Homebrew
Happiness
Home
My Writing
#coaching
#creative writing
#culture
#mental health
#running
#science
#tech
#training
#TransFemTrailGuide
Coaching
Contact
My Portfolio
About Me
My Strava
The Tale of Training for Testosterone
2025-10-19
Exercise scientists, athletes, single men, and rapidly aging grandparents all share at least one common interest. They want the answer to the question, “How do I build bigger muscles?” The answer is simple in theory. Lift weights, take care of yourself, and hope for the best. But the more detailed answers can be as complicated and theoretical as any of science’s other great mysteries: the age of the universe, human consciousness, or how Dr Pepper fits all those flavors in a single can of soda. **A Bit of History** From the 1980s until the mid-2000s, some prominent exercise hormone scientists (endocrinologists) believed that the best way to stimulate muscle growth—also known as hypertrophy—was to lift heavy weights with little rest for as long as possible (*Kraemer & Ratamess, 2005*). In essence, they believed the harder the workout, the bigger muscles would grow. In their tests, high intensity resistance training would increase the concentration of testosterone within the blood for 15 to 60 minutes following the workout (*Kraemer & Ratamess, 2005*). Since scientists largely agree that more testosterone tends to lead to greater muscle hypertrophy (*Bhasin et al., 2003*), these exercise endocrinologists assumed that the transient increase in testosterone levels would positively impact workout recovery and muscle growth (*Kraemer & Ratamess, 2005*). Decades of research and likely millions of dollars went into studying the post-high intensity exercise increase in testosterone concentration (*Kraemer & Ratamess, 2005*). The field became something of an echo chamber where studies and methods were replicated a hundred times over. Each study would feature a rotating cast made up of a small handful of labs and researchers. Their findings turned into textbooks and training manuals, and now many coaches and athletes consider their theories and practices to be practical science (*Fleck & Kraemer, 2014*). However, their conclusions haven’t held up as new labs and researchers entered the field of exercise endocrinology. At the time, exercise scientists worked from the belief that testosterone only impacted muscle hypertrophy through directly stimulating muscle protein synthesis (*Bhasin et al., 2003*). In other words, testosterone would bind with receptors in the muscle fibers and increase the rate at which the fiber would build the proteins that perform the act of muscle contractions. Later research found that testosterone also plays a large role in specialized stem cells called mesenchymal stem cells (MSCs) (*Bhasin et al., 2003*). MSCs have the unique ability to become either fat cell precursors, which add to the body’s fat stores, or muscle cell precursors, which add muscle mass (hypertrophy). In the early 2000s, a group of researchers discovered that testosterone would increase the rate at which MSCs would produce muscle precursors and slow the production rate of fat cell precursors (*Bhasin et al., 2003*). This stem cell commitment mechanism of testosterone-mediated muscle growth helps explain a large portion of why muscle growth can scale linearly with circulating testosterone levels (*Bhasin et al., 2003*). Later research would use this theory for helping to determine what effect the transient rise in testosterone concentration may or may not have on muscle hypertrophy. **The Confounding Variable** Prior to the wave of research on testosterone’s acute response to high-intensity resistance training, Collins et al. (*1989*) and Collins et al. (*1986*) found that high-intensity exercise caused a phenomenon called hemoconcentration. These studies suggest that the more intense a workout was, the greater a rise in blood pressure and high-powered muscle contractions would force blood plasma out of the bloodstream and into the surrounding compartments. Blood plasma, which is primarily made up of water, leaving the bloodstream would artificially increase the concentrations of things like red blood cells and hormones within the vascular system (*Pullinen et al., 2002*). In other words, the transient increase of testosterone following high-intensity resistance exercise was likely a product of hemoconcentration—blood plasma loss while retaining hormones—rather than an increase in testosterone production (*Pullinen et al., 2002*). As plasma volume returns to the bloodstream, concentration normalizes and the body returns to baseline (*Collins et al., 1986*). A study published by Pullinen et al. in 2002 demonstrated that much of the supposed hormonal spikes were products of shifts in plasma volume. They utilized the Dill and Costill (*1974*) method to correct for any changes in blood plasma volume during their analysis. By applying this correction, they discovered that transient changes to testosterone markers largely disappeared. Their results demonstrated that the body didn’t actually create more testosterone in response to the workout and that other researchers’ claims of rising testosterone following high-intensity workouts were mostly a product of more concentrated blood (*Pullinen et al., 2002*). **Practical Implications** Does acute hemoconcentration impact training response like the scientists in the nineties had hoped? In practice, a drop in blood plasma and increase in testosterone concentration seems to have no effect on muscle hypertrophy. In 2010, a lab from McMaster University led by Daniel West (*2010*) used a unique within-subject training protocol in which untrained men would exercise each arm on different days. Their goal was to determine what effect, if any, testosterone concentration spikes would have on the outcome of a 12-week training program in untrained young men. This study had participants perform single arm exercises at a low intensity. On one day, the participants would train one arm at a low intensity to avoid causing a hormone concentration increase. On another day, the participants would train the other arm identically, but following the exercises, they would complete a series of fatiguing leg exercises to induce the acute testosterone concentration increase. If the transient testosterone concentration increase were meaningful, the exercises done in the context of the testosterone spike would cause greater hypertrophy than the exercises performed without the preceding high-intensity exercise (*West et al., 2010*). However, West and his team determined that the two arms gained muscle mass and strength at identical rates suggesting that the assumptions of prior research were inconsequential (*West et al., 2010*). More recently, a group of researchers attempted to answer the question of how hemoconcentration may impact muscle growth via testosterone-sensitive muscle precursors (*Luk et al., 2019*). In their study, they measured both markers of hormone concentration and markers of muscle cell precursor (satellite cell) proliferation and differentiation, key stages in the life cycle of a muscle cell precursor. Their results showed that, in men, early portions of satellite cell proliferation would increase in the context of hemoconcentration, but as hormone concentrations returned to normal, the later stages of satellite cell differentiation were unaffected (*Luk et al., 2019*). In other words, the transient rise in testosterone concentration caused by shifts in plasma volume is sufficient to provide a brief signal to the body’s muscle growth and repair system, but not with enough magnitude or duration to affect the eventual outcome of that process (*Luk et al., 2019*). These results are consistent with the earlier conclusions of West et al. (*2010*) that hemoconcentration does not impact training outcomes and Bhasin et al. (*2004*) that testosterone concentrations impact stem cell commitment to induce hormone-mediated muscle hypertrophy. **Conclusion** Based on the findings of recent research within the exercise endocrinology field, training systems that use high-intensity exercise to induce hemoconcentration are likely not any more effective than less intense programs at inducing muscle hypertrophy. While some science supports using a given amount of weight, lifting to failure, or performing a certain number of sets per week to optimize hypertrophy, the best answer to the question “How do I build bigger muscles?” may be the simplest. Lift weights, take care of yourself, and be patient. **Bibliography** *Bhasin, S., Taylor, W. E., Singh, R., Artaza, J., Sinha-Hikim, I., Jasuja, R., Choi, H., & Gonzalez-Cadavid, N. F. (2003). The mechanisms of androgen effects on body composition: mesenchymal pluripotent cell as the target of androgen action. The Journals of Gerontology. Series A, Biological Sciences and Medical Sciences, 58(12), M1103-1110. https://doi.org/10.1093/gerona/58.12.m1103* *Collins, M. A., Hill, D. W., Cureton, K. J., & DeMello, J. J. (1986). Plasma volume change during heavy-resistance weight lifting. European journal of applied physiology and occupational physiology, 55(1), 44–48. https://doi.org/10.1007/BF00422891* *Collins, M. A., Cureton, K. J., Hill, D. W., & Ray, C. A. (1989). Relation of plasma volume change to intensity of weight lifting. Medicine and Science in Sports and Exercise, 21(2), 178–185. https://doi.org/10.1249/00005768-198904000-00011* *Dill, D. B., & Costill, D. L. (1974). Calculation of percentage changes in volumes of blood, plasma, and red cells in dehydration. Journal of applied physiology, 37(2), 247–248. https://doi.org/10.1152/jappl.1974.37.2.247* *Fleck, S. J., & Kraemer, W. J. (2014). Designing resistance training programs. Human Kinetics.* *Kraemer, W. J., & Ratamess, N. A. (2005). Hormonal responses and adaptations to resistance exercise and training. Sports medicine, 35(4), 339–361. https://doi.org/10.2165/00007256-200535040-00004* *Luk, H. Y., Levitt, D. E., Boyett, J. C., Rojas, S., Flader, S. M., McFarlin, B. K., & Vingren, J. L. (2019). Resistance exercise-induced hormonal response promotes satellite cell proliferation in untrained men but not in women. American Journal of Physiology. Endocrinology and Metabolism, 317(2), E421–E432. https://doi.org/10.1152/ajpendo.00473.2018* *Pullinen, T., Mero, A., Huttunen, P., Pakarinen, A., & Komi, P. V. (2002). Resistance exercise-induced hormonal responses in men, women, and pubescent boys. Medicine and science in sports and exercise, 34(5), 806–813. https://doi.org/10.1097/00005768-200205000-00013* *West, D. W., Burd, N. A., Tang, J. E., Moore, D. R., Staples, A. W., Holwerda, A. M., Baker, S. K., & Phillips, S. M. (2010). Elevations in ostensibly anabolic hormones with resistance exercise enhance neither training-induced muscle hypertrophy nor strength of the elbow flexors. Journal of applied physiology (Bethesda, Md. : 1985), 108(1), 60–67. https://doi.org/10.1152/japplphysiol.01147.2009*