Can low energy availability from endurance training lower testosterone in men?

High-volume endurance training combined with low energy availability (LEA) and depleted body fat triggers profound neuroendocrine adaptations, culminating in a state known as exercise-hypogonadal male condition (EHMC).

Neuroendocrine mechanisms

• HPG Axis Downregulation: Severe energy deficits suppress hypothalamic gonadotropin-releasing hormone (GnRH) pulsatility, reducing both its pulse frequency and amplitude. This central downshifting blunts downstream stimulation of the testes.
• Inappropriately Normal Gonadotropins: While total, free, and bioavailable testosterone levels drop significantly, luteinizing hormone (LH) and follicle-stimulating hormone (FSH) characteristically remain within standard laboratory reference ranges. Because the primary defect is central (hypothalamic suppression), the expected compensatory rise in gonadotropins is absent, presenting as "inappropriately normal" relative to the low testosterone.
• Thyroid Suppression: As a parallel metabolic adaptation to conserve energy under high physical demand, LEA also suppresses thyroid function, leading to decreased circulating free triiodothyronine (fT3) levels.

Clinical and systemic impacts

• Skeletal Integrity: The chronic deficit in total, free, and bioavailable testosterone directly compromises skeletal homeostasis. Over time, this functional hypogonadism leads to reduced bone mineral density (BMD) and an elevated risk of stress fractures.

Bottom line

• Low energy availability and low body fat centrally suppress the hypothalamic-pituitary-gonadal axis, driving down total, free, and bioavailable testosterone while leaving LH and FSH in an "inappropriately normal" range. This central suppression is accompanied by metabolic adaptations like lowered fT3 and elevates the long-term risk of bone density loss.