The Effect of Exercise Training on Testicular Function

The Effect of Exercise Training on Testicular Function

Written by Ben Bunting: BA, PGCert. (Sport & Exercise Nutrition) // British Army Physical Training Instructor // S&C Coach.


Endurance (or aerobic) exercises like jogging and swimming can improve heart, lung and circulatory health, while strength-based resistance training strengthens muscles. Balance and flexibility exercises such as yoga can keep limber.

Exercise has been shown to reverse the declines seen with obesity or aging in testosterone, luteinizing hormone and follicle-stimulating hormone levels as well as sperm parameters. This effect likely stems from decreased oxidative stress and inflammation responses.

Effects of Exercise Training on Testicular Function

Exercise training's impact on the hypothalamus-pituitary-gonadal axis, testosterone, luteinizing hormone and follicle stimulating hormone levels and sperm parameters is complex.

Research demonstrates that it can depend on the type, intensity, duration and characteristics of an athlete's training program.

Furthermore, certain intrinsic characteristics (such as body mass index or age) may alter response to exercise training.

Though some studies demonstrate a beneficial impact of moderate-load exercise on testicular function, others do not.

This could be attributable to different experimental settings and exercises being utilized, or investigations that focus more on seminal fluid biomarkers rather than its structure and functionality of the testis itself.

Studies have demonstrated that oxidative stress levels increase as one ages. Yet its role in impaired testicular function remains uncertain, though diets low in fat could reduce this form of oxidative stress and improve testicular health.

Testicular volume can be determined by numerous factors, including water and protein intake in semen, as well as levels of testosterone, luteinizing hormone, and sex hormone-binding globulin hormones.

They're all controlled by various hormones including adipose tissue hormones and glucocorticoids steroids. In addition, insulin/glucose levels influence how much protein and water in semen is present.

The testicle contains multiple cell types, such as Leydig cells, germ cells (spermatogonia and spermatocytes), and spermatozoa.

Their functioning depends on mitochondrial activity which in turn is affected by levels of lipid peroxidation as well as antioxidant enzyme systems in place within each testicle.

Studies have shown that long-term endurance training increases testicular volume in men.

One such study showed an inverse relationship between total testis volume and cycling miles for elite triathletes, suggesting there may be a minimum testicular volume below which exercise has no positive effects on reproductive function.

Another showed endurance training positively impacting testis mass-to-body weight ratio ratio in male rats but these results weren't replicated during subsequent experiments.

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Effects of Exercise Training on Spermatogenesis

Exercise training, particularly low-intensity exercises, has been shown to significantly improve sperm parameters for both infertile and subfertile men alike, though its exact mechanisms remain unknown.

Elevated scrotal temperatures caused by sports may play a part here as exercise can hinder secretion of testosterone and gonadotropins.

But high-intensity training has also been linked to impaired sperm production among healthy males, possibly as a result of increasing oxidative stress in the testes and its consequent reduction of testosterone biosynthesis and count.

Furthermore, studies have also suggested a correlation between higher body mass index (BMI) and impaired testicular function resulting in lower free testosterone serum levels, decreased gonadotropin secretion, and impaired sperm maturation.

Recent mice research suggests that long-term exposure to high-fat diets leads to obesity, an accumulation of lipids in non-traditional places and increased oxidative stress in testis tissue.

This leads to a decrease in antioxidant enzyme mRNA expression and activation of an inflammatory response via nuclear factor-kB and proinflammatory cytokines, and inhibition of testosterone synthases' mRNA expression and serum testosterone level, impacting on sperm quality.

Lifelong moderate-load exercise was shown to significantly reduce body fat, relieve obesity-induced high oxidative stress and inflammation responses in testis tissues.

Moderate exercise also downregulates nuclear factor-kB expression as well as proinflammatory cytokine expression, restores testosterone synthases mRNA expression levels as well as serum testosterone level and quality in testis tissues.

One study sought to assess the effects of lifelong moderate-intensity exercise on spermatogenesis in rats, as well as to explore its protective mechanism against impaired testicular function caused by food withdrawal or low-calorie diets.

Rats exposed to diet with and without exercise exhibited that repression of Nrf1 mRNA and protein expression served as a key buffer against loss of spermatogenesis between diet groups with exercise (DR, ET and DR+ET) versus control rats.

This was also associated with a decrease in phosphorylation of p70S6 kinase 1 (mTORC1) in both DR and ET groups; inhibition of this pathway activates autophagy to suppress spermatogenesis.

Effects of Exercise Training on Testosterone

Exercise training may affect spermatogenesis by increasing or decreasing testosterone levels, with its effects being determined by various factors such as total testicular volume, androgen receptor status and metabolic state of the body.

These variables will vary between individuals depending on intensity, frequency, duration and recovery from exercise sessions. Exercise also has an influence on cortisol production which has significant ramifications on health outcomes.

Long and intense physical activity has long been known to decrease testosterone in men, likely as a result of an inhibition in endogenous gonadotropin release and/or accumulation of fat cells.

This may contribute to dysfunction of the hypothalamic-pituitary-testicular axis and thus impair spermatogenesis.

Additionally, changes in HPT are affected by numerous other biomarkers, including changes in oxidative stress and inflammation responses.

Therefore, when researching exercise's effect on spermatogenesis it is crucial to account for all these variables.

Studies have demonstrated that exercise training can restore the HPT axis from any detrimental effects it might have had on spermatogenesis and semen production, with different intensities, frequencies, durations, and combinations achieving similar results as non-trained control groups.

These studies indicate that the HPT axis can be reversed with lifestyle modification including diet, sleep patterns and supplementation.

One study demonstrated how moderate-load exercise could significantly enhance sperm quality for obese mice fed a high-fat diet, via alleviating obesity-induced oxidative stress.

Thus downregulating expressions of nuclear factor-kB and proinflammatory cytokines, restoring mRNA expression for testosterone synthases, increasing serum testosterone levels and reducing apoptosis of sperm cells.

According to this research, long-term moderate exercise could mitigate negative impacts associated with obesity on male reproductive function by preventing cell apoptosis of sperm cells.

Authors believe long-term moderate-load exercise can mitigate negative impacts associated with obesity by preventing cell apoptosis of sperm cells.

Hence long-term, moderate load exercise can mitigate negative impacts related to obesity-induced oxidative stress by preventing cell apoptosis of sperm cells.

Restoration of mRNA expression of testosterone synthases; increased serum testosterone levels and reduced sperm cell apoptosis.

Author of study suggest long term moderate load exercise can mitigate its detrimental effect by preventing sperm cell apoptosism. 

Effects of Exercise Training on Testicular Development

Exercise has long been recognized to influence the hypothalamus-pituitary-gonadal axis and improve male reproductive function, particularly through its impact on testosterone levels and the secretion of gonadotropins such as luteinizing hormone (LH) and follicle stimulating hormone (FSH).

However, the precise mechanisms by which these changes take place remain obscure.

Furthermore, exercise training may either negatively or positively influence hypothalamus-pituitary-gonadal function depending on intensity, duration and type of training program chosen.

Exercise training may alter sperm parameters in blood and seminiferous tubules, due to direct and indirect effects on testicular growth, spermatogenesis, testosterone production and LH levels as well as their influence on endocrine environments in which sperm are formed.

Humans and other mammals typically progress through three distinct phases when developing postnatal testis.

  1. The first one is known as testicular growth stage, in which genes associated with nerve, blood vessel and cell junction development are highly expressed.
  2. Next comes transitional stage with downregulation of growth-related genes while gradual elevation in spermatogenesis-related genes gradually occurring over time.
  3. Finally comes spermatogenesis-driven phase with formation of spermatogenic epithelium and spermia within seminiferous tubules.

Testicular seminiferous tubules are lined by Sertoli cells that serve as blood-testis barriers to protect spermatogenic epithelium and maintain the immunoprivileged environment of the testis.

Furthermore, tubular myoid cells surround seminiferous tubules on their peripheries to provide mechanical force necessary to transport sperm through them.

One study conducted transcriptome analysis in early-puberty Yiling goats to investigate dynamic changes in testicular development at organ, tissue and transcriptome levels.

Theri findings demonstrated that exercise training had an impactful change on transcription of most genes involved with testicular growth.

This includes spermatogenesis and cell structure as well as significant increases in gene expression for steroid and lipid metabolism, cell signaling, immune response as well as hub genes predicted by WGCNA: most associated with spermatogenesis, steroid biosynthesis or other functions of testis development.


Aerobic exercise not only strengthens and tones the muscles, but it also improves circulation throughout the body by providing oxygen-rich blood to your heart and lungs.

This allows your body to efficiently burn fat and build muscle more efficiently - helping lower resting heart rates and cholesterol levels, increasing energy, and making you feel better overall.

Studies on the effects of exercise on semen quality have yielded inconsistent findings.

While some reports have noted how high-intensity endurance training may cause plasma LH, FSH, and T concentrations to drop as well as an overall decrease in sperm parameters due to exercise, others have discovered no such effects from exercising at high intensities.

One possible cause for the inconsistent findings may lie with the types and intensities of exercises employed.

For instance, strenuous long-term HIE may increase scrotal temperatures which interfere with testicular thermoregulation, thus hindering sperm production.

Furthermore, certain forms of vigorous exercise cause an increase in ROS (reactive oxygen species) levels which trigger DNA damage that blocks production.

To further examine the relationship between testicular function and exercise, this study investigated the effects of lifelong moderate-intensity endurance (MIE) training vs high-intensity endurance (HIE) training on testicular structure and molecular characteristics in a rat model.

The research team found that MIE training provided protection from age-induced testicular atrophy as well as favorable effects on sperm concentration as well as percentage with normal morphology.

Moreover MIE group showed increased mRNA expression of antioxidant transcription factor Nrf1 while HIE group showed decreased expression as well as reduction of OXPHOS complex subunits mRNA expression/protein levels of OXPHOS respectively.

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