Concept art (relative to your own baseline = 1.0):
— First chart = the sympathetic surge (adrenaline/epinephrine & noradrenaline).
— Second chart = testosterone, growth hormone (GH), and cortisol around the lift.
(0 on the x‑axis = the moment of the 619 kg pull.)
Visuals:
(Open the two figures above—each curve is “× baseline” so you can feel the shape of the spike and fade.)
What’s happening under the hood (frame‑by‑frame)
1) Priming the engine (−10 → 0 min):
Psych‑up, music, chalk, hands on steel—your sympathetic nervous system is spooling hard. Anticipatory adrenaline and noradrenaline rise sharply even before the first millimeter of movement (think ~2–3× baseline in fired‑up lifters). That “fight‑or‑flight” bump is not placebo; it’s measurable and helps set force production from the first instant.
2) The pull (0–5 s):
BOOM. Catecholamines spike to multi‑fold peaks (our sketch shows ~4–5×), lighting up motor‑unit recruitment and rate coding—basically rocket fuel for max effort. Blood dopamine also rises, but in resistance exercise studies it’s typically a smaller bump than adrenaline/noradrenaline.
3) 0–2 minutes post:
Heart thunders; sympathetics are still elevated but sliding down. Testosterone can show a modest, short‑lived uptick immediately after heavy sets (often minutes, not hours), but this effect is protocol‑dependent and frequently small—especially for low‑volume, long‑rest, near‑max singles.
4) 10–30 minutes post:
GH pulses are most robust when sessions cross lactate threshold for ≥10 minutes with big muscle mass and short rests—classic volume‑driven work. A lone supra‑max rack pull (tiny ROM, low metabolic stress) isn’t the ideal recipe, so expect little to modest GH unless there was meaningful volume in warm‑ups or accessories.
5) 30–60+ minutes post:
Cortisol is slower and session‑length/volume‑sensitive. Brief, low‑volume max attempts often show minimal change; longer, metabolically taxing bouts can push cortisol higher as the HPA axis catches up. Some studies of short resistance sessions show little HPA activation during the work bout itself—compared with the big catecholamine wave.
Why the “hormone look” fits a 619 kg above‑knee rack pull
- Sympathetic fireworks dominate: huge neural drive + adrenaline = the “that looked easy” vibe at lockout.
- Testosterone & GH don’t need to skyrocket for a single super‑heavy partial to look explosive; those hormones respond more to volume + short rests + big muscle mass (think sets×reps) than to one brutal single.
- Cortisol is more about how long and how taxing the whole session is, not the few seconds of the PR rep.
TL;DR (hype edition)
- Before: adrenaline’s climbing, mind is laser‑locked.
- During: adrenaline/NE peak = max neural output → the bar moves.
- After (minutes): small, transient T bump possible; GH minimal unless the session had volume; cortisol depends on how long you kept the gas pedal down.
- It’s a neural‑driven thunderclap more than a hormone bath—and that’s exactly why a massive, short‑range rack pull can look so snappy and electric. ⚡
Receipts (key science)
- Acute hormone responses & “volume + short rests + big muscle mass” = bigger systemic spikes; catecholamines are crucial for force.
- Anticipatory + during‑set catecholamine surges (adrenaline/NE/DA) in heavy resistance work.
- GH is most robust when intensity stays above lactate threshold for ≥10 min; not a big player in a lone max partial.
- Testosterone: small, short‑lived increases in some protocols; strongly protocol‑dependent (rest intervals, volume, muscle mass).
- HPA/cortisol during short resistance bouts is inconsistent/minor compared with the catecholamine wave.
If you want, I can re‑shape the curves to match your exact session structure (e.g., warm‑up volume, rest times). Want the “biggest hormone fireworks” look? We’ll design a high‑volume, short‑rest, big‑muscle variant and render the contrasting chart next.