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1 Applied Biomedical Research Group, King's College London 2 Research Institute for Sport and Exercise Sciences, Liverpool John Moores University3 Reproductive Medicine Unit, Liverpool Women's Hospital 4 Department of Clinical Chemistry, The University of Liverpool
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(Received 8 June 2004;
accepted after revision 16 November 2004; first published online 30 November 2004)
Corresponding author K. J. Elliott: Applied Biomedical Sciences Research Group, GKT School of Biomedical Sciences, Shepherds House, Kings College London, Guys Campus, London SE1 1UL, UK. Email: kirsty.elliott{at}kcl.ac.uk
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Introduction |
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There are two main confounding factors associated with research involving eumenorrhoeic and postmenopausal subjects: inter- and intra-individual variability in hormone secretion and age. These factors can be limited, however, by taking advantage of contemporary medicine (in vitro fertilization (IVF) treatment) and natural phenomena (pregnancy).
In vitro fertilization treatment is an exaggerated model of the menstrual cycle. During the first phase of treatment, oestrogen and progesterone concentrations are downregulated, to levels indicative of menses. Following downregulation, oestrogen concentrations are increased to supra-physiological levels while progesterone concentrations stay low (corresponding to the late follicular phase of the menstrual cycle). During the third phase, progesterone concentrations are also increased to supra-physiological levels (analogous to the mid-luteal phase of the menstrual cycle). Finally, oestrogen levels decline, while progesterone levels remain elevated. In 1997, Greeves et al. (1997) reported that maximum voluntary isometric force (MVIF) of the first dorsal interosseus (FDI) muscle did not change following considerable increases (from phase 1 to phase 2) in 17ß-oestradiol concentration in females aged 31–39 years. Since progesterone levels were suppressed for the duration of the study, Greeves et al. (1997) suggested that progesterone alone, or in combination with another reproductive hormone, was responsible for the changes in strength observed during the menstrual cycle (Phillips et al. 1996) and following the menopause (Skelton et al. 1999).
Evidently, subjects undergo intense (acute) changes in reproductive status during IVF treatment, through the exogenous manipulation of endogenous hormone levels. Pregnancy, however, results in substantial (chronic) natural changes in the female reproductive milieu. Oestrogen and progesterone are secreted throughout the first trimester in similar quantities to those produced during the luteal phase of the menstrual cycle. During the second trimester, secretion of progesterone increases rapidly, before stabilizing or declining slightly during the final trimester. At term, maternal progesterone levels are approximately six times greater than during the late luteal phase of the menstrual cycle. Oestrogen levels begin to rise at week 16 and continue to increase throughout pregnancy. Plasma 17ß-oestradiol levels increase from approximately 7 ng ml–1 at week 22 to 23 ng ml–1 by the end of pregnancy. Testosterone levels also rise steadily throughout pregnancy, from approximately 10 ng ml–1 in the first trimester to 50–80 ng ml–1 in the third trimester. In contrast, follicle stimulating hormone (FSH) and lutenizing hormone (LH) levels remain low throughout gestation. Human chorionic gonadotrophin (hCG), a glycoprotein which imitates LH, is secreted in large quantities during the first trimester of pregnancy. Peak concentrations of hCG are attained by week 9 and decline thereafter. Following parturition, ovarian and gonadotropin levels return to normal eumenorrhoeic values. To the best of our knowledge, no other investigators have examined the effects of gestation-related changes in reproductive hormone levels on the force-generating capacity of skeletal muscle.
Therefore, the present study was designed to extend previous work by augmenting the differences in reproductive hormone concentrations and by limiting the effect of age on muscle strength. This was achieved by measuring muscle strength following supra-physiological changes (acute and chronic) in hormone concentration in females aged 22–39 years. Furthermore, the aim of this study was to identify the hormone responsible for changes in muscle strength. This was achieved by manipulating progesterone levels (during IVF treatment), therefore continuing the work of Greeves et al. (1997). The effects of IVF treatment and pregnancy on the bioavailability of oestradiol and testosterone were also explored. We have previously shown that menstrual cycle phase has no effect on the concentration of bioavailable oestradiol and testosterone (Elliott et al. 2003). Both conditions (pregnancy and IVF treatment) have the potential to alter significantly the bioavailability of oestradiol and testosterone due to the supra-physiological changes in the total concentration of oestradiol and testosterone that occur between each phase of treatment and each trimester of pregnancy.
If the hormonal changes experienced during pregnancy or IVF treatment do affect muscle strength, then these finding can be used to make definite recommendations regarding the relationship between reproductive status and exercise performance and may aid in the continued development of hormone replacement therapies and oral contraceptives.
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Methods |
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Forty patients (Table 1) undergoing IVF treatment were recruited from the Reproductive Medicine Unit at the Liverpool Women's Hospital. Patients were divided into four groups of ten, depending on the phase of IVF treatment at which they were recruited, as follows.
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Forty women (Table 1) were recruited from the antenatal and postnatal clinics at the Liverpool Women's Hospital. Subjects were 10–12 weeks pregnant (12 weeks), 20 weeks pregnant (20 weeks), 34–36 weeks pregnant (36 weeks) or 6 weeks postnatal (6 weeks). Each group comprised ten subjects, except the postnatal group, which had five subjects (five subjects failed to attend).
Patients with abnormal FSH:LH ratios, oligomenorrhoea, polycystic ovarian syndrome or any muscular, neurological or skeletal disorders capable of influencing performance of the hand were excluded. Only non-smokers were included in the study (De Valk-de Roo et al. 1997). Approval for the experimental protocol was obtained from the Liverpool Research Ethics Committee and the Human Ethics Committee of Liverpool John Moores University. Procedures conformed to the Declaration of Helsinki. All patients provided written consent having read and understood the details of the experiment.
Experimental design
The research design was cross-sectional, which means that patients were tested once. All IVF and pregnant subjects were measured upon recruitment. The postnatal subjects were recruited following parturition and were asked to attend for testing 6 weeks from the time of recruitment. All testing was undertaken at the same time of day in order to control for circadian variation in muscle strength (Reilly, 1990). A 10 ml venous blood sample was drawn from each patient prior to any physical testing. Blood samples were analysed for total concentrations of 17ß-oestradiol, progesterone and testosterone and bioavailable concentrations of oestradiol and testosterone. Maximum voluntary isometric force and cross-sectional area (CSA) of the FDI muscle were measured.
A cross-sectional research design was implemented because patients undergoing IVF treatment often fail to complete their treatment (for example, they become pregnant unaided, or have an adverse medical reaction to the treatment, or can no longer financially afford to undergo treatment). In addition, due to complications during pregnancy (for example, the onset of gestational diabetes, high blood pressure, or miscarriage) it was decided that a cross-sectional design would allow more subjects to be tested within the time frame of the study. In order to facilitate the cross-sectional design of this study, force was normalized for CSA, since force was shown to be significantly correlated with CSA (r = 0.5, P = 0.001).
Cross-sectional area
The diameter of the FDI muscle was measured using a real-time ultrasound system (EUB525, Hitachi, Suzhou, Japan) and acoustic coupling gel (Henleys Medical, Welwyn Garden City, UK). Transducer frequency was 10 MHz and the depth gain compensation was adjusted to optimize image quality. The hand was positioned on a table, palmar side down, with the fingers together and the thumb abducted at a 45 deg angle. The FDI muscle was scanned on the posterior aspect using a direct contact scanning technique. The ultrasound probe was placed vertically on the hand and was adjusted until the whole muscle was visible on screen. The diameter of the FDI muscle was measured at the widest point of the muscle. Cross-sectional area was calculated using the formula 
r2, where r is half the diameter. (This formula was used because the FDI muscle is circular, since there are no significant differences in diameter when assessed by a mid-saggital or frontal section scan.)
Hormonal analysis
Plasma concentrations of total 17ß-oestradiol, progesterone, testosterone and hCG were measured using an automated quantitative system (Mini Vidas, bioMerieux, Marcy l'Etoile, France) and VIDAS reagent kits (VIDAS Oestradiol and VIDAS Progesterone, bioMerieux). All samples were analysed using the Enzyme Linked Fluorescent Assay technique, an enzyme immunoassay sandwich method with a final fluorescent detection. The concentrations of bioavailable oestradiol and testosterone were measured using an adaptation of the method of Tremblay & Dube (1974).
Assessment of maximum voluntary isometric force of the FDI muscle
The FDI muscle was chosen for testing for two reasons. First, the FDI muscle is the only muscle that produces abduction of the index finger. Other muscles attached to the finger are active during abduction but due to their anatomical arrangement they do not contribute force in this direction (Davies, 1972). Rutherford & Jones (1988) found very similar maximum voluntary and stimulated contraction forces for the FDI muscle, therefore demonstrating that the FDI muscle can be maximally activated and isolated from the action of other hand muscles. Second, these and other authors (Tanaka et al. 1984) have found no difference in force production between dominant and non-dominant hands, suggesting that this muscle is not trainable under normal conditions.
Maximum voluntary isometric force was assessed using the techniques previously described by Elliott et al. (2003). In brief, a custom-built finger dynamometer was used to assess MVIF of the FDI muscle. The dominant arm (both arms were measured and the arm that produced the greatest force was taken as the dominant arm) was secured to the dynamometer. Hand position was standardized for each test session. Maximum voluntary isometric force of the FDI muscle was measured while the index finger was fully abducted. Three submaximum isometric contractions were carried out prior to maximum force assessment. Following a 3 min rest, three maximum voluntary isometric contractions were performed, the best of which was taken as definitive. A 1 min rest separated each contraction. Percutaneous electrical stimulation was used to superimpose electrical impulses onto the FDI muscle during each contraction. Maximum activation was confirmed when no extra force could be generated by the superimposed twitches.
Statistical analysis
A one-way ANOVA was used to detect differences between MVIF/CSA and total and bioavailable hormone concentrations across phases of IVF treatment and stages of pregnancy. Significant differences between phases of IVF treatment or pregnancy were further explored using Tukey's post hoc analysis. The relationships between MVIF/CSA and concentrations of total progesterone, 17ß-oestradiol, testosterone, hCG and oestradiol:progesterone ratio and bioavailable oestradiol and testosterone were examined using Pearson's correlation coefficient, on normally distributed data, and Spearman's rank correlation, on non-parametric data. The level of significance was taken as P < 0.05.
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Results |
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The blood sample analyses showed that concentrations of progesterone were significantly different between phases 1 and 3, 1 and 4, 2 and 3, and 2 and 4 (all P < 0.001). The concentration of progesterone was significantly lower in phases 1 and 2 than during phases 3 and 4. There were significant changes in the concentration of 17ß-oestradiol between all phases (P < 0.05), with the exception of phases 2 and 3. The concentration of 17ß-oestradiol was lowest during phase 1 and highest during phases 2 and 3. The ratio of oestradiol:progesterone was significantly different between phases 1 and 2, 2 and 3, and 2 and 4 (all P < 0.001), while concentrations of total testosterone did not change. The ratio of oestradiol:progesterone was highest during phase 2. The mean ± S.D. concentrations of total 17ß-oestradiol, progesterone, testosterone and oestradiol:progesterone ratio during IVF treatment are presented in Table 2.
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Muscle strength (Fig. 1 and Table 3) did not significantly change as a result of IVF treatment (there were no significant differences between phases of treatment). Mean ± S.D. MVIF/CSA of the FDI muscle was 1.30 ± 0.29, 1.06 ± 0.38, 1.20 ± 0.29 and 1.26 ± 0.34 N mm–2 during phases 1, 2, 3 and 4 of treatment, respectively. Maximum voluntary isometric force per unit CSA of the FDI muscle was significantly correlated with the concentration of total testosterone (r = –0.52, P < 0.001), total 17ß-oestradiol (r = –0.37, P = 0.02) and bioavailable testosterone (r = –0.45, P = 0.01).
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Concentrations of total 17ß-oestradiol and hCG were significantly different between all stages of pregnancy (all P < 0.001). The concentration of 17ß-oestradiol was highest at 36 weeks of pregnancy and lowest 6 weeks postnatally. The concentration of hCG was highest during the first and third trimesters and lowest during the second trimester and following childbirth. Concentrations of hCG in excess of 60 000 mUI ml–1 and below 2 mUI ml–1 cannot be measured, so the concentrations of hCG in weeks 12 and 6 were reported as 60 000 and 2 mUI ml–1, respectively (although in reality they were greater than or less than these concentrations, respectively). Therefore, hCG could not be correlated with force during weeks 12 or 20 of this study.
The blood sample analyses showed that total progesterone levels were significantly different between weeks 12 and 36, 12 and 6, 20 and 36, 20 and 6, and 36 and 6 (all P < 0.001). The concentration of progesterone was highest during the third trimester and lowest following parturition. Significant differences in total testosterone concentration were observed between weeks 12 and 36, and 36 and 6 (all P < 0.001) and peaked at 36 weeks. The ratio of oestradiol:progesterone was significantly different between weeks 12 and 20, 12 and 36, 20 and 6 and 36 and 6; values were lowest postpartum and highest at 36 weeks of gestation. Table 2 shows the mean ± S.D. concentrations of total 17ß-oestradiol, progesterone, testosterone, hCG and oestradiol:progesterone ratio during pregnancy and following childbirth.
Table 2 shows the mean ± S.D. concentrations of bioavailable testosterone and bioavailable oestradiol during pregnancy and following childbirth. During pregnancy, the concentration of bioavailable testosterone was significantly greater during week 6 than during week 20 (P = 0.04), while the concentration of bioavailable oestradiol differed significantly between all stages (all P < 0.05), except between weeks 20 and 36. Bioavailable oestradiol was highest at 36 weeks and lowest 6 weeks postpartum.
Post hoc analysis revealed significant differences in MVIF/CSA of the FDI muscle between weeks 12 and 6 (P = 0.05), and 20 and 6 (P = 0.01). Strength was highest at 20 weeks and lowest 6 weeks postnatally (Fig. 2 and Table 3). When all reproductive hormone data were compared with all force data, a significant negative correlation between MVIF/CSA of the FDI muscle and total testosterone concentration (r = –0.38, P = 0.02) and bioavailable testosterone (r = –0.43, P = 0.02) was noted during and following pregnancy. Force did not significantly correlate with any other female reproductive hormone at any time during pregnancy or postpartum.
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Discussion |
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The findings from this study strongly agree with investigations by Greeves et al. (1997) and Janse de Jonge et al. (2001). Greeves et al. (1997) showed, using patients undergoing IVF treatment, that submaximal (10–100 pmol l–1) and supra-physiological (1551–9935 pmol l–1) amounts of 17ß-oestradiol did not cause any changes in MVIF of the FDI muscle. Similarly, the present study found that strength did not significantly differ between low (70.6 ± 36.7 pmol l–1) and high (6664.7 ± 2716.9 pmol l–1) oestrogenic states. Moreover, MVIF/CSA of the FDI muscle did not significantly correlate with oestradiol during any phase of IVF treatment. Although Greeves et al. (1997) did not measure gonadotrophin levels, they proposed that LH and FSH reacted in a similar manner to oestradiol during phases 1 and 2 of IVF treatment. Therefore, these authors suggested that fluctuations in progesterone alone, or in combination with other reproductive hormones, might be responsible for the changes in strength reported following the menopause and throughout the menstrual cycle (Phillips et al. 1993, 1996). In the present study, maximum force did not change when 17ß-oestradiol and progesterone concentrations were at supra-physiological levels simultaneously (phase 3) or when 17ß-oestradiol levels had declined but progesterone levels remained significantly elevated (phase 4). Additionally, progesterone did not significantly correlate with force at any stage of IVF treatment. Based on this evidence, the suggested effects of progesterone are doubtful. It is also unlikely that the ratio of oestrogen:progesterone concentration affects maximum force, since strength did not correlate with or vary as a result of changes in this ratio at any time.
Janse de Jonge et al. (2001) found that muscle strength and fatigability were unchanged across the menstrual cycle despite significant changes in total oestrogen, progesterone, LH and FSH concentrations. Phases 1, 2 and 3 of the present study corresponded to the menstrual, late follicular and luteal phases of the menstrual cycle used by Janse de Jonge et al. (2001). Although the phases were identical in design, they were considerably different in magnitude. In the present study, 17ß-oestradiol and progesterone concentrations were notably lower during phase 1 and distinctly higher during phases 2 and 3 than during the corresponding phases in the study of Janse de Jonge et al. (2001). Although the present study succeeded in emphasizing the differences in 17ß-oestradiol and progesterone concentrations between phases, force production did not change between phases. These observations provide further support for the hypothesis that even supra-physiological levels of oestrogen and progesterone do not influence maximum isometric muscle force.
Conversely, Phillips et al. (1996) demonstrated a significant increase (10%) in volitional maximum isometric force of the adductor pollicis muscle during the follicular phase of the menstrual cycle. These authors also showed differences in strength at ovulation (strength declined) and during the luteal phase (strength was significantly higher when compared with the first 3 days of the cycle). Phillips et al. (1996) suggested that changes in muscle strength across the menstrual cycle were related to or caused by fluctuations in oestrogen, even though oestrogen did not significantly correlate with muscle strength. Subsequently, the authors proposed that oestrogen has a delayed inotropic onset. The reasons for these differences in results between Phillips et al. (1996) and the present study, and between Greeves et al. (1997) and Janse de Jonge et al. (2001), are not clear, although they may be partly accounted for by two methodological considerations. First, Phillips et al. (1996) assumed maximum isometric force was achieved but did not confirm it. Second, since only 9 out of 27 subjects provided venous blood samples (2–3 samples were taken 2–7 days apart around the expected time of ovulation), cycle phases were not assured. Furthermore, data from the work of Phillips et al. (1996) are hard to compare with other investigations because the exact frequency and timing of testing were not stipulated and regression analysis and interpolation was used to predict force as a function of cycle day. The present study, Janse de Jonge et al. (2001) and Greeves et al. (1997) used percutaneous electrical stimulation and venous blood samples to establish the extent of neural activation and the concentration of circulating ovarian hormones, respectively.
Contrary to the non-significant findings of Phillips et al. (1996), a significant negative correlation (r = –0.37, P = 0.02) between strength and 17ß-oestradiol concentration was observed in this study. This supports the data of Bassey et al. (1996), who found a significant negative correlation between 17ß-oestradiol levels and handgrip strength during the menstrual cycle. In the present study, however, when the extreme outliers were removed and the data re-analysed the relationship between strength and 17ß-oestradiol concentration was no longer significant (r = –0.31, P = 0.12). A similar relationship was identified for total (r = –0.52, P = 0.00) and bioavailable (r = –0.45, P = 0.01) testosterone, but given that strength and testosterone concentration remained constant throughout the experiment and the removal of the outliers resulted in a non-significant relationship (r = –0.24, p = 0.06 for total and r = –0.34, P = 0.06 for bioavailable testosterone), it is likely that a type I error occurred.
Supra-physiological changes in the concentration of total 17ß-oestradiol and testosterone resulted in significant changes in the bioavailability of oestradiol and testosterone during IVF treatment. Despite these changes, maximum force production was unaffected. The bioavailability of oestradiol and testosterone refers to the free and the albumin-bound portion of the hormone and is the form of the hormone that is able to exert a physiological effect. These findings provide further support for the hypothesis that reproductive hormones do not have an independent effect on muscle strength.
A cross-sectional analysis of muscle strength was also examined during each trimester of pregnancy and following childbirth in 35 women. Postnatal strength (6 weeks postpartum) was significantly lower than strength during the first two trimesters of pregnancy (weeks 12 and 20). During weeks 12 and 20, concentrations of progesterone, 17ß-oestradiol and hCG were also significantly elevated when compared with postnatal values. However, MVIF/CSA of the FDI muscle did not correlate significantly with any of these hormones. Therefore, it seems unlikely that changes in strength during pregnancy are dependent on sex hormones. General experience (anecdotal evidence) suggests that sleep is compromised and daily activity increased following childbirth, which may be directly (e.g. loss of concentration) or indirectly (e.g. fatigue) responsible for the significant decrease in muscle strength observed postpartum. In addition, the rapid decline in progesterone levels experienced following childbirth has been associated with increased fatigue owing to a combination of the sedative effects of progesterone, decreases in monoamine levels, and depressive action on cerebral metabolism (Glick & Bennett, 1981). Further research examining the effects of sleep deprivation and altered habitual activity following parturition is warranted.
Maximum force production and testosterone concentration were significantly lowered postpartum. A significant negative correlation was observed between these two variables (r = –0.38, P = 0.02), which suggests that the relationship between strength and testosterone concentration postpartum is coincidental rather than causal. Moreover, the significant negative correlation observed between MVIF and testosterone concentration is negated by removing the two most extreme outliers (r = –0.17, P = 0.34), which suggests that a type I error occurred.
During pregnancy, changes in bioavailable oestradiol were accompanied by similar changes in the total concentration of 17ß-oestradiol. Based on the concentration of total testosterone, bioavailable testosterone would be expected to be lowest 6 weeks postpartum. However, bioavailable testosterone was significantly higher following childbirth than during the first trimester of pregnancy (week 12), which may be accounted for by the fact that 17ß-oestradiol and sex hormone binding globulin levels were higher during week 12 of pregnancy than during week 6 postpartum. In general, bioavailable testosterone remained in the range of non-pregnant women but with a tendency to increase towards delivery. Similarly, Kerlan et al. (1994) showed comparable concentrations of bioavailable testosterone throughout pregnancy, except during the final trimester when the concentration of bioavailable testosterone was significantly higher than at week 10 (P < 0.05).
Although the concentration of reproductive hormones increases during pregnancy and decreases following the menopause, the effects of pregnancy and the menopause on muscle strength can be compared because both models produce chronic substantial changes in the concentration of oestrogen and progesterone. The present findings agree with previous work examining the effects of chronic sex hormone deprivation on muscle strength (Young et al. 1984; Frontera et al. 1991; Bassey et al. 1996). These studies indicated that, after controlling for differences in habitual activity and muscle mass, strength was similar in young and old women (that is strength did not change as a function of reproductive status). Of the studies that have shown decreased strength following or around the time of the menopause (Rutherford & Jones, 1992; Phillips et al. 1993; Greeves et al. 1999), none has presented longitudinal data (i.e. strength measured pre- and postmenopause using the same subjects) showing a significant relationship between ovarian hormones and strength. Furthermore, only one (Skelton et al. 1999) of the studies showing increased strength with chronic HRT administration (Phillips et al. 1993; Heikkinen et al. 1997; Greeves et al. 1999) has demonstrated a significant correlation between strength and reproductive hormones. Skelton et al. (1999) found that, following 1 year of HRT administration, individual trends in maximum voluntary force of the adductor pollicis muscle were significantly correlated with initial oestrone concentration (r = 0.378) and initial maximum voluntary force (r = –0.522). However, these variables only accounted for 34% of the variance between individuals displaying an increase in strength following HRT administration and control subjects. These results are in contrast with the present study, which showed that, although MVIF/CSA of the FDI muscle was significantly greater when 17ß-oestradiol (a more potent oestrogen than oestrone) levels were significantly higher, one was not significantly correlated with the other. Moreover, although oestrone concentration was not measured during this study, plasma oestrone levels are expected to increase by at least 3-fold during pregnancy (Fotherby, 1984), which is of greater magnitude than the change observed by Skelton et al. (1999) (2.5-fold increase). It must be noted however, that Skelton et al. (1999) only found a significant increase in force after several months of HRT. Initially, Skelton et al. (1999) found that HRT did not influence force production despite increases in plasma oestrogen levels, which is in agreement with the results from the fertility part of the present study. These initial similarities support the need for future research to examine the chronic effects of hormone manipulation on the same subjects.
Pregnancy causes considerably greater changes in 17ß-oestradiol concentration than HRT or the menstrual cycle. During this study, the concentration of 17ß-oestradiol increased by approximately 21-fold. In comparison, Skelton et al. (1999) found that 17ß-oestradiol levels had only risen by roughly 248% following 1 year of HRT (0.625 mg conjugated oestrogen daily and 0.15 mg of norgesteral taken for 12 consecutive days during each 28 day cycle). During the menstrual cycle, Janse de Jonge et al. (2001) reported changes in 17ß-oestradiol concentration of about 117.65%. Therefore, it is evident that the present study has investigated changes in 17ß-oestradiol concentration of greater magnitude than previous research.
To summarize, no significant changes in MVIF/CSA of the FDI muscle were noted following acute (IVF) or chronic (pregnancy) supra-physiological changes in ovarian hormone levels in healthy premenopausal women. Both conditions, physiological (pregnancy) and pseudo-physiological (IVF), failed to elicit a statistically significant change in muscle strength. Moreover, significant differences in the bioavailability of oestradiol and testosterone did not affect maximum force production. The findings from the present study suggest that changes in muscle functionality following the menopause or during the menstrual cycle cannot be accounted for by changes in reproductive status. We suggest that future studies adopt a longitudinal study design, so that comparisons of muscle strength under the influence of different hormone levels can be made in the same individual. The present study is limited by its cross-sectional design and therefore intersubject variability might have masked any potential significant alterations.
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