Hormones, Hypertrophy, and Hype: An Evidence-Guided Primer on Endogenous Endocrine Influences on Exercise-Induced Muscle Hypertrophy

Abstract

We review the evidence indicating that endogenous changes in these hormones, including testosterone, growth hormone, insulin growth factor-1, and estrogen, and their proposed anabolic effects contribute to and augment resistance exercise training (RET)-induced hypertrophy. Additionally, we provide recommendations for gold-standard methodological rigor to establish best practices for verifying menstrual phases as part of their research, ultimately enhancing our understanding of the impact of ovarian hormones on RET-induced adaptations.

Figure 1

Somatic hormonal profiling panel depicting the concentrations of various proposed anabolic hormones among various physiological and supraphysiological states (,–51). From left to right: (A) testosterone, (B) growth hormone, (C) estradiol. GHD, growth hormone deficiency; HA PCOS, hyperandrogenic polycystic ovarian syndrome. This figure was created using BioRender.com.

Figure 2

A schematic diagram of the compounds, enzymes, and locations of the human steroidogenesis pathways. The red rectangle highlights hormones of interest. [Adapted from Häggström M, Richfield D. Diagram of the pathways of human steroidogenesis. WikiJournal of Medicine 2014:1(1). doi:10.15347/wjm/2014.005. https://en.wikiversity.org/wiki/WikiJournal_of_Medicine/Diagram_of_the_pathways_of_human_steroidogenesis.]

Figure 3

A. Mechanistic actions of estrogen. B. Hypothesized mechanistic action of progesterone in antagonizing estrogen action. The red X’s indicate points where progesterone is theorized to inhibit estrogen’s action. Specifically, progesterone is hypothesized to block estrogen binding to its receptor, inhibit receptor dimerization, and prevent the activation of estrogen target genes, ultimately inhibiting muscle protein synthesis. Additionally, progesterone is thought to block estrogen binding to GPER, thereby inhibiting GPER-mediated nongenomic signaling. GPER, G-protein coupled estrogen receptor; MPB, muscle protein breakdown; MPS, muscle protein synthesis. This figure was created using BioRender.com.