The Female Athlete Triad (Triad) and the more encompassing Relative Energy Deficiency in Sport (RED-S) are disorders caused by low energy availability (LEA). LEA is a state of insufficient energy intake by an athlete relative to their energy expenditure. Persistent LEA results in the deleterious consequences to health and performance that comprise RED-S. With respect to both the Triad and RED-S, researchers have called for more education of those involved with sport, particularly coaches, to help reduce the incidence of these disorders. Recent studies have shown that as few as 15% of coaches are aware of the Triad, with up to 89% unable to identify even one of its symptoms. RED-S is a more recently established concept such that coach knowledge regarding it has only begun to be assessed, but the results of these initial studies indicate similar trends as for the Triad. In this review, we synthesize research findings from 1986 to 2021 that pertains to LEA and RED-S, which coaches should know so they can better guide their athletes.

Insulin promotes protein accretion in cardiac and skeletal muscle through a stimulation of the mRNA translation initiation phase of protein synthesis. The present set of experiments examined the regulatory TSC2 signaling pathway that potentially contribute to the myocardial responsiveness of protein synthesis to insulin in post-absorptive male Sprague-Dawley rats in vivo. Heart and skeletal muscle were sampled from rats up to one hour following intravenous injection of various doses of insulin. In cardiac muscle, TSC2 phosphorylation was elevated only at the highest plasma insulin concentration (386 ng/ml). In contrast, the extent of mTOR phosphorylation on either Ser( 2448 ) or Ser( 2481 ) was raised at 24-fold less concentration of insulin and corresponded with increased phosphorylation of PKB(Thr 308 ) or PKB(Ser 473 ). In gastrocnemius, TSC2 phosphorylation was elevated at plasma insulin concentrations (16 ng/ml) lower than observed in cardiac muscle (386 ng insulin/ml). The increased TSC2 phosphorylation corresponded with a marked stimulation of PKB phosphorylation. However, mTOR(Ser 2448 ) or mTOR(Ser 2481 ) phosphorylation was not elevated until the plasma insulin concentration reached 97 ng/ml. The results indicate there is a dissociation of TSC2 and mTOR phosphorylation in vivo.

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