Heat stress due to climate warming can significantly affect the synthesis of sex hormones in male adolescents, which can impair the ability of the hypothalamus to secrete gonadotropin-releasing hormone on the hypothalamic-pituitary-gonadal axis, which leads to a decrease in luteinizing hormone and follicle-stimulating hormone, which ultimately negatively affects spermatogenesis and testosterone synthesis. Heat stress directly affects the testes, damaging them and reducing testosterone synthesis. Low levels of testosterone in male adolescents lead to delayed puberty and incomplete sexual maturation, negatively affect height growth and bone mineral density, and can lead to a decrease in lean body mass and an increase in fat mass.

Heat stress has been shown to reduce testosterone synthesis by damaging the testicles, which is due to various mechanisms, such as increased oxidative stress, disruption of steroidogenic enzyme expression, and apoptosis of Leydig cells. Heat stress due to climate warming can significantly affect the synthesis of sex hormones in male adolescents, which can impair the ability of the hypothalamus to secrete gonadotropin-releasing hormone on the hypothalamic–pituitary–gonadal axis, which leads to a decrease in luteinizing hormone and follicle-stimulating hormone, which ultimately negatively affects spermatogenesis and testosterone synthesis. It has been drawing attention that the dysfunction of HPG axis caused by heat stress can ultimately lead to decreased testosterone levels.

“Stress increases serum glucocorticoids, and a number of in vitro studies have shown that glucocorticoid directly inhibits testosterone production by Leydig cells.” The authors note that “stress-mediated elevations in circulating glucocorticoid levels lead to corresponding rapid declines in testosterone production by Leydig cells in the testis.” They further state that “glucocorticoids act directly on Leydig cells to inhibit testosterone biosynthesis… Elevations in circulating glucocorticoids during stress including restraint stresses and psychosocial stresses of subordinate rats can, therefore, cause suppression in androgen secretion at the level of the testis.”

The hypothalamic–pituitary–adrenal (HPA) axis and glucocorticoids are major regulators of the organism’s responses to stress. Numerous studies report **sex differences in glucocorticoid (cortisol in humans) responses to stress and in stress-related pathologies**. The review notes that **testosterone exposure during the prepubertal period is important for the masculinization of glucocorticoid responses to stress in adulthood**, and that various molecular mechanisms explain sex-specific glucocorticoid stress responses.

This review states that “elevated levels of glucocorticoids are also associated with decreased testosterone biosynthesis by Leydig cells.” It explains that glucocorticoids “directly inhibit the transcription of genes encoding testosterone biosynthetic enzymes, such as… steroidogenic acute regulatory protein (StAR)… and CYP17” and that “glucocorticoid treatment in mouse Leydig cells can inhibit cAMP formation within 15 minutes, and a rapid decline in testosterone production is seen by 30 minutes.” In humans, the authors note that males in high-stress military training with “elevated levels of serum cortisol demonstrate maximal testosterone suppression but levels of LH similar to baseline,” indicating a direct testicular effect.

Prolonged or severe stress has been found to inhibit the hypothalamic-pituitary-gonadal axis (HPG) and its testosterone release. In particular, during short- and long-term military field exercises with physical stress, a significant increase in cortisol levels and a simultaneous decrease in testosterone levels have been found. Various acute stressors in the military environment resulted in a transient co-activation of both the HPA and HPG axes and their hormone release, whereas intense and prolonged stress resulted in inhibition of the HPG axis and its testosterone release.

In contrast, acute stress induces a rapid increase in serum concentrations of cortisol followed by a decrease in the serum concentration of testosterone. This study demonstrated that beyond stress, the key stress system genes might affect cortisol levels, which in turn affect testosterone figures via the Gαs-cAMP/PKA signaling pathway. These findings imply that increased CYP17 and FKBP5 expression may cause SHBG suppression in the testes, which results in a drop in testosterone levels.

The abstract summarizes that “glucocorticoid (GC) inhibits testosterone production in adult Leydig cells by the glucocorticoid receptor (GR).” The study shows that treatment with synthetic glucocorticoid “significantly suppressed hCG-stimulated testosterone production” in rat Leydig cells and that this suppression was mediated by GR signaling, reducing the expression of key steroidogenic genes. The authors conclude that glucocorticoids “suppress steroidogenesis” in Leydig cells, providing a mechanism for stress-related decreases in androgen production.

This review summarizes data showing that **acute physical and psychological stressors elevate cortisol and can transiently suppress testosterone in men**. It reports that intense exercise and overtraining are associated with **increased cortisol and decreased resting testosterone**, altering the testosterone:cortisol ratio which is often used as an index of anabolic–catabolic balance in athletes.

This clinical review states that **both exogenous glucocorticoids and chronic activation of the HPA axis (elevated cortisol) can suppress the hypothalamic–pituitary–gonadal axis in men**. It explains that glucocorticoids reduce GnRH and LH secretion and can act directly on Leydig cells, **resulting in reduced testosterone levels**, impaired spermatogenesis and reduced fertility.

The paper notes that **chronic glucocorticoid therapy or endogenous Cushing’s syndrome (excess cortisol) is frequently associated with male hypogonadism**, characterized by **low serum testosterone**. Mechanistically, glucocorticoids suppress hypothalamic and pituitary function and can have direct inhibitory effects on Leydig cells, leading to reduced testosterone production and typical hypogonadal features such as decreased muscle mass and reduced secondary sexual characteristics.

In this classic human study, administration of pharmacological doses of hydrocortisone (a glucocorticoid) to healthy men **reduced basal and GnRH-stimulated LH secretion and led to a significant fall in plasma testosterone levels**. The authors concluded that glucocorticoids can acutely inhibit the hypothalamic–pituitary–gonadal axis and decrease circulating testosterone in men.

Results: Our data show a delayed effect of exercise in cold after 7 days of recovery in the total plasma levels of testosterone (56% increase vs baseline) and cortisol (54% increase vs baseline), with no difference immediately after physical training in cold. Conclusion: A 5-day period of daily exercise in a cold environment showed no immediate effects, but a potential to elicit adaptive changes delayed for up to 7 days, leading to a significant increase in steroid hormones, without changing the testosterone/cortisol ratio.

This review notes that “through their receptors at each level of hypothalamo-pituitary-gonadal axis glucocorticoid excess, either endogenous or administered or stress-induced, could affect steroid production in the testis and thus male fertility.” It emphasizes that “a number of studies dealt with various aspects of GC effect on Leydig cell steroidogenesis. A decrease of testosterone production after GC treatment was observed… Later studies on rats definitely proved direct inhibitory effect of GC on expression on two enzymes of testosterone biosynthesis, namely 3β- and 17β-hydroxysteroid dehydrogenase.” The authors state that glucocorticoids “affect expression and function of steroidogenic enzymes” and that local 11β-hydroxysteroid dehydrogenase regulates glucocorticoid access to testicular cells.

Air temperature significantly affected the human salivary cortisol concentration. The more comfortable the environment, the lower the cortisol concentration. When compared to cold and warm temperature conditions, the thermal sensation vote and thermal comfort vote of subjects exposed to comfortable temperature conditions for a short time were more neutral and comfortable, with the lowest cortisol levels.

In men, prolonged exposure to extreme temperatures inhibits testicular steroidogenesis and spermatogenesis, and results in reduced circulating testosterone and semen quality. In males, sustained exposure to high heat levels can hinder testicular steroidogenesis and spermatogenesis, which in turn reduces testosterone levels and semen quality. Heat stress disrupts the production of hormones crucial for male reproductive health.

In this paper summarizing steroid cross talk, the authors state that “glucocorticoid binds to GR to inhibit testosterone production in Leydig cells.” They discuss that adrenal glucocorticoids, acting via glucocorticoid receptors, negatively regulate Leydig cell steroidogenesis, while other steroid receptors (such as mineralocorticoid receptors) can have stimulatory effects, highlighting a direct inhibitory pathway of glucocorticoids on testosterone synthesis within Leydig cells.

This overview reports that **physical and psychological stress can impair male reproductive function through activation of the HPA axis and elevated glucocorticoids**. It notes that stress-induced glucocorticoids can suppress GnRH and gonadotropin secretion and reduce Leydig cell steroidogenesis, thereby **lowering circulating testosterone** and contributing to reduced libido, impaired spermatogenesis, and other changes in male secondary sexual characteristics.

Gonadal steroids play an important role in the development and expression of sexually dimorphic traits, including differences in HPA axis responses to stress. Testosterone and estradiol modulate central HPA axis regulation, contributing to sex differences in stress reactivity and downstream physiological and behavioral outcomes. Alterations in gonadal steroid levels can therefore influence sexually dimorphic traits that depend on these hormones.

This experimental study reports that treatment of adult rat Leydig cells with glucocorticoids “resulted in a significant increase in Leydig cell apoptosis” and that chronic exposure “decreased serum testosterone levels by reducing the numbers of Leydig cells per testis.” The authors link chronic glucocorticoid excess with both functional suppression of steroidogenesis and loss of testosterone-producing cells, suggesting a mechanism by which prolonged stress hormones can lower circulating testosterone.

In this in vitro study, rat Leydig cells exposed to physiologically relevant corticosterone concentrations showed “dose-dependent inhibition of testosterone production.” The authors report that corticosterone treatment reduced LH/hCG-stimulated testosterone synthesis and that the effect was blocked by a glucocorticoid receptor antagonist, indicating a receptor-mediated action. They conclude that stress-level increases in glucocorticoids can directly inhibit Leydig cell testosterone secretion.

High levels of the stress hormone cortisol play a critical role in blocking testosterone's influence on competition and domination. The findings show that when cortisol increases, the body is mobilized to escape danger, rather than respond to any influence that testosterone is having on behavior. According to research, chronically elevated cortisol levels can produce impotence and loss of libido by inhibiting testosterone production in men. In women, chronically high levels of cortisol can produce severe fertility problems and result in an abnormal menstrual cycle.

Reviewing human and animal data, the authors note that “acute and chronic stressors are associated with elevated cortisol levels and concomitant suppression of circulating testosterone.” They describe that glucocorticoids “inhibit testicular steroidogenesis at multiple levels,” including direct actions on Leydig cells and modulation of hypothalamic–pituitary signaling. The review highlights studies in which psychological or physical stress raised cortisol and led to reduced testosterone concentrations without major changes in gonadotropins, indicating a peripheral effect.

This article explains that activation of the hypothalamic–pituitary–adrenal (HPA) axis during stress elevates cortisol, which “exerts inhibitory effects on the hypothalamic–pituitary–gonadal axis and directly on the testis.” The authors summarize that cortisol and other glucocorticoids “suppress Leydig cell steroidogenesis, resulting in reduced testosterone production.” They also discuss how chronic stress-related hypogonadism can influence secondary sexual characteristics and reproductive function in males.

In a study of males undergoing combat training, the authors found that “sustained physical and psychological stress produced persistent elevations in cortisol accompanied by significant reductions in serum testosterone.” They report that despite reduced testosterone, “LH concentrations remained within the normal range,” suggesting that increased glucocorticoids during stress suppressed testicular testosterone production rather than pituitary drive. The paper links stress-induced cortisol with hypogonadal changes in young men.

Generally speaking, chronic stress is likely to lower your testosterone levels. Because of this, and the negative feedback loops we discussed earlier, persistently high cortisol can dampen the HPG axis too, preventing testosterone release. Cortisol is also thought to reduce testosterone production directly by acting on the Leydig cells (found in the testes). Some short-term stressors, like exam stress, may temporarily increase testosterone levels up to a certain threshold, but chronic stress with persistently high cortisol tends to lower testosterone.

Chronic cortisol suppresses testosterone production through a complex biological rivalry between your stress response system and reproductive hormone pathways. When cortisol remains elevated, it directly suppresses the hypothalamus from releasing gonadotropin-releasing hormone (GnRH). This creates a domino effect: reduced GnRH leads to lower luteinizing hormone (LH) and follicle-stimulating hormone (FSH), which are essential signals that tell your testicles to produce testosterone. A comprehensive 2023 analysis published in Nature revealed that cortisol spikes predict testosterone drops occurring 0.5 to 3 days later, establishing a clear temporal relationship between stress hormone elevation and testosterone suppression.

The paper states that **high levels of testosterone are primarily responsible for development of masculine facial morphologies**, such as pronounced brow ridges and jawlines, which are classic **sexually dimorphic traits**. It discusses how variation in testosterone-related development influences the degree of facial sexual dimorphism across populations.

Chronic stress increases cortisol which in turn can reduce your testosterone levels. Increased cortisol levels due to stress can negatively impact your testosterone production. When your cortisol levels spike under stress, your body blocks testosterone as a response. Excess cortisol can lead to a decrease in testosterone. Chronically high cortisol levels due to chronic stress can lead to constantly low testosterone levels, which can significantly impact your body and result in chronic symptoms and health issues.

The thesis reviews literature showing that **elevated cortisol levels are correlated with decreased testosterone levels in men, and with increased testosterone levels in women** (citing both human and rodent studies). It further notes that testosterone is an important anabolic factor that counteracts deleterious effects of elevated cortisol on muscle, and that sex hormones have important interactions with cortisol and its effects on muscle, a sexually dimorphic tissue.

In Pacific abalone, the authors report that **thermal stress (high water temperature) significantly decreased hemolymph testosterone levels** compared to normal temperature conditions. The study concludes that **thermal stress has a repressive effect on gonadal maturation and reproduction**, partly through changes in GnRH-related gene expression and testosterone, a key sex steroid mediating sexually dimorphic reproductive traits.

Larvae maintained at a masculinizing high temperature (29 °C) **had higher cortisol, 11-ketotestosterone, and testosterone titres** than those at a feminizing temperature (17 °C). Administration of cortisol and a glucocorticoid receptor agonist at a neutral temperature **increased the proportion of males**, and the authors conclude that their results "provide clear evidence of a relationship between stress (cortisol) and gonadal masculinization" during thermal sex determination. This shows that **thermal stress–induced cortisol can modulate sex steroid pathways and sexually dimorphic gonadal traits**, although in this species it increases androgens rather than decreasing them.

Acute stress is a short-term problem, while chronic stress is prolonged, during which cortisol levels stay high for an extended period. Both forms of stress can suppress your testosterone levels in different ways, but testosterone reduction caused by acute stress is temporary. Elevated cortisol levels can disrupt hypothalamic-pituitary-testicular (HPT) function and, eventually, testosterone production. Cortisol can reduce the production of luteinizing hormone (LH) from the pituitary, which is required to activate the testes for testosterone formation, and raised cortisol levels increase the aromatase enzyme activity that converts testosterone into oestrogen.

Research indicates that under stressful conditions, cortisol acts to suppress testosterone production. Increased cortisol levels suppress endocrine signaling, leading to decreased testosterone. Studies show that increased cortisol directly inhibits testosterone production by inhibiting the Leydig cells in the testes. Testosterone levels are reduced in response to psychological, physical, and acute (e.g., surgery) stress, and the processes that regulate cortisol and testosterone levels are antagonistic.

This study in a fish model investigates high-temperature stress and sex reversal. It cites previous work showing that **cortisol and androgen pathways cross-talk in high temperature–induced masculinization**, and that **environmental stress-induced testis differentiation can involve androgen production as a by-product of cortisol inactivation**. The authors emphasize that high temperature stress can change sex ratios and sexually dimorphic gonadal traits via interactions between cortisol and androgens.

Testosterone is a key androgen underlying sexually dimorphic traits such as increased muscle mass, body hair, and male-pattern facial features. Chronic suppression of testosterone, whether via direct testicular effects or via hypothalamic-pituitary-gonadal axis inhibition by elevated cortisol, is associated with reduced secondary sexual characteristics over time, including decreased muscle mass, changes in fat distribution, and reduced libido. These traits are part of the sexually dimorphic phenotype in humans and other vertebrates.

Chronic stress triggers the hypothalamic-pituitary-adrenal axis leading to the release of corticotropin-releasing hormone from the hypothalamus, stimulating the anterior pituitary to produce adrenocorticotropic hormone and promote the adrenal glands to secrete cortisol. Elevated cortisol levels inhibit the hypothalamic-pituitary-gonadal axis, causing a disruption to the regulation of testosterone production through decreased GnRH secretion, reduced LH release from the pituitary gland, and impaired Leydig cell function in the testes, ultimately resulting in diminished testosterone synthesis. Cortisol actually competes with testosterone for binding to carrier proteins such as sex hormone binding globulin, so as cortisol levels rise, more binding globulin becomes occupied, leading to a decrease in free bioavailable testosterone.