Do low androgen levels reduce muscle synthesis, cause fatigue, and increase central fat in women?

In women, the relationship between circulating androgens—such as testosterone and DHEA-S—and muscle preservation, energy, and body composition is complex and often differs from male physiology.

Muscle protein synthesis and recovery

• Androgens stimulate muscle protein synthesis (MPS) via androgen receptor signaling and the Akt-mTOR pathway.
• While supraphysiologic testosterone can acutely elevate MPS rates, endogenous testosterone fluctuations within the normal female range do not associate with differences in muscle mass. Women maintain robust basal MPS rates despite having significantly lower absolute testosterone levels than men.
• Physiological-dose androgen replacement (e.g., DHEA or low-dose testosterone) has largely failed to improve protein synthesis, muscle mass, or physical performance in clinical trials.

Fat distribution and adipose biology

• Rather than low levels driving adiposity, a highly androgenic milieu (elevated free testosterone) correlates with central, visceral, and abdominal fat accumulation in women.
• During the menopause transition, estrogen deficiency—not a decline in androgens—is the primary hormonal driver shifting fat storage from gynoid subcutaneous depots to android visceral fat. Higher free testosterone relative to estradiol is associated with expanded visceral fat and larger waist circumferences.

Clinical fatigue and energy

• Although observational studies link low androgen levels to subjective fatigue, randomized controlled trials of physiologic testosterone replacement in women consistently fail to demonstrate a robust benefit for fatigue, mood, or quality of life compared to placebo.
• Verified clinical benefits of androgen therapy in women are primarily restricted to sexual function, specifically hypoactive sexual desire disorder.

Bottom line

• In female physiology, low androgen levels do not drive central fat gain (which is promoted by estrogen deficiency and relative androgen excess) or significantly impair muscle synthesis, and correcting low levels does not reliably resolve clinical fatigue.