Prenatal exercise in fetal development: a placental perspective

Abstract

gestational diabetes mellitus (GDM); glucose transporters (GLUTs); G protein-coupled receptor (GPCR); human chorionic gonadotropin (hCG); hypoxia inducible factor-1a (HIF-1a); luteinizing hormone/choriogonadotropin receptor (LHCGR); maternal exercise (ME); maternal obesity (MO); maximal oxygen consumption rates (VO 2 max); metastatic lymph node 64 (MLN64); superoxide dismutase 3 (SOD3); mitochondrial transcription factor A (TFAM); peroxisome proliferator-activated receptor  coactivator-1 (PGC-1); placental lactogen (PL); placental growth hormone (PGH); protein kinase A (PKA); vascular endothelial growth factor (VEGFA); voluntary wheel running (VWR).

The role of enriched environment in neural development and repair

“…Given that voluntary physical activity is an essential component of EE, we separately analyzed the positive effects of a prenatal exercise intervention on neurodevelopment. More and more studies have shown that reasonable physical exercise during pregnancy is not only conducive to reducing the incidence of gestational diabetes and hypertension and the percentage of body fat in pregnant women but also conducive to promoting fetal development reflected in the increase of placental survival rate and placental hormone secretion (Hopkins et al, 2011 ; Rosa et al, 2011 ; Davies and Artal, 2019 ; Chae et al, 2021 ). Treadmill training in pregnant rats significantly increased cell proliferation, BNDF, and apoptosis inhibition protein expression in the hippocampus of adolescent and adult progeny rats (Kim et al, 2021 ), which may explain the high spatial learning ability in neonatal rat pup on the premise of voluntary exercise of maternal rats (Parnpiansil et al, 2003 ).…”

Possible roles of exercise and apelin against pregnancy complications

“…On the other hand, the abundance of apelin and APJ in the placenta is strongly related to placental AMPK signaling and causes the transfer of maternal glucose to the fetus because all effects in mice treated with apelin are eliminated by inactivating AMPK ( 33 , 92 ). In addition, during AMPK activation, ACC is inhibited, then the concentration of malonyl-coenzyme A (CoA) decreases, and beta-oxidation of fatty acids increases in muscle ( 15 , 93 , 94 ). In the human placenta, ACC is phosphorylated via p-AMPK to enhance fatty acid oxidation and reduce fatty acid synthesis ( 95 ).…”

“…In obese pregnant mice, daily exercise on a treadmill reduces weight gain, lowers serum glucose and fat, and increases insulin sensitivity ( 4 , 14 ). In humans, exercising (40 to 60% of VO2max) during pregnancy reduces the risk of gestational hypertension and preeclampsia and increases energy consumption ( 15 , 16 ). The fetal and maternal cardiac response to aerobic, anaerobic, and circular exercise activities has been reported to be safe and beneficial during pregnancy in humans and animals ( 17 – 19 ).…”

“…It seems that one of the reasons for these improvements is due to the placentokines such as apelin, leptin, apela, irisin, and adiponectin, but the placentokine we review in this study is apelin. The release of apelin due to exercise also is more than the other placentokines ( 15 ). Apelin also is known as exerkine (exercise + cytokine) and placentokine (placenta + cytokine) ( 15 , 20 , 21 ).…”

“…The release of apelin due to exercise also is more than the other placentokines ( 15 ). Apelin also is known as exerkine (exercise + cytokine) and placentokine (placenta + cytokine) ( 15 , 20 , 21 ). Apelin as an exerkine reverses obesity-related placental dysfunction by increasing mitochondrial biogenesis in mice ( 22 ).…”