Written by: Adam Tzur
Updated: July 24, 2019 – Added West et al., 2012 | September 16, 2018 – Added Morton et al., 2018 | 20.05.2018 – Updated quotes | 16.05.2017 – Citation(s) added for cortisol
Acknowledgements: Greg Nuckols of Strengtheory.

Summary

Expand Table →

Post-exercise hormone secretion will, per the research today, not predict gains. Even if the hormones secreted are anabolic.
Designing training programs around testosterone maximization and cortisol minimization is most likely not a sound way to do programming.
Intramuscular IGF-1 might be related to gains if measured properly.

Introduction to hormones

Our body uses hormones for sending “slow” long-range signals. Hormones act systemically, meaning they affect the body as a whole. This is in contrast to short-distance cell communication (Tortora & Derrickson, 2012). You have probably heard of hormones like cortisol and testosterone and associate these hormones with stress and growth, respectively.

In my experience, people commonly believe these hormones function in an independent, linear fashion. Meaning more testosterone equals more masculinity and growth, while more cortisol equals stress and catabolism. However, this point of view ignores the fact that hormones have a physiological range where they help the body function optimally (Tortora & Derrickson, 2012). By trying to minimise or maximise certain hormonal responses we ignore the whole-body context in which they exist. Indeed, hormones have many functions. For example, testosterone is a regulator of mental health (Celec et al., 2015). Trying to shoehorn a hormone into one role is overly reductionistic. We all know about hormones like insulin, growth hormone, adrenaline, and cortisol. We probably also have a general idea of their purpose in the body. But were you also aware that these hormones are linked to sleep regulation (McGinnis & Young., 2016)? People who inject hormones like insulin, GH, testosterone, etc. might be inadvertently altering organ functionality in their bodies. This could lead to unwanted and unintended consequences which could be detrimental to their overall health (Lamb, 1984; ACSM, 1987; Su et al., 1993; Sullivan et al., 1998; Hartgens & Kuipers, 2004; Maravelias et al., 2005; Achar et al., 2010; Piacentino et al., 2015; Frati et al., 2015; Grönbladh et al., 2016).

Trying to min-max your hormones like the stats of an RPG character is probably not a good idea given that hormones are essential regulators of homeostasis. By interfering with their natural balance you change a ton of homeostatic parameters, causing butterfly effects. But this review isn’t about the effects of steroids, so let’s get back on topic.

Research now shows that different, and perhaps unexpected, types of tissues can secrete hormones. For example, fat tissue can secrete inflammatory products 1 and hormones 2. In addition to fat, muscle tissue can secrete beneficial hormones (Egan and Zierath, 2013) called myokines 3. This means that muscles and fat can communicate messages to the whole body.

Quote 1: Obesity is characterized by a state of mild inflammation, and [inflammation] generally rises as adipose tissue expands (Trayhurn, 2005)

Quote 2: The fat surrounding the liver and other abdominal organs, so-called visceral fat, is very metabolically active. It releases fatty acids, inflammatory agents, and hormones that ultimately lead to higher LDL cholesterol, triglycerides, blood glucose, and blood pressure (The Harvard School of Public Health)

Quote 3: Myokines have been suggested to mediate anti-inflammatory and metabolic effects (…) It is possible that myokines contribute to mediate the preventive effects of exercise against chronic diseases, such as cardiovascular diseases, type 2 diabetes, cancer, and dementia (Karstoft & Pedersen, 2016)

Can systemic hormones predict hypertrophy after exercise?

After challenging exercise, our body secretes various hormones like cortisol, testosterone, GH, and IGF-1 (Volek et al., 1997; Copeland et al., 2002; Leal-Cerro et al., 2003; Goto et al., 2005; Hill et al., 2008; Leite et al., 2011; Conceição et al., 2014; Rubin et al., 2015; Gonzalez, 2015; Kraemer and Castracane, 2015; Kraemer et al., 2016; Seifi-skishahr et al., 2016; González-Badillo et al., 2016; Hooper et al., 2017; Walker et al., 2017). Since several of these hormones are associated with hypertrophy, it makes intuitive sense that we improve our gains the higher our anabolic hormones spike after exercise (Goto et al., 2005; Villanueva et al., 2012). By accepting this hypothesis, we assume there is a positive relationship between acute post-exercise hormonal secretion and hypertrophy.

There is only one issue. Most studies and systematic reviews agree that temporary post-exercise increases in anabolic hormones do not predict hypertrophy (Wilkinson et al., 2006; Velloso, 2008; West et al., 2009; West et al., 2010; West et al., 2012; West and Phillips, 2010; Schroeder et al., 2013; Mitchell et al., 2013; Henselmans and Schoenfeld, 2014; Gonzalez et al., 2015a; Mangine et al., 2015; Morton et al, 2016; Fink et al., 2016; Mckendry et al., 2016; Hooper et al., 2017; Walker et al., 2017; Morton et al., 2018). Though some studies disagree when it comes to GH (McCall et al., 1999; Goto et al., 2005; West and Phillips, 2012) and cortisol being negatively associated with fat mass and LBM (Longland et al., 2016). GH might be indirectly tied to hypertrophy (Goto et al., 2005).

“Our findings are in line with a recent study showing no correlation between acute systemic hormonal elevations and muscle hypertrophy (Morton et al. , 2016). Furthermore, a recent study recorded inferior myofibrillar protein synthesis in a RT protocol triggering acute hormonal elevations as compared to a protocol in which hormonal levels did not increase (McKendry et al. , 2016). Indeed, according to previous findings, the hypertrophic effects of GH are strongly regulated by IGF-1 which can be triggered by GH elevations (Cameron et al. , 1988; Goldspink, 1999). Acute local IGF-1 increases in muscle tissue have been shown to be correlated to muscle fibre area increase (Suetta et al. , 2010).”

“…our data demonstrate that exercise-induced increases in MPS are dissociated from postexercise testosteronemia and that stimulation of MPS occurs effectively with low systemic testosterone concentrations in women” West et al., 2012

“However, systemic GH alone does not appear to be directly related to muscle hypertrophy but rather exerts its influence by regulating fat and carbohydrate metabolism (Gravholt et al. , 1999). Further, it is important to make the difference between acute endogenous hormonal elevations and chronic supraphysiological hormonal levels (Bhasin et al. , 1996; Ehrn- borg et al. , 2005). We suggest that the small acute endogenous increases in hormones cannot imitate the anabolic effects of high chronic supraphysiological hormonal levels. Nevertheless, even though acute GH elevations cannot be directly related to muscle hypertrophy, acute GH elevations may be used as metabolic stress marker (Goto et al. , 2005).”

“… our data add to a growing body of evidence demonstrating that exercise-induced circulating GH and T concentrations are not related to MPS (West et al. 2009; West & Phillips, 2012; Mitchell et al. 2013) (…) Given recent evidence that acute resistance exercise-induced MPS rates do not predict chronic training- induced muscle hypertrophy (Mitchell et al. 2014), the suggestion that the blunted MPS and intracellular signalling response in the early recovery period for 1M may be indicative of impaired long-term muscle hypertrophy is tenuous. However, exercise-induced elevations in MPS persist for 24–72 h postexercise (Phillips et al. 1997; Miller et al. 2005; Burd et al. 2011 a ), which may explain the discord between acute assessment of MPS over several hours postexercise and long-term hypertrophy.”

“No hormone measured before exercise, after exercise, pre-intervention, or post-intervention was consistently significant or consistently selected in the final model for the change in: type 1 cross sectional area (CSA), type 2 CSA, or fat- and bone-free mass (LBM).” – Morton et al., 2018

The figure shows the non-link between CSA (hypertrophy) and growth hormone secretion post-exercise by Fink et al., 2016

Several of the authors agree that local mechanisms are more important than systemic mechanisms 4. Others say there is not enough evidence to make conclusive statements about hormonal changes and gains (Schoenfeld, 2013; Kraemer et al., 2016). Schoenfeld speculates that “the purpose of post-exercise hormonal elevations is to mobilize fuel stores rather than promote tissue anabolism”, which is a hypothesis that fits with AMPK and the “energy crisis of the cell”. Additionally, Schoenfeld presents us with the idea that our genetics determine whether we respond to post-exercise increases in anabolic hormones 5. It’s possible that some people are genetically hardwired to react favourably with endogenous anabolic hormones, while others won’t.

Quote 4: “Intramuscular rather than systemic processes [mediate] hypertrophy (Mitchell et al., 2013)”

Quote 5: “It has been estimated that genetic differences can account for approximately half of the variation in athletic performance. This is consistent with studies showing that the hypertrophic response to resistance training displays tremendous variance between individuals. It is therefore conceivable that acute hormonal responses may be more relevant to certain lifters as opposed to others. There is some evidence to support this contention as a strong trend for a significant association has been shown between IGF-1 and those who respond favorably to hypertrophy-type training”
(Schoenfeld, 2013)

A very recent study challenges these arguments, because it finds that acute post-exercise testosterone secretion is related to hypertrophy in 26 resistance trained men over an 8 week training period (Mangine et al., 2016). The authors criticize some of the aforementioned studies because some of them were underpowered (i.e. too few participants) and because they used non-optimal statistical procedures. These are valid arguments. However, I get a bit suspicious when Mangine et al. imply that the research is biased or erroneous 6. This is a bit odd since such a critique could apply to pretty much every study out there. There’s always the possibility of bias and error. If bias and error were present in the hormone studies, they would be interfering with the efforts of several independent research teams. Mangine et al’s findings are very interesting but until they are replicated and supported by other studies, we have to slow-pedal their conclusions.

The validity of this [research] is based upon the assumption that the related variables were collected without systematic or random error (…) data were collected or analyzed using procedures that were dependent upon technician reliability and were therefore subject to error (Mangine et al., 2016)

Beyond hypertrophy, there are studies that suggest there is a link between testosterone secretion and strength gains (Beaven et al., 2008). Though the focus of this article is hypertrophy and not strength, so I won’t go in-depth on this.

With all the research taken into account, designing a training program around hormonal responses is not a good way to do programming or periodization (Gonzalez, 2015b; Mangine et al., 2015; Walker et al., 2017). Any program that promises maximal testosterone or GH secretion using (for example) very short rest periods (Goto et al., 2005; Willardson, 2006; Villanueva et al., 2012; Henselmans and Schoenfeld, 2014) probably won’t do more good than regular, intelligent programming (Henselmans and Schoenfeld, 2014; Walker et al., 2017). Intense training to failure can actually lead to T-levels that fall below baseline, 48 hours post-exercise (González-Badillo et al., 2016) 7. Though this reduction in testosterone might be a temporary overreaching-response. See table below for details.

Quote 7: … subjects with lower testosterone values at 48 h-Post, induced by the 3 × 8(8) protocol, also showed lower HRV. Furthermore, the relationship observed between velocity loss and the changes in testosterone at 48 h-Post (r = − 0.70) suggest that greater velocity loss during the set, like that induced by the 3 × 8(8) protocol, results in lower testosterone at 48 h-Post, even below resting levels. All these observations might reflect a temporal status of fatigue, sometimes termed overreaching (González-Badillo et al., 2016)

With that said, we shouldn’t discount hormones completely. Just because temporary changes in hormonal secretion doesn’t predict gains, doesn’t mean your long-term hormonal profile is unimportant (Kvorning et al., 2006; Mouser et al., 2016; Mangine et al., 2016; Hooper et al., 2017; Bermon, 2017). For example, men have 10x more circulating testosterone than women, which is one of the reasons it might be easier for men to build and maintain muscle mass after puberty (Schroeder et al., 2013). Androgenic hormones seem to be important for performance (Kvorning et al., 2006; Bermon, 2017). Though some disagree that gender differences in performance and muscle mass are related to anabolic hormones (Healy et al., 2014).

Insulin

Atherton and Smith have described insulin as an anti-catabolic hormone that lowers MPB and thus “protects” the body from muscle wasting. Insulin could act synergistically with essential amino acids (EAA), where insulin decreases MPB while EAAs increase MPS (Atherton and Smith, 2012; Everman et al., 2016).

Many studies have measured post-exercise insulin concentrations, and haven’t found any connection to gains. However, their results might be affected by the fact that insulin responds strongly to protein and carbohydrates. In fact, insulin concentrations actually decrease (Schwarz et al., 2011; Mangine et al., 2015) or remain unchanged (Marliss et al., 2002) during exercise. So it makes little sense that insulin would predict hypertrophy when measured right after exercise. But, if exercise was combined with feeding, it’s possible insulin might be correlated with gains.

Insulin secretion is therefore part of the nutrient timing hypothesis which states that consuming carbohydrates and protein around the the exercise window (before, during, after), could lead to improved gains (Kerksick et al., 2008). This hypothesis has been thoroughly researched in the last twenty years. I will write a separate nutrient timing article on this topic specifically.

Can local hormones predict hypertrophy after exercise?

Local hormones can also be described as intramuscular hormones. They exist in contrast to circulating hormones which flow freely in the bloodstream. Some authors think local hormonal concentrations are better at predicting gains compared to circulating hormones.

Insulin-like Growth Factor 1 (IGF-1)

Like insulin, IGF-1 is a hormone that is an exception to the rule. We can measure “circulating” IGF-1 in the blood, or we can measure intramuscular IGF-1 (IMIGF-1). The studies that dismissed IGF-1 as a predictor of gains measured circulating IGF-1. IMIGF-1 is different because it functions locally in cell-to-cell communication (Adams, 2002; Velloso, 2008; Wang et al., 2013). It’s possible that IMIGF-1 levels predict strength gains (Kraemer et al., 2016) and hypertrophy better than circulating IGF-1 (Häkkinen et al., 2001; Adams, 2002; Velloso, 2008; Frystyk, 2010; Schoenfeld, 2013; Mangine et al., 2016; Fink et al., 2016). Sadly, there hasn’t been a ton of human studies on this question as of yet (Velloso, 2008).

Conclusion

As per the research presented in this article, there’s little reason to believe temporary changes in hormonal secretion predicts gains. Future research is needed to confirm or deny the hormone hypothesis.