Meek, Shon E.

Context: Testosterone is a steroid hormone produced primarily in the testes in men and ovaries in women, playing crucial roles in androgenic, anabolic, and psychological functions, including muscle growth, bone formation, erythropoiesis, risk-taking, and aggression, making it important for athletes. Sports performance is linked closely to testosterone level, prompting athletes to explore legal and illegal ways to boost testosterone. This review examines testosterone physiology and legal strategies for optimizing testosterone levels in athletes, as well as their practical applications. Evidence Acquisition: Database search. Study Design: Narrative review. Level of Evidence: Level 5. Results: Maintaining healthy testosterone levels requires energy balance and optimal nutrition with adequate macronutrients and micronutrients, especially for athletes prone to dieting and food restriction. Testosterone boosters are marketed widely but lack strong evidence for efficacy and may pose risks. While some substances show promise, further research is needed. Sleep is critical as testosterone secretion is linked to the rapid eye movement phase, highlighting the need for proper sleep hygiene and addressing sleep disorders. Moderate-to-high intensity free-weight resistance exercises are most effective for increasing testosterone, while the effects of sexual activity remain unclear. Endocrine-disrupting chemicals can lower testosterone levels and should be avoided. While cold-water immersion may decrease testosterone, sauna bathing appears to be neutral. Radiofrequency electromagnetic radiation from modern electronic devices may harm the hypothalamic-pituitary-gonadal axis, warranting limited use. Over-the-counter analgesics, such as nonsteroidal anti-inflammatory drugs and acetaminophen, may decrease testosterone levels, suggesting cautious use. Seasonal changes in testosterone levels require further study. Testosterone-optimizing strategies excluding banned substances may aid in treating functional low testosterone or reducing harm in anabolic-androgenic steroid users. Conclusion: Educating athletes on safe and effective strategies to increase testosterone is crucial, with ongoing research needed to explore additional methods. Strength-of-Recommendation Taxonomy: B.

Phenylalanine (Phe) kinetics are increasingly used in studies of amino acid kinetics, because the metabolic fate of Phe is limited to incorporation into protein (protein synthesis, Sp) and catabolism via hydroxylation ( Q pt) to tyrosine (Tyr). Besides an infusion of labeled Phe to measure Phe flux ( Q p), a priming dose of Tyr and an independent Tyr tracer are used to measure Tyr flux ( Q t) and Q pt. Alternatively, Q t, Q pt, and Sp can be approximated by using equations, based on Phe and Tyr concentrations in body proteins, that eliminate the need for a Tyr tracer. To evaluate the accuracy of this approach, data were obtained from 12 type I diabetic patients and 24 nondiabetic control subjects who were studied with the full complement of tracers both with and without insulin infusion. Sp approximations closely matched measured values in both groups (mean difference <2%, all values <5%), but the agreement was poor for Q pt (error range = −8 to +43%) and Q t (error range −22 to +41%). Insulin status had no effect on these comparisons. The lower approximation error for Sp vs. Q pt is due to the small contribution (∼10%) of Q pt to Q p. Approximation error for Q pt( r > 0.99) can be explained by variability in the ratio of Tyr to Phe coming from protein breakdown, ( Q t − Q pt)/ Q p. Ideally, all fluxes should be directly measured, but these data suggest that whole body Sp can be approximated with an acceptably small margin of error. However, the same equations do not yield reliably accurate values for Q pt or Q t.

Synthesis of Tyr in the human body occurs by hydroxylation of the indispensable amino acid Phe. Until now, it was believed that in humans, this process was restricted to the liver, but we provide compelling evidence of production of Tyr from Phe in the kidney. To determine whether the human kidney produces Tyr, we measured Tyr balance, the Tyr appearance rate, and the Phe-to-Tyr conversion in 12 healthy human subjects by using [ 15 N]Phe and [ 2 H 4 ]Tyr as tracers. Renal plasma flow was measured by using paraaminohippurate, and sampling from the femoral artery and renal veins was performed. The results were compared with those obtained in 12 control subjects undergoing hepatic vein catheterization and infusion of identical tracers. In all 12 subjects, there was a net uptake of Phe by the kidney (2.2 ± 1.2 μmol/min), whereas Tyr was released (5.3 ± 1.5 μmol/min). In contrast, there was a net uptake of both Phe (9.5 ± 1.2 μmol/min) and Tyr (14.3 ± 1.3 μmol/min) by the splanchnic bed. Phe conversion to Tyr occurred at a rate of 5.2 ± 1.2 μmol/min in kidney and 3.0 ± 0.7 μmol/min in the splanchnic bed. The kidney contributed a substantial amount of Tyr to the systemic circulation where the splanchnic bed was a net remover of Tyr. Our results demonstrate that the kidney is the major donor of Tyr to the systemic circulation by its conversion of Phe to Tyr. This observation may have important clinical implications for patients with both renal and hepatic disease, who may be at risk of Phe overloading and Tyr deficiency, and it should be considered when parenteral or enteral nutrients are administered rich in Phe and low in Tyr.