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1 Molecular, Cellular, and Developmental Biology, University of Colorado at Boulder, Boulder, CO, USA
* To whom correspondence should be addressed. E-mail: Leslie.Leinwand{at}colorado.edu.
How sex and genetic background modify cardiac adaptation to increased workload is a topic of great interest. We systematically evaluated morphologic and physiologic cardiac adaptation in response to voluntary and forced exercise. We find that sex/gender is a dominant factor in exercise performance (in two exercise paradigms and two mouse strains) and that females of one of these strains have greater capacity to increase their cardiac mass in response to similar amounts of exercise. To explore the biochemical mechanisms for these differences, we examined signaling pathways previously implicated in cardiac hypertrophy. Calcium/Calmodulin-dependent protein kinase (CaMK) activity was significantly greater in males compared to females and increased following voluntary cage wheel exposure in both sexes, but the proportional increase in CaMK activity was 2-fold higher in females compared to males. Phosphorylation of glycogen-synthase kinase-3
(GSK-3) was evident after 7 days of cage wheel exposure in both sexes and remained elevated by 21 days of exercise but in females only. Despite moderate increases in myocyte enhancer factor 2 transcriptional activity, a downstream effector of CaMK, and phosphorylation of Akt with exercise there were no sex differences. MAPK signaling components (p38-MAPK and ERK1/2) were not different between male and female mice and were not affected by exercise. We conclude that females have increased exercise capacity and an increased hypertrophic response to exercise. We have also identified sex-specific differences in hypertrophic signaling within the cardiac myocyte that may contribute to sexual dimorphism in exercise and cardiac adaptation to exercise.
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