ONLINE DRIVERS MEDIA

Dont fall for someone who overgeneralizes, misreports or -interprets study results to tell you that healthy mid-range testosterone levels were a major trigger of cancer development.

I just got an email from my good friend Carl Lanore who hosts the Super Human Radio Show I am sure you have already seen in the sidebar of the SuppVersity. He pointed me towards the results of a recent study from the Copenhagen University Hospital saying "Adel have you seen this? Im sure the media will be all over it." Since Carl is usually pretty good at identifying things that "news" make headlines, I would like to leapfrog the mass media craze before any of you consider cutting off their best parts to end up in the allegedly healthy depth of quasi zero testosterone.

You have no clue what I am talking about? Well, I am about to elaborate. You just have to stay with me for the rest of a comparatively long, but insightful (I promise) analysis of the study and related contemporary evidence.
So, where do I begin?  The "mass media compatible message" of the abstract (and this is usually not even as far as most headline producers read) says: Having normal testosterone levels increases your risk of dying from cancer before your time by at least 30%! The more testosterone, the likelier you will pass away before your expiry date."

Well, as I said, this is the mainstream interpretation. And interpretation anyone could identify as being fundamentally flawed by simply reading the abstract carefully. In fact, you dont even have to read the whole 268 words! It would suffice to read the end of the first line of the result section, where it says:

"For risk of early death after cancer, for men [...]" (Ørsted. 2014)

Did you notice it? There is an "after cancer" in this sentence. This means, your risk of dying, if you develop cancer is increased, if [whatever follows]. Now, that which follows is ...

• if you are in the 2nd quartile, your risk will be increased by 30%,
• if you are in the 3rd quartile, your risk will be increased by 31%,
• if you are in the 4th quartile, your risk will be increased by 52% and
• if you are in the 5th quartile, your risk will be increased by 80%.

So, if you happen to be unlucky enough to develop cancer and your testosterone levels are high there is in fact an increased risk you could die from cancer.

So testosterone is still bad, right? Yes, but anything that is "anabolic", i.e. promotes the growth of all cells in your body is "bad" for someone who has cancer. Guess what chemotherapy will to do your testosterone levels and the amount of other pro-anabolic factors in your body? It will wreak havoc on your testes (Wallace. 1997), reduce their size to that of dried raisins, increase your risk of gynecomastia and reduce your testosterone levels to exactly those 6-10 nmol/L (Whitehead. 1982) of which the previously cited study by Ørsted et al. found that they are associated with the least risk of dying from already existing cancer in your body.

Figure 1: If you look at a random assemble of the myriad of risk associations that have been established for low T, the results of the study at hand do no longer appear to be that frightening - right?

A result that conceals the established negative effects of having low testosterone (see Figure 1) or depressing it which androgen deprivation therapy which may reduce the testosterone levels to the allegedly desirable range, but is associated with a 350% (!) increased risk of dieing from cardiovascular disease in prostate cancer patients (Tsai. 2007). I guess this should make you reconsider the "usefulness" of low testosterone levels.

But there is also an increase in cancer risk, no?

Yes, there is. According to the scientists it is (I quote) "1.07 (95% CI 0.98–1.18) and 1.06 (0.93–1.22) for men and women" if you compare say a man with 10nmol/L to a man with 20nmol/L. Now, as far as I can remember a 95% confidence interval, which is what you see in brackets, i.e. for men 0.98-1.18, defines the range in which the chance that the hypothesis that is tested, i.e. "testosterone influences the risk of prostate cancer" has a 5% chance of not being bullocks... ah, I mean statistical significant.
So, the scientists are 95% sure that a 2x higher testosterone level will be associated with a 2% decrease and 18% increase in... does this ring a bell? Yeah, thats not exactly a reliable prediction considering the fact that the researchers adjusted for smoking status, cumulative smoking, body mass index, alcohol consumption, level of education, and level of income for men and women, but "forgot" to adjust for...

• family history of cancer, which is one of the, if not the main correlate of your risk of developing various cancer, such as prostate cancer (1000% increase, no typo | Steinberg. 1990), colon cancer (up to 59% risk increase depending on the region | Slattery. 1994) or breast cancer (145% risk increase with first-degree relative having breast cancer | Slattery. 1993) 
• diabetes, which has been found to be associated with a 60% increase in colorectal cancer risk in patients who have been diagnosed with diabetes 10+ years ago (La Vecchia. 1997), a
• the level of visceral fat, where high levels (relative to total body fat) are associated with 850% increased risk of breast cancer (Schapira. 1994) and up to 1000% increased prostate cancer risk (Hafe. 2004)
• low sleep duration and quality, which has been associated with an increased risk of developing almost every form of cancer you can think of (Blask. 2009), including 60% increased breast cancer risk for women working the "graveyard shift" (Davis. 2001)

I could go on with all sorts of nutritional factors, medication (specifically hormonal contraceptives) the amount of exercise, the area you live in, your year of birth and hundreds of other factors that have previously been associated with an increase of cancer risk, but I guess the above should suffice to make you less confident that a "confidence interval" of 0.98–1.18 in men and 0.93–1.22 in women was enough to make the claim that "having a high testosterone level would [mechanistically!] trigger the development of cancer.
References:

• Araujo, Andre B., et al. "Endogenous testosterone and mortality in men: a systematic review and meta-analysis." The Journal of Clinical Endocrinology & Metabolism 96.10 (2011): 3007-3019.
• Blask, David E. "Melatonin, sleep disturbance and cancer risk." Sleep medicine reviews 13.4 (2009): 257-264.
• Davis, Scott, Dana K. Mirick, and Richard G. Stevens. "Night shift work, light at night, and risk of breast cancer." Journal of the national cancer institute 93.20 (2001): 1557-1562.
• Garavello, Werner, et al. "Family history and the risk of oral and pharyngeal cancer." International journal of cancer 122.8 (2008): 1827-1831.
• Hafe, Pedro, et al. "Visceral fat accumulation as a risk factor for prostate cancer." Obesity research 12.12 (2004): 1930-1935.
• La Vecchia, Carlo, et al. "Diabetes mellitus and colorectal cancer risk." Cancer Epidemiology Biomarkers & Prevention 6.12 (1997): 1007-1010.
• Morgentaler, Abraham. "Testosterone and prostate cancer: an historical perspective on a modern myth." european urology 50.5 (2006): 935-939.
• Raynaud, Jean-Pierre. "Prostate cancer risk in testosterone-treated men." The Journal of steroid biochemistry and molecular biology 102.1 (2006): 261-266.
• Roddam, Andrew W., et al. "Endogenous sex hormones and prostate cancer: a collaborative analysis of 18 prospective studies." Journal of the National Cancer Institute 100.3 (2008): 170-183.
• Slattery, Martha L., and Richard A. Kerber. "A comprehensive evaluation of family history and breast cancer risk: the Utah Population Database." Jama 270.13 (1993): 1563-1568.
• Slattery, Martha L., and Richard A. Kerber. "Family history of cancer and colon cancer risk: the Utah Population Database." Journal of the National Cancer Institute 86.21 (1994): 1618-1626.
• Schapira, David V., et al. "Visceral obesity and breast cancer risk." Cancer 74.2 (1994): 632-639.
• Shores, Molly M., et al. "Low serum testosterone and mortality in male veterans." Archives of internal medicine 166.15 (2006): 1660-1665.
• Stattin, Pär, et al. "High levels of circulating testosterone are not associated with increased prostate cancer risk: a pooled prospective study." International journal of cancer 108.3 (2004): 418-424.
• Steinberg, G. D., Carter, B. S., Beaty, T. H., Childs, B. and Walsh, P. C. (1990), Family history and the risk of prostate cancer. Prostate, 17: 337–347. doi: 10.1002/pros.2990170409 
• Tsai, Henry K., et al. "Androgen deprivation therapy for localized prostate cancer and the risk of cardiovascular mortality." Journal of the National Cancer Institute 99.20 (2007): 1516-1524. 
• Ujpál, Márta, et al. "Diabetes and Oral Tumors in Hungary Epidemiological correlations." Diabetes care 27.3 (2004): 770-774.
• Wallace, Euan M., et al. "Effects of chemotherapy-induced testicular damage on inhibin, gonadotropin, and testosterone secretion: a prospective longitudinal study." The Journal of Clinical Endocrinology & Metabolism 82.9 (1997): 3111-3115.
• Whitehead, E., et al. "The effects of Hodgkins disease and combination chemotherapy on gonadal function in the adult male." Cancer 49.3 (1982): 418-422.

High fat + high carbohydrate foods like mini doughnuts are exactly what you should not eat on a refeed day, let alone during weeks of bulking.

Do you want to know what happens during days and weeks of gluttony? How the effects "bulking" will have on your body weight and composition, depending on where those extra calories come from? Have you wondered what the optimal nutrient composition on refeed days may look like. And are you concerned about the potential the health consequences of bulking?

Yes? In this case, I would suggest you take a closer look at the following overview of the research. An overview that is probably not complete, but it should suffice to provide preliminary answers to the aforementioned questions.

• The amount of weight you gain depends on your genes: They are not the only determinant. Thats for sure. A 1990 study by Bouchard et al. still leaves no doubt that your genes are one of the most important determinants of the quantity of weight you gain.
  
  In said study the researchers from the Laval University fed 24 sedentary young male twins 1,000kcal extra for six out of seven days of the week. In that the study is not the first to investigate the effects of overfeeding on weight gain in twins. It is yet the first and only one that did this over a period of 100 days and thus with a total energy excess of 84,000 kcal on a diet that contained 50 percent carbohydrate, 35 percent fat, and 15 percent protein.
  

  Figure 1: Comparison of the weight (left) and visceral fat (right) gains in twin pairs; high correlations were observed for both, but the correlation was significantly more pronounced for the unhealthy visceral fat than it was for the mere body weight (Bouchard. 1990).

  The data in Figure 1 does probably not need any extra explanations. In view of the fact that similar results have also been observed in previous studies like Poehlman et al. (1986), it should be obvious that the difference between the weight (left) and visceral fat (right) two identical twins gained was significantly smaller the difference between one twin from pair A and one twin from pair B. The statistical analysis of body fat and waist circumference data revealed similar correlations which were most significant for the visceral fat mass and the waist hip sizes, i.e. those quantities that predict the ill health effects of weight gain best.
  
  According to Ukkola, et al. (2001), the genetic differences may partly be mediated by differences in the genetic make-up of ones beta-2 adrenoreceptors with specific variants being associated with greater increases in insulin resistance, body weight and subcutaneous fatness. Other candidates are the cholesterol ester transfer protein (CETP) gene which appears to affect adiposity in response to long-term overfeeding (Terán-García. 2008). Other scientists use similar genetic polymorphisms to explain a general resistance to weight gain during overfeeding via genetically determined variations in nonexercise activity thermogenesis (Vanltallie. 2001).
• Overfeeding fat, carbohydrate or protein, does it make a difference? Studies that compare isocaloric overfeeding are quasi non-existent. What we do have are studies like the one by Horton et al. (1995) that compared high fat vs. high carbohydrate diets (see Figure 2 for macronutrient composition), where the additional energy came from fat or carbohydrates.
  
  In the Horton study this was a 50% extra that was added in form of fat or carbohydrates on top of the baseline diets of the normal-weight and obese subjects. A 50% extra that lead to significant weight gain.
  

  Figure 3: Weight gain (left) and increase in energy expenditure (right) in obese and lean subjects in response to carbohydrate and fat overfeeding (Horton. 1995).

  As you can see in Figure 3, both diets led to a rapid increase in body weight, but the trajectory was different. The main and maybe practically relevant difference, though, was that the rapid increase in water and glycogen in the high carbohydrate group was less resilient weight loss in the post-overfeeding period.

• Figure 4: Proportion of the energy that was stored as body fat (Horton. 1995).

  If we take a look at the proportion of energy that was stored as body fat in Figure 4, it is obvious why the fat gains lasted longer than the carbohydrate gains. Why? Well, simply because the 14-day overfeeding on fat lead to a significantly higher relative increase in body fat.
  
  Last but not least, it may also be worth mentioning that the the fat gain in the obese group was 89% and 57% higher in the carbohydrate and fat overfeeding group, respectively. An intriguing result that appears to stand in line with dieting studies, where high fat diets are superior to high carbohydrate diets in the obese, but not in lean individuals.
  
  What was not different for obese and lean individuals, though, was the the fact that the carbohydrate overfeeding lead to higher gains in lean mass than the fat overfeeding. A result that should remind you of a previously reported study here at the SuppVersity, in which a no fat bulk lead to significantly greater muscle and significantly lower fat gains than a low fat bulk (see "If You Go "High Carb", You Better Go Really High!" | more). Overall, "bulking", i.e. eating more than you need on any mixed diet, has repeatedly been shown to produce significant increases plasma Somatomedin-C/Insulin-like Growth Factor (SM-C/IGF-l) and testosterone concentrations as well as insulin, of which Forbes et al. speculate that they promote the lean mass increases that are particularly pronounced when overfeeding is combined with resistance training.
  
  In a more nutrient-type specific study b by Dirlewanger that did not focus on the weight gain or anabolism, but on the leptin response and the increase in resting energy expenditure the subjects experienced a significant increase in leptin (+28%) and resting energy only in the high carbohydrate, yet not in the fat overfeeding arm of their study in young, lean individuals (Dirlewanger. 2000). Other studies, without clear distinction between high carb and high fat overfeeding, indicate that fast food like burgers or fries is an effective short-term leptin stimulator, too - at least if its consumed in a single binge (Kolaczynski,. 1996).
  

  Figure 5: Energy partitioning in young men upon overfeeding with ~5,000kcal per day - mostly carbohydrates, i.e. 1% protein, 3% fat, and 86% carbohydrate (Acheson. 1988).

  In the short run, like on refeed days, for example, carbohydrate overfeeding has another advantage over fat overfeeding, because it takes roughly 500g of carbohydrates (thats 2,000kcal) before even a single gram of those carbs is converted to fat and potentially, but not necessarily stored as body fat (Acheson. 1988) - at "only" 400kcal extra from carbs for one day there was no net lipogenesis at all (see Figure 5). This result is corroborated by data from McDevitt et al. (2000) who observed that the fat gain with fat overfeeding starts with day 1, while there is a time gap in the increase in body fat with carbohydrate overfeeding (McDevitt. 2000).

• Figure 6: Schematic representation of the main lipid metabolic pathways affected in skeletal muscle during 4 weeks of fat overfeeding. Genes indicated in white boxes were down-regulated during the dietary study, whereas genes indicated in gray boxes were up-regulated (Meugnier. 2007).

  Fat overfeeding, on the other hand, has been show to favor fat storage not just because the dietary fat can be stored without being converted to triglycerides, but also because metabolic and genomic investigations show that the lipid oxidation rate tends to decrease, and 55 genes in the skeletal muscle were modified.
  
  Modifications of which Meugnier et al. show that they stimulate the synthesis of triacylglycerol, inhibit lipolysis and reduce the oxidation of fatty acid oxidation, while promoting the development of adipocytes with an excess of only ~550kcal/day from fat per day (see Figure 6).
  
  Another potential explanation is the change in thyroid hormones, of which the data in Figure 7 from an overfeeding study by Danforth Jr., et al. (1979) tells you that the high protein overfeeding despite a 29.8% lower total energy intake triggered the most, the carbohydrate diet the 2nd most favorable (=in favor of greater energy expenditure) effects on the thyroid hormone.
  

  Figure 7: Effects of overfeeding with carbohydrates, fats, and protein on thyroid hormones (Danforth, Jr. 1979).

  Accordingly, high protein diets, of which we know for sure that they are the most satiating hypercaloric diets (followed by high carb and high fat | Johnstone. 1996) and have the highest thermogenic effect (see Figure 8) and can help dieters avoid the yoyo effect after a diet (Lejeune. 2005), should have the least negative impact on your physique.
  

  Figure 8: Estimates thermic effect of carbohydrates fats, protein, and alcohol in % energy of the energy thats ingested in form of the respective nutrients (Joosen. 2006).

  And in fact, Jose Antonio et al. (2014) have recently been able to show that a diet that contains fivefold more protein than the FDA recommends (4.4g/kg | 307g/day) is not just benign but will, in conjunction with exercise, will have significant beneficial effects on the physique of healthy resistant trained men (learn more). Furthermore studies indicate that a high protein content may also ameliorate negative effects such as an increase in intrahepatocellular lipid deposition in humans (Bortolotti. 2009).

• Classic overfeeding studies with protein as a single nutrient are yet unfortunately rare. Even less, namely nothing, is known about the effects of ketogenic diets, which is why its at the moment impossible to tell whether a hypercaloric high fat diet that is devoid of carbs and low enough in protein to actually induce ketosis will have the same negative effects as a high fat diet that still contains 15-30% carbohydrates and some protein.
  Based on the studies we have, its yet quite certain that the combination of some carbs and a high amount of fat is the most obesogenic variety of "bulking" you could possibly select. Therefore - with the exception of ketogenic diets, where corresponding data is still missing, the rule of thumb is: The more fat in the diet, the more rapid the body fat, but not necessarily the body weight gain.

• MCT overfeeding is less obesogenic - The reason that rodents that are overfed with medium-chain triglycerides (Geliebter. 1983) and assumable human beings store less fat than on long-chain triglycerides as you will find them in your bacon, sausages, dairy & co is an increase in thermogenesis that has been observed in both rodent and human studies.
  

  Figure 10: Metabolic rate in healthy men after the ingestion of isocaloric fat meals containing MCTs or long chain triglycerides (Hill. 1989).

  As you can see in Figure 10, this effect does not diminish over time - at least, when only the effect of the infusion of MCTs versus long-chain fatty acids is concerned. In view of the rodent study by Geliebter et al. (1983) and the results of the study by Hill et al. (1989), it appears to be quite obvious that MCTs constitute a valuable addition to hypercaloric diets. The often-heard claim that they cannot be stored as fat is yet misleading - even if they are oxidized in the liver, the increase in available energy will increase the storage of energy from other nutrients. The dream of eating as much as you want without gaining weight does therefore remain a dream - at least for all of us who dont harbor a gene defect that blunts the storage of fat.
  
  Still, in theory it would appear as if using MCTs in a dieting context makes sense. In reality, studies have shown that using MCTs as a major source of your dietary fats does not lead to significant long-term improvements in  fat or general weight loss - even if 27% of an 800kcal/day starvation diet were pure MCT oil (Yost. 1989).

References:

• Acheson, K. J., et al. "Glycogen storage capacity and de novo lipogenesis during massive carbohydrate overfeeding in man." The American journal of clinical nutrition 48.2 (1988): 240-247. 
• Antonio, Jose, et al. "The effects of consuming a high protein diet (4.4 g/kg/d) on body composition in resistance-trained individuals." Journal of the International Society of Sports Nutrition 11.1 (2014): 19.
• Bouchard, Claude, et al. "The response to long-term overfeeding in identical twins." New England Journal of Medicine 322.21 (1990): 1477-1482. 
• Danforth Jr, E., et al. "Dietary-induced alterations in thyroid hormone metabolism during overnutrition." Journal of Clinical Investigation 64.5 (1979): 1336.
• Dirlewanger, M., et al. "Effects of short-term carbohydrate or fat overfeeding on energy expenditure and plasma leptin concentrations in healthy female subjects." International journal of obesity and related metabolic disorders: journal of the International Association for the Study of Obesity 24.11 (2000): 1413-1418.
• Faeh, David, et al. "Effect of fructose overfeeding and fish oil administration on hepatic de novo lipogenesis and insulin sensitivity in healthy men." Diabetes 54.7 (2005): 1907-1913.
• Forbes, Gilbert B., et al. "Hormonal response to overfeeding." The American journal of clinical nutrition 49.4 (1989): 608-611.
• Geliebter, Ae al, et al. "Overfeeding with medium-chain triglyceride diet results in diminished deposition of fat." The American journal of clinical nutrition 37.1 (1983): 1-4.
• Hill, James O., et al. "Thermogenesis in humans during overfeeding with medium-chain triglycerides." Metabolism 38.7 (1989): 641-648.
• Horton, Tracy J., et al. "Fat and carbohydrate overfeeding in humans: different effects on energy storage." The American journal of clinical nutrition 62.1 (1995): 19-29. 
• Johnstone, A. M., R. J. Stubbs, and C. G. Harbron. "Effect of overfeeding macronutrients on day-to-day food intake in man." European journal of clinical nutrition 50.7 (1996): 418-430. 
• Joosen, A. M., and Klaas R. Westerterp. "Energy expenditure during overfeeding." Nutr Metab (Lond) 3 (2006): 25.
• Kolaczynski, JERZY W., et al. "Response of leptin to short-term and prolonged overfeeding in humans." The Journal of Clinical Endocrinology & Metabolism 81.11 (1996): 4162-4165.
• Lejeune, Manuela PGM, Eva MR Kovacs, and Margriet S. Westerterp-Plantenga. "Additional protein intake limits weight regain after weight loss in humans." British Journal of Nutrition 93.02 (2005): 281-289.
• McDevitt, Regina M., et al. "Macronutrient disposal during controlled overfeeding with glucose, fructose, sucrose, or fat in lean and obese women." The American journal of clinical nutrition 72.2 (2000): 369-377.
• McDevitt, Regina M., et al. "De novo lipogenesis during controlled overfeeding with sucrose or glucose in lean and obese women." The American journal of clinical nutrition 74.6 (2001): 737-746.
• Meugnier, Emmanuelle, et al. "Changes in gene expression in skeletal muscle in response to fat overfeeding in lean men." Obesity 15.11 (2007): 2583-2594. 
• Minehira, K., et al. "Effect of carbohydrate overfeeding on whole body macronutrient metabolism and expression of lipogenic enzymes in adipose tissue of lean and overweight humans." International journal of obesity 28.10 (2004): 1291-1298.
• Poehlman, Eric T., et al. "Genotype-controlled changes in body composition and fat morphology following overfeeding in twins." The American journal of clinical nutrition 43.5 (1986): 723-731. 
• Roberts, Susan B., et al. "Effects of age on energy expenditure and substrate oxidation during experimental overfeeding in healthy men." The Journals of Gerontology Series A: Biological Sciences and Medical Sciences 51.2 (1996): B148-B157.
• Terán-García, Margarita, et al. "Effects of cholesterol ester transfer protein (CETP) gene on adiposity in response to long-term overfeeding." Atherosclerosis 196.1 (2008): 455-460.
• Ukkola, Olavi, A. Tremblay, and C. Bouchard. "Beta-2 adrenergic receptor variants are associated with subcutaneous fat accumulation in response to long-term overfeeding." International journal of obesity and related metabolic disorders: journal of the International Association for the Study of Obesity 25.11 (2001): 1604-1608.
• Vanltallie, Theodore B. "Resistance to weight gain during overfeeding: a NEAT explanation." Nutrition reviews 59.2 (2001): 48-51.
• Yost, Trudy J., and R. H. Eckel. "Hypocaloric feeding in obese women: metabolic effects of medium-chain triglyceride substitution." The American journal of clinical nutrition 49.2 (1989): 326-330.

You wont see the same effects with pineapple/juice (Aiyegbusi. 2011).

Proteases are as any Wikipedia user will lean enzymes that break down proteins (proteolysis) by hydrolyzing the peptide bonds that link amino acids together in the polypeptide chain forming the protein.

Proteases have evolved multiple times, and different classes of protease can perform the same reaction by completely different catalytic mechanisms. Proteases can be found in animals, plants, bacteria, archaea and viruses. And proteases can be found on among the favorite supplements of naturopath.
Up to today, however proteases could not be found on the list of scientifically proven performance enhancers. With the latest study from the University of Tasmania, the latter has changed: According to the results Shing et al. published in the latest issue of the European Journal of Sport Science, bromelain, a protease that can be found among others in several foods, most prominently pineapple, can reduce (a) the subjective feelings of fatigue and (b) help to maintain testosterone concentration in competitive cyclists taking part in a six-day cycle stage race.

The former is what Shing et al. conclude based on the results of a study that involved fifteen highly trained cyclists [age: 22, years, height: 1.79, body mass: 68.69]. In the corresponding randomized, double-blind, placebo-controlled trial

• 8 of the cyclist 1000mg of bromelain per day, while
• 7 of the cyclists got a visually identical placebo supplement

which was consumed daily across six days of competitive racing. Blood was collected from each cyclist on days one, three and six of racing and analysed for creatine kinase (CK), myoglobin, lactate dehydrogenase (LDH) and testosterone.

Figure 1: Changes in CK and testosterone during the 6 days of competitive cycling (Shing. 2015).

The results of the study show significant elevations in CK activity (this protein is indicative of muscle damage), LDH activity (this protein is necessary to get rid of lactate) and myoglobin concentration in both groups. What was different, though was that the testosterone concentrations of the athletes who received the bromelain supplement tended to maintain stable, while those of the subjects in the placebo group decreased significantly over the course of the 6-day race period.

In conjunction with the perceived feeling of fatigue with was lower in the bromelain group on day four of racing (P = 0.01), the results of the study at hand to this in fact suggest that the consumption of 1,000mg of bromelain can have beneficial effects on some, albeit not directly performance relevant parameters in trained athletes.
References:

• Aiyegbusi, Ayoola I., et al. "A comparative study of the effects of bromelain and fresh pineapple juice on the early phase of healing in acute crush achilles tendon injury." Journal of medicinal food 14.4 (2011): 348-352.
• Pavan, Rajendra, Sapna Jain, and Ajay Kumar. "Properties and therapeutic application of bromelain: a review." Biotechnology research international 2012 (2012).
• Shing, Cecilia M., et al. "Acute protease supplementation effects on muscle damage and recovery across consecutive days of cycle racing." European journal of sport science ahead-of-print (2015): 1-7.

Its obviously to have the 24h effects on testosterone and cortisol than only those measured after the workout , but can we make solid conclusions based on the additional data?

In spite of the fact that the acute testosterone and cortisol response to exercise appears to have little direct effects on the overall training outcome (Schoenfeld. 2013), acute increase in cortisol and reductions in testosterone, i.e. a decrease in the testosterone:cortisol ratio is a classic feature of overtraining and can very well blunt, if not reverse the beneficial effects of exercise on your health and body composition.

Against that background a recent experiment that was conducted by researchers from the University of Chieti-Pescara in Italy could be of great interest to everyone who is performing high intensity interval training on a regular basis. Why?

Well, in contrast to previous studies, Blasio et al. investigated both the acute and 24h effects of a high intensity interval resistance training regimen in trained young men.
To characterize the effects on heart rate and hormonal responses the subjects, eight trained, healthy trained men (28.61 ±3.51 yrs), performed three different workouts which had the same exercises, the same load and number of repetitions for each exercise, but different exercise order, recovery and speed of execution.

• RANDOM workout: the assigned goal was to complete the assigned repetitions respecting only two duties. The first one was don’t stop until all of the repetitions were completed; the second was that there were no assigned order of execution of exercises and no assigned consecutive repetitions to complete.
  
  Participants were thus free to choose both the order of exercises and number of consecutive repetitions for each exercise (i.e. 2 repetitions of kettlebell swing, 10 repetitions of medicine ball slam, 20 repetitions of squat, 4 repetitions of spin with Bulgarian bag, etc.).
  
  No recovery period was assigned, except the time necessary to move from a station to another, and no speed of execution of exercises was assigned: participants were free to choose the preferred speed. 
• LADDER workout: respecting the following order of execution, kettlebell swing, medicine ball slam, spin with Bulgarian bag, squat, pull-up, burpee, participants had to complete the total repetitions according to a pyramidal scheme (e.g. 1st lap 10 repetitions at each exercise, 2nd lap 9 repetitions at each exercise) until the total number of repetitions of each exercise was executed.
  
  Each lap of the circuit was followed by 1 minute of recovery. No speed of execution of exercises was assigned: participants were free to choose the preferred speed. 
• AS SOON AS POSSIBLE (ASAP) workout : respecting the following order of execution, kettlebel swing, medicine ball slam, spin with Bulgarian bag, squat, pull-up, burpee, participants had to complete the total volume in six laps executed as soon as possible.
  
  During each lap participants had to complete the sixth part of total number of repetitions of each exercise without rest among exercises. Each lap of the circuit was followed by 1 minute of recovery.

Salivary samples were collected before and after each workout, at 11:00 p.m. and at 7:00 a.m. of the following day. Salive was also collected during a non-training day. Similarly, before and after the workout, plasma lactate was measured while a beat-to-beat heart rate recording was executed during each workout. Cortisol (C) and testosterone (T) were measured in salivary samples.

2h before the workouts the subjects who had to abstain from sexual intercourse, stimulants and alcohol from 2 days before to the experimental days and until 9:00 a.m. of the following day, consumed a standardized meal that was lower to 400 and consisted of 33 cl of water, 35 cl of orange juice and two 30 g energy bars (Power Sport Double Use, Enervit, Milan, Italy).

Lets look at the results

While the protocols elicited the same heart rate response (the major part of each workout was spent between 80 and 100% of maximal heart rate, confirming the high cardiovascular intensity of the workouts), they elicited different hormonal and lactate variations with the LADDER workout producing the lowest lactate increase and the RANDOM workout eliciting the highest lactate, cortisol and testosterone increases.

Figure 1: Relative changes in hormone and lactate concentration in response to the workouts (Di Blasio. 2014)

When C was considered in ratio with T no significant differences have been shown among workouts-induced variations. Results of the analysis of covariance, executed on significantly modified variables, confirmed that basal hormonal and lactate values did not influence their variations.

When they studied the effects of workouts on prolonged hormones production (i.e. until the morning following the morning, di Blasio et. al. found that observed that observed that

"C had both time (F=179.723; p < 0.001) and group × time effect (F=10.942; p < 0.001): while during non-training day there is a physiological decline of C production at 11:00 p.m., during training days its decline is not present but seems to have a continuous increase from 7:00 p.m. to 7:00 a.m." (Di Blasio. 2014)

For the testosterone production the authors found both time (F=443.340; p < 0.001) and group × time effect (F=3.254; p=0.008) even if the group × time effect seems determined by the samples collected at 7:00 p.m., so that the effects cannot be ascribed fully / exclusively to the workout.

Figure 2: 23h hormone profile after the RANDOM, LADDER, ASAP workouts on a control day (di Blasio. 2014)

What is most interesting, though, is the cortisol to testosterone ratio. It shows the greatest inter-group differences and could potentially be of great physiological relevance (Crowley. 1996). In that, the LADDER workout has the most negative effect, as it will totally blunt the natural decline of the C:T ratio at noon.
References:

• Crowley, Michael A., and Kathleen S. Matt. "Hormonal regulation of skeletal muscle hypertrophy in rats: the testosterone to cortisol ratio." European journal of applied physiology and occupational physiology 73.1-2 (1996): 66-72. 
• Schoenfeld, Brad J. "Postexercise hypertrophic adaptations: a reexamination of the hormone hypothesis and its applicability to resistance training program design." The Journal of Strength & Conditioning Research 27.6 (2013): 1720-1730.