Journal of Gynecology and Reproductive Health
ISSN: 2574-2728 | DOI: 10.64030/2574-2728
Herman Weiss
Background: Polycystic ovary syndrome (PCOS), recently predesignated polyendocrine metabolic ovarian syndrome (PMOS), affects approximately one in eight women of reproductive age. Insulin resistance is its cardinal metabolic feature, present across phenotypic subtypes and independent of body mass index. Skeletal muscle, responsible for approximately 80% of insulinmediated postprandial glucose disposal, is the dominant tissue in which this insulin resistance is mechanistically expressed— yet skeletal muscle has received comparatively little attention in PCOS clinical practice and research frameworks organized around ovarian pathology.
Objective: This narrative review synthesizes the peer-reviewed literature on skeletal muscle mass and quality, muscular fitness, structured exercise training, and their relationships with insulin resistance and reproductive outcomes in women with PCOS, with a comparative analysis of exercise versus pharmacological metabolic intervention and a secondary section on male reproductive parallels.
Methods: MEDLINE, Web of Science, and Scopus were searched from inception through April 2026 using the following primary search terms: PCOS, polycystic ovary syndrome, skeletal muscle, lean body mass, insulin resistance, exercise training, resistance training, ovulation, fertility, myokines, GLUT4, sarcopenic obesity, and male infertility. Randomized controlled trials, systematic reviews, meta-analyses, and mechanistic studies were prioritized. Reference lists of identified key papers were hand-searched for additional relevant publications. No language restriction was applied. Approximately 240 publications were reviewed, with primary emphasis on human RCTs, systematic reviews, meta-analyses, and mechanistic studies directly evaluating skeletal muscle function, exercise intervention, or body composition in women with PCOS. Animal and in vitro studies were included where they provide essential molecular context not yet available from human trials.
Results: Women with PCOS demonstrate an intrinsic, BMI-independent 27% reduction in whole-body insulin sensitivity, attributable to skeletal muscle signaling defects at IRS-1, PI3K-Akt, and GLUT4, compounded by intramuscular lipid accumulation and mitochondrial dysfunction. The lean PCOS phenotype insulin-resistant at normal BMI exemplifies the independence of muscle metabolic dysfunction from adiposity: lean women with PCOS demonstrate 25% lower insulin sensitivity by clamp, intramuscular lipid accumulation (40% higher triacylglycerol, 50% higher diacylglycerol, 300% higher ceramide), and reduced AMPK expression and activation compared with BMI-matched healthy controls. Sarcopenic obesity present in over 50% of women with PCOS in some cohorts amplifies metabolic and inflammatory burden in a pattern invisible to BMI-based assessment. Structured exercise training improves insulin sensitivity, reduces hyperandrogenemia, normalizes anti-Müllerian hormone (AMH), and restores ovulatory cyclicity. In the most direct fertility evidence available, six weeks of structured exercise tripled ovulation probability in obese clomiphene-resistant women with PCOS. Lifestyle modification and metformin produce comparable effects on pregnancy rate and menstrual cyclicity, while lifestyle intervention more effectively improves insulin resistance and SHBG. Physical activity's effect on ART live birth rate remains statistically uncertain in current meta-analytic evidence. In men, adequate muscle mass and favorable body composition are associated with higher endogenous testosterone and better semen parameters.
Conclusions: The available evidence supports skeletal muscle as an underrecognized metabolic organ in PCOS whose improvement through structured exercise including progressive resistance training may represent an important strategy for improving reproductive outcomes. These findings support integration of muscle-targeted lifestyle therapies as a key component of first-line management in PCOS fertility care. Adequately powered RCTs using live birth rate as a primary endpoint are needed to establish the full clinical scope of this benefit.