Midfollicular Research Articles

Impact of Follicular Menstrual Phase on Body Composition Measures and Resting Metabolism.

This study aimed to identify the effects of early follicular (EF) and midfollicular (MF) menstrual phases on body composition, resting metabolic rate (RMR), and respiratory quotient (RQ) assessment accuracy to identify an optimal testing period. Body composition was obtained from a four-compartment (4C) criterion model (fat mass (FM), fat-free mass, body fat percent, and dual-energy x-ray absorptiometry (DXA; FM, lean mass (LM), trunk FM, and trunk LM) in 19 eumenorrheic females (mean ± SD: age, 21.3 ± 3.1 yr, body mass index, 23.6 ± 1.8 kg·m-2). RMR (kcal·d-1) and RQ (a.u.) were measured via indirect calorimetry for 25 min. Body composition, RMR, and RQ were measured during the EF and MF phases. Dependent-samples t-tests were used to compare outcomes between EF and MF. 4C outcomes were similar between phases (P > 0.05). During EF, the following 4C components were significantly greater (P < 0.05): body volume (mean difference (MD) ± SD, 0.70 ± 1.05 L), extracellular fluid (MD ± SD, 0.27 ± 0.51 L), and body mass (MD ± SD, 0.56 ± 0.80 kg). DXA-measured LM, body fat percent, trunk LM, and trunk FM were similar (P > 0.05); however, DXA FM was significantly greater during EF (MD ± SD, 0.29 ± 0.40 kg; P = 0.005), yet within measurement error of the device. Although RMR was not significantly different between phases (MD ± SD, 6.0 ± 190.93 kcal·d-1; P > 0.05), RQ was significantly higher during EF (mean ± SD, 0.03 ± 0.06 a.u.; P = 0.029) compared with MF. Body composition from 4C and DXA do not seem to be affected beyond measurement error as a result of compartmental changes from the menstrual cycle. During MF, women oxidized more fat as demonstrated by a lower RQ. Researchers should aim to be more inclusive and schedule testing for females within 11-12 d from the onset of menstruation.

Aerobic Exercise Performance is Reduced in the Mid‐luteal Compared to the Mid‐follicular Phase of the Menstrual Cycle in Eumenorrheic Women

PurposeUp to 40% of women believe their menstrual cycle affects their aerobic exercise performance. Fluctuations in sex hormone concentrations heighten many physiological and psychological responses to aerobic exercise in the mid‐luteal (ML) compared to the mid‐follicular (MF) phase of the menstrual cycle, which can promote reductions in aerobic exercise performance in the ML phase. However, the literature is equivocal regarding whether aerobic exercise performance differs between the ML and MF phases. Therefore, we tested the hypothesis that aerobic exercise performance is impaired in the ML compared to the MF phase of the menstrual cycle.MethodsTwelve recreationally active eumenorrheic women (25 ± 6 y) completed three familiarization and two experimental exercise sessions across the span of 3 consecutive menstrual cycles during the MF and ML phases. Saliva samples were collected at the beginning of each test session for analysis of progesterone and estrogen concentration. Each exercise session consisted an 8 km time trial that was preceded by 5 min of constant load exercise at a power output both 10% below (88 ± 19 W) and 10% above (108 ± 19 W) the gas exchange threshold (GET). Total mood disturbance was calculated from the Profile of Mood States administered prior to exercise. Heart rate, ventilation, and oxygen uptake were continuously recorded throughout exercise. Ratings of perceived exertion (RPE) and ratings of fatigue were assessed during the time trial using visual analogue scales.ResultsProgesterone concentration was 250± 386 pg/ml higher in the ML phase compared to the MF phase (P = 0.04), while estrogen concentration did not differ between phases (4.1 ± 1.6 vs. 5.7 ± 1.6 pg/ml, P = 0.32). Total mood disturbance was greater during the ML compared with the MF phase (123 ± 19 vs. 112 ± 22 a.u., P = 0.03) indicating a more negative mood state during the ML phase. During constant load exercise 10% below GET, ventilation (38.2 ± 5.0 vs. 35.4 ± 4.7 L/min, P = 0.03) and oxygen uptake (1.4 ± 0.2 vs. 1.3 ± 0.2 L/min, P = 0.03) were higher during the ML phase, but heart rate did not differ between phases (P = 0.67). Ventilation (P =0.11), oxygen uptake (P = 0.23), and heart rate (P =0.50) did not differ between phases during exercise at 10% above GET. Mean power output was lower during the ML phase (115 ± 28 vs. 125 ± 27 W, P&lt;0.01) which led to a slower time trial in the ML phase (18.3 ± 2.0 min) compared to the MF phase (17.8 ± 1.7 min, P=0.03). Ratings of fatigue were greater during the ML phase from 4–8 km (P ≤0.05), while RPE did not differ between phases (P = 0.09). Heart rate (P = 0.85), ventilation (P = 0.53), and oxygen uptake (P = 0.32) did not differ between phases during the time trial.ConclusionAerobic exercise performance is reduced in the ML phase compared to the MF phase of the menstrual cycle in recreationally active eumenorrheic women. This is likely explained by a negative mood state pre‐exercise in the ML phase along with increased ratings of fatigue that persisted during the self‐paced exercise.

Menstrual cycle phase does not affect whole body peak fat oxidation rate during a graded exercise test.

Female sex hormones fluctuate in a predictable manner throughout the menstrual cycle in eumenorrheic women. In studies conducted in both animal and humans, estrogen and progesterone have been found to exert individual metabolic effects during both rest and exercise, suggesting that estrogen may cause an increase in fat oxidation during exercise. However, not all studies find these metabolic changes with the natural physiological variation in the sex hormones. To date, no studies have investigated whether whole body peak fat oxidation rate (PFO) and maximal fat oxidation intensity (FATmax) are affected at different time points [mid-follicular (MF), late-follicular (LF), and mid-luteal (ML)] in the menstrual cycle, where plasma estrogen and progesterone are either at their minimum or maximum. We hypothesized that an increased plasma estrogen concentration together with low progesterone concentration in LF would result in a modest but significant increase in PFO. We found no differences in body weight, body composition, or peak oxygen uptake (V̇o2peak) between any of the menstrual phases in the 19 healthy, young eumenorrheic women included in this study. PFO [MF: 0.379 (0.324-0.433) g/min; LF: 0.375 (0.329-0.421) g/min; ML: 0.382 (0.337-0.442) g/min; mean ± (95% CI)] and resting plasma free fatty acid concentrations [MF: 392 (293-492) µmol/l; LF: 477 (324-631) µmol/l; ML: 396 (285-508) µmol/L] were also similar across the menstrual cycle phases. Contrary to our hypothesis, we conclude that the naturally occurring fluctuations in the sex hormones estrogen and progesterone do not affect the whole body PFO and FATmax in young eumenorrheic women measured during a graded exercise test.NEW & NOTEWORTHY Menstrual cycle phase does not affect the peak fat oxidation rate during a graded exercise test. Natural physiological fluctuations in estrogen do not increase peak fat oxidation rate. FATmax is not influenced by menstrual cycle phase in healthy, young eumenorrheic women.

Effectiveness of Fish Oil Supplementation in Attenuating Exercise-Induced Muscle Damage in Women During Midfollicular and Midluteal Menstrual Phases.

McKinley-Barnard, SK, Andre, TL, Gann, JJ, Hwang, PS, and Willoughby, DS. Effectiveness of fish oil supplementation in attenuating exercise-induced muscle damage in females during midfollicular and midluteal menstrual phases. J Strength Cond Res 32(6): 1601-1612, 2018-The purpose of this study was to determine whether the differences in estrogen levels during the female menstrual cycle and fish oil supplementation would attenuate eccentric exercise-induced muscle damage and delayed-onset muscle soreness (DOMS). In a double-blind fashion, 22 physically active females (20.9 ± 1.4 years, 63.5 ± 9.0 kg, 165.2 ± 7.5 cm) were randomly assigned to ingest either 6 g of fish oil (n = 11) or placebo (n = 11) daily for 21 days. Participants underwent an eccentric exercise bout of the knee extensors on 2 occasions during the midfollicular (MF) and midluteal (ML) phases of the 28-day menstrual cycle. Before (PRE), at 6 (6HRPOST), and at 24 hours postexercise (24HRPOST) for each session, participants underwent assessments of DOMS, muscle strength, and had venous blood samples and muscle biopsies obtained. Data were analyzed using a 2 × 2 × 3 repeated-measures multivariate analysis of variance for each criterion variable (p ≤ 0.05). Further analysis of the main effects for the test was performed using separate 1-way analyses of variance. Delayed-onset muscle soreness was significantly greater at the 6HRPOST and 24HRPOST timepoints compared with PRE (p < 0.001). Superoxide dismutase and tumor necrosis factor-alpha (TNF-α) concentrations were significantly higher at the MF phase compared with the ML phase (p < 0.001 and p = 0.05, respectively). There were no statistically significant differences observed for muscle strength, myoglobin, NF-Kβ p50, or NF-Kβ p65. This study demonstrates that higher levels of estrogen may exert a cytoprotective effect on the sarcolemma.

Effects of cycle stage on regionalised galanin, galanin receptors 1–3, GNRH and GNRH receptor mRNA expression in the ovine hypothalamus

The neurotransmitter galanin has been implicated in the steroidogenic regulation of reproduction based on work mainly conducted in rodents. This study investigated the temporal changes in the expression of galanin and its three receptor isoforms and GNRH and GNRHR mRNA in specific hypothalamic nuclei known to be involved in the regulation of reproductive cyclicity, namely the medial pre-optic area (mPOA), the rostral mPOA/organum vasculosum of the lamina terminalis, the paraventricular nucleus and the arcuate nucleus using an ovine model. Following synchronisation of their oestrous cycles, tissues were collected from ewes at five time points: the early follicular, mid follicular (MF) and late follicular phases and the early luteal and mid luteal phases. The results indicated significant differences in regional expression of most of the genes studied, with galanin mRNA expression being highest during the MF phase at the start of the GNRH/LH surge and the expression of the three galanin receptor (GalR) isoforms and GNRH and its receptor highest during the luteal phase. These findings are consistent with a role for galanin in the positive feedback effects of oestradiol (E(2)) on GNRH secretion and a role for progesterone induced changes in the pattern of expression of GalRs in the regulation of the timing of E(2)'s positive feedback through increased sensitivity of galanin-sensitive systems to secreted galanin.

Predominance of Distal Skin Temperature Changes at Sleep Onset across Menstrual and Circadian Phases

Menstrual cycle-associated changes in reproductive hormones affect body temperature in women. We aimed to characterize the interaction between the menstrual, circadian, and scheduled sleep-wake cycles on body temperature regulation. Eight females entered the laboratory during the midfollicular (MF) and midluteal (ML) phases of their menstrual cycle for an ultradian sleep-wake cycle procedure, consisting of 36 cycles of 60-minute wake episodes alternating with 60-minute nap opportunities, in constant bed-rest conditions. Core body temperature (CBT) and distal skin temperature (DT) were recorded and used to calculate a distal-core gradient (DCG). Melatonin, sleep, and subjective sleepiness were also recorded. The circadian variation of DT and DCG was not affected by menstrual phase. DT and DCG showed rapid, large nap episode-dependent increases, whereas CBT showed slower, smaller nap episode-dependent decreases. DCG values were significantly reduced for most of the wake episode in an overall 60-minute wake/60-minute nap cycle during ML compared to MF, but these differences were eliminated at the wake-to-nap lights-out transition. Nap episode-dependent decreases in CBT were further modulated as a function of both circadian and menstrual factors, with nap episode-dependent deceases occurring more prominently during the late afternoon/evening in ML, whereas nap episode-dependent DT and DCG increases were not significantly affected by menstrual phase but only circadian phase. Circadian rhythms of melatonin secretion, DT, and DCG were significantly phase-advanced relative to CBT and sleep propensity rhythms. This study explored how the thermoregulatory system is influenced by an interaction between circadian phase and vigilance state and how this is further modulated by the menstrual cycle. Current results agree with the thermophysiological cascade model of sleep and indicate that despite increased CBT during ML, heat loss mechanisms are maintained at a similar level during nap episodes, which may allow for comparable circadian sleep propensity rhythms between menstrual phases.

Salivary estradiol, interleukin-6 production, and the relationship to substrate metabolism during exercise in females

Estradiol (E(2)) has been documented to have anti-inflammatory effects on the immune system. Interleukin-6 (IL-6), is classified as a "myokine", and has known metabolic consequences. Thus, the purpose of this study was to determine the effects of menstrual phase and exercise on the interaction of E(2) and IL-6, and the role of IL-6 in substrate metabolism. Ten female subjects completed three separate testing sessions: baseline evaluation, and 1h of treadmill exercise at 65% of peak [Formula: see text] during both the midfollicular (MF) and midluteal (ML) menstrual phases. Saliva was collected prior to, during, and post-exercise for determination of E(2) and IL-6. Expired gases and an additional saliva sample were collected 30min post-exercise. No significant differences were observed in any of the measured variables across menstrual phase. Exercise resulted in an acute rise in estradiol and IL-6; however, E(2) was not related to IL-6 at baseline or in response to exercise. IL-6 remained elevated at the end of exercise and was found to be related to energy expenditure from fat, and to total energy expenditure at 60min, and 30min post-exercise. No relationships were found between the anti-inflammatory estrogen E(2) and the cytokine IL-6. However, relationships were found between IL-6 and indices of substrate metabolism. Based on the data from the current research, IL-6 likely plays a metabolic role in healthy individuals during exercise when released from the muscle as a result of reduced energy availability, acting as a "myokine", in comparison to inflammation-induced IL-6 release.

INCREASED SENSITIVITY TO LIGHT-INDUCED MELATONIN SUPPRESSION IN PREMENSTRUAL DYSPHORIC DISORDER

Increased sensitivity to light-induced melatonin suppression characterizes some, but not all, patients with bipolar illness or seasonal affective disorder. The aim of this study was to test the hypothesis that patients with premenstrual dysphoric disorder (PMDD), categorized as a depressive disorder in Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition (DSM-IV), have altered sensitivity to 200 lux light during mid-follicular (MF) and late-luteal (LL) menstrual cycle phases compared with normal control (NC) women. As an extension of a pilot study in which the authors administered 500 lux to 8 PMDD and 5 NC subjects, in the present study the authors administered 200 lux to 10 PMDD and 13 NC subjects during MF and LL menstrual cycle phases. Subjects were admitted to the General Clinical Research Center (GCRC) in dim light (<50 lux) to dark (during sleep) conditions at 16:00 h where nurses inserted an intravenous catheter at 17:00 h and collected plasma samples for melatonin at 30-min intervals from 18:00 to 10:00 h, including between 00:00 and 01:00 h for baseline values, between 01:30 and 03:00 h during the 200 lux light exposure administered from 01:00 to 03:00 h, and at 03:30 and 04:00 h after the light exposure. Median % melatonin suppression was significantly greater in PMDD (30.8%) versus NC (−0.2%) women (p = .040), and was significantly greater in PMDD in the MF (30.8%) than in the LL (−0.15%) phase (p = .047). Additionally, in the LL (but not the MF) phase, % suppression after 200 lux light was significantly positively correlated with serum estradiol level (p = .007) in PMDD patients, but not in NC subjects (p > .05). (Author correspondence: bparry@ucsd.edu)

Circadian variation of sleep during the follicular and luteal phases of the menstrual cycle.

Women experience insomnia more frequently than men. Menstrual cycle changes in reproductive hormones and circadian rhythms may contribute to sleep disruptions. Our aim, therefore, was to clarify the interaction between menstrual and circadian processes as it affects sleep. Participants entered the laboratory during the mid-follicular (MF) and mid-luteal (ML) phases of their menstrual cycle for an ultra-rapid sleep-wake cycle (URSW) procedure, consisting of 36 cycles of 60-min wake episodes alternating with 60-min nap opportunities. This procedure concluded with an ad libitum nap episode. Time-isolation suite. Eight unmedicated, physically and mentally healthy females with regular ovulatory menstrual cycles. N/A. Polysomnographic sleep from nocturnal sleep episodes and 60-min naps; subjective alertness; core body temperature (CBT); salivary melatonin; urinary estradiol; and urinary progesterone. Increased CBT values at night and decreased CBT amplitude were observed during ML compared to MF. Circadian phase of CBT and the circadian melatonin profile were unaffected by menstrual phase. All analyzed sleep parameters showed a circadian variation throughout the URSW procedure, with no menstrual phase differences observed for most, including slow wave sleep (SWS). The circadian variation of REM sleep duration, however, was sensitive to menstrual phase, with reduced REM sleep during ML at circadian phase 0 degrees and 30 degrees. Moderate but significant changes in REM sleep across the menstrual and circadian cycles were observed. These results support an interaction between circadian and menstrual processes in the regulation of REM sleep.

Late, but not early, wake therapy reduces morning plasma melatonin: Relationship to mood in Premenstrual Dysphoric Disorder

Wake therapy improves mood in Premenstrual Dysphoric Disorder (PMDD), a depressive disorder in DSM-IV. We tested the hypothesis that the therapeutic effect of wake therapy in PMDD is mediated by altering sleep phase with melatonin secretion. We measured plasma melatonin every 30 min (18:00–09:00 h) in 19 PMDD and 18 normal control (NC) women during mid-follicular (MF) and late luteal (LL) menstrual cycle phases, and during LL interventions with early wake therapy (EWT) (sleep 03:00–07:00 h)(control condition) vs. late wake therapy (LWT) (sleep 21:00–01:00 h)(active condition). Melatonin offset was delayed and duration was longer in the symptomatic LL vs. asymptomatic MF phase in both NC and PMDD subjects. LWT, but not EWT, advanced offset and shortened duration vs. the LL baseline, although they improved mood equally. Later baseline LL morning melatonin offset was associated with more depressed mood in PMDD patients, and longer melatonin duration in the MF phase predicted greater mood improvement following LWT. That LWT, but not EWT, advanced melatonin offset and shortened duration while they were equally effective in improving mood suggests that decreasing morning melatonin secretion is not necessary for the therapeutic effects of wake therapy in PMDD.

Carbohydrate Loading and Female Endurance Athletes: Effect of Menstrual-Cycle Phase

This study compared 3 d of carbohydrate loading (CHOL; 8.4 g x kg(-1) x d(-1) carbohydrate) in female eumenorrheic athletes with 3 d of an isoenergetic normal diet (NORM; 5.2 g x kg(-1) x d(-1) carbohydrate) and examined the effect of menstrual-cycle phase on performance, muscle-glycogen concentration [glyc], and substrate utilization. Nine moderately trained eumenorrheic women cycled in an intermittent protocol varying in intensity from 45% to 75% VO2max for 75 min, followed by a 16-km time trial at the midfollicular (MF) and midluteal (ML) phases of the menstrual cycle on NORM and CHOL. Time-trial performance was not affected by diet (CHOL 26.10 +/- 1.04 min, NORM 26.16 +/- 1.35 min; P = 0.494) or menstrual-cycle phase (MF 26.05 +/- 1.10 min, ML 26.23 +/- 1.33 min; P = 0.370). Resting [glyc] was lowest in the MF phase after NORM (575 +/- 145 mmol x kg(-1) x dw(-1)), compared with the MF phase after CHOL (728 mmol x kg(-1) x dw(-1)) and the ML phase after CHOL and NORM (756 and 771 mmol x kg(-1) x dw(-1), respectively). No effect of phase on substrate utilization during exercise was observed. These data support previous observations of greater resting [glyc] in the ML than the MF phase of the menstrual cycle and suggest that lower glycogen storage in the MF phase can be overcome by carbohydrate loading.

No effect of menstrual cycle phase on glycerol or palmitate kinetics during 90 min of moderate exercise

The systemic flux of glycerol and palmitate [a representative nonesterified free fatty acid (NEFA)] was assessed in three different phases of the menstrual cycle at rest and during moderate-intensity exercise. It was hypothesized that circulating glycerol and NEFA turnover would be greatest in the midfollicular (MF) phase of the menstrual cycle, when estrogen is elevated but progesterone low, followed by the midluteal phase (ML; high estrogen and progesterone), and lowest in the early follicular (EF) phase of the menstrual cycle (low estrogen and progesterone). Subjects included moderately active, eumenorrheic, healthy women. Testing occurred after 3 days of diet control and after an overnight fast (12-13 h). Resting and exercise (50% maximal oxygen uptake, 90 min) measurements of tracer-determined glycerol and palmitate kinetics were made. There was a significant increase in both glycerol and palmitate turnover from rest to exercise in all phases of the menstrual cycle (P<0.0001). No significant differences, however, were observed between cycle phases in the systemic flux of glycerol or palmitate, at rest or during exercise. Maximal peripheral lipolysis during exercise, as represented by glycerol rate of appearance at 90 min, equaled 8.45+/-0.96, 8.35+/-1.12, and 7.71+/-0.96 micromol.kg-1.min-1 in the EF, MF, and ML phases, respectively. Circulating free fatty acid utilization also peaked at 90 min of exercise, as indicated by the palmitate rate of disappearance (3.31+/-0.35, 3.17+/-0.39, and 3.47+/-0.26 micromol.kg-1.min-1) in the EF, MF, and ML phases, respectively. In conclusion, systemic rates of glycerol and NEFA turnover (as represented by palmitate flux) were not significantly affected by the cyclic fluctuations in estrogen and progesterone that occur throughout the normal menstrual cycle, either at rest or during 90 min of moderate exercise.

Cortisol circadian rhythms during the menstrual cycle and with sleep deprivation in premenstrual dysphoric disorder and normal control subjects

Background: In this study we extended previous work by examining whether disturbances in the circadian rhythms of cortisol during the menstrual cycle distinguish patients with premenstrual dysphoric disorder (PMDD) from normal control (NC) subjects. In addition, we tested the differential response to the effects of early and late partial sleep deprivation on cortisol rhythms. Methods: In 15 PMDD and 15 NC subjects we measured cortisol levels every 30 min from 6:00 pm to 9:00 am during midfollicular (MF) and late luteal (LL) menstrual cycle phases and also during a randomized crossover trial of early (sleep 3:00 am–7:00 am) versus late (sleep 9:00 pm–1:00 am) partial sleep deprivation administered in two subsequent and separate luteal phases. Results: In follicular versus luteal menstrual cycle phases we observed altered timing but not quantitative measures of cortisol secretion in PMDD subjects, compared with NC subjects: in the LL versus MF phase the cortisol acrophase was a mean of 1 hour earlier in NC subjects, but not in PMDD subjects. The effect of sleep deprivation on cortisol timing measures also differed for PMDD versus NC subjects: during late partial sleep deprivation (when subjects’ sleep was earlier), the cortisol acrophase was almost 2 hours earlier in PMDD subjects. Conclusions: Timing rather than quantitative measures of cortisol secretion differentiated PMDD subjects from NC subjects both during the menstrual cycle and in response to early versus late sleep deprivation interventions.

Sleep EEG studies during early and late partial sleep deprivation in premenstrual dysphoric disorder and normal control subjects

In this study of 23 patients with premenstrual dysphoric disorder (PMDD) and 18 normal comparison (NC) subjects, we examined sleep EEG measures during baseline midfollicular (MF) and late luteal (LL) menstrual cycle phases and after early sleep deprivation (ESD), in which subjects slept from 03.00 to 07.00 h, and late sleep deprivation (LSD), in which subjects slept from 21.00 to 01.00 h. Each sleep deprivation night was followed by a night of recovery sleep (ESD-R, LSD-R) (sleep 22.30–06.30 h) and was administered in the late luteal phase of separate menstrual cycles. During baseline studies, sleep EEG measures differed significantly by menstrual cycle phase, but not group. Both PMDD and NC groups showed longer REM latencies and less REM sleep (minutes and percent) during the luteal compared with the follicular menstrual cycle phase. PMDD subjects, however, did not show sleep architecture changes similar to those of patients with major depressive disorders. Sleep quality was better during recovery nights of sleep in PMDD compared with NC subjects. REM sleep measures changed in association with clinical improvement in responders to sleep deprivation. Both early and late sleep deprivation may help to correct underlying circadian rhythm disturbances during sleep in PMDD, although differential sleep changes during ESD vs. LSD did not correlate with clinical response. Further sleep studies addressing additional circadian variables may serve to elucidate mechanisms mediating the therapeutic effects of sleep deprivation in PMDD.

Neuroendocrine effects of light therapy in late luteal phase dysphoric disorder

In 20 late luteal phase dysphoric disorder (LLPDD) and in 11 normal control (NC) subjects, circadian profiles of cortisol, prolactin, thyrotropin-stimulating hormone (TSH), and core body temperature were measured during midfollicular (MF) and late luteal (LL) menstrual cycle phases and after 1 week of light therapy either with (1) bright (τ2500 lux) white morning (6:30 am to 8:30 am), (2) bright white evening (7 pm to 9 pm) or (3) dim (<10 lux) red evening light, randomly administered in three separate luteal phases. In NC but not PMDD subjects, the cortisol peak significantly delayed in the LL compared with the MF phase. In PMDD, prolactin peak and amplitude were higher, prolactin acrophase earlier, and temperature amplitude higher during both the MF and LL phases. After light treatment, prolactin amplitude remained higher in LLPDD than in controls. In both groups, bright light shifted the cortisol acrophase, and am light increased the prolactin nadir. Bright pm light increased the TSH nadir in LLPDD, but decreased it in controls. Thus, menstrual cycle phase, diagnosis, and light therapy may differentially affect neuroendocrine systems.

Physiological responses to submaximal exercise at the mid-follicular, ovulatory and mid-luteal phases of the menstrual cycle.

This study examined the responses of eumenorrheic women to 60 min of submaximal exercise at the mid-follicular (MF), ovulatory (OV) and mid-luteal (ML) phases of the menstrual cycle. Blood metabolite-hormonal measures, cardiorespiratory responses and ratings of perceived exertion (RPE) (local, legs only; and total, entire body) were monitored at 15-min intervals throughout exercise. No significant effects for phase were observed in the blood measures or the cardiorespiratory responses, except for the respiratory exchange ratio (RER). The overall exercise OV RER (0.86 ± 0.02; mean ± SEM) was lower than at MF (0.94 ± 0.02) but not at ML (0.89 ± 0.01). Substrate utilization (%) and oxidation (g/min) calculations indicated that more fat was used during OV than at MF but not ML. Conversely, more carbohydrate was used during MF than OV. Additionally, local RPE was higher in OV than in the MF or ML trials at 30-60 min of exercise. These findings suggest that menstrual cycle hormonal fluctuations influence metabolic substrate usage and effort perception during submaximal exercise in eumenorrheic women.

Circulating Luteinizing Hormone Pulse Frequency in Women with Polycystic Ovary Syndrome

To determine whether pulsatile LH frequency is altered in patients with the polycystic ovary syndrome (PCO) serum LH was measured every 10 min for 12 h (0800-2000 h) in nine patients. Six cycling women studied in the midfollicular (MF) or early follicular (EF) phases of their cycle served as controls. Three of these women were studied in both phases, yielding a total of nine control studies. In the PCO patients the mean LH pulse frequency was 12.1 +/- 0.7 (+/- SE) pulses/12 h. This value was indistinguishable from that of normal EF (12.1 +/- 0.4 pulses/12 h) or MF women (12.0 +/- 0.7 pulses/12 h). In contrast, the mean LH pulse amplitude in the PCO patients (12.2 +/- 2.7 mIU/mL) was higher (P less than 0.05) than that in normal women in either phase (EF, 6.2 +/- 0.8 mIU/mL; MF, 6.4 +/- 0.6 mIU/mL). These results suggest that the elevations in serum LH levels that occur in PCO patients are due primarily to increased LH pulse amplitude rather than increased pulse frequency.

Circulating luteinizing hormone pulse frequency in women with polycystic ovary syndrome.

To determine whether pulsatile LH frequency is altered in patients with the polycystic ovary syndrome (PCO) serum LH was measured every 10 min for 12 h (0800-2000 h) in nine patients. Six cycling women studied in the midfollicular (MF) or early follicular (EF) phases of their cycle served as controls. Three of these women were studied in both phases, yielding a total of nine control studies. In the PCO patients the mean LH pulse frequency was 12.1 +/- 0.7 (+/- SE) pulses/12 h. This value was indistinguishable from that of normal EF (12.1 +/- 0.4 pulses/12 h) or MF women (12.0 +/- 0.7 pulses/12 h). In contrast, the mean LH pulse amplitude in the PCO patients (12.2 +/- 2.7 mIU/mL) was higher (P less than 0.05) than that in normal women in either phase (EF, 6.2 +/- 0.8 mIU/mL; MF, 6.4 +/- 0.6 mIU/mL). These results suggest that the elevations in serum LH levels that occur in PCO patients are due primarily to increased LH pulse amplitude rather than increased pulse frequency.