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Skeletal muscle macrophages regulate angiogenesis and tissue remodeling and may contribute to early alterations in muscle structure and function during cardiac pressure overload. We tested whether chronic pressure-overload induces sex-specific skeletal muscle remodeling and alters macrophage abundance and paracrine signaling in male and female Sprague Dawley rats that underwent transverse aortic constriction (TAC) or sham surgery at 4 weeks of age and were studied after 40 wk. TAC induced 12% greater heart mass (\n                    <jats:italic>p<\/jats:italic>\n                    \u2009=\u20090.049) and 17% greater heart-to-body mass ratio (\n                    <jats:italic>p<\/jats:italic>\n                    \u2009=\u20090.018) in males, while females showed minimal cardiac remodeling. In extensor digitorum longus (EDL) muscle, TAC males exhibited\u2009~\u200910% smaller fiber perimeter corresponding with higher capillary-to-fiber perimeter exchange (\n                    <jats:italic>p<\/jats:italic>\n                    \u2009&lt;\u20090.05 for both), while female TAC rats had no difference in fiber size and 17% lower capillary-to-fiber ratio than female sham (\n                    <jats:italic>p<\/jats:italic>\n                    \u2009=\u20090.033). In soleus muscle, TAC rats had higher capillarization indices (\n                    <jats:italic>p<\/jats:italic>\n                    \u2009&lt;\u20090.05) regardless of sex. Muscle macrophage abundance was 19% lower in TAC males than sham males (\n                    <jats:italic>p<\/jats:italic>\n                    \u2009=\u20090.005). TAC macrophages secreted less MCP-1 (\u2212\u200935%,\n                    <jats:italic>p<\/jats:italic>\n                    \u2009=\u20090.0058), IL-1\u03b2 (\u2212\u200916%,\n                    <jats:italic>p<\/jats:italic>\n                    \u2009=\u20090.0167), TNF-\u03b1 (\u2212\u200916%,\n                    <jats:italic>p<\/jats:italic>\n                    \u2009=\u20090.0337), and VEGF-A (\u2212\u200916%,\n                    <jats:italic>p<\/jats:italic>\n                    \u2009=\u20090.0120) and produced less complex endothelial networks (18% larger mesh size,\n                    <jats:italic>p<\/jats:italic>\n                    \u2009=\u20090.001). These findings indicate that TAC is associated with skeletal muscle remodeling and macrophage immunosuppression, with some changes occurring in a sex-specific manner. This suggests the potential for immune-microvascular coupling in peripheral adaptations to cardiac pressure overload.\n                  <\/jats:p>","DOI":"10.1007\/s00424-026-03220-w","type":"journal-article","created":{"date-parts":[[2026,10,10]],"date-time":"2026-10-10T10:28:04Z","timestamp":1791628084000},"update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["Sex-specific skeletal muscle fiber atrophy and reduced macrophage inflammation in a rodent transverse aortic constriction model"],"prefix":"10.1007","volume":"478","author":[{"given":"William S.","family":"Evans","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Maria Canellas","family":"da Silva","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Gabriel","family":"Pena","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Sarah","family":"Kuzmiak-Glancy","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Steven J.","family":"Prior","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"297","published-online":{"date-parts":[[2026,10,10]]},"reference":[{"issue":"2","key":"3220_CR1","doi-asserted-by":"publisher","first-page":"286","DOI":"10.1161\/CIRCHEARTFAILURE.114.001825","volume":"8","author":"BP Dhakal","year":"2015","unstructured":"Dhakal BP et al (2015) Mechanisms of exercise intolerance in heart failure with preserved ejection fraction: the role of abnormal peripheral oxygen extraction. 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