Acute Changes in Cortisol and Muscle Steroids in Resistance-Trained People
Written by Ben Bunting: BA, PGCert. (Sport & Exercise Nutrition) // British Army Physical Training Instructor // S&C Coach.
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Neither the high hormone (HH) nor low hormone (LH) protocols induced serum steroid concentration increases that seemed related to muscle steroid concentration changes (cortisol only). This may have been caused by an extended interval between preexercise measurements and postexercise evaluations.
Network analyses of gene expression profiles regulated by acute ECC and CON in exercise-habituated muscle revealed a generic ECC response characterized by upregulation of genes involved in cytoskeletal organisation.
Cortisol
Cortisol is a hormone produced by your adrenal glands located on top of each kidney that controls your body's stress response. Like most hormones, cortisol serves multiple functions and has many complex processes within its matrix - it suppresses inflammation throughout all body tissues while controlling metabolism in muscle, fat, liver and bone cells, impacting sleep-wake cycles and even acting as a powerful anabolic agent when its levels match with stress-inducement levels.
Cortisol's effects depend on other steroid hormones present in working muscle. Testosterone stimulates protein synthesis but needs molecules called somatomedins in order to do so; similarly DHEA and DHT increase cortisol's effects by interacting with these same somatomedins - this combination is key to resistance training's overall effect on protein synthesis and muscular growth.
When your immune system encounters large quantities of antigen, your brain sends signals to your adrenal glands for them to produce cortisol in order to manage an excessive response from it. Ideally, the amount produced should match up with the level of antigen exposure so as to prevent overreacting of your immune system - this process is known as negative feedback loop. Unfortunately, however, regular exposure can make it hard for us to maintain the right level of cortisol production and may prevent it from matching.
Research has demonstrated that an acute increase in cortisol following resistance exercise does not result in significant changes to skeletal muscle steroid hormone concentrations, likely as a result of exercise and recovery periods being relatively brief, thus not significantly depleting liver glycogen and muscle tissue.
Cortisol may increase after resistance exercise, yet this increase may be offset by increases in growth hormone, testosterone and muscle specific somatomedins - which will preserve protein balance of muscles. Therefore, conducting an in-depth investigation of how resistance exercise affects serum and intramuscular steroid concentrations will allow us to gain a better understanding of how the interaction between the glucocorticoid hormone system and muscle steroid hormones works together.
Testosterone
Steroids are naturally-occurring hormones produced by our bodies to support physiological functions. They fall into two groups: anabolic and androgenic steroids, which promote muscle growth; and corticosteroids, which reduce inflammation. Steroids can either be natural or synthetic and administered either via injection, pill, or liquid form for treatment of various conditions.
Researchers have investigated the effects of testosterone on resistance training-induced increases in lean body mass, cross-sectional area of type 2 muscle fibers and strength; however, results have often been conflicting and inconsistent. To further clarify this discrepancy between studies by studying acute changes in serum and skeletal muscle steroid concentrations during and immediately following resistance exercise (RE), as well as examine its influence on muscle steroidogenesis capacity of skeletal muscles using this study as well.
Serum and skeletal muscle total and free testosterone, dehydroepiandrosterone, and dihydrotestosterone levels were measured using commercially available EIA kits from Cayman in Ann Arbor Michigan USA; ENZO Life Sciences in Farmingdale New York USA and IBL international in Hamburg Germany). For aromatization control injections of androstenedione were given, while muscle samples were homogenized using RIPA buffer and stored at -80 degC until analysis took place -all samples were analyzed twice for accuracy.
RE-induced increases in skeletal muscle testosterone, dehydroepiandrosterone and dihydrotestosterone concentrations were accompanied by an equally acute increase in the ratio of free to total testosterone concentrations. This change may reflect an increased ability of muscle cells to synthesize androgens from androstenedione; their production contributes to enhanced protein synthesis and anabolic effects within muscles.
Steroid medication works to decrease immune system response and lower rejection risks after organ transplant. Steroid medication may also be effective at relieving inflammation caused by conditions like COVID-19, asthma or other autoimmune diseases like Lupus and Vasculitis; and can even prevent kidney damage after heart attacks or stroke. Side effects vary according to dosage taken; local side effects can occur while systemic effects spread throughout your system and aid other parts of the body.
DHEA
Dehydroepiandrosterone (DHEA) is a naturally-occurring steroid hormone that serves as a precursor for androgens like testosterone and dihydrotestosterone, as well as estrogens like estradiol. Additionally, DHEA can be converted to cortisol - another glucocorticoid hormone responsible for managing stress reactions and blood pressure - by being converted back into its original state through conversion into cortisol.
DHEA levels may be low among certain individuals, particularly those living with ulcerative colitis and Crohn's disease. Studies indicate that taking DHEA supplements could improve these conditions; more research needs to be conducted. Furthermore, taking DHEA may have positive effects on memory; one study revealed that adults living with HIV who took supplementation improved both memory function and mental capacity as a result.
Though DHEA has long been seen as a "natural anabolic steroid" that promotes muscle growth, there is no scientific basis to this claim. DHEA does not act as a performance enhancer nor raise testosterone or luteinizing hormone (LH), yet does promote estrogen production among female athletes and increases bone mineral density among both premenopausal women and post-menopausal women alike - protecting against osteoporosis by aiding in calcium and phosphorous absorption.
Some researchers have proposed that DHEA supplements could help alleviate depression symptoms, though further study is required. Others have discovered that it can reduce inflammation, improve memory in older people with Alzheimer's disease and reduce symptoms associated with systemic lupus erythematosus (lupus). Some advocates claim DHEA can reverse aging while providing energy and motivation boosts while helping combat obesity prevention efforts; it may even enhance quality-of-life for postmenopausal women by reducing sexual drive and vaginal dryness during postmenopausal years.
The authors used a counterbalanced, within-subject, crossover design to assess the effects of resistance exercise on serum and skeletal muscle steroids. Participants performed single arm lateral raise or squat exercises at three laboratory visits; blood and muscle samples were obtained before exercise bout, immediately post bout, 45 min post session as well as 45 minutes later post exercise session using an ELISA assay system with intra-assay CV%'s of 6.38% for total DHEA, 8.32% for free DHEA respectively;
DHT
DHT (dihydrotestosterone) is an androgen that plays a significant role in male sexual organ and sex characteristic development. Produced by 5-alpha reductase and binding to testosterone receptors on testicles and other tissues, low DHT levels may cause males to suffer gynecomastia or testicular atrophy; male pattern baldness; androgen insensitivity syndrome is another possible consequence.
DHT exerts a direct effect on the growth of both penis and scrotum and is thus responsible for puberty in boys. Furthermore, DHT plays an integral role in hair growth during adolescence both body-wide and facially as well as its formation through androgen receptor formation on skin and prostate gland. Mutations which increase DHT production could lead to overactive prostates, larger breasts, or male pattern baldness among other adverse consequences.
DHT, as an androgen, interacts with androgen receptors on the scalp of growing hair follicles by binding to them, inhibiting protein, vitamin and mineral intake while decreasing size of follicle and miniaturizing hair shaft - leading to thin and sparse hair as follicles lose ability to produce thick, dense locks. Furthermore, it acts as an androgen by binding with androgen receptors in sebaceous glands, stimulating their expansion. Furthermore, its binding also causes changes to cell membranes as well as protein synthesis inhibition and cell turnover - leading to further hair thinning as follicles lose ability to produce thick dense locks.
Sensitivity to DHT differs greatly among individuals. Unfortunately, its cause remains elusive; genetic or environmental influences could play a part in this variance, perhaps through gene variants affecting 5-alpha reductase activity or changes to receptors for androgens.
Resistance exercise (RE) was found to increase serum concentrations of testosterone, DHEA and DHT; cortisol also rose significantly at specific postexercise time points; however RE did not appear to change steroid hormone concentrations in skeletal muscle due to albumin's ability to bind with circulating steroids.
Conclusion
Heavy resistance exercise (RE) has been demonstrated to generate high anabolic hormone concentrations; however, their exact mechanism remains unknown. A 2023 assessed acute changes in serum cortisol and growth hormone concentrations following different fatiguing RE protocols that featured short and long rest intervals between sets.
Six resistance-trained males participated in a counterbalanced within-subject design using either lateral raise (ten sets of 12 repetitions to failure, followed by three minutes rest) or squat exercises (5 sets of 8-12 repetitions, with 1 minute rest between sets) using immunoassays to measure serum and muscle testosterone, dehydroepiandrosterone sulfate dihydrotestosterone and cortisol levels.
Serum growth hormone (GH) and cortisol concentrations were significantly greater after exercising with either protocol, both at 15 min postexercise and 30 min postexercise, when compared to their levels following LH protocol exercise. Serum testosterone and dehydroepiandrosterone concentrations, however, did not show any increase postexercise regardless of which protocols were employed.
After performing the HH protocol, testosterone concentrations appeared to rise more than cortisol concentrations; suggesting that either RE type was not responsible for their rise, or that contractility did not influence this hormonal increase. Muscle steroid concentrations showed no change after both protocols, suggesting they weren't affected by either.
