Small (~5%) amounts of T are secreted from the prostrate, liver and adrenal cortex but the majority is secreted from the testes. The secretion at the testes is controlled via a complex pathway involving three other intermediary hormones. Initially, the arcuate and preoptic areas of the hypothalamus release pulses of Gonadotropin Releasing Hormone (GNRH). GNRH stimulates the basophilic cells of the anterior pituitary at the base of the brain to secrete Leutinizing Hormone (LH) and Follicle Stimulating Hormone (FSH). LH hormone stimulates the Leydig cells, in the interstitial tissue of the testes, to convert cholesterol into T. Specifically, LH promotes the synthesis of a protein that transports cholesterol into the mitochondria, the site of the conversion. The conversion is a complex enzymatic process involving numerous intermediates but the key, and ‘limiting’ stage, is the conversion of cholesterol to Pregnenolone (2,8,10,11).
FSH stimulates the production of Androgen Binding Protein (ABP) in the Sertoli cells also of the testes. ABP is located intra-testicularly and sustains spermatogenesis by maintaining androgen concentration at more than two hundred times that found in the blood (11).
T and LH secretion is circadian but highly individual and variable (10). Both hormones are secreted in pulses between eight and fourteen times per day, T usually lagging LH by approximately sixty minutes. T is controlled via a negative feedback loop whereby higher serum T causes a decrease in LH and GNRH secretion. Serum T levels are greatest in the morning upon waking and decrease by approximately 25% throughout the day (10). A young adult typically has serum concentrations of between 14 and 28nmol/L. From the age of thirty aging causes a significant decrease in average serum T. An average sixty year old typically has serum T concentrations of less than 12nmol/L (10).
Since steroid hormones are only sparingly soluble in blood only approximately 2% of T is in the free, unbound form. Approximately 60% is bound to a protein synthesised in the liver called Sex Hormone Binding Globulin (SHBG). Due to the strength of the bond to this carrier the T is biologically inactive. The remaining T is bound to albumin but these bonds are weaker and hence the T remains bio-available. An increase in T secretion will not necessarily cause an increase in bio-available testosterone if a greater percentage is bound to SHBG (10, 11, 12).. The ratio between total and bio-available T has been hypothesised to reflect individual trainability (5).
T is a powerful anabolic hormone that increases and limits muscle protein synthesis by increasing transport of amino acid across cell membranes and by increasing mRNA and DNA synthesis (10). It is also an anti-catabolic hormone that inhibits cortisol by competing for receptor sites (7, 11). (One of cortisol’s functions is to promote the breakdown of muscle by converting amino acids to carbohydrates) In addition to these anabolic effects, T is also beneficial for strength and power athletes since it contributes to the conversion of type IIa muscle fibres into faster type IIb. T increases the secretion of the other anabolic hormones, growth hormone and Insulin-Like Growth Factors from the liver (13). Lastly T stimulates of erythropoietin synthesis and hence explains the higher hematocrit value in males versus females (11). This latter effect highlights a potential performance benefit of steroid abuse by endurance athletes.
T is androgenic, meaning it promotes masculine characteristics. The significant rise in testosterone production during male adolescence induces secondary sex characteristics. These include the growth of pubic hair, deepening of the voice, reproductive maturation, sperm production and, as one would expect, an increase in lean muscle mass. Contradictorily T both increases bone growth and terminates growth by promoting epiphyseal closure (10, 11).
The androgenic effects side effects of anabolic steroids are especially significant to females. Females who chronically abuse steroids undergo irreversible physical changes including clitoral hypertrophy, deepening of the voice and male pattern baldness (2).
Factors Effecting Serum Testosterone
1. Resistance Training
Appropriate resistance exercise causes an increase in serum T post exercise of up to 70% (5,6,8,9,10). T response to an identical workout can however fluctuate widely (10). This suggests that resistance exercise interacts with other factors to cause elevated serum T. There are a number of conflicting theories as to the possible cause of this increase. Renal blood flow is reduced and this may lead to decreased metabolic clearance of T. There may also be an alteration in testicular blood flow causing an increase in secretion from the Leydig cells. Lastly a decrease in plasma volume due to movement of water out of the cardiovascular system, would cause an increase in T concentration without an increase in total T (8,9,10).
Further increases in strength, in highly trained strength athletes, are highly correlated with increases in bioavailable T (that not bonded to SHGH) and LH (5). The T: SHGH ratio may therefore reflect individual trainability at a given time and positive changes in the ratio may be a long term adaptation to training (5). Periods of overtraining (over-reaching) cause a decrease in serum T but an increase in LH suggesting a reduced utilisation of LH in the Leydig cells. Overtraining also causes a significant increase in the catabolic hormone cortisol. The cortisol:T ratio has been suggested as an indicator of the balance between anabolic and catabolic mechanisms (7).
Multi-joint exercises, such as squats, that utilise large muscle masses are more effective than isolation exercises of smaller muscle groups (6). Some evidence suggests T concentrations decrease after around one hour of intense resistance training. Further research is required to determine the optimum volume, intensity and recovery to induce the greatest increase in T. One regularly quoted study compared the following popular lifting protocols (9):
1. 10 reps, 1 minute recovery
2. 5 reps; 3 minute recovery
It was found that the second workout caused the greatest elevation in T. This suggests that providing intensity remains sufficiently high, increases in volume through higher repetitions and/or decreased recovery induces the greater elevation in serum T (8,9).
2. Alcohol and Analgesics
One of the most powerful T suppressors is alcohol. There is a direct, negative correlation between blood alcohol and T concentrations such that T concentration is lowest when blood alcohol concentration is highest (2, 11). This is caused by enzyme inhibition in the testes that reduces conversion of cholesterol to T. ‘Intoxication’ decreases serum T by more than 25% and for between 10 and 16 hours after blood alcohol concentrations return to normal. LH concentrations however increase in response to alcohol as the body increases secretion in an attempt to regain T homeostasis. Another group of drugs that suppress T are analgesics such as aspirin and codeine. These act not at the testes, but at the pituitary where they reduce LH secretion. The more powerful the analgesic the more effective it is in inhibiting T production (2, 11).
T has been shown to be extremely sensitive to an individual’s emotional state. Life stresses such as those caused by work and relationships can cause a sustained reduction in testosterone secretion (unlike adrenal hormone secretion which initially increases but returns to base levels if stress persists). Conversely positive emotional states increase T production (4).
Emotional state can invoke ‘viscous cycles’ for example poor performance could induce anxiety and hence further declines in performance. Understanding of these hormonal responses may allow athletes to pre-empt and accept declines in performance and adapt there training accordingly.
Insulin is a hormone secreted from the beta cells of the Islets of Langerhans in the pancreas. Its secretion is influenced by a number of factors but most significantly by high plasma glucose concentration. It promotes cellular uptake of glucose and amino acids and inhibits protein degradation (11). Elevation in blood insulin above ‘baseline’ levels causes a decrease in serum T. There is however, no correlation between insulin elevation and the degree of T decrease. The decreased serum T is believed to occur due to an increase in utilisation at muscle cells rather than a decrease in secretion. Supporting evidence to this theory includes LH concentration, which remain unaffected by elevated insulin (1). The popular idea of consuming large amounts of protein and carbohydrate post exercise to take advantage of elevated serum T therefore appears to be correct..
5. Energy Deficit
Energy deficit due to calorie expenditure is greater than calorie consumption. When the deficit is greater than ‘threshold’ serum T decreases. This occurs due to a decrease in LH secretion and an increase in binding proteins that decreases bio-available T (4). When multiple stresses are present such as sleep deprivation and psychological stress, energy deficit appears to be limiting factor to suppress serum T (4). The decrease in T and increase in cortisol caused by energy deficit contribute to a decrease in lean body mass. Sports people who are attempting to reduce body fat or to make body weight categories may be advised to reduce calorie intake to just above threshold. Further research is therefore required to ascertain typical thresholds and any factors that influence them.
ZMA is a mineral supplement, containing magnesium and zinc, marketed as a supplement to optimise testosterone production. Exercise stress causes zinc and magnesium deficiencies and hence these are common in athletic populations (12). These minerals may also be deficient due to the difficulty in attaining the RDA from typical Western diets. Zinc deficiency reduces serum T and magnesium depletion increases cortisol secretion (12). Preliminary evidence in ZMA supplementation does appear to suggest an increase an average circulating free and total T by up to 30%.
T physiology and the factors influencing serum concentrations are not fully understood at this time. None-the-less, I hope that this review has provided some useful suggestions as to natural means to optimise blood testosterone concentrations. I hope that further research into areas discussed will permit more precise guidelines in future.
Author Pat Bateman
Categories: Anabolic Steroid Information