
Receptor education
Fat-loss receptors, and what actually hits them
β2 and β3 turn lipolysis on. α2 turns it off. Then you have to burn what you released. Most stalls are not a missing peptide. They are food in the fasted window, no deficit, sleep, alcohol, or stacking two β2 drugs. Tap the chart. Compounds are named. Pairing and doses stay with coaching.
Fat cell · tap to explore
This diagram is live
Tap any circle. The panel updates with what that receptor does and which compounds hit it.
Green = gas · Red = brake · Gray = heart spill
Tap a compound. Matching docks light up.
β-AR → Gs → cAMP → PKA → HSL / ATGL → FFA released. Oxidize it or it is stored again.
Problem areas
Why that spot will not move
These depots run high α2 and often low blood flow. Extra β2 still fights a locked brake. Tap a spot to light the whole circuit: brake off, gas, shuttle, fasted work, deficit.
Compounds
What each one does
Same taps as the chips on the fat cell. What it is, what dock it hits. Pairing and doses are coaching.
Circuit
Mobilize, then shuttle, then oxidize
1 · Mobilize
Press β2 and/or β3. Take α2 off. That is lipolysis. Released is not burned.
- β2 gas
- β3 gas
- α2 brake off
2 · Shuttle
Move FFA into mitochondria or they re-esterify.
- L-carnitine
3 · Oxidize
Burn it. Deficit is required. Released FFA that is not oxidized is stored again.
- Calorie deficit
- Fasted cardio
- Fasted HIIT
Beyond adrenergic
HIIT hits more than this clock
The four docks are adrenergic. Higher-intensity work also opens a fifth fat-cell dock and two hormone axes. Still fasted. Still a deficit.
Catecholamines → β2 / β3
HIIT dumps more epinephrine/NE than a walk. Same gas pedals as clen-class, from work instead of a pill. β1 is on some fat cells. The useful gas is still β2/β3. β1 is the heart cost.
NPR-A (ANP / BNP)
Heart stretch peptides bind NPR-A on fat cells. Guanylyl cyclase → cGMP → PKG → HSL and perilipin. Same lipolysis endpoint, different pipe than cAMP. This is the extra dock. Stronger when insulin is low.
GH receptor
HIIT spikes GH. JAK2/STAT5, not adrenergic. Lipolytic and insulin-antagonizing for a window. Tesamorelin is the peptide version of this axis, not this map.
Not equal docks
Glucagon is mostly liver in humans. Cortisol/GR can help acutely by sensitizing cAMP, and wrecks a cut if it stays high. Do not chase either as a fat-loss receptor.
LISS still oxidizes. HIIT is the pulse, not a replacement for the deficit or the walk. Morning, not night, so sympathetic load can come down before sleep. Heart-limited clients do not use HIIT as the stim substitute.
Who uses what
Daily job vs coach-directed receptors
Every client
This is the fat-loss job. Receptors do not replace it.
- Calorie deficit you can repeat
- Protein target daily
- Lift. Do not swap it for extra cardio
- Sleep
- Caffeine if it helps the morning session
- Fasted walk or LISS to oxidize. Fasted HIIT if they recover, morning, for the catecholamine and ANP pulse
- No alcohol in a hard cut
Coach-directed only
Compounds that hit these docks are coach-directed. Pairing and doses are not on this page.
Timing
When the receptors actually work
Fasted block
Yohimbine, then movement, then the first meal. That is the α2 unlock. Food first locks the brake.
HIIT morning
The catecholamine and ANP pulse belongs early. Evening HIIT keeps sympathetic load up into sleep. Sleep is the cut.
Eat to keep training
The deficit is around the session, not a reason to miss protein or collapse under the bar.
What kills fat loss
These stall the circuit. Tap one.
Hit matrix
What hits which receptor
| Compound | Step | ||||
|---|---|---|---|---|---|
| Clenbuterol | Gas | — | — | Spill | mobilize |
| Yohimbine | — | — | Blocks | — | mobilize |
| Caffeine | Indirect | Indirect | Indirect | Indirect | mobilize |
| Nicotine gum | Indirect | Indirect | — | Indirect | mobilize |
| Bronkaid (ephedrine) | Gas | Indirect | Indirect | Spill | mobilize |
| Salbutamol (albuterol) | Gas | — | — | Spill | mobilize |
| Mirabegron | — | Gas | — | Spill | mobilize |
| CL-316243 | — | Gas | — | — | mobilize |
| L-carnitine | — | — | — | — | shuttle |
| Fasted cardio | — | — | — | — | oxidize |
| Fasted HIIT | Indirect | Indirect | — | — | mobilize · oxidize |
| Calorie deficit | — | — | — | — | oxidize |
| T3 | — | — | — | — | oxidize |
| ATX-304 | — | — | — | — | oxidize |
| SLU-PP-332 / 915 | — | — | — | — | oxidize |
| GLP-1 / reta | — | — | — | — | oxidize |
| MOTS-c | — | — | — | — | oxidize |
Stubborn fat
Why lower belly ignores extra clen
High α2 density
Those depots have more brake than gas. More β2 still fights a locked brake.
Insulin locks the brake
Yohimbine needs a fasted window. Eat first and α2 stays on.
Released is not burned
Without carnitine, cardio, and a deficit, FFA returns to the cell.
Outside this map
Useful tools. Different job.
SANA
Creatine-cycle heat. Not adrenergic.
Tesamorelin
GH pulse, visceral fat.
5-Amino-1MQ
NNMT. Outside this map.