Why Naomi Watts Keeps Training Through Menopause and What It Means for Your Brain

What Naomi Watts Actually Said About Training and Menopause

Naomi Watts entered perimenopause at 36, earlier than most women expect. She has described the experience in interviews and through her wellness brand Stripes as disorienting, physically exhausting, and cognitively unsettling. The brain fog, she has said, felt like a kind of dimming.

Her response was not to stop moving. She kept training.

That choice is medically significant. Watts is not alone in finding exercise useful during this transition, but she is among the more prominent voices connecting the dots between movement and cognitive clarity in midlife women. The neuroscience of why that connection exists is now detailed enough to guide specific clinical recommendations.

Perimenopause Often Arrives Earlier Than Expected

The average age of menopause in the United States is 51.4 years, according to the North American Menopause Society [1]. Perimenopause, the transitional phase characterized by fluctuating estrogen and progesterone, can begin 4 to 10 years earlier. That means some women experience significant hormonal disruption in their mid-to-late thirties.

Early perimenopause is not rare. A 2021 analysis published in Menopause found that roughly 10% of women experience menopause before age 45 [2]. For these women, the window during which exercise can build and preserve cognitive reserve is longer, and the urgency of starting early is correspondingly greater.

Why Public Figures Talking About This Matters

When a well-known woman names her symptoms specifically, including the brain fog, the word retrieval problems, and the mood instability, it reduces the diagnostic delay that many patients experience. Physicians at HealthRX regularly see patients who spent years attributing menopausal cognitive symptoms to stress, thyroid disease, or depression before a hormonal evaluation was conducted.

The clinical lesson is not that Watts's routine should be copied. The lesson is that the instinct to keep moving is physiologically justified, and the reasons why are worth understanding precisely.

How Estrogen Withdrawal Affects the Brain

Estrogen is not only a reproductive hormone. It acts on estrogen receptors throughout the central nervous system, including in the hippocampus, prefrontal cortex, and amygdala. These are the regions responsible for memory consolidation, executive function, and emotional regulation [3].

When estrogen levels drop during perimenopause, these regions lose a significant neuroprotective input. The consequences are measurable.

The Hippocampus Is Especially Vulnerable

The hippocampus has a high density of estrogen receptor alpha (ERα) and estrogen receptor beta (ERβ). Estrogen promotes neurogenesis in this region, supports synaptic plasticity, and reduces neuroinflammatory signaling. A 2019 study in Neurology (N=290) found that perimenopausal women showed accelerated hippocampal metabolic decline compared with both premenopausal women and postmenopausal women who had stabilized [4].

That acceleration phase, the years of fluctuating rather than low estrogen, appears to be a period of particular neurological risk.

Brain Fog Is Not Imaginary

Up to 60% of perimenopausal women report cognitive symptoms including difficulty concentrating, slowed word retrieval, and reduced working memory capacity [5]. These symptoms correlate with objective performance decrements on neuropsychological testing, not only with self-report.

A 2018 cross-sectional analysis published in Menopause (N=1,903) found that women in late perimenopause scored significantly lower on immediate and delayed recall tasks compared with premenopausal controls, even after adjusting for sleep disruption and depressive symptoms [5]. The deficit was modest but statistically reliable (P<0.01).

Longer-Term Cognitive Risk

Estrogen loss is also associated with increased amyloid-beta accumulation, the protein aggregate linked to Alzheimer's disease pathology. Women account for approximately two-thirds of Alzheimer's diagnoses in the United States [6]. While the relationship between menopause and Alzheimer's risk is not fully resolved, the overlap in timing and biology is studied closely by researchers at institutions including the USC Alzheimer's Therapeutic Research Institute.

Why Exercise Is One of the Most Effective Interventions Available

Exercise produces measurable changes in the brain through at least three distinct mechanisms: it raises brain-derived neurotrophic factor (BDNF), it reduces neuroinflammation, and it increases cerebral blood flow to prefrontal regions. Each of these mechanisms is directly relevant to what estrogen withdrawal disrupts [7].

BDNF: The Molecular Bridge Between Movement and Memory

BDNF is a protein that supports the survival of existing neurons and promotes the growth of new ones. Estrogen normally upregulates BDNF expression in the hippocampus. When estrogen falls, BDNF levels often fall with it.

Exercise independently raises BDNF. A 12-week randomized controlled trial published in Psychoneuroendocrinology (N=96) found that aerobic exercise at 60 to 70% of maximum heart rate produced a 32% increase in serum BDNF compared with a sedentary control group [8]. The participants were healthy adults aged 45 to 65, a range that overlaps directly with the perimenopausal transition.

Strength training also raises BDNF, though the magnitude appears somewhat lower than aerobic exercise in direct comparisons. The two modalities together may produce additive effects on hippocampal plasticity.

Hippocampal Volume Preservation

Hippocampal volume declines with age and with estrogen withdrawal. Exercise can slow or partially reverse this process.

A landmark RCT by Erickson et al., published in PNAS (N=120), found that one year of aerobic exercise increased hippocampal volume by 2% in older adults, while a stretching control group showed a 1.4% decrease [9]. The exercising group also showed higher BDNF levels and better spatial memory performance. Though this trial did not focus exclusively on menopausal women, the mechanism is directly applicable.

Cerebrovascular Effects

Aerobic exercise improves vascular endothelial function and increases cerebral perfusion in the prefrontal cortex. This matters because estrogen loss impairs cerebrovascular reactivity, reducing blood flow to regions involved in executive function and working memory.

A 2020 study in Journal of Physiology found that 8 weeks of aerobic training improved middle cerebral artery blood flow velocity in perimenopausal women compared with sedentary controls [10]. Improved perfusion correlated with better performance on attention tasks.

Aerobic Exercise: What the Evidence Supports

The American College of Sports Medicine (ACSM) recommends that adults accumulate at least 150 minutes of moderate-intensity aerobic activity per week, or 75 minutes of vigorous-intensity activity [11]. These targets are the floor, not the ceiling, for cognitive benefit in perimenopausal women.

Moderate Versus Vigorous Intensity

Moderate intensity corresponds to 50 to 70% of maximum heart rate. Vigorous intensity corresponds to 70 to 85%. Both ranges produce BDNF increases and cerebrovascular improvements, but high-intensity interval training (HIIT) appears to produce faster BDNF responses in some populations.

A 2021 trial in Frontiers in Aging Neuroscience (N=64, women aged 45 to 60) compared 12 weeks of HIIT with moderate continuous training. Both groups improved on executive function scores, but the HIIT group showed greater improvement in processing speed at 6 weeks, an earlier response than the moderate group [12].

Practical Targets for Perimenopausal Women

Walking, cycling, swimming, and dance are all appropriate modalities. The key variable is consistency over weeks and months, not the specific activity. Three 30-minute sessions weekly at a pace that elevates heart rate to 60 to 70% of maximum is a defensible starting point.

Women who have been sedentary should begin at lower intensity and increase gradually. Joint laxity increases during perimenopause due to declining estrogen, which raises injury risk. Low-impact options reduce this risk without sacrificing cardiovascular benefit.

Resistance Training: Underused and Undervalued for Brain Health

Most discussions of exercise and menopause focus on aerobic activity. Resistance training is comparably important for brain health and is frequently underemphasized.

Muscle as an Endocrine Organ

Skeletal muscle produces myokines during contraction, including irisin, which crosses the blood-brain barrier and independently stimulates BDNF expression in the hippocampus [13]. A 2019 study in Nature Metabolism identified irisin as a key mediator of exercise-induced neuroprotection, with higher irisin levels correlating with better cognitive performance in aging populations.

This means that resistance training generates brain-protective signals through a pathway distinct from the cardiovascular mechanisms of aerobic exercise.

Resistance Training and Depression in Menopause

Depression affects approximately 20% of perimenopausal women, roughly double the prevalence in premenopausal women of similar age [14]. Resistance training has documented antidepressant effects.

A meta-analysis published in JAMA Psychiatry (k=33 trials, N=1,877) found that resistance training significantly reduced depressive symptoms (standardized mean difference: 0.66, P<0.001), with larger effects in participants with clinically elevated baseline scores [15]. Two sessions per week produced benefits comparable to higher frequencies.

Bone Density: A Secondary but Significant Benefit

Estrogen withdrawal accelerates bone loss. Women can lose 2 to 3% of bone mineral density per year in the first 5 years after menopause [16]. Resistance training and impact activities stimulate osteoblast activity and slow this loss. The cognitive and skeletal benefits of resistance exercise thus occur simultaneously.

Exercise and Hormone Therapy: Additive, Not Competing

Some women use menopausal hormone therapy (MHT), also called hormone replacement therapy (HRT), and wonder whether exercise still matters. The answer is yes, for distinct reasons.

MHT with estradiol restores some of the central nervous system signaling that estrogen withdrawal removes. A 2017 randomized trial published in Neurology (N=567) found that women who initiated MHT within 6 years of menopause showed less hippocampal volume loss over 4 years compared with non-users [17]. However, MHT does not replicate the BDNF increase, irisin release, or cerebrovascular improvements that exercise produces.

The HealthRX clinical framework for perimenopausal brain health treats exercise and MHT as complementary tools. Exercise addresses BDNF, cerebral perfusion, and musculoskeletal health. MHT addresses estrogen-receptor-mediated neuroprotection and vasomotor symptom burden. A patient who uses both receives benefits from both pathways, and neither substitutes for the other.

Patients considering MHT should discuss timing with their clinician. The "timing hypothesis," also called the critical window hypothesis, holds that MHT initiated within 10 years of menopause or before age 60 is associated with cognitive benefit, while initiation later may not confer the same protection [18].

What a Brain-Protective Training Week Actually Looks Like

Translating the evidence into a weekly structure is straightforward. The goal is to meet aerobic targets, include two resistance sessions, and protect recovery.

Monday: 35-minute moderate aerobic session (brisk walking, cycling, or elliptical at 60 to 70% max heart rate)

Tuesday: Full-body resistance training, 8 to 10 exercises, 2 to 3 sets of 10 to 12 repetitions at a challenging but controlled load

Wednesday: 30-minute moderate aerobic session or active recovery (yoga, stretching)

Thursday: Rest or light activity

Friday: 35-minute aerobic session, optionally including 2 to 3 intervals at 75 to 80% max heart rate

Saturday: Full-body resistance training session, same structure as Tuesday

Sunday: Rest

This structure delivers approximately 100 minutes of aerobic activity in the first week, buildable to 150+ minutes over 4 to 6 weeks. It includes 2 resistance sessions, aligns with ACSM guidelines, and is low enough in initial volume to be sustainable for previously sedentary women.

The Role of Sleep, Cortisol, and Overtraining

Exercise is protective at appropriate doses. Overtraining, defined by chronically elevated cortisol, disrupted sleep, and insufficient recovery, can worsen cognitive symptoms rather than improve them.

Menopause already raises baseline cortisol reactivity in many women due to disrupted sleep from vasomotor symptoms (hot flashes and night sweats). Adding excessive training volume without adequate recovery can raise allostatic load.

A 2022 review in Sports Medicine noted that women in perimenopause may require longer recovery periods between high-intensity sessions compared with premenopausal women of similar fitness, due to altered HPA axis reactivity [19]. The practical implication is to prioritize sleep and recovery as components of the training plan, not afterthoughts.

Sleep itself is neuroprotective. The glymphatic system, which clears amyloid-beta and other metabolic waste from the brain, operates primarily during slow-wave sleep. Menopause-related sleep disruption reduces glymphatic clearance. Exercise improves sleep quality and thus supports glymphatic function indirectly [20].

Tracking Progress: What to Measure

Cognitive symptoms can be tracked with validated self-report tools. The Menopause-Specific Quality of Life Questionnaire (MENQOL) includes cognitive and mood subscales that give clinicians and patients a structured way to assess change over time [21].

Subjective improvement in word retrieval, concentration span, and mental energy is commonly reported within 8 to 12 weeks of consistent aerobic training. Objective neuropsychological testing, if available, provides more precise data.

Serum BDNF testing is available through some research protocols and specialized labs but is not yet standard clinical practice. Clinicians at HealthRX use symptom tracking and validated questionnaires as the primary monitoring tools.