (p < 0.01), hypercapnia (p < 0.01) and acidosis (p < 0.025). Fetal blood gases are therefore related to umbilical circulatory function and cerebral vasodilatation, suggesting fetal vascular redistribution.

To investigate the relationship between maternal exercise and fetal circulatory responses in humans during the third trimester of pregnancy, changes in uterine, umbilical and fetal cerebral circulations were measured by pulsed-Doppler ultrasound method in 14 healthy volunteer pregnant women before and just after a moderate non-exhaustive exercise. Maternal heart rate increased significantly reaching 80% of the theoretical maximal heart rate (TMHR) while uterine resistance indices did not change. The fetal heart rate and umbilical mean velocity were unchanged while umbilical resistance index decreased slightly (0.58 +/- 0.06 versus 0.62 +/- 0.07, P < 0.05). The fetal internal carotid artery mean velocity increased (23.2 +/- 5.3 versus 20.4 +/- 4.1 cm/s, P < 0.02) and the cerebral resistance index decreased (0.71 +/- 0.11 versus 0.80 +/- 0.10, P < 0.01). We conclude that submaximal maternal exercise at 80% of TMHR does not significantly alter uterine perfusion but involves a slight fetal cerebral vasodilation which could be due to a moderate fetal hemoglobin desaturation.