Exercise boosts testosterone in two important ways. First, specific types of exercise actually cause our body to produce more testosterone. We’ll talk more about those in a bit. Second, exercise helps to increase muscle mass and decrease body fat. As we’ve discussed previously, adipose tissue converts testosterone into estrogen. The less fat we get, the more T we have.

Men can experience a range of symptoms if testosterone decreases more than it should. Low testosterone, or low T, is diagnosed when levels fall below 300 nanograms per deciliter (ng/dL). A normal range is typically 300–1000 ng/dL, according to the U.S. Food and Drug Administration. A blood test called a serum testosterone test is used to determine your level of circulating testosterone.


A 2010 study published in the journal Hormones and Behavior first suggested this when researchers evaluated the “dual-hormone hypothesis” clinically. (11) They discovered that when cortisol is elevated, testosterone responds by elevating as well but soon after bottoms out at a much lower level than before cortisol kicked in! That means you want to find ways to relieve stress to keep your testosterone levels up.
Intramuscular testosterone injections were first used around fifty years ago. Commercially available preparations contain testosterone esters in an oily vehicle. Esterification is designed to retard the release of testosterone from the depot site into the blood because the half life of unmodified testosterone would be very short. For many years intramuscular preparations were the most commonly used testosterone therapy and this is still the case in some centers. Pain can occur at injection sites, but the injections are generally well tolerated and free of major side effects. Until recently, the available intramuscular injections were designed for use at a frequency of between weekly and once every four weeks. These preparations are the cheapest mode of testosterone treatment available, but often cause supraphysiological testosterone levels in the days immediately following injection and/or low trough levels prior to the next injection during which time the symptoms of hypogonadism may return (Nieschlag et al 1976). More recently, a commercial preparation of testosterone undecanoate for intramuscular injection has become available. This has a much longer half life and produces testosterone levels in the physiological range throughout each treatment cycle (Schubert et al 2004). The usual dose frequency is once every three months. This is much more convenient for patients but does not allow prompt cessation of treatment if a contraindication to testosterone develops. The most common example of this would be prostate cancer and it has therefore been suggested that shorter acting testosterone preparations should preferably used for treating older patients (Nieschlag et al 2005). Similar considerations apply to the use of subcutaneous implants which take the form of cylindrical pellets injected under the skin of the abdominal wall and steadily release testosterone to provide physiological testosterone levels for up to six months. Problems also include pellet extrusion and infection (Handelsman et al 1997).

Testosterone has two major effects on bones: (a) through conversion to estradiol by way of the enzyme, aromatase, testosterone inhibits osteoclastic activity and hence bone resorption; and (b) through conversion to DHT via 5-α-reductase, it stimulates osteoblastic activity and so enhances the laying down of bone (Tivesten et al 2004; Davey and Morris 2005). Hypogonadal men are at risk for the development of osteopenia or osteoporosis and hence for subsequent fracture (Fink et al 2006). About one-third of all osteoporotic hip fractures occur in men and the risk of any osteoporotic fracture in men over 50 is as high as 25 percent (Seeman 1997; Adler 2006). Although treatment with testosterone in hypogonadal men increases bone mineral density (Katznelson et al 1996), it has not yet been established that this results in a reduction in fracture rate.


Many clinical studies have looked at the effect of testosterone treatment on body composition in hypogonadal men or men with borderline low testosterone levels. Some of these studies specifically examine these changes in older men (Tenover 1992; Morley et al 1993; Urban et al 1995; Sih et al 1997; Snyder et al 1999; Kenny et al 2001; Ferrando et al 2002; Steidle et al 2003; Page et al 2005). The data from studies, on patients from all age groups, are consistent in showing an increase in fat free mass and decrease in fat mass or visceral adiposity with testosterone treatment. A recent meta-analysis of 16 randomized controlled trials of testosterone treatment effects on body composition confirms this pattern (Isidori et al 2005). There have been less consistent results with regard to the effects of testosterone treatment of muscle strength. Some studies have shown an increase in muscle strength (Ferrando et al 2002; Page et al 2005) with testosterone whilst others have not (Snyder et al 1999). Within the same trial some muscle group strengths may improve whilst others do not (Ly et al 2001). It is likely that the differences are partly due to the methodological variations in assessing strength, but it also possible that testosterone has different effects on the various muscle groups. The meta-analysis found trends toward significant improvements in dominant knee and hand grip strength only (Isidori et al 2005).
DHEA (dehydroepiandrosterone) extract - this is a chemical that used in your body which a ‘hormone precursor’. This means it’s the chemical used by the body to create hormones like oestrogen or testosterone. When taken as supplement it is believed to boost testosterone levels, but DHEA has not been shown to increase testosterone in men. DHEA comes in two form:

Pellets. Your doctor will place the testosterone pellets under the skin of your upper hip or buttocks. Your doctor will give a shot of local anesthesia to numb your skin, then make a small cut and place the pellets inside the fatty tissues underneath your skin. This medication dissolves slowly and is released over about 3-6 months, depending on the number of pellets. 


14. Volek JS, Volk BM, Gómez AL, Kunces LJ, Kupchak BR, Freidenreich DJ, Aristizabal JC, Saenz C, Dunn-Lewis C, Ballard KD, Quann EE, Kawiecki DL, Flanagan SD, Comstock BA, Fragala MS, Earp JE, Fernandez ML, Bruno RS, Ptolemy AS, Kellogg MD, Maresh CM, Kraemer WJ. Whey protein supplementation during resistance training augments lean body mass. J Am Coll Nutr. 2013;32(2):122-35. PMID: 24015719


Unfortunately, in the modern world, stresses and emotional exhaustion lie in wait for men at every step. Nowadays, burnout is a constant state for many men. Of course, this causes great harm to the men’s health. Stresses drain of vitality and affect emotional state. Besides, they are also very dangerous for the nervous system. The nature is wise. And the body of a man who is not subject to stress can produce more testosterone.
The sex hormone testosterone is far more than just the stuff of the alpha male's swagger. Though it plays a more significant role in the life of the biological male, it is actually present in both sexes to some degree. Despite popular perceptions that testosterone primarily controls aggression and sex drive—although it does play a role in both of those things—research has shown that individual levels of testosterone are also correlated with our language skills and cognitive abilities. Testosterone occurs in the body naturally, but can be administered as a medication, too: its most common uses are in the treatment of hypogonadism and breast cancer, as well as in hormone therapy for transgender men.
First, it’s important to note that these tactics and practices to boost testosterone naturally probably won’t work with men who have hypoandrogenism. If the glands and cells responsible for producing testosterone are damaged or defective, no amount of eggs or sleep will help you raise testosterone levels. You’ll likely need to use testosterone replacement therapy to get your T levels to a healthy place.
A related issue is the potential use of testosterone as a coronary vasodilator and anti-anginal agent. Testosterone has been shown to act as a vasodilator of coronary arteries at physiological concentrations during angiography (Webb, McNeill et al 1999). Furthermore men given a testosterone injection prior to exercise testing showed improved performance, as assessed by ST changes compared to placebo (Rosano et al 1999; Webb, Adamson et al 1999). Administration of one to three months of testosterone treatment has also been shown to improve symptoms of angina and exercise test performance (Wu and Weng 1993; English et al 2000; Malkin, Pugh, Morris et al 2004). Longer term studies are underway. It is thought that testosterone improves angina due its vasodilatory action, which occurs independently of the androgen receptor, via blockade of L-type calcium channels at the cell membrane of the vascular smooth muscle in an action similar to the dihydropyridine calcium-channel blockers such as nifedipine (Hall et al 2006).
Type 2 diabetes is an important condition in terms of morbidity and mortality, and the prevalence is increasing in the developed and developing world. The prevalence also increases with age. Insulin resistance is a primary pathological feature of type 2 diabetes and predates the onset of diabetes by many years, during which time raised serum insulin levels compensate and maintain normoglycemia. Insulin resistance and/or impaired glucose tolerance are also part of the metabolic syndrome which also comprises an abnormal serum lipid profile, central obesity and hypertension. The metabolic syndrome can be considered to be a pre-diabetic condition and is itself linked to cardiovascular mortality. Table 1 shows the three commonly used definitions of the metabolic syndrome as per WHO, NCEPIII and IDF respectively (WHO 1999; NCEPIII 2001; Zimmet et al 2005).
When females have a higher baseline level of testosterone, they have higher increases in sexual arousal levels but smaller increases in testosterone, indicating a ceiling effect on testosterone levels in females. Sexual thoughts also change the level of testosterone but not level of cortisol in the female body, and hormonal contraceptives may affect the variation in testosterone response to sexual thoughts.[51]

It is a natural hormone present in the body known as Dehydroepiandrosterone (DHEA). It reduces the estrogen levels while boosting testosterone levels. It has been in use since so long to raise testosterone levels. Among all supplements, it is one of the famous and many researchers are working on it to tell how it stimulates testosterone production. It is banned for athletes and professional players.
Sleep apnea is another frequently listed contraindication to testosterone treatment. There have been a few reports of the development, or worsening, of sleep apnea during testosterone therapy (Matsumoto et al 1985) but sleep apnea is actually associated with lower serum testosterone levels (Luboshitzky et al 2002). The reduction in fat mass during treatment with testosterone could potentially be beneficial for sleep apnea, so many specialists will still consider patients for treatment with appropriate monitoring. It is wise to take a clinical history for sleep apnea during testosterone treatment in all men and perform sleep studies in those who develop symptoms.

Sprinting has been shown numerous times that it has positive effects on testosterone levels. One 2011 study (ref 84) looked at weightlifters who performed 4x35m sprints twice a week. In contrast to the control group (who continued lifting but did not sprint), it was found that “After the 4-week training program, total testosterone and the total testosterone/cortisol ratio increased significantly in the (sprinters) EXP group”.


Epidemiological studies suggest that many significant clinical findings and important disease states are linked to low testosterone levels. These include osteoporosis (Campion and Maricic 2003), Alzheimer’s disease (Moffat et al 2004), frailty, obesity (Svartberg, von Muhlen, Sundsfjord et al 2004), diabetes (Barrett-Connor 1992), hypercholesterolemia (Haffner et al 1993; Van Pottelbergh et al 2003), hypertension (Phillips et al 1993), cardiac failure (Tappler and Katz 1979; Kontoleon et al 2003) and ischemic heart disease (Barrett-Connor and Khaw 1988). The extent to which testosterone deficiency is involved in the pathogenesis of these conditions, or to which testosterone supplementation could be useful in their treatment is an area of great interest with many unanswered questions.
This summary is intended for general informational purposes only, and should not be interpreted as specific medical advice. The U.S. Food and Drug Administration does not strictly regulate herbs and supplements. There is no guarantee of purity, strength, or safety of the products. As a result, effects may vary. You should read product labels. In addition, if you are taking medications, herbs, or other supplements you should consult with a qualified healthcare provider before taking a supplement as supplements may interact with other medications, herbs, and nutritional products. If you have a medical condition, including if you are pregnant or nursing, you should speak to your physician before taking a supplement. Consult a healthcare provider if you experience side effects.

The changes in average serum testosterone levels with aging mean that the proportion of men fulfilling a biochemically defined diagnosis of hypogonadism increases with aging. Twenty percent of men aged over 60 have total testosterone levels below the normal range and the figure rises to 50% in those aged over 80. The figures concerning free testosterone are even higher as would be expected in view of the concurrent decrease in SHBG levels (Harman et al 2001).


Erectile dysfunction is a common finding in the aging male. A prevalence of over 70% was found in men older than 70 in a recent cross-sectional study (Ponholzer et al 2005). Treatment with phosphodiesterase-5 (PDE-5) inhibitors is proven to be effective for the majority of men but some do not respond (Shabsigh and Anastasiadis 2003). The condition is multi-factorial, with contributions from emotional, vascular, neurological and pharmacological factors. The concept of erectile dysfunction as a vascular disease is particularly interesting in view of the evidence presented above, linking testosterone to atherosclerosis and describing its action as a vasodilator.


Epidemiological data has associated low testosterone levels with atherogenic lipid parameters, including lower HDL cholesterol (Lichtenstein et al 1987; Haffner et al 1993; Van Pottelbergh et al 2003) and higher total cholesterol (Haffner et al 1993; Van Pottelbergh et al 2003), LDL cholesterol (Haffner et al 1993) and triglyceride levels (Lichtenstein et al 1987; Haffner et al 1993). Furthermore, these relationships are independent of other factors such as age, obesity and glucose levels (Haffner et al 1993; Van Pottelbergh et al 2003). Interventional trails of testosterone replacement have shown that treatment causes a decrease in total cholesterol. A recent meta-analysis of 17 randomized controlled trials confirmed this and found that the magnitude of changes was larger in trials of patients with lower baseline testosterone levels (Isidori et al 2005). The same meta-analysis found no significant overall change in LDL or HDL cholesterol levels but in trials with baseline testosterone levels greater than 10 nmol/l, there was a small reduction in HDL cholesterol with testosterone treatment.
If testosterone deficiency occurs during fetal development, then male characteristics may not completely develop. If testosterone deficiency occurs during puberty, a boy’s growth may slow and no growth spurt will be seen. The child may have reduced development of pubic hair, growth of the penis and testes, and deepening of the voice. Around the time of puberty, boys with too little testosterone may also have less than normal strength and endurance, and their arms and legs may continue to grow out of proportion with the rest of their body.
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