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Effect of gender on the development of hypocapnic apnea/hypopnea during NREM sleep.

We hypothesized that a decreased susceptibility to the development of hypocapnic central apnea during non-rapid eye movement (NREM) sleep in women compared with men could be an explanation for the gender difference in the sleep apnea/hypopnea syndrome. We studied eight men (age 25-35 yr) and eight women in the midluteal phase of the menstrual cycle (age 21-43 yr); we repeated studies in six women during the midfollicular phase. Hypocapnia was induced via nasal mechanical ventilation for 3 min, with respiratory frequency matched to eupneic frequency. Tidal volume (VT) was increased between 110 and 200% of eupneic control. Cessation of mechanical ventilation resulted in hypocapnic central apnea or hypopnea, depending on the magnitude of hypocapnia. Nadir minute ventilation in the recovery period was plotted against the change in end-tidal PCO(2) (PET(CO(2))) per trial; minute ventilation was given a value of 0 during central apnea. The apneic threshold was defined as the x-intercept of the linear regression line. In women, induction of a central apnea required an increase in VT to 155 +/- 29% (mean +/- SD) and a reduction of PET(CO(2)) by -4.72 +/- 0.57 Torr. In men, induction of a central apnea required an increase in VT to 142 +/- 13% and a reduction of PET(CO(2)) by -3.54 +/- 0.31 Torr (P = 0.002). There was no difference in the apneic threshold between the follicular and the luteal phase in women. Premenopausal women are less susceptible to hypocapnic disfacilitation during NREM sleep than men. This effect was not explained by progesterone. Preservation of ventilatory motor output during hypocapnia may explain the gender difference in sleep apnea.

Adult↗

Effects of gender on neuroendocrine and metabolic counterregulatory responses to exercise in normal man.

Significant, sexual dimorphisms exist in counterregulatory responses to commonly occurring stresses, such as hypoglycemia, fasting, and cognitive testing. The question of whether counterregulatory responses differ during exercise in healthy men and women remains controversial. The aim of this study was to determine whether a sexual dimorphism exists in neuroendocrine, metabolic, or cardiovascular responses to prolonged moderate exercise. Sixteen healthy (eight men and eight women) subjects matched for age (28+/-2 yr), body mass index (22+/-1 kg/m2), nutrient intake, and spectrum of physical fitness were studied in a randomized fashion during 90 min of exercise on a cycle ergometer at 80% of their anaerobic threshold (approximately 50% VO2 max). Respiratory quotient and oxygen consumption relative to body weight were identical in men and women. Glycemia was equated (5.3+/-0.2 mmol/L) during exercise via an exogenous glucose infusion. Gender had significant effects on counterregulatory responses during exercise. Arterialized epinephrine (1.05+/-0.2 vs. 0.45+/-0.04 nmol/L), norepinephrine (9.2+/-1.1 vs. 5.8+/-1.1 nmol/L), and pancreatic polypeptide (52+/-6 vs. 37+/-6 pmol/L) were significantly (P<0.01) increased in men compared to women, respectively. Plasma glucagon, cortisol, and GH levels responded similarly in men and women. Insulin values were higher at baseline in men and fell by a greater amount to reach similar levels during exercise compared to those in women. Endogenous glucose production, measured with [3-3H]glucose was similar in men and women. Carbohydrate oxidation was significantly increased in men relative to women (21.2+/-2 vs. 15.6+/-2 mg/kg fat free mass x min; P<0.05). Despite reduced sympathetic nervous system (SNS) drive, lipolytic responses were increased in women. Arterialized blood glycerol (215+/-30 vs. 140+/-20 micromol/L), beta-hydroxybutyrate (54+/-9 vs. 25+/-10 micromol/L), and plasma nonesterified fatty acids (720+/-56 vs. 469+/-103 micromol/L) were significantly (P<0.01) increased in women. In keeping with increased SNS activity, systolic blood pressure and mean arterial pressure were significantly increased (P<0.01) in men. In summary, this study demonstrates that a significant sexual dimorphism exists in neuroendocrine, metabolic, and cardiovascular counterregulatory responses to prolonged moderate exercise in man. We conclude that during exercise, men have increased autonomic nervous system (epinephrine, norepinephrine, pancreatic polypeptide), cardiovascular (systolic, mean arterial pressure) and certain metabolic (carbohydrate oxidation) counterregulatory responses, but that women have increased lipolytic (glycerol, nonesterified fatty acids) and ketogenic (beta-hydroxybutyrate) responses. Women may compensate for diminished SNS activity during exercise by increased lipolytic responses.

Adult↗

Warm-up prior to undertaking a dynamic psychomotor task: does it aid performance?

AIM: The purpose of this study was to examine the effect of differing types of warm-up on the performance of a psychomotor skill that required quick reaction and movement times (MTs), and whole-body co-ordination. METHODS: Subjects (n=12) carried out a psychomotor task which involved reacting to 1 of 3 lights, then running through a slalom course before kicking a mini-soccer ball at a target. The task was completed following rest, a physical warm-up, a skill-specific warm-up and a skill plus physical warm-up. In the physical, and skill plus physical warm-ups the subjects cycled on an ergometer at a workload calculated to induce exercise at their lactate threshold. The outcome dependent variables were time to initiate a movement (reaction time), time to complete the slalom run (MT) and two measures of passing accuracy(constant error and variable error. Biomechanical variables(knee, hip and ankle angles, and horizontal and vertical ankle velocities at contact(were also compared. RESULTS: A repeated measures analysis of variance showed no significant effect of warm-up type on any of the dependent variables. Stepwise multiple regression analyses showed that changes in heart rate from resting values to those before performance of the skill test (D HR pre-performance) and those after performance of the test (D HR post-performance) combined were significant predictors of MT (R(2)=0.31, P<0.001), while D HR post-performance significantly predicted reaction time (R(2)=0.12, P<0.02). CONCLUSIONS: It was concluded that warm-up provided no significant benefit in performance for a task that was dynamic in nature but that physical arousal probably aids reaction and MTs.

Adult↗

The effects of prelatent/latent iron deficiency on physical work capacity.

In order to examine the effects of mild iron deficiency on physical work capacity, 40 prelatent iron-deficient female endurance runners were studied before and after 8 wk of supplementation with either oral iron (320 mg ferrous sulfate) or a matching placebo. Subjects underwent the following physical work capacity tests: the Wingate cycle ergometer test, the anaerobic speed test, the ventilatory threshold, VO2max, and maximal treadmill velocity during the VO2max test. Muscle biopsy samples pre- and post-treatment were obtained from 17 of the subjects, and these were assayed for citrate synthase and cytoplasmic alpha-glycerophosphate dehydrogenase activity. Subjects were randomly assigned to one of the treatment groups, and a double-blind method of administration of the supplements was used. The differences in improvement scores between the two groups on the work capacity and enzyme activity variables were statistically nonsignificant (P greater than 0.05). Serum ferritin values rose from a mean of 12.4 +/- 4.5 to 37.7 +/- 19.7 ng.ml-1 for the experimental group and from 12.2 +/- 4.3 to 17.2 +/- 8.9 ng.ml-1 for the controls (P = 0.0025), whereas hemoglobin levels remained fairly constant for both groups (P = 0.6). Eight weeks of iron supplementation to prelatent/latent iron-deficient, physically active females did not significantly enhance work capacity. Within the limitations of this study, the presence of a serum ferritin below 20 ng.ml-1 does not pose a significant handicap to physical work capacity.

Adolescent↗

Effect of the menstrual cycle on standard achromatic and blue-on-yellow visual field analysis of women with migraine.

BACKGROUND: It has been postulated that migraine and glaucoma may have common vascular causative factors. Significant sex-based differences in the incidence of many important ocular conditions raise the possibility that estrogens may have direct effects on the eye. We performed a study to determine the effect of the menstrual cycle on standard achromatic automated perimetry (SAP) and short-wavelength automated perimetry (SWAP) (blue-on-yellow perimetry) of women with migraine. METHODS: Both eyes of 73 normally menstruating women (31 subjects with migraine and 42 healthy control subjects) were included in the study. Subjects underwent a complete ocular examination including SAP and SWAP in both the follicular phase (12th to 13th day of the cycle) and the luteal phase (1 to 2 days before the onset of bleeding) of two consecutive menstrual cycles.We performed visual field analysis using the Humphrey Field Analyzer II with the full-threshold central 30-2 program. Mean sensitivity was calculated for the superior temporal, inferior temporal, superior nasal and inferior nasal regions separately. RESULTS: Thirteen subjects were lost to follow-up (5 in the migraine group and 8 in the control group), leaving 26 subjects and 34 subjects respectively. There was no significant difference in mean age between the two groups (33.9 years [standard deviation (SD) 3.4 years] vs. 35.1 years [SD 3.3 years]). The mean duration of migraine was 7.6 (SD 3.1) years (range 3-14 years). In both groups, serum estradiol levels were significantly lower (p = 0.001) and serum progesterone levels were significantly higher (p < 0.001) in the luteal phase than in the follicular phase. In the control group, the mean sensitivity values with SWAP were significantly lower in the luteal phase than in the follicular phase (p = 0.04). A similar decrease was observed for the subjects with migraine with both SAP and SWAP (p = 0.01). There was no difference in regional mean sensitivity between the two phases with either perimetric test in the control group. For the subjects with migraine, there was no difference in regional mean sensitivity between the two phases with SAP. However, with SWAP, the mean sensitivity for the nasal visual field locations was significantly lower in the luteal phase than in the follicular phase (p = 0.01). INTERPRETATION: Our study provides further evidence of an effect of sex hormones on the visual field of women with migraine. In addition to assessment of intraocular pressure, menstrual cycle phases should be considered in women with migraine at risk for glaucomatous optic neuropathy.

Adult↗

Modification of the recovery-cycle of human median nerve by ischemia.

Variations in excitability have been shown to follow single activation of sensory and motor axons in human peripheral nerve, with a sequence of refractoriness, supernormal and subnormal excitability ("recovery cycle"). Modifications of the recovery cycle of nerve excitability by ischemia have been investigated in the present study in sensory fibers of human median nerve. During ischemia, there is an initial fall in the nerve threshold to a brief electric pulse, followed by a progressive rise in threshold until the nerve becomes inexcitable. These ischemia-induced threshold changes interact with the impulse-induced variations in nerve excitability during the recovery period, leading to a characteristic alteration of the recovery cycle with a progressive reduction of the magnitude and duration of the supernormal period. Conduction velocity becomes progressively reduced, probably because of a slowed conduction of the action potential in the fastest conducting fibres, due to ischemic depolarization of the resting membrane potential. In the postischemic phase the magnitude and duration of supernormality are increased, probably because of the hyperpolarization of the resting membrane potential in this condition. Conduction velocity only returns to normal values after 12-25 min.

Action Potentials↗

A modelling study of locomotion-induced hyperpolarization of voltage threshold in cat lumbar motoneurones.

During fictive locomotion the excitability of adult cat lumbar motoneurones is increased by a reduction (a mean hyperpolarization of approximately 6.0 mV) of voltage threshold (Vth) for action potential (AP) initiation that is accompanied by only small changes in AP height and width. Further examination of the experimental data in the present study confirms that Vth lowering is present to a similar degree in both the hyperpolarized and depolarized portions of the locomotor step cycle. This indicates that Vth reduction is a modulation of motoneurone membrane currents throughout the locomotor state rather than being related to the phasic synaptic input within the locomotor cycle. Potential ionic mechanisms of this locomotor-state-dependent increase in excitability were examined using three five-compartment models of the motoneurone innervating slow, fast fatigue resistant and fast fatigable muscle fibres. Passive and active membrane conductances were set to produce input resistance, rheobase, afterhyperpolarization (AHP) and membrane time constant values similar to those measured in adult cat motoneurones in non-locomoting conditions. The parameters of 10 membrane conductances were then individually altered in an attempt to replicate the hyperpolarization of Vth that occurs in decerebrate cats during fictive locomotion. The goal was to find conductance changes that could produce a greater than 3 mV hyperpolarization of Vth with only small changes in AP height (< 3 mV) and width (< 1.2 ms). Vth reduction without large changes in AP shape could be produced either by increasing fast sodium current or by reducing delayed rectifier potassium current. The most effective Vth reductions were achieved by either increasing the conductance of fast sodium channels or by hyperpolarizing the voltage dependency of their activation. These changes were particularly effective when localized to the initial segment. Reducing the conductance of delayed rectifier channels or depolarizing their activation produced similar but smaller changes in Vth. Changes in current underlying the AHP, the persistent Na(+) current, three Ca(2+) currents, the "h" mixed cation current, the "A" potassium current and the leak current were either ineffective in reducing Vth or also produced gross changes in the AP. It is suggested that the increased excitability of motoneurones during locomotion could be readily accomplished by hyperpolarizing the voltage dependency of fast sodium channels in the axon hillock by a hitherto unknown neuromodulatory action.

Animals↗

Progressive accumulation of mitochondrial DNA mutations and decline in mitochondrial function lead to beta-cell failure.

A key adaptation enabling the fetus to survive in a limited energy environment may be the reprogramming of mitochondrial function, which can have deleterious effects. Critical questions are whether mitochondrial dysfunction progressively declines after birth, and if so, what mechanism might underlie this process. To address this, we developed a model of intrauterine growth retardation (IUGR) in the rat that leads to diabetes in adulthood. Reactive oxygen species (ROS) production and oxidative stress gradually increased in IUGR islets. ATP production was impaired and continued to deteriorate with age. The activities of complex I and III of the electron transport chain progressively declined in IUGR islets. Mitochondrial DNA point mutations accumulated with age and were associated with decreased mitochondrial DNA content and reduced expression of mitochondria-encoded genes in IUGR islets. Mitochondrial dysfunction resulted in impaired insulin secretion. These results demonstrate that IUGR induces mitochondrial dysfunction in the fetal beta-cell, leading to increased production of ROS, which in turn damage mitochondrial DNA. A self-reinforcing cycle of progressive deterioration in mitochondrial function leads to a corresponding decline in beta-cell function. Finally, a threshold in mitochondrial dysfunction and ROS production is reached, and diabetes ensues.

Adenosine Triphosphate↗

Experimentally induced pain perception is acutely reduced by aerobic exercise in people with chronic low back pain.

This study examined whether subjects with chronic low back pain demonstrate exercise-induced analgesia to experimentally induced pressure pain. We employed a repeated measures design to study eight subjects with chronic low back pain (mean +/- standard deviation age = 40 +/- 10, duration of pain = 7 +/- 4 years). Pain ratings were measured immediately before and 2 minutes and 32 minutes after 25 minutes of cycle ergometry (5 minutes at 50% peak oxygen uptake, then 20 minutes at 70% peak oxygen uptake). We based the pain ratings on subject input on a visual analog scale at 10-second intervals during the 2-minute pressure pain stimulus to the nondominant index finger. Compared with preexercise values, pain ratings were significantly (p < 0.05) decreased after exercise at both 2 and 32 minutes postexercise. We conclude that pressure pain perception can be reduced for more than 30 minutes following aerobic exercise from leg cycling among people with chronic low back pain.

Adult↗

The effect of endurance training on the ventilatory response to exercise in elite cyclists.

The purpose of this study was to investigate the effects of endurance training on the ventilatory response to acute incremental exercise in elite cyclists. Fifteen male elite cyclists [mean (SD) age 24.3 (3.3) years, height 179 (6) cm, body mass 71.1 (7.6) kg, maximal oxygen consumption (VO2max) 69 (7) ml x min(-1) x kg(-1)] underwent two exercise tests on a cycle ergometer. The first test was assessed in December, 6 weeks before the beginning of the cycling season. The second test was performed in June, in the middle of the season. During this period the subjects were expected to be in a highly endurance-trained state. The ventilatory response was assessed during an incremental exercise test (20 W x min(-1)). Oxygen consumption (VO2), carbon dioxide production (VCO2), minute ventilation (VE), and heart rate (HR) were assessed at the following points during the test: at workloads of 200 W, 250 W, 300 W, 350 W, 400 W and at the subject's maximal workload, at a respiratory exchange ratio (R) of 1, and at the ventilatory threshold (Th(vent)) determined using the V-slope-method. Post-training, the mean (SD) VO2max was increased from the pre-training level of 69 (7) ml x min(-1) x kg(-1) (range 61.4-78.6) to 78 (6) ml x min(-1) x kg(-1) (range 70.5-86.3). The mean post-training VO2 was significantly higher than the pre training value (P < 0.01) at all work rates, at Th(vent) and at R = 1. VO2 was also higher at all work rates except for 200 W and 250 W. VE was significantly higher at Th(vent) and R = 1. Training had no effect on HR at all workloads examined. An explanation for the higher VO2 cost for the same work rate may be that in the endurance-trained state, the adaptation to an exercise stimulus with higher intensity is faster than for the less-trained state. Another explanation may be that at the same work rate, in the less-endurance-trained state power is generated using a significantly higher anaerobic input. The results of this study suggest the following practical recommendations for training management in elite cyclists: (1) the VO2 for a subject at the same work rate may be an indicator of the endurance-trained state (i.e., the higher the VO2, the higher the endurance-trained capacity), and (2) the need for multiple exercise tests for determining the HR at Th(vent) during a cycling season is doubtful since at Th(vent) this parameter does not differ much following endurance training.

Adult↗

Plasma cyclic AMP and blood lactate responses to incremental cycling in untrained male subjects.

Recently, it has been suggested that epinephrine influences blood lactate and the lactate threshold during incremental exercise through a beta-adrenergic adenylate cyclase dependent mechanism. We sought to characterize the relationship between the changes in the beta-adrenergic adenylate cyclase system and blood lactate during incremental exercise indirectly through the measurement of plasma cAMP. The relationships of plasma cAMP to blood lactate levels and the lactate threshold were examined in nine untrained male subjects. Each subject performed an incremental exercise test to volitional exhaustion on an electronically-braked cycle ergometer. Although plasma cAMP was rising at the lactate threshold, it did not demonstrate the classic threshold response usually seen in blood lactate. Pairwise matched t-tests were used as a post-hoc test to determine if the successive changes in blood lactate and plasma cAMP between 21.4, 38.6, 58.7, 81.2 and 100% of VO2max were significant. Plasma cAMP was rising between 38.6% and 58.7% and between 58.7% and 81.2% of VO2max, but these changes in plasma cAMP did not reach statistical significance (p > 0.0125) with Bonferoni adjustment. The change in plasma cAMP compared to its previous value as well as the change in plasma cAMP above the resting value was not statistically significant until 81.2% of VO2max. A moderate but significant correlation was observed between blood lactate and plasma cAMP levels (r = 0.612) using blood samples obtained at each workstage in all subjects. The mean correlation between blood lactate and plasma cAMP was 0.75 (S.E. = 0.05) and ranged between 0.58 and 0.97 in individual subjects.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

Effects of prior exercise and recovery duration on oxygen uptake kinetics during heavy exercise in humans.

Prior heavy exercise (above the lactate threshold, LT) reduces the amplitude of the pulmonary oxygen uptake (VO2) slow component during heavy exercise, yet the precise effect of prior heavy exercise on the phase II VO2 response remains to be established. This study was designed to test the hypotheses that (1) prior heavy exercise increases the amplitude of the phase II VO2 response independently of changes in the baseline VO2 value and (2) the effect of prior exercise depends on the amount of external work done during prior exercise, irrespective of the intensity of the prior exercise. Nine subjects performed two 6 min bouts of heavy cycling exercise separated by 6 min baseline pedalling recovery (A), two 6 min heavy exercise bouts separated by 12 min recovery (6 min rest and 6 min baseline pedalling, B), and a bout of moderate exercise (below the LT) in which the same amount of external work was performed as during the prior heavy exercise, followed by 6 min heavy exercise (C). In both tests A and B, prior heavy exercise significantly increased the absolute VO2 amplitude at the end of phase II (by approximately 150 ml x min(-1)), and reduced the amplitude of the VO2 slow component by a similar amount. Following 12 min of recovery (B), baseline VO2, but not blood [lactate], had returned to pre-exercise levels, indicating that these effects occurred independently of changes in baseline VO2. Prior moderate exercise (C) had no effect on either the VO2 or blood [lactate] responses to subsequent heavy exercise. The VO2 response to heavy exercise was therefore dependent on the intensity of prior exercise, and the effects on the amplitudes of the phase II and slow VO2 components persisted for at least 12 min following prior heavy exercise.

Adult↗

Muscle metabolism during heavy-intensity exercise after acute acetazolamide administration.

Carbonic anhydrase (CA) inhibition is associated with a lower plasma lactate concentration ([La(-)](pl)), but the mechanism for this association is not known. The effect of CA inhibition on muscle high-energy phosphates [ATP and phosphocreatine (PCr)], lactate ([La(-)](m)), and glycogen was examined in seven men [28 +/- 3 (SE) yr] during cycling exercise under control (Con) and acute CA inhibition with acetazolamide (Acz; 10 mg/kg body wt iv). Subjects performed 6-min step transitions in work rate from 0 W to a work rate corresponding to approximately 50% of the difference between the O(2) uptake at the ventilatory threshold and peak O(2) uptake. Muscle biopsies were taken from the vastus lateralis at rest, at 30 min postinfusion, at end exercise (EE), and at 5 and 30 min postexercise. Arterialized venous blood was sampled from a dorsal hand vein and analyzed for [La(-)](pl). ATP was unchanged from rest values; no difference between Con and Acz was observed. The fall in PCr from rest [72 +/- 3 and 73 +/- 3.6 (SE) mmol/kg dry wt for Con and Acz, respectively] to EE (51 +/- 4 and 46 +/- 5 mmol/kg dry wt for Con and Acz, respectively) was similar in Con and Acz. At EE, glycogen (mmol glucosyl units/kg dry wt) decreased to similar values in Con and Acz (307 +/- 16 and 300 +/- 19, respectively). At EE, no difference was observed in [La(-)](m) between conditions (46 +/- 6 and 43 +/- 5 mmol/kg dry wt for Con and Acz, respectively). EE [La(-)](pl) was higher during Con than during Acz (11.4 +/- 1.0 vs. 8.2 +/- 0.6 mmol/l). The similar [La(-)](m) but lower [La(-)](pl) suggests that the uptake of La(-) by other tissues is enhanced after CA inhibition.

Acetazolamide↗

Silent period induced by cutaneous stimulation.

An electrical stimulus applied to a cutaneous nerve during isometric muscle contraction causes a suppression of EMG activity (silent period) followed by a rebound. The extent of inhibition is related to the stimulus intensity as the silent period is more evident when stimulation is perceived as painful. The silent period is present in different limb and cranial muscles after stimulation of the same cutaneous nerve and in the same muscle after stimulation of distant cutaneous nerves. It also occurs synchronously in antagonist muscles. Within the silent period induced after cutaneous stimulation the maximal inhibition on the opponens pollicis motor neuron pool, as tested by the motor response evoked after transcranial cortical stimulation, occurs between 50 and 70 msec. Using the double stimulus technique to study the recovery cycle, the silent period is present at interstimulus intervals as low as 100 msec, and does not habituate with trains of stimuli at frequencies up to 5 Hz. Our results suggest that motor neuron inhibition from nociceptive stimulation may be mediated by Renshaw cells directly activated by high threshold cutaneous afferents.

Adolescent↗

A proposed test for determining physical working capacity at the oxygen consumption threshold (PWCVO2).

The purpose of this study was 3-fold: (a) to determine if the mathematical model used to estimate the electromyographic fatigue threshold (EMGFT) and physical working capacity at the heart rate threshold (PWCHRT) could be applied to VO2 measurements, (b) to propose a new fatigue threshold called the physical working capacity at the oxygen consumption threshold (PWCVO2), and (c) to compare the power output at the PWCVO2 to those of the EMGFT, PWCHRT, and ventilatory threshold (VT). Fifteen adult volunteers (mean age +/- SD = 22 +/- 2 years) performed a maximal cycle ergometer test to determine VO2peak and VT as well as 4 8-minute submaximal work bouts for the determination of PWCHRT, EMGFT, and PWCVO2. A 1-way repeated measures analysis of variance (ANOVA) with Tukey post hoc comparison indicated that PWCHRT (84 +/- 36) was significantly (p < 0.05) less than EMGFT (126 +/- 51), but there were no differences for PWCVO2 (111 +/- 44) and VT (111 +/- 60) versus PWCHRT or EMGFT. The results of this study indicated that (a) the mathematical model used to determine the PWCHRT and EMGFT was applicable to the measurement of VO2 and could be used to estimate the PWCVO2 during cycle ergometry, (b) there was a difference in the mean power outputs that corresponded to the fatigue thresholds determined from EMG and heart rate measurements, and (c) the PWCVO2 test may provide a useful submaximal technique for estimating the VT.

Adult↗

Resumption of pituitary and ovarian activity post-partum: endocrine and ultrasonic observations in bromocriptine-treated women.

The resumption of pituitary and ovarian activity was investigated by hormonal measurements and ultrasound scanning in 45 healthy post-partum women who were treated with bromocriptine. Bromocriptine, 50 mg (Parlodel LAR) was administered within 24 h post-partum. Plasma luteinizing hormone, follicle stimulating hormone, oestradiol, progesterone and prolactin concentrations were measured repeatedly and correlated with ultrasound measurements. Forty-one of the 45 women completed the study. A prompt fall in prolactin levels to normal (non-pregnant) values was observed within 24 h post-partum. Hereafter, a rapid return of the normal menstrual cycle was observed. Endocrine evidence of ovulation was obtained in 19/41 women within 1 month post-partum. Ultrasound measurements started at day 10 and were repeated regularly in 40 women. Ultrasound evidence of ovulation was found in 25/40 women. Ultrasound findings appeared not to correspond with the hormonal measurements. It is concluded that the resumption of pituitary and ovarian secretory functions post-partum is not always paralleled by a concomitant recovery of normal follicular growth and ovulation. Application of a progesterone threshold to judge resumption of ovulation post-partum should be reconsidered.

Adolescent↗

Spontaneous electrical and contractile activity correlated to 86Rb+ efflux in smooth muscle of guinea-pig mesotubarium.

1. The spontaneous mechanical activity of guinea-pig mesotubarium consists of fused tetanic contractions lasting about 6 min, with a frequency of about four per hour. The muscle is completely relaxed between the contractions. Stretching the relaxed muscle elicits a contraction of the same appearance as the spontaneous ones. Comparison of preparations from oestrus (day 1 of the hormonal cycle), dioestrus (days 9-11) and prooestrus (days 14-15) showed no variation in the pattern of mechanical activity. 2. The resting membrane potential, measured by intracellular microelectrodes, did not differ with hormonal phase (prooestrus: -63.5 +/- 0.84 (n = 16); oestrus: -63.7 +/- 1.6 (n = 5); dioestrus: -61.6 +/- 0.77 (n = 17]. In most recordings a depolarization of a few millivolts occurred during the relaxation period (5-10 min), but in a few cells a more pronounced spontaneous depolarization of 10-15 mV was found. Ouabain (1 microM) caused depolarization by about 9 mV, both in pro- and dioestrus, leading to the initiation of maintained repetitive spiking. 3. Contraction is preceded by a depolarization lasting 10-30 s, and when a threshold is reached a train of slow waves and spikes is elicited. The frequency of slow waves and the number of spikes on each slow wave progressively decrease during the contraction, until spiking eventually ceases. 4. The spikes are resistant to tetrodotoxin (0.5 microM) and disappear in Ca2+-free medium, which also causes membrane depolarization. The duration of contractions increased with Ca2+ concentration in the range 1-5 mM. 5. The rate of 86Rb+ efflux, expressed as fractional release in 2 min intervals, showed a consistent variation during the contractile cycle in preparations with regular spontaneous activity. Relative to the value at the end of the relaxed period the efflux rate increased by about twofold during the contraction. From the beginning of the relaxed period after the contraction the efflux rate decreased by about 25% until the beginning of the next contraction. 6. It is concluded that the contractile activity in the mesotubarium, as opposed to that of the fallopian tube (Lydrup & Hellstrand, 1986a), is independent of the hormonal phase, including the period around ovulation. The mechanism for initiation of the trains of action potentials associated with spontaneous contractions may involve a gradual decrease of permeability of K+ channels or activity of the Na+-K+ pump during the relaxed period.

Action Potentials↗

Magnesium prophylaxis of menstrual migraine: effects on intracellular magnesium.

The effects of oral Magnesium (Mg) pyrrolidone carboxylic acid were evaluated in 20 patients affected by menstrual migraine, in a double-blind, placebo controlled study. After a two cycles run-in period, the treatment (360 mg/day of Mg or placebo) started on the 15th day of the cycle and continued till the next menses, for two months. Oral Mg was then supplemented in an open design for the next two months. At the 2nd month, the Pain Total Index was decreased by both Placebo and Mg, with patients receiving active drug showing the lowest values (P less than 0.03). The number of days with headache was reduced only in the patients on active drug. Mg treatment also improved premenstrual complaints, as demonstrated by the significant reduction of Menstrual Distress Questionnaire (MDQ) scores. The reduction of PTI and MDQ scores was observed also at the 4th month of treatment, when Mg was supplemented in all the patients. Intracellular Mg++ levels in patients with menstrual migraine were reduced compared to controls. During oral Mg treatment, the Mg++ content of Lymphocytes (LC) and Polymorphonucleated cells (PMN) significantly increased, while no changes in plasma or Red Blood Cells were found. An inverse correlation between PTI and Mg++ content in PMN was demonstrated. These data point to magnesium supplementation as a further means for menstrual migraine prophylaxis, and support the possibility that a lower migraine threshold could be related to magnesium deficiency.

Administration, Oral↗