LH

Luteinizing Hormone (LH) is a glycoprotein gonadotropin secreted by anterior pituitary gonadotroph cells in response to hypothalamic GnRH pulses. In adult males, LH binds the LH receptor (LHCGR) on testicular Leydig cells, activating cAMP signalling that triggers steroidogenic enzyme expression and testosterone synthesis from cholesterol via the StAR-CYP17A1-HSD3B2-CYP17A1-HSD17B3 cascade.

Reference range, adult male:

– Serum LH: 1.7–8.6 mIU/mL
– Pulsatile pattern: peaks every 90–120 minutes; trough draws underestimate true integrated secretion
– Diurnal variation: modest; morning draw standard for consistency

Suppression kinetics on AAS protocols:

Exogenous testosterone administration suppresses LH below detection limit (<0.2 mIU/mL on most assays) within 14 days at any dose above replacement (200 mg/week or higher). The suppression is dose-saturating — 200 mg/week and 600 mg/week produce equivalent LH shutdown despite the threefold dose difference. Bhasin et al. 1996, NEJM dose-response data documented the kinetics across the 25–600 mg/week testosterone range.

Nandrolone-containing protocols produce deeper LH suppression with slower recovery — the progestogenic activity of 19-nor compounds adds suppressive signal beyond pure androgen feedback. Trenbolone produces similarly extended suppression. SARMs at therapeutic dose suppress LH more variably depending on tissue selectivity profile.

Recovery interpretation:

LH measurement post-PCT distinguishes the failure modes:

– Low LH + low testosterone: central signal has not restarted. Hypothalamic-pituitary suppression persists. Extend SERM intervention; consider hCG bridge if duration exceeds 12 weeks.
– Normal LH + low testosterone: primary testicular failure. Leydig cells are not responding to restored LH signal — desensitisation from extended exposure or unmasked pre-existing testicular insufficiency. hCG protocol may restore function; formal endocrinology referral if no response.
– Normal LH + normal testosterone + low free T: SHBG rebound. Resolves over 4–8 weeks without intervention. The “low libido despite normal testosterone” pattern often resolves here.
– Elevated LH (>10 mIU/mL) with low testosterone: primary hypogonadism unmasked or developed during cycle. Warrants endocrine workup including FSH, inhibin B, and possibly testicular ultrasound.

Pulsatile pattern matters more than single-point reading:

Veldhuis et al. 2013, J Clin Endocrinol Metab documented that pulsatile LH secretion is the operative central signal — single-point measurement underrepresents the recovery state. Detectable LH with appropriate pulse pattern is functional recovery; flat-line LH at low-detectable values represents partial recovery only. Clinical settings rarely measure pulsatility directly; the practical surrogate is LH stability across multiple draws within a 2–3 week window.

hCG as LH analogue:

Human chorionic gonadotropin shares the α-subunit with LH and binds the same LHCGR. Exogenous hCG bypasses hypothalamic-pituitary signalling and stimulates Leydig cells directly. Useful for on-cycle Leydig preservation (250–500 IU 2× weekly) or pre-PCT bridge to restore Leydig responsiveness before SERM intervention. The mechanism distinction matters clinically: hCG restores testicular testosterone synthesis without restarting the central signal; SERMs restart the central signal but require responsive Leydig cells to work.