Laverne Hildebrand
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The gonadal axis suppression transient and the axis functional, as the effect, can be reversible with weight gain; although the rate of testosterone returning to normal seems highly individualistic (96–98). In the case of the second proposed mechanism, several researchers' decades ago demonstrated short- and long-term caloric deficient results in testosterone reductions in men (92–94). In these scenarios the inhibitory effect of cortisol appears twofold; i.e., to impact LH and FSH via GnRH suppression as well as a compromise of Leydig cell function via direct steroidogenesis inhibition (79, 83). The development of the Overtraining Syndrome has been reported in a multitude of sports, regardless of the emphasis on training modality employed (e.g., runners vs. weight lifters vs. tennis players) although the specific symptoms and frequency of select symptoms can be somewhat sports specific (74, 75). The syndrome results in a chronic under-performance, negative health consequences (see Table 6), and typically can end or curtail an athlete's competitive season (56, 57, 77). Many coaches and exercise scientists would be surprised to find that this topic has been recognized and discussed for nearly 100 years (56).
Although it is important to remember that low testosterone-hypogonadism can exist in athletes-exercisers due to other scenarios such as TBI events or AAS use, and should always be ruled-out before assuming other causalities. It is proposed herein, that the development of exercise relative hypogonadism from training can be generalized into one of two categories; an acute, transient phenomenon (overtraining, Triad/RED-S … etcetera) or a more chronic phenomenon reflective of a training-induced adaptation (EHMC). The evidence clearly indicates that exercise training can result in the development of low testosterone in men, and at times the level of reductions reaches the clinical definition of hypogonadism. Finally, and importantly to the present discussion, in most clinical diagnosis settings, much of the assessment and detection of reproductive dysfunction relies on evaluating hormonal status in a resting, basal condition and not in response to an exercise session (53). In general, these acute-chronic exercise endocrine principles for hormonal response hold true for the reproductive and non-reproductive hormones (52).
In the same group, the I-postT T-Testo were also increased and remained elevated at 30 min into the recovery. Compared to the baseline levels, the T-Testo concentrations were increased at I-preT in middle-aged men only. Arazi et al. studied young and middle-aged men who underwent an 8-week-long progressive resistance training program. Kraemer et al. examined the acute effect of heavy resistance exercise on T-Testo in young (29.8 ± 5.3 years), and older (62 ± 3.2 years) men. Studies in older participants refer to studies in men with an average age of 60 ± 5 years. This is secondary to the decreasing capacity of aging Leydig cells to produce testosterone in response to LH stimulation .
This recommended terminology was targeted to exercising men who displayed functional hypogonadotropic hypogonadism and met certain criteria and was not intended for universal application to all exercising men with low testosterone. Interestingly, earlier researchers had drawn an analogy between the development of menstrual disruptions in exercising women and the observation of low testosterone in men but had never applied the Triad terminology to men (111, 112). It is well-known traumatic brain injuries (TBI), such as concussions, can result in the development of low testosterone; specifically, a secondary hypogonadism usually develops due to a pituitary dysfunction (106, 107). That is, their reduced caloric intakes plus high exercise expenditures lead to extreme negative energy balances and an HPG axis suppression—specifically, a hypogonadotropic hypogonadism state development—see preceding section discussion (105). Mechanistically the reason for this reduction in testosterone most likely is related to the practice of many athletes in these sports to use extreme weight loss tactics (e.g., semi-starvation) in attempting to reach a specific competitive weigh category.
Hollywood actors, professional bodybuilders, fitness models, you know, all those basic juice heads that claim they workout 2 times a day every single day, eating a 6000 calorie diet. That threshold varies a lot from person to person, and one key factor that makes the difference is your hormonal profile. And then those ‘experts’ tell to low-average testosterone guys that they should work out 7 days a week doing crazy Hollywood programs and diets.
Although it is important to remember that low testosterone-hypogonadism can exist in athletes-exercisers due to other scenarios such as TBI events or AAS use, and should always be ruled-out before assuming other causalities. It is proposed herein, that the development of exercise relative hypogonadism from training can be generalized into one of two categories; an acute, transient phenomenon (overtraining, Triad/RED-S … etcetera) or a more chronic phenomenon reflective of a training-induced adaptation (EHMC). The evidence clearly indicates that exercise training can result in the development of low testosterone in men, and at times the level of reductions reaches the clinical definition of hypogonadism. Finally, and importantly to the present discussion, in most clinical diagnosis settings, much of the assessment and detection of reproductive dysfunction relies on evaluating hormonal status in a resting, basal condition and not in response to an exercise session (53). In general, these acute-chronic exercise endocrine principles for hormonal response hold true for the reproductive and non-reproductive hormones (52).
In the same group, the I-postT T-Testo were also increased and remained elevated at 30 min into the recovery. Compared to the baseline levels, the T-Testo concentrations were increased at I-preT in middle-aged men only. Arazi et al. studied young and middle-aged men who underwent an 8-week-long progressive resistance training program. Kraemer et al. examined the acute effect of heavy resistance exercise on T-Testo in young (29.8 ± 5.3 years), and older (62 ± 3.2 years) men. Studies in older participants refer to studies in men with an average age of 60 ± 5 years. This is secondary to the decreasing capacity of aging Leydig cells to produce testosterone in response to LH stimulation .
This recommended terminology was targeted to exercising men who displayed functional hypogonadotropic hypogonadism and met certain criteria and was not intended for universal application to all exercising men with low testosterone. Interestingly, earlier researchers had drawn an analogy between the development of menstrual disruptions in exercising women and the observation of low testosterone in men but had never applied the Triad terminology to men (111, 112). It is well-known traumatic brain injuries (TBI), such as concussions, can result in the development of low testosterone; specifically, a secondary hypogonadism usually develops due to a pituitary dysfunction (106, 107). That is, their reduced caloric intakes plus high exercise expenditures lead to extreme negative energy balances and an HPG axis suppression—specifically, a hypogonadotropic hypogonadism state development—see preceding section discussion (105). Mechanistically the reason for this reduction in testosterone most likely is related to the practice of many athletes in these sports to use extreme weight loss tactics (e.g., semi-starvation) in attempting to reach a specific competitive weigh category.
Hollywood actors, professional bodybuilders, fitness models, you know, all those basic juice heads that claim they workout 2 times a day every single day, eating a 6000 calorie diet. That threshold varies a lot from person to person, and one key factor that makes the difference is your hormonal profile. And then those ‘experts’ tell to low-average testosterone guys that they should work out 7 days a week doing crazy Hollywood programs and diets.
