Dbol Cycle: Guide To Stacking, Dosages, And Side Effects

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, https://i-medconsults.com/ 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.