Pathway Glossary

Neurotransmitter–DA/NE

Catecholamine signaling. DA/NE bind GPCRs (D1–D5, α/β-adrenergic) → ↑ cAMP/PKA, Ca²⁺ influx. ↑ arousal, motivation, locomotion.

Neurotransmitter–ACh

ACh acts via nicotinic ion channels (fast depolarization) and muscarinic GPCRs (M1–M5). Supports learning, memory, neuromuscular drive.

CNS–Stimulant

Blockade of monoamine reuptake transporters → ↑ extracellular DA/NE in cortex/striatum → ↑ wakefulness, psychomotor drive.

ATP–PCr System

Creatine kinase transfers phosphate from PCr → ADP. Rapid ATP regeneration during short maximal effort (<10s).

Ca²⁺–Signaling

Ca²⁺ enters via L-type VGCCs and released from SR (RyR). Triggers contraction, calmodulin, CaMK, and mitochondrial enzymes.

Osmolyte–Cell Volume

Small molecules (creatine, taurine, betaine) regulate osmotic stress, stabilize proteins, modulate mTOR and apoptosis.

Methylation–Homocysteine

Betaine donates methyl via BHMT → homocysteine → methionine → SAM. Supports DNA/protein methylation, lowers vascular risk.

IGF1–mTOR Axis

IGF-1 activates PI3K–Akt → mTORC1 → phosphorylation of p70S6K/4EBP1 → ↑ translation, hypertrophy.

Vitamin–Hormone Signaling

Vitamin D binds VDR (nuclear receptor) → ↑ Ca²⁺ channels/transporters. Vitamin K2 carboxylates osteocalcin/MGP → bone mineralization.

Bone–Mineralization

Osteoblasts secrete osteocalcin, ALP. Hydroxyapatite crystal deposition requires Ca²⁺, phosphate, vitamin D/K synergy.

NFkB–Inflammation

TNFα/IL-1 activate IKK → NF-κB released from IκB → nuclear translocation → transcription of pro-inflammatory cytokines.

Membrane–Fluidity

PUFAs (EPA/DHA) incorporate into phospholipid bilayers → ↑ receptor mobility, ↓ lipid raft rigidity → improved insulin/GPCR signaling.

MPS–Sensitivity

ω-3s and leucine ↑ mTOR responsiveness → reduced leucine threshold for muscle protein synthesis.

NMDA–GABA Balance

Mg²⁺ blocks NMDA at rest. Glycine/taurine = NMDA co-agonists + GABA-A agonists → adjust excitatory/inhibitory tone → anxiolysis, sleep.

Sleep–Regulation

Adenosine buildup, melatonin (MT1/MT2), and GABAergic tone regulate sleep onset, SWS, REM cycles.

Thermoregulation

Glycine modulates NMDA in preoptic hypothalamus → vasodilation, ↓ core temperature → sleep induction.

ECM–Remodeling

Fibroblasts remodel collagen/elastin via MMPs/TIMPs. Promoted by GH/IGF1, BPC-157, TB-500.

Collagen–Crosslinking

Vit C–dependent hydroxylases stabilize collagen triple helices → tendon/ligament resilience.

Adenosine–Blockade

Caffeine antagonizes A1/A2A adenosine receptors → ↑ DA/NE release, ↓ sleep pressure → ↑ alertness, performance.

GABA–Agonism

Taurine/glycine weakly activate GABA-A receptors → ↑ Cl⁻ influx → hyperpolarization → sedation, relaxation.

Circadian–Rhythm

Light input via retinal melanopsin → SCN activation → regulation of PER/CRY clock genes → synchronizes sleep–wake cycles.

Antioxidant–Defense

Melatonin, taurine, curcumin directly scavenge ROS + activate Nrf2 → ↑ SOD, catalase, glutathione.

GH–IGF1 Axis

GHRH → GH (pituitary) → IGF-1 (liver) → anabolic tissue effects, ECM repair. Pulsatile during sleep.

LH–FSH Axis

GnRH → pituitary LH/FSH → gonadal testosterone + spermatogenesis. Suppressed by estrogen feedback.

Estrogen–ER Pathway

Estrogens bind ERα/β (nuclear receptors) → gene transcription for reproduction, bone, metabolism. Blocked by SERMs → ↑ GnRH.

p70S6K–mTOR

Central growth regulator. mTORC1 activates p70S6K/4EBP1 → ↑ translation, hypertrophy. Sensitive to AA, IGF-1, ATP/AMP ratio.

AMPK–Energy Sensing

AMPK activated by ↑ AMP/ATP → ↑ GLUT4, FAO, autophagy. Inhibits mTOR. Master regulator of cellular energy.

NO–Perfusion

Arginine → NO (via eNOS) → cGMP → smooth muscle relaxation → vasodilation → ↑ perfusion, ↓ BP.

Urea Cycle

Ammonia detox: NH₃ + CO₂ → urea. Supported by arginine/citrulline → reduced fatigue, improved performance.

Mitochondrial Efficiency

Nitrates → NO → cytochrome c oxidase modulation → less O₂ cost per ATP produced.

FAO–CPT1

Carnitine shuttle via CPT1/2 imports FA into mitochondria → β-oxidation. ↑ endurance, fat use.

Acyl–Carnitine Shuttle

Carnitine binds long-chain FA → acyl-carnitine transported into mitochondria → re-converted → β-oxidation.

Adrenergic–β

β-AR (Gs GPCR) → ↑ cAMP → PKA → HSL/ATGL activation → lipolysis, ↑ HR, contractility.

Adrenergic–α2

α2-AR (Gi GPCR) presynaptic autoreceptor → ↓ NE release → suppresses lipolysis, sympathetic tone.

Glutamate–GABA Balance

Theanine antagonizes NMDA, ↑ GABA, balances excitatory glutamate → relaxation, anxiolysis.

Androgen Receptor

Ligand-activated nuclear receptor. Testosterone/SARMs → ↑ AR binding → hypertrophy, bone density ↑.

Ubiquitin–Proteasome

E3 ligases (atrogin-1, MuRF1) tag proteins → proteasomal degradation. HMB/IGF-1 inhibit → anti-catabolic.

COX2–Eicosanoid

COX2 converts AA → prostaglandins → inflammation, pain. Curcumin ↓ COX2 → anti-inflammatory.

Angiogenesis

VEGF/FGF → endothelial cell migration → new capillaries. BPC/TB-500 stimulate → healing ↑.

Cell Migration

Thymosin β4 regulates actin polymerization → ↑ cell motility, tissue regeneration.

Immune–Antiviral

Zn²⁺ inhibits viral RNA polymerase and modulates IFN response → ↓ viral replication.

HPA–Cortisol

Hypothalamic CRH → pituitary ACTH → adrenal cortisol. Cortisol follows a circadian rhythm, peaking after waking, suppressed by darkness.

Serotonin–5HT

Tryptophan → serotonin via TPH. Acts on 5HT receptors (GPCRs/ion channels). Modulates mood, cognition, circadian entrainment.

Melatonin–MT1/MT2

Melatonin binds MT1/MT2 GPCRs in SCN → inhibits neuronal firing, shifts circadian phase, promotes sleep onset and maintenance.


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The material presented here is strictly a matter of theoretical scientific inquiry.
It is written for educational purposes only, to analyze mechanisms, pathways, and research findings.
Any mention of substances (including SARMs, peptides, or other experimental agents) is made in the spirit of scientific discussion, not in the context of real-world usage.
This site does not provide medical advice, treatment recommendations, or instructions for application.
All content should be understood as part of a conceptual, academic-style exploration.