The effect of reproductive hormones on muscle function in young and middle-aged females.
The menopause is associated with a deficiency of reproductive hormones, and accompanied by a
significant loss of bone mass. This bone loss is accelerated within the first five years post-menopause.
Muscle strength at this time would have important clinical implications for correcting imbalance and
preventing falls. The aim of the studies within this thesis were to 1) determine the rate and time course
of force loss of the quadriceps muscle group over 12 months in three groups of women with varying
hormonal status 2) establish the role of oestrogen in this weakness and 3) investigate the effectiveness of
hormone replacement therapy (HRT) in maintaining muscle function.
The reliability of an isokinetic dynamometer and a strain gauge assembly was examined initially to
determine the inherent variability of muscle function assessment. Strength of the knee extensors
measured on the isokinetic dynamometer was deemed reliable in middle-aged women, although at 1.05
rad/s more practice trials were needed to attain peak torque. Measurements of the knee flexors were
highly variable. Maximal voluntary isometric contractions were repeatable using the strain gauge
system, for both the knee extensors and first dorsal interosseus (FOI) muscle. There was greater
variability in force production generated from electrically stimulated contractions.
Maximal strength of the knee extensors declined by 9.3±4.6 and I0.3±3.1% (mean±SE) for dynamic
(1.05 radls) and isometric strength respectively over 9 months in hypoestrogenic post-menopausal
women. There were no changes at higher angular velocities, or for handgrip strength. These results
support the role of reproductive hormones in influencing force production, which is further endorsed by
the observation that females on HRT did not experience a reduction in strength over this time. The force
loss was significant only when the post-menopausal and HRT group were compared (p<0.05). The postmenopausal
group were within I to 3 years past the menopause, the time period in which bone loss is
rapid. This rapid loss of strength would therefore be expected to level out, similarly to bone.
The menopause is an oestrogen-deficient and progesterone-deficient endocrinopathy. It is not possible to
identify which hormone, if not both, is responsible for these observed changes in strength. To explore
the relationship between acute changes in oestrogen and progesterone and strength, maximal force
production of the quadriceps and first dorsal interosseus (FOI) was measured across the menstrual cycle.
Maximal strength of the quadriceps was lowest prior to the surge in luteinizing hormone (LH) and
reached its peak mid-luteal, a difference of 12.6±4.3% (mean±SE). These changes were significantly
different (pO.OS).The difficulty in isolating oestrogen during the menstrual cycle does not render this a
good model to assess its effects upon force production. Maximal strength and fatiguability of the FDI
were examined in young women undergoing in vitro fertilisation (IVF) treatment when acute, massive
changes in oestrogen are induced. There were no differences in muscle function of the FDI when
assessed under very low or high oestrogen changes (p>O.05). The independent effects of oestrogen upon
muscle function were not demonstrated here.
Hormone replacement therapy is the most efficacious treatment for preventing menopausally-related
bone loss. The results from the longitudinal study suggest that HRT confers protection against muscle
weakness as a consequence of ovarian failure. Whether HRT maintains or restores strength was
examined in the FDI of post-menopausal women (n=9). The oestrogen only and oestrogen-progestogen
phases were compared with baseline measurements. A positive change in strength was observed,
although this did not reach significance (p