Скачать или смотреть IGF-1LRG: Atrophy Command Sequence

2,879.250 Hz — Primary Peptide Backbone Signature
• Mirrors the alpha-helix structural rhythm of IGF-1 LR3
• Models long-chain peptide extension behavior
• Acts as the core “molecular skeleton carrier”
• Provides lengthened peptide-field coherence

1,439.625 Hz — Disulfide Bridge Echo Tone
• Reflects IGF-1 disulfide linkage clusters
• Models fold-locking stability mechanisms
• Functions as a bond-stabilizer harmonic
• Supports tertiary-shape integrity

719.8125 Hz — Receptor-Binding Impression Layer
• Echoes ligand-docking vibrational behavior
• Represents side-chain rotational harmonics
• Functions as the receptor interface frequency
• Provides a “surface communication” signature

11,517 Hz — Amino-Terminal Extension Band
• Models LR3 N-terminal extension oscillations
• Enhances binding-freedom simulation
• Adds molecular high-definition detail
• Sharpens peptide field precision

10,819 Hz — Beta-Sheet Micro-Stability Tone
• Represents secondary sheet-like vibrational patterns
• Contributes surface-tension micro-stability
• Balances the alpha-helix carrier frequencies
• Adds structural refinement

11,727 Hz — Signal-Cascade Spark Frequency
• Mirrors cascade-initiation shimmer patterns
• Simulates activation charge distribution
• Acts as the “ignition” layer of the stack
• Adds dynamic intracellular-motion analogues

Iso 3.5 Hz
• Resonates with regenerative slow-wave tempos
• Adds deep anabolic-style rhythmic grounding

Iso 6.0 Hz
• Mirrors theta-band activation windows
• Provides the best biological communication tempo

Iso 11.0 Hz
• Reflects low-alpha readiness rhythms
• Enhances activation-style fields

Binaural: 2,879.250 Hz L / 2,885.250 Hz R
• Creates a 6 Hz motion field
• Models molecular interference dynamics
• Adds movement and micro-phase shifts
• Animates the peptide backbone pattern

Molecular Process Driving Muscle Atrophy

Primary mechanism: increased protein breakdown.

Key molecular pathways:
• Ubiquitin–Proteasome System (UPS) – tags muscle proteins with ubiquitin and sends them to be degraded; the main engine of atrophy.
• Autophagy–Lysosome System – breaks down cell components during disuse, starvation, or disease.
• Myostatin Signaling (SMAD2/3) – suppresses muscle cell growth; elevated during inactivity.
• FOXO Transcription Factors – activate muscle-wasting genes (atrogin-1, MuRF1).
• Inflammatory cytokines (TNF-α, IL-6) – promote catabolic breakdown.
• Reduced IGF-1/AKT activity shuts down growth pathways and removes inhibition on FOXO.

Summary:
Atrophy occurs when protein breakdown protein synthesis through UPS + autophagy + myostatin + FOXO activation.


Molecular Process Driving Muscle Growth (Hypertrophy)

Primary mechanism: increased protein synthesis.

Key molecular pathways:
• IGF-1 / AKT / mTOR Pathway – the core anabolic pathway; increases translation, ribosome activity, and muscle-fiber growth.
• mTORC1 activation – increases protein synthesis rate and muscle-cell enlargement.
• Satellite Cell Activation (Pax7, MyoD) – muscle stem cells fuse to fibers to increase nuclei and capacity for growth.
• Mechanical Tension MAPK Signaling – detects load and increases anabolic gene expression.
• Amino Acid Signaling (especially leucine) – feeds directly into mTOR activation.
• Hormonal Support (testosterone, GH/IGF-1) – boosts protein synthesis and recovery.
• Reduced myostatin activity – removes growth inhibition.

Summary:
Muscle growth occurs when protein synthesis protein breakdown driven by IGF-1/AKT/mTOR + satellite cell fusion + mechanical-load signaling.

Sanskrit to English Subliminal

5 8 7 7 9 2. 5 8 7 7 9 2. 5 8 7 7 9 2.
उबिक्विटिन्–प्रोटिओसोम विघटन-क्रमं सक्रियय
अौताफ़जी–लाइसोज़ोम अपघटन-प्रक्रियाम् आवर्तय
मायोस्टैटिन्–SMAD2/3 नियमन-क्षेत्रं प्रवर्तय
FOXO-चालित् अपचय-जीवनुच्चारणं सक्षमय
IGF-1/AKT सञ्चारण-निर्गमं न्यूनीयकरोतु
स्थितिम् स्थापय— प्रोटीन-अपचयः प्रोटीन-संश्लेषणात् अधिकः

Activate the ubiquitin–proteasome breakdown sequence
Engage the autophagy lysosome degradation protocol
Trigger the myostatin–SMAD2/3 regulation field
Enable FOXO-driven catabolic gene expression
Reduce IGF-1 AKT signaling output
Set the system state: protein breakdown greater than protein synthesis