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Better sleep and improved body composition have obvious downstream effects on mood and energy levels. Start with regular exercise, which boosts your body's sensitivity to hormones. Common options include TSH (thyroid-stimulating hormone) tests to evaluate thyroid function, as well as tests for growth hormone and IGF-1, which tend to decrease naturally as we age. For example, growth hormone secretion diminishes by about 14% per decade after age 30, while DHEA levels plummet to just 10–20% of their peak by the age of 80. This physical transformation correlates with a 50% drop in growth hormone production by the age of 60. Resistance training helps counteract muscle loss, and modest caloric restriction (reducing intake to 75–80% of baseline) can further support hormonal balance and insulin function. Free testosterone levels drop even faster due to a yearly 2.7% increase in Sex Hormone-Binding Globulin (SHBG), which limits hormone availability.
On the other hand, treatable disorders often involve more noticeable issues, such as ongoing fatigue, unexpected weight changes, or challenges with sexual function. While hormone replacement therapy might seem like an easy fix, it’s not a one-size-fits-all solution. They also blur the line between normal aging and treatable endocrine disorders, making accurate clinical assessment even more crucial. The endocrine system experiences noticeable shifts as we age, with hormonal changes influencing almost every aspect of health.
Conversely, impaired testosterone responsiveness to RE in older adults, likely attenuates the AR response, due to lack of testosterone mediated AR increases, and subsequently, limits muscle mass gains with RET. Given the concentration of SHBG increases across the lifespan in men (Liu et al., 2007) and only increase after ~60 y in women (Maggio et al., 2008), bioavailable testosterone (free plus albumin-bound testosterone) concentrations decline even more markedly than total testosterone levels with aging (Matsumoto, 2002). That being said, the importance of testosterone in women remains unclear since while there is an indispensable role e.g., on bone health, in older males (Mohamad et al., 2016), a reduction in testosterone generally does not occur independently of other hormones (such as the oestrogens) in females (e.g., following the menopause) (Chakravarti et al., 1976). Whilst the majority of investigations into the role of testosterone in muscle adaptive response have been performed in males (reflecting male biology), the importance of circulating concentrations of testosterone in adult women should not be underestimated based on its biological role in the conversion of progesterone to the principal oestrogens—oestradiol and oestrone (Cui et al., 2013). In an attempt to better understand the discrepancies between testosterone and muscle adaptive responses, Phillips and colleagues devised a unique experimental approach, whereby they compared a "high" vs. "low" hormone environment (induced by working distinct muscle bulk) (West et al., 2010). For example, immediately following RE, serum testosterone levels peak ~from 13 (resting levels) to 38 (at ~30 mins) nmol.L−1 with a concomitant upregulation of AR mRNA and protein content within the muscle (Willoughby and Taylor, 2004; Hooper et al., 2017). RE has been shown to increase the concentration of these hormones which activate several different signaling pathways in the muscle.
Hormonal patterns are obviously physiologically distinct in females and males, complicating true clarity of the isolated effects e.g., of the sex hormones (higher testosterone levels may play an important role for the adaption to RET in men; whereas in premenopausal women, estrogen may enhance the sensitivity to anabolic stimuli). The effects of acute estrogen release may relate to a reduction in exercise-induced muscle damage and improved recovery (Hansen, 2018), possibly via its indirect antioxidant properties and stabilization of cell membranes (Paroo et al., 2002) and decreased post-exercise production of protein chaperones- i.e., heat shock protein (HSP) 72 (Paroo et al., 1999) and HSP70 (Enns and Tiidus, 2010). While the acute response of testosterone returns to baseline rapidly post exercise and has been shown to not be elevated chronically following repeated bouts of RE (Hooper et al., 2017); the acute upregulation of AR mRNA and protein content can last up to 1–2 days post RE (Ratamess et al., 2005), thereby augmenting testosterone uptake into the muscle, and potentiating the anabolic effects of testosterone over longer periods (Murphy and Koehler, 2020; Tinline-Goodfellow et al., 2020). Maintenance of skeletal muscle mass throughout the life course is key for the regulation of health, with physical activity a critical component of this, in part, due to its influence upon key hormones such as testosterone, estrogen, growth hormone (GH), and insulin-like growth factor (IGF). However, there is growing evidence for selected anabolic hormones to influence the form and function of the motoric system, and, as such, there is a need for increased research in this area. Human studies examining increased muscle strength and physical function with elevated endogenous hormone levels or exogenous hormone replacement have examined muscle function, but to our knowledge, none have placed particular emphasis on endocrine actions on components of the motoric system.
Although blockade of IGF-1 reduced axon outgrowth, the CSMNs were still viable, suggesting cell death and axon morphology were dissociated. The remaining IGF-1 in the body is extrahepatic, and a study in mouse cell lines suggests IGF-1 is produced locally in tissues to have autocrine/paracrine actions (Tollefsen et al., 1989). Furthermore, compared to normal untreated specimens, saporin causes 63% dendrite morphology reduction in quadriceps motor neurons of treated female rats. However, ARs are found in all spinal motor neurons of adult male and female rats (Sar and Stumpf, 1977, MacLusky et al., 1987, Lumbroso et al., 1996), which confer other important androgen-mediated properties to motor neurons.

Gender: Female