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Updated: May 31, 2026

Swimming Exercise Protocol and Care Methods for Pregnant Rats
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Maternal exercise reduces hyperthermia-induced apoptosis in developing mouse brain.

Jin Lee1, Joon Yong Cho, Sang Duk Oh

  • 1Department of Anatomy and Cell Biology, College of Medicine, Hanyang University, Seoul, Korea.

International Journal of Hyperthermia : the Official Journal of European Society for Hyperthermic Oncology, North American Hyperthermia Group
|July 16, 2011
PubMed
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Maternal exercise protects embryos from heat stress by reducing cell death. Regular exercise up-regulates heat shock proteins (HSPs), crucial for this protective effect during pregnancy.

Area of Science:

  • Reproductive biology
  • Developmental toxicology
  • Cellular stress response

Background:

  • Hyperthermia induces apoptosis in neuroepithelial cells via the mitochondrial pathway.
  • Regular exercise increases heat shock proteins (HSPs) that inhibit apoptosis.
  • The protective role of maternal exercise against prenatal heat exposure is not fully understood.

Purpose of the Study:

  • To investigate the protective effects of maternal exercise against hyperthermia-induced embryo apoptosis.
  • To examine the expression of apoptosis-related factors and HSPs in response to maternal exercise and heat exposure.
  • To elucidate the role of HSPs in mediating embryo protection during pregnancy.

Main Methods:

  • Pregnant mice (Hsp70 knockout) were divided into control, exercise, hyperthermia, and hyperthermia-after-exercise groups.

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  • Maternal swimming exercise (5-10 min/day) was performed from embryonic day 1 to 8.
  • Hyperthermia (43°C, 5 min) was induced on embryonic day 8; apoptosis-related factors and HSPs were analyzed via western blotting and electron microscopy.

    • Main Results:

    • Maternal exercise significantly reduced the number of apoptotic cells in embryos exposed to hyperthermia.
    • Key apoptosis factors (Caspase-9, -7, -3, Bax) were down-regulated in the hyperthermia-after-exercise group.
    • Anti-apoptotic proteins (Bcl-2) and HSPs (Hsp27, Hsp110) were up-regulated, indicating a protective cellular response.

    Conclusions:

    • Maternal exercise is crucial for inhibiting apoptotic cell death in embryos exposed to hyperthermia during pregnancy.
    • Exercise-induced up-regulation of HSPs plays a significant role in protecting embryos from heat stress.
    • This study highlights a potential non-pharmacological intervention to mitigate risks associated with prenatal hyperthermia.