Which gland makes what, how a hormone actually gets a message into a cell, and — the part the exam leans on hardest — exactly which workout variables move testosterone, growth hormone, and cortisol.
What this chapter is actually tested on
The endocrine system is the body's slow, broadcast communication network: ductless glands release chemical messengers — hormones — directly into the bloodstream, and any cell carrying the matching receptor can pick up the signal, no matter how far it sits from the gland that sent it. That's the core contrast with the nervous system: nerves fire a signal down a dedicated wire to one specific target in milliseconds; hormones broadcast to the whole body and let the receptor do the filtering, over seconds to hours.
Every hormone gets released because something triggered the gland to secrete it, and that trigger falls into one of three categories.
| Mechanism | The trigger | Example |
|---|---|---|
| Humoral | A direct change in the blood level of an ion or nutrient | Rising blood glucose triggers insulin release from the pancreas — no nerve or second hormone is involved |
| Neural | Direct stimulation by a nerve | Sympathetic nerves synapsing on the adrenal medulla trigger epinephrine release almost instantly |
| Hormonal (trophic) | Release of one hormone commanding release of another, further down a gland axis | Hypothalamic CRH → pituitary ACTH → adrenal cortisol |
That third row is worth sitting with: it describes a whole chain of command, not a single step. The hypothalamus sits at the top issuing releasing hormones (and, for some axes, inhibiting hormones), the anterior pituitary responds by releasing its own trophic hormone into general circulation, and only then does the actual target gland — thyroid, adrenal cortex, or gonad — put out the hormone that does the work at the tissue. Three tiers, two hormones in between the brain and the payoff hormone.
Once a hormone is in the bloodstream, not all of it is available to act. Steroid hormones especially travel largely hitched to carrier (binding) proteins — testosterone and estrogen ride mostly on sex hormone-binding globulin (SHBG), cortisol rides mostly on corticosteroid-binding globulin, and IGF-1 travels almost entirely bound to a family of IGF-binding proteins. Only the small unbound, or free, fraction can leave the bloodstream and actually reach a receptor — the bound fraction is inert cargo until it's released.
A hormone can only act on a cell that's built a matching receptor for it — that specificity is usually taught as a lock-and-key relationship: one hormone shape, one receptor shape, and nothing else fits. Where that receptor sits is dictated almost entirely by whether the hormone can cross a cell membrane on its own, which in turn comes down to solubility.
| Hormone class | Solubility | Receptor location | Examples |
|---|---|---|---|
| Steroid | Lipid-soluble | Intracellular (cytoplasm or nucleus) | Testosterone, cortisol, aldosterone, estrogen |
| Thyroid | Lipid-soluble (the exception among amine-derived hormones) | Intracellular (nuclear) | T3, T4 |
| Peptide/protein | Water-soluble | Cell-surface (membrane) | Insulin, growth hormone, ACTH, LH, FSH, glucagon |
| Catecholamine | Water-soluble | Cell-surface (membrane) | Epinephrine, norepinephrine |
A lipid-soluble hormone diffuses straight through the membrane, binds its receptor inside the cell, and the hormone–receptor complex itself goes on to bind DNA and change which genes get transcribed — a genomic mechanism that's powerful but slow, playing out over minutes to hours. A water-soluble hormone can't get through the membrane at all, so it binds a receptor sitting on the surface, and that binding event triggers a second-messenger cascade inside the cell (commonly cyclic AMP) that changes an already-existing enzyme's activity in seconds — fast, but shorter-lived and non-genomic.
The simple lock-and-key picture is a fine starting point, but two refinements matter for how you actually reason about training:
Where people lose points
Downregulation: when a cell is chronically exposed to high levels of a hormone, it responds by reducing its own receptor number or sensitivity, blunting the signal rather than amplifying it. This is backwards from what intuition suggests, and it's exactly what happens in insulin resistance — chronically elevated insulin (from chronically elevated blood glucose) leaves cells progressively less responsive to insulin's signal, not more.
This is the single table the exam leans on hardest in this chapter. Learn it by gland, in order down the body.
| Gland | Hormone(s) | Primary action |
|---|---|---|
| Hypothalamus | GHRH, GnRH, CRH, TRH (+ inhibiting hormones, e.g. somatostatin) | Trophic control of the anterior pituitary |
| Anterior pituitary | Growth hormone (GH) | Drives tissue growth and liver IGF-1 release; mobilizes fat for fuel |
| Anterior pituitary | ACTH | Stimulates cortisol release from the adrenal cortex |
| Anterior pituitary | TSH | Stimulates T3/T4 release from the thyroid |
| Anterior pituitary | LH, FSH | Drive testosterone production (Leydig cells) and ovarian hormone production/gametogenesis |
| Posterior pituitary | ADH (vasopressin), oxytocin | Water reabsorption in the kidney; uterine contraction/milk ejection — both hormones are made in the hypothalamus and only stored and released here |
| Thyroid | T3, T4 | Set basal metabolic rate; permissive for other hormones' effects |
| Thyroid | Calcitonin | Lowers blood calcium |
| Parathyroid | Parathyroid hormone (PTH) | Raises blood calcium |
| Adrenal cortex | Cortisol | Mobilizes fuel; catabolic/stress-response hormone |
| Adrenal cortex | Aldosterone | Sodium retention; regulates blood volume and pressure |
| Adrenal medulla | Epinephrine, norepinephrine | Fight-or-flight response; glycogenolysis and lipolysis; raises heart rate and contractility |
| Pancreas (islets) | Insulin | Lowers blood glucose; promotes glucose/amino-acid uptake and storage |
| Pancreas (islets) | Glucagon | Raises blood glucose |
| Gonads | Testosterone (testes) / estrogen & progesterone (ovaries) | Anabolic tissue effects; reproductive function |
Keeping cortex and medulla straight
The adrenal cortex is the outer layer and makes steroid hormones (cortisol, aldosterone) under slow hormonal control from ACTH. The adrenal medulla is the inner core and makes catecholamines under fast, direct neural control — it's functionally an extension of the sympathetic nervous system itself.
Beyond memorizing the gland table, it helps to know how far a hormone's signal actually travels, because that changes how you interpret a blood sample. Hormonal action splits into three ranges.
| Mode | Where the signal goes | Example |
|---|---|---|
| Endocrine | Released into blood, acts on distant target cells | Testosterone released from the testes acting on skeletal muscle |
| Paracrine | Diffuses locally, acts on neighboring cells | Locally produced IGF-1 acting on nearby satellite cells within the same muscle |
| Autocrine | Acts back on the very cell that secreted it | A cytokine released by a muscle fiber that then binds receptors on that same fiber |
Two more descriptors matter for how hormones combine: a permissive effect is when one hormone must be present in adequate amounts for a second hormone to produce its full effect (thyroid hormone is permissive for several of catecholamines' and GH's actions), and a synergistic effect is when two hormones acting together produce a bigger effect than either would alone. Overall, resistance training leans on the endocrine system for four broad jobs: mobilizing fuel to match demand, coordinating the balance between tissue breakdown and repair, managing fluid/electrolyte shifts during a session, and — cumulatively, bout after bout — helping drive the chronic adaptations training is meant to produce.
A venous blood draw showing a higher hormone concentration after a workout looks like straightforward evidence that the gland secreted more of it. It isn't always that simple, and the exam likes to test the nuance.
A trap worth knowing
For years, the size of the acute post-workout hormone spike (especially testosterone and GH) was assumed to directly drive how much muscle a session would build — the "hormone hypothesis" of hypertrophy. More recent evidence has weakened that link considerably: local, muscle-level signaling triggered by mechanical tension appears to matter more than the size of the systemic spike. Don't assume "bigger acute hormone response = more growth" is settled fact — it's a much shakier claim than it used to be treated as.
Testosterone is the hormone most associated with resistance training's anabolic effects, and it's tested from three angles: where it comes from, how it travels in blood, and how it actually changes a muscle fiber.
In men, the overwhelming majority of circulating testosterone comes from the Leydig cells of the testes, under LH stimulation from the anterior pituitary; the adrenal cortex contributes a smaller amount in both sexes, and peripheral tissue can convert some circulating precursors as well. Women produce testosterone too — from the ovaries and adrenal cortex — but at a fraction of male circulating levels.
Testosterone's anabolic effect works through more than one channel. The classic route is genomic: free testosterone diffuses into a target cell, binds an intracellular androgen receptor, and the complex moves into the nucleus to upregulate genes for protein synthesis. Research also points to faster, non-genomic signaling that can interact with the same mechanical-loading pathways a set of heavy squats triggers directly. Testosterone is also reported to indirectly support growth hormone release and may sharpen CNS drive and motivation during training — effects that are harder to quantify but plausibly contribute to performance. Critically, the receptor-level anabolic effect concentrates in the tissue that was actually mechanically loaded — a hormone circulating at a higher level doesn't uniformly grow every muscle in the body; it amplifies what recruited, loaded fibers are already primed to do.
Applied — what actually raises the acute testosterone response
The acute rise tends to be largest with protocols that combine: large muscle-mass, multi-joint exercises (squat, deadlift-pattern lifts) over small-muscle isolation work; moderate-to-heavy loads and high total volume (multiple sets); and short rest intervals (around 1 minute), pushed toward or to fatigue/relative failure. Any one of these alone produces a smaller response than combining several together — this stacking effect is one of the most commonly tested applied points in the chapter.
Growth hormone (GH) is secreted from somatotroph cells in the anterior pituitary, under dual hypothalamic control: GHRH stimulates release, somatostatin inhibits it. "Growth hormone" is also not one single molecule — it's a family of related isoforms, which matters for how research on it gets interpreted.
| Form | Approximate share of circulating GH | Note |
|---|---|---|
| 22-kDa monomer | Majority form | The isoform most immunoassays are built to detect |
| 20-kDa monomer | Minor form | Splice variant, less consistently captured by older assays |
| Aggregates/oligomers and fragments | Remainder | Larger and smaller variants; different assays capture different subsets |
Because different immunoassay generations detect different mixes of these isoforms, studies measuring "growth hormone" haven't always been measuring quite the same thing — a detail worth knowing conceptually even without memorizing assay names.
Applied — what drives the acute GH response
GH is unusually sensitive to metabolic stress — protocols that build up lactate and acidosis produce the biggest GH spikes. That favors moderate loads (roughly 10RM range), high volume, and short rest intervals (around 1 minute or less), similar to the testosterone recipe but leaning even harder on accumulated fatigue rather than raw load. A very heavy, low-rep, long-rest protocol — great for maximal strength — typically produces a comparatively small acute GH response despite the higher loads used.
Insulin-like growth factors (IGF-1 being the one relevant here) are structurally related to insulin and act as one of the main downstream mediators of GH's tissue-building effects — but "downstream of GH" is only half the story.
Two IGF-1 pools, two different triggers
Liver-made IGF-1 answers to the GH axis. Muscle-made IGF-1 answers to mechanical tension. The local pool is thought to matter more for the hypertrophy response than the number that shows up on a blood panel.
Functionally, IGF-1 promotes protein synthesis, drives satellite cell proliferation and differentiation, and suppresses protein breakdown — putting it near the center of the signaling cascade that turns a loaded muscle fiber into a bigger one.
Cortisol is released from the zona fasciculata of the adrenal cortex, under command of the hypothalamic-pituitary-adrenal (HPA) axis: hypothalamic CRH stimulates pituitary ACTH, which stimulates the adrenal cortex to release cortisol. (The adrenal cortex has two neighboring zones with their own jobs: the outer zona glomerulosa makes aldosterone, and the inner zona reticularis contributes adrenal androgens.)
Cortisol is one of the clearest examples in the whole endocrine chapter of a hormone whose value depends entirely on the time horizon.
| Function | Single training bout (acute) | Sustained overexposure (chronic) |
|---|---|---|
| Blood glucose | Supports gluconeogenesis to protect glucose availability during the session | Persistent hyperglycemia and insulin resistance |
| Protein metabolism | Frees amino acids to support glucose production and tissue remodeling | Net muscle protein breakdown — catabolic wasting |
| Reproductive axis | Minimal short-term effect | Suppresses GnRH/LH and blunts testosterone production |
| Inflammation/immunity | Helps regulate exercise-induced inflammation | Broadly suppresses immune function, raising illness/injury risk |
| Fat storage pattern | Minimal short-term effect | Promotes central (visceral) fat deposition |
Don't treat cortisol as simply "bad"
A cortisol response to a hard training session is normal and necessary — without it, fuel mobilization and remodeling stall. The problem is duration and recovery, not the hormone's existence. Chronically elevated cortisol — from inadequate recovery, poor sleep, or excessive training load — is the mechanism most often cited behind overreaching and overtraining syndrome. Some programs track a cortisol-to-testosterone ratio over time as a rough proxy for whether an athlete is trending anabolic or catabolic.
Epinephrine and norepinephrine are released from the adrenal medulla, and the release mechanism is worth calling out again here because it's unlike every other hormone in this chapter: the adrenal medulla is directly innervated by sympathetic preganglionic neurons, so a "release command" doesn't route through a releasing hormone at all — sympathetic activation triggers catecholamine release essentially instantly. (Norepinephrine is also released locally as a neurotransmitter at sympathetic nerve terminals throughout the body; only a fraction of that local release spills over into general circulation and shows up on a blood draw.)
Because their release is intensity-linked rather than volume-linked in the same way cortisol and GH are, catecholamine responses scale most closely with how hard and how anaerobic an effort is — short-rest, high-intensity resistance protocols and sprint-type efforts drive the largest spikes.
Two more hormones round out the picture, and neither one is typically thought of as "exercise hormones" the way testosterone or cortisol are — but both set the stage the other hormones act on.
| Hormone | Source | Role relevant to resistance training |
|---|---|---|
| T3 / T4 | Thyroid, under TSH control | Set the metabolic rate the whole training response operates against; permissive for GH's and catecholamines' full effects — without adequate thyroid hormone, those other hormones underperform |
| Insulin — during a bout | Pancreatic beta cells | Secretion typically drops during exercise as glucagon and catecholamines rise, which helps permit fuel mobilization rather than storage |
| Insulin — after a bout | Pancreatic beta cells | Insulin sensitivity rises post-exercise, which speeds glycogen resynthesis and supports amino-acid uptake into muscle during recovery |
Insulin is worth remembering as fundamentally anabolic at the cellular level — it drives glucose and amino acid uptake and glycogen/protein synthesis — even though its secretion is actively suppressed during the exercise bout itself.
A coach explains that sympathetic nerves synapse directly on the adrenal medulla, so epinephrine release doesn't wait for a releasing hormone from the hypothalamus. Which release mechanism is being described?
B — neural. Direct nerve stimulation of the gland is the defining feature. Humoral release is triggered by a blood ion/nutrient change, and hormonal (trophic) release is triggered by a different hormone further up an axis.
Which pair of hormones binds a receptor located inside the target cell rather than on its surface?
C. Cortisol and testosterone are both steroid hormones — lipid-soluble, so they cross the membrane and bind an intracellular receptor. The other three options are all peptide hormones or catecholamines, which are water-soluble and bind cell-surface receptors.
ACTH is released from which structure, and what does it stimulate?
B. ACTH is a trophic hormone from the anterior pituitary that travels to the adrenal cortex and triggers cortisol release — CRH from the hypothalamus is what triggers ACTH release in the first place.
Roughly what share of total circulating testosterone is free (unbound) and therefore immediately bioactive?
C. Only about 1–2% circulates free. Roughly 44% is bound tightly to SHBG (essentially unavailable) and the remainder rides loosely on albumin, which is often lumped with the free fraction as "bioavailable."
Two lifters have identical total testosterone on a lab panel. Lifter A has much higher SHBG than Lifter B. What follows?
B. Higher SHBG means more testosterone is locked onto the tightly-bound carrier, leaving less free/bioavailable at the same total — a good illustration of why total hormone numbers alone can mislead.
Which resistance training protocol would be expected to produce the largest acute testosterone and growth hormone response?
B. Large muscle mass, multiple sets, moderate load, and short rest intervals stack together to produce the largest acute anabolic-hormone response — more so than very heavy low-rep work, isolation exercises, or long rest periods, even though those can be superior for other goals like maximal strength.
Which statement about cortisol is most accurate?
C. The acute response is a normal, necessary part of the stress response to a training bout. It's sustained, chronic elevation — usually from inadequate recovery — that drives muscle wasting and suppresses the reproductive/testosterone axis.
A researcher finds that a muscle's local IGF-1 response to a resistance training bout doesn't track closely with the athlete's circulating growth hormone level. What best explains this?
B. There are two IGF-1 pools: liver-derived, GH-dependent systemic IGF-1, and locally produced, mechanically-triggered muscle IGF-1 (including the mechano growth factor splice variant) — the local pool doesn't have to track circulating GH.
Blood drawn immediately after a heavy training session shows a higher concentration of a hormone than a pre-exercise sample. Which factor could inflate that number without any increase in actual secretion?
B. Exercise-induced plasma volume shifts concentrate whatever hormone remains in circulation, which can raise a measured concentration even with no change — or even a drop — in actual secretion rate. Clearance rate changes can do the same thing.
What typically happens to insulin secretion during a bout of exercise, and why?
B. Insulin secretion typically drops during exercise as glucagon and catecholamines rise, which favors releasing fuel rather than storing it. Insulin sensitivity then rises afterward, which is what speeds glycogen resynthesis during recovery.
This chapter is original study material covering topics also addressed in Essentials of Strength Training and Conditioning, 5th edition (NSCA/Human Kinetics). It is an independent work, not a reproduction or paraphrase of that text. This guide is not affiliated with, endorsed by, or sponsored by the National Strength and Conditioning Association (NSCA). CSCS® and Certified Strength and Conditioning Specialist® are registered trademarks of the NSCA.