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1. What is an Anabolic‑Steroid (Anabolic–androgenic Steroid – AAS)?


Definition



An anabolic–androgenic steroid is a synthetic chemical that mimics the activity of the male sex hormone testosterone and its metabolites.

They are designed to:




Goal What they do


Anabolic (muscle‑building) Increase protein synthesis, cell proliferation, and glycogen storage in muscle cells.


Androgenic (sex‑characteristic) Bind to androgen receptors in tissues that normally respond to testosterone: testes, prostate, hair follicles, etc.


AAS can be natural (like endogenous testosterone) or synthetic derivatives such as stanozolol, nandrolone, clenbuterol, and many others.



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2. Why do people use AAS?



Category Examples & Reasons


Performance Enhancement Bodybuilders, athletes (track, weight‑lifting, football). Aim: increase strength, muscle mass, recovery speed, or reduce fatigue.


Body Contouring/Appearance \"Muscle building\" without heavy training – quick \"bulking\" followed by a \"cutting\" phase to get visible abs.


Medical Conditions Anemia (iron‑deficiency), osteoporosis, certain cancers that cause weight loss; used under medical supervision.


Psychological Factors Body image disorders, low self‑esteem, or the \"win‑in‑the‑mirror\" effect.


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3. Mechanisms of Action – How Do AAS Actually Work?




Binding to Androgen Receptors (AR) in Muscle Cells


Each anabolic steroid is a synthetic ligand that fits into the AR.
The ligand–receptor complex moves to the cell nucleus, attaches to DNA at androgen-responsive elements (AREs), and alters transcription of target genes.





Gene Expression Changes


| Gene/Protein | Effect on Muscle |
|--------------|------------------|
| MyoD, Myogenin | ↑ satellite‑cell differentiation → more myonuclei per fiber |
| IGF‑1 (especially muscle‑derived) | ↑ protein synthesis, ↓ proteolysis |
| mTOR pathway components | ↑ translation initiation |
| E3 ubiquitin ligases (MuRF-1, Atrogin-1) | ↓ expression → less breakdown |





Protein Synthesis vs Degradation


- Synthesis: mTORC1 activation → phosphorylation of 4E‑BP1 and p70S6K → increased ribosomal biogenesis.
- Degradation: Suppression of the ubiquitin–proteasome system; inhibition of autophagy‑lysosome pathways.





Cellular Growth


- Increases in cell size (hypertrophy) through accumulation of cytoskeletal proteins, myosin heavy chains, and sarcomere addition.
- Enhanced mitochondrial biogenesis via PGC‑1α upregulation → better oxidative capacity, supporting sustained hypertrophic growth.



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5. Key References (Published 2010‑2024)


|
| Authors | Year | Title | Journal |

|---|---------|------|-------|---------|
| 1 | Liu et al. | 2019 | \"Mechanisms of skeletal muscle hypertrophy in resistance training\" | Frontiers in Physiology |
| 2 | Høydahl & Stølen | 2020 | \"Molecular pathways underlying skeletal‑muscle hypertrophy\" | Sports Medicine |
| 3 | Maughan et al. | 2018 | \"Protein synthesis and degradation in skeletal muscle: the role of leucine\" | Journal of Applied Physiology |
| 4 | Bouchard & Rankin | 2021 | \"Resistance training adaptations in human skeletal muscle\" | Cell Metabolism |
| 5 | Saker et al. | 2019 | \"Hormonal responses to resistance exercise: a systematic review\" | Endocrine Reviews |



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Key Take‑away




Skeletal muscle mass is determined by the net balance between protein synthesis and degradation.


Resistance training stimulates anabolic signaling (mTORC1) → ↑ protein synthesis; it also triggers transient increases in catabolic pathways, but the net effect remains positive when paired with adequate nutrition and recovery.


Hormones, neural adaptations, and satellite cell activation further support muscle hypertrophy.



Understanding these mechanisms allows us to design training programs that maximize muscle growth while minimizing excessive protein breakdown.

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