Mid-luteal Menstrual Phases Research Articles

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.

Sex hormones and the nervous system, do they matter for physical performance?

There are well-known oscillations in circulating sex hormones that occur in both men and women on daily and monthly cycles, as well as across the lifespan. The non-reproductive effects of estrogen and progesterone, particularly in women, on physical performance have been an area of intense debate. This presentation will examine the evidence that sex hormones can modulate the nervous system from the cellular-level to a whole-body perspective and impact human physical performance. The cell-level and animal literature clearly indicates sex hormones have the capability to directly modulate the excitability of the nervous system through gamma-Aminobutyric acid (GABA) receptors. Pregnenolone, a first-order metabolite of progesterone, is able to directly activate GABA receptors creating either a neuro-excitatory or inhibitory effect depending on whether pregnenolone is sulfonated. Progesterone is able to enhance the GABA receptor response in the presence of GABA, increasing neural inhibition. Additionally, estrogen creates an excitatory effect on the nervous system by attenuating the release of GABA from neurons. Research from our work group has shown that the discharge of motor neurons are altered across the menstrual cycle 1 Tenan M.S. Peng Y.L. Hackney A.C. Griffin L. MSSE. 2013; 45: 2151-2157 Google Scholar and that quadriceps MVC may decrease by as much as 23% in the mid luteal phase of the menstrual cycle, when both estrogen and progesterone are high. 2 Tenan M.S. Hackney A.C. Griffin L. EJAP. 2016; 116: 153-160 Google Scholar In relative time to exhaustion, the mid luteal menstrual phase also has the least stable force production across the entire isometric task. At the cellular level, sex hormones clearly have the capability to modulate nervous system function. Our research indicates that this translates to measurable effects on human performance; however, this finding is not uniform across all studies. In conclusion, sex hormones have the theoretical ability to modify physical performance but the inconsistent findings at the clinical level may be a result of individual variability in the level of sex hormones both in circulation and uniquely within the central nervous system, making broad generalizations across a population of men or women challenging.

The effect of estrogen on muscle damage biomarkers following prolonged aerobic exercise in eumenorrheic women.

This study assessed the influence of estrogen (E2) on muscle damage biomarkers [skeletal muscle - creatine kinase (CK); cardiac muscle - CK-MB] responses to prolonged aerobic exercise. Eumenorrheic women (n=10) who were physically active completed two 60-minute treadmill running sessions at ∼60-65% maximal intensity during low E2 (midfollicular menstrual phase) and high E2 (midluteal menstrual phase) hormonal conditions. Blood samples were collected prior to exercise (following supine rest), immediately post-, 30 min post-, and 24 hours post-exercise to determine changes in muscle biomarkers. Resting blood samples confirmed appropriate E2 hormonal levels Total CK concentrations increased following exercise and at 24 hours post-exercise were higher in the midfollicular low E2 phase (p<0.001). However, CK-MB concentrations were unaffected by E2 level or exercise (p=0.442) resulting in the ratio of CK-MB to total CK being consistently low in subject responses (i.e., indicative of skeletal muscle damage). Elevated E2 levels reduce the CK responses of skeletal muscle, but had no effect on CK-MB responses following prolonged aerobic exercise. These findings support earlier work showing elevated E2 is protective of skeletal muscle from exercise-induced damage associated with prolonged aerobic exercise.

Urinary estrogens and estrogen metabolites and subsequent risk of breast cancer among premenopausal women.

Endogenous estrogens and estrogen metabolism are hypothesized to be associated with premenopausal breast cancer risk but evidence is limited. We examined 15 urinary estrogens/estrogen metabolites and breast cancer risk among premenopausal women in a case-control study nested within the Nurses' Health Study II (NHSII). From 1996 to 1999, urine was collected from 18,521 women during the mid-luteal menstrual phase. Breast cancer cases (N = 247) diagnosed between collection and June 2005 were matched to two controls each (N = 485). Urinary estrogen metabolites were measured by liquid chromatography-tandem mass spectrometry and adjusted for creatinine level. Relative risks (RR) and 95% confidence intervals (CI) were estimated by multivariate conditional logistic regression. Higher urinary estrone and estradiol levels were strongly significantly associated with lower risk (top vs. bottom quartile RR: estrone = 0.52; 95% CI, 0.30-0.88; estradiol = 0.51; 95% CI, 0.30-0.86). Generally inverse, although nonsignificant, patterns also were observed with 2- and 4-hydroxylation pathway estrogen metabolites. Inverse associations generally were not observed with 16-pathway estrogen metabolites and a significant positive association was observed with 17-epiestriol (top vs. bottom quartile RR = 1.74; 95% CI, 1.08-2.81; P(trend) = 0.01). In addition, there was a significant increased risk with higher 16-pathway/parent estrogen metabolite ratio (comparable RR = 1.61; 95% CI, 0.99-2.62; P(trend) = 0.04). Other pathway ratios were not significantly associated with risk except parent estrogen metabolites/non-parent estrogen metabolites (comparable RR = 0.58; 95% CI, 0.35-0.96; P(trend) = 0.03). These data suggest that most mid-luteal urinary estrogen metabolite concentrations are not positively associated with breast cancer risk among premenopausal women. The inverse associations with parent estrogen metabolites and the parent estrogen metabolite/non-parent estrogen metabolite ratio suggest that women with higher urinary excretion of parent estrogens are at lower risk.

The impact of menstrual cycle phase on cardiac autonomic regulation

This study investigated menstrual cycle phase differences in heart rate (HR) and RR interval variability (RRV) in 49 healthy, premenopausal, eumenorrheic women (age 30.2+/-6.2 years). HR and RRV were computed from ambulatory 24-h electrocardiogram, collected for up to 6 days, with at least 1 day each during early to midfollicular and midluteal menstrual phases. Phase effects on HR and RRV were assessed using linear mixed effects models with a random intercept to account for the correlation of observations within each subject as well as intrasubject variation. During follicular phase monitoring, women had significantly lower average HR (-2.33 bpm), and higher standard deviation, the root mean squared successive difference, and high frequency (0.04-0.15 Hz) and low frequency (0.15-0.40 Hz) RRV than during the luteal phase. These results provide strong support for the influence of menstrual phase on cardiac autonomic regulation in premenopausal women.

Sex Hormone Suppression Reduces Resting Energy Expenditure and β-Adrenergic Support of Resting Energy Expenditure

Resting energy expenditure (REE) decreases with aging and may decrease in women as a result of the menopause, potentially contributing to weight gain. REE has been observed to fluctuate during the menstrual cycle, suggesting regulation by sex hormones. The aim of the present study was to determine the effects of suppressing estrogen and progesterone on REE. Fourteen premenopausal women, 29 +/- 5 yr old (mean +/- sd), were studied in the midluteal menstrual phase (ML) and after 6 d of GnRH antagonist therapy (GnRHant) administered in the follicular menstrual phase. REE was measured by indirect calorimetry in the morning after a 12-h fast and again during beta-adrenergic blockade to determine sympathetic nervous system (SNS) support of REE. Treatment with GnRHant significantly decreased REE (1405 +/- 42 vs. 1334 +/- 36 kcal/d, mean +/- se, ML vs. GnRHant; P = 0.002). Additionally, SNS blockade tended to alter REE more during ML than during GnRHant (-19 +/- 10 vs. 5 +/- 11 kcal/d; P = 0.14). Suppression of sex hormones to postmenopausal levels by GnRHant reduced REE in young healthy women. These findings suggest that the withdrawal of estrogen and/or progesterone attenuates REE, possibly through a SNS-mediated mechanism.

Effects of menstrual cycle and physical training on heat loss responses during dynamic exercise at moderate intensity in a temperate environment

We evaluated the effects of the menstrual cycle and physical training on heat loss (sweating and cutaneous vasodilation) responses during moderate exercise in a temperate environment. Ten untrained (group U) and seven endurance-trained (group T) women (maximal O2 uptake of 36.7+/-1.1 vs. 49.4+/-1.7 ml.kg-1.min-1, respectively; P<0.05) performed a cycling exercise at 50% maximal O2 uptake for 30 min during both the midfollicular and midluteal menstrual phase in a temperate environment (ambient temperature of 25 degrees C, relative humidity of 45%). In group U, plasma levels of estrone, estradiol, and progesterone at rest and esophageal temperature (Tes) during exercise were significantly higher during the midluteal than during the midfollicular phase (P<0.05). Sweating rate and cutaneous blood flow (measured via laser-Doppler flowmetry) on the chest, back, forearm, and thigh were lower during the midluteal than during the midfollicular phase during exercise. Tes threshold for heat loss responses was significantly higher and sensitivity of the heat loss responses was significantly lower in the midluteal than in the midfollicular phase, regardless of body site. These effects of the menstrual cycle in group U were not observed in group T. The sweating rate and cutaneous blood flow were significantly higher in group T than in group U, regardless of menstrual phase or body site. Tes threshold for heat loss responses was significantly lower and sensitivity of heat loss responses was significantly greater in group T than in group U in the midluteal phase; however, sensitivity of the sweating response was significantly greater in the midfollicular phase. These results suggest that heat loss responses in group U were inhibited in the midluteal phase compared with in the midfollicular phase. Menstrual cycle had no remarkable effects in group T. Physical training improved heat loss responses, which was more marked in the midluteal than in the midfollicular phase.

Enhanced response to ozone exposure during the follicular phase of the menstrual cycle.

Exposure to ozone (O3), a toxic component of photochemical smog, results in significant airway inflammation, respiratory discomfort, and pulmonary function impairment. These effects can be reduced via pretreatment with anti-inflammatory agents. Progesterone, a gonadal steroid, is known to reduce general inflammation in the uterine endometrium. However, it is not known whether fluctuations in blood levels of progesterone, which are experienced during the normal female menstrual cycle, could alter O3 inflammatory-induced pulmonary responses. In this study, we tested the hypothesis that young, adult females are more responsive to O3 inhalation with respect to pulmonary function impairment during their follicular (F) menstrual phase when progesterone levels are lowest than during their mid-luteal (ML) phase when progesterone levels are highest. Nine subjects with normal ovarian function were exposed in random order for 1 hr each to filtered air and to 0.30 ppm O3 in their F and ML menstrual phases. Ozone responsiveness was measured by percent change in pulmonary function from pre- to postexposure. Significant gas concentration effects (filtered air versus O3) were observed for forced vital capacity (FVC), forced expiratory volume in 1 sec (FEV1), and forced expiratory flow between 25 and 75% of FVC (FEF25-75; p < .05). More importantly, the pulmonary function flow rates, FEV1 and FEF25-75, showed a significant menstrual phase and gas concentration interaction effect, with larger decrements observed in the F menstrual phase when progesterone concentrations were significantly lower. We conclude that young, adult females appear to be more responsive to acute O3 exposure during the F phase than during the ML phase of their menstrual cycles.(ABSTRACT TRUNCATED AT 250 WORDS)

Enhanced Response to Ozone Exposure during the Follicular Phase of the Menstrual Cycle

Exposure to ozone (O3), a toxic component of photochemical smog, results in significant airway inflammation, respiratory discomfort, and pulmonary function impairment. These effects can be reduced via pretreatment with anti-inflammatory agents. Progesterone, a gonadal steroid, is known to reduce general inflammation in the uterine endometrium. However, it is not known whether fluctuations in blood levels of progesterone, which are experienced during the normal female menstrual cycle, could alter O3 inflammatory-induced pulmonary responses. In this study, we tested the hypothesis that young, adult females are more responsive to O3 inhalation with respect to pulmonary function impairment during their follicular (F) menstrual phase when progesterone levels are lowest than during their mid-luteal (ML) phase when progesterone levels are highest. Nine subjects with normal ovarian function were exposed in random order for 1 hr each to filtered air and to 0.30 ppm O3 in their F and ML menstrual phases. Ozone responsiveness was measured by percent change in pulmonary function from pre- to postexposure. Significant gas concentration effects (filtered air versus O3) were observed for forced vital capacity (FVC), forced expiratory volume in 1 sec (FEV1), and forced expiratory flow between 25 and 75% of FVC (FEF25-75; p &lt; .05). More importantly, the pulmonary function flow rates, FEV1 and FEF25-75, showed a significant menstrual phase and gas concentration interaction effect, with larger decrements observed in the F menstrual phase when progesterone concentrations were significantly lower. We conclude that young, adult females appear to be more responsive to acute O3 exposure during the F phase than during the ML phase of their menstrual cycles.(ABSTRACT TRUNCATED AT 250 WORDS)