How to Stay Fit During Menopause | Stacy Sims PhD

Sims distinguishes this from the pre-cardio protocol: resistance training primarily demands protein signaling (muscle protein synthesis) whereas cardio demands blood glucose access. The protein pre-resistance training ensures that when training stress spikes cortisol, there is adequate substrate to maintain muscle protein balance rather than tipping into net catabolism. In perimenopausal women who already have reduced anabolic sensitivity to protein due to declining estrogen, this pre-training protein signal is even more critical.

Sims explains that women's estrogen and progesterone shuttle carbohydrates away from metabolic use during the high-hormone phase, meaning women are naturally fat-adapted. Adding fasted cardio on top of this provides no additional fat-oxidation benefit but does raise cortisol and suppress kisspeptin neurons — producing hormone dysfunction. The pre-cardio carbohydrate drops cortisol and allows blood glucose access so the training session can be executed at sufficient intensity to generate the cardiovascular adaptations required for menopausal metabolic health.

Sims frames this explicitly against the cultural default: most women entering menopause instinctively apply the eat-less-train-more equation and end up in low energy availability. The correct inversion is: fuel training aggressively, let the training drive metabolic adaptation, and apply only modest caloric restriction at night when the body is already transitioning to rest-state metabolism. This approach preserves thyroid function, muscle mass, and bone density — the three assets most at risk in the menopausal transition.

Sims is explicit that this prescription crosses athletic archetypes: an endurance athlete in perimenopause drops volume-based training blocks and substitutes quality sessions while reducing easy aerobic volume. A strength athlete changes set/rep schemes toward heavier, lower-rep work and adds metabolic sprint intervals. The common thread is the same: volume out, intensity in. The physiological rationale is that high-intensity work provides a more potent hormetic signal relative to the metabolic cost, which matters when the hormonal milieu supporting recovery has degraded.

Sims updated ROAR second edition (2023) specifically with this cycling-based periodization and added new data on how HRV changes across the menstrual cycle and how that differs between naturally cycling, IUD-using, and oral-contraceptive-using women. Professional athletes who use this data to schedule competition blocks in the follicular phase have a measurable performance advantage. The deload before menstruation is not rest — it is skill refinement, technique work, and reaction training that develops quality without the recovery cost of load.

Sims frames this as the opposite of the typical endurance athlete's instinct: when performance regresses in perimenopause, the first response is usually to add volume. The correct response is to cut volume and add sprint intervals, then reintroduce volume only in race-specific blocks. The rationale is that moderate-intensity aerobic work is metabolically costly and requires good hormonal recovery support — which perimenopause progressively removes. High-intensity intervals provide a stronger hormetic stimulus relative to their recovery cost in this context.

A heavier bleed signals estrogen dominance relative to progesterone (insufficient luteal phase progesterone). A shorter or lighter bleed may signal insufficient follicular-phase estrogen. Either pattern, combined with fatigue, brain fog, poor training recovery, and body composition changes despite no dietary change, constitutes an early warning stack that warrants evaluation even before the clinical 12-consecutive-months-without-period definition is met. Catching this early enables proactive adjustment of training (volume down, intensity up), nutrition (fuel training adequately), and evaluation for menopausal hormone therapy.

Sims explains that women have two populations of kisspeptin neurons in the hypothalamus: one governing appetite and nutrient sensing, the other governing endocrine function. Under caloric stress + exercise load, the nutrient-sensing neurons go quiet, which feeds forward to suppress the endocrine kisspeptin neurons, which then suppresses thyroid — the beginning of low energy availability. This is why fasted women in research cohorts accumulate more hormone dysfunction than fed women doing the same training program. In the male dataset, the same fasted training protocol produces better metabolic control without the endocrine cascade, because male hypothalamic kisspeptin organization differs.

Sims describes the physiological chain reaction: undereating under training load creates a low energy state, thyroid downregulation, muscle catabolism (losing the metabolic tissue that burns fat at rest), bone catabolism (bone is a metabolically expensive tissue the body sacrifices early), and increased body fat as the body shifts to fat storage mode for survival. The entry point into this spiral is the culturally conditioned response to eat less and train more. The exit is fueling adequately around training, then — only if caloric deficit is needed — applying a modest 10-20% restriction at night, away from training windows.

Sims specifies this across three athlete archetypes: (1) Endurance-oriented women drop total volume, keep quality sessions (high-intensity intervals), and become race-specific in volume only during peaking; (2) Strength-oriented women vary sets and rep schemes and add sprint intervals for metabolic control; (3) General fitness (training 3x/week) prioritizes two sprint interval sessions and three heavy lifting sessions — these can be combined in one session for time efficiency. The unifying principle is that declining estrogen and progesterone mean the body's stress-resilience and recovery capacity are reduced; moderate-intensity, high-volume work is inefficient and accumulates fatigue without the adaptive return.

The immune mechanism: pre-ovulation, the immune system is highly reactive to bacteria and viruses — the body can sustain heavy stress. Post-ovulation, a pro-inflammatory shift occurs because the body needs to avoid attacking a potentially fertilized egg. This means recovery is slower, injury risk is elevated, and intense training accumulates more cortisol. The deload window right before menstruation is when HRV data typically shows the most suppressed recovery markers. Sims emphasizes that cycle tracking (using HRV and subjective markers) is critical because the pattern varies significantly between women using oral contraceptives, IUDs, and naturally cycling women.

Sims explains the physiology of the lengthening cycle: the follicular phase extends because the body is working harder to mature a viable egg as ovarian reserve depletes. But some women never see cycle length change — their bleed pattern shifts instead. A heavier bleed signals estrogen dominance relative to progesterone. A shorter or lighter bleed may signal insufficient follicular-phase estrogen. Either pattern, stacked with the classic symptom cluster (fatigue, brain fog, poor recovery, body comp changes), suggests perimenopause is underway even before the 12-consecutive-months-without-period definition is met.

Sims notes the estrobolome — the subset of gut microbiota that metabolizes estrogens — processes endogenous estrogens via one pathway and exogenous/synthetic estrogens (ethinyl estradiol in OCP) via another, producing different ratios of active to inactive estrogen metabolites. The downstream consequences include different inflammatory profiles, different degrees of oxidative stress, and different body composition outcomes. This distinction matters particularly for perimenopausal women deciding between continuing oral contraceptives versus transitioning to menopausal hormone therapy.