Exercise enhances placental labyrinth trophoblast development by activation of PGC-1α and FNDC5/irisin†.

Placental chorion/labyrinth trophoblasts are energy demanding which is met by the mitochondrial oxidative phosphorylation. Exercise enhances placental development and mitochondrial biogenesis, but the underlying mechanisms remain poorly understood. To address, female C57BL/6 J mice were randomly assigned into two groups: a control group and an exercise (EX) group.

Exercise improves homeostasis of the intestinal epithelium by activation of apelin receptor-AMP-activated protein kinase signalling.

Intestinal remodelling is dynamically regulated by energy metabolism. Exercise is beneficial for gut health, but the specific mechanisms remain poorly understood. Intestine-specific apelin receptor (APJ) knockdown (KD) and wild-type male mice were randomly divided into two subgroups, with/without exercise, to obtain four groups: WT, WT with exercise, APJ KD and APJ KD with exercise.

Stage-specific nutritional management and developmental programming to optimize meat production.

Over the past few decades, genetic selection and refined nutritional management have extensively been used to increase the growth rate and lean meat production of livestock. However, the rapid growth rates of modern breeds are often accompanied by a reduction in intramuscular fat deposition and increased occurrences of muscle abnormalities, impairing meat quality and processing functionality. Early stages of animal development set the long-term growth trajectory of offspring.

AMP-activated protein kinase inhibition in fibro-adipogenic progenitors impairs muscle regeneration and increases fibrosis.

Background: Following muscle injury, fibro-adipogenic progenitors (FAPs) are rapidly activated and undergo apoptosis at the resolution stage, which is required for proper muscle regeneration. When excessive FAPs remain, it contributes to fibrotic and fatty infiltration, impairing muscle recovery. Mechanisms controlling FAP apoptosis remain poorly defined.

Maternal exercise improves epithelial development of fetal intestine by enhancing apelin signaling and oxidative metabolism.

Obesity in pregnancy is currently the leading cause of gestational complications for the mother and fetus worldwide. Maternal obesity (MO), common in western societies, impedes development of intestinal epithelium in the fetuses, which causes disorders in the nutrient absorption and intestine-related immune responses in offspring. Here, using a mouse model of maternal exercise (ME), we found that exercise during pregnancy protects the impairment of fetal intestinal morphometrical formation and epithelial development due to MO.

Obesity induces adipose fibrosis and collagen cross-linking through suppressing AMPK and enhancing lysyl oxidase expression.

Collagen is the main component of connective tissue surrounding adipocytes. Collagen cross-linking affects adipose remodeling, which is crucial for maintaining function and metabolic homeostasis of adipose tissue. However, the effects of obesity on collagen cross-linking and adipose fibrosis remain to be examined.

Exerkine apelin reverses obesity-associated placental dysfunction by accelerating mitochondrial biogenesis in mice.

Maternal exercise (ME) protects against adverse effects of maternal obesity (MO) on fetal development. As a cytokine stimulated by exercise, apelin (APN) is elevated due to ME, but its roles in mediating the effects of ME on placental development remain to be defined. Two studies were conducted.

Maternal exercise intergenerationally drives muscle-based thermogenesis via activation of apelin-AMPK signaling.

Background: Sarcolipin and uncoupling protein 3 (UCP3) mediate muscle-based non-shivering thermogenesis (NST) to improve metabolic homeostasis. The impacts of maternal obesity (MO) and maternal exercise (ME) on NST in offspring muscle remain unexamined.

Methods: Female mice were fed with a control diet or high fat diet to induce obesity.

Prenatal exercise in fetal development: a placental perspective.

Maternal obesity (MO) and gestational diabetes mellitus (GDM) are common in Western societies, which impair fetal development and predispose offspring to metabolic dysfunction. Placenta is the organ linking the mother to her fetus, and MO suppresses the development of vascular system and expression of nutrient transporters in placenta, thereby affecting fetal development. For maintaining its proper physiological function, placenta is energy demanding, which is met through extensive oxidative phosphorylation.

Treadmill Running of Mouse as a Model for Studying Influence of Maternal Exercise on Offspring.

Epidemiological studies robustly show the beneficial effects of maternal exercise in reducing maternal birth complications and improving neonatal outcomes, though underlying mechanisms remain poorly understood. To facilitate mechanistic exploration, a protocol for maternal exercise of mice is established, with the regimen following the exercise guidelines for pregnant women. Compared to volunteer wheel running, treadmill running allows precise control of exercise intensity and duration, dramatically reducing variations among individual mouse within treatments and facilitating translation into maternal exercise in humans.

Maternal Inactivity Programs Skeletal Muscle Dysfunction in Offspring Mice by Attenuating Apelin Signaling and Mitochondrial Biogenesis.

Although maternal exercise (ME) becomes increasingly uncommon, the effects of ME on offspring muscle metabolic health remain largely undefined. Maternal mice are subject to daily exercise during pregnancy, which enhances mitochondrial biogenesis during fetal muscle development; this is correlated with higher mitochondrial content and oxidative muscle fibers in offspring muscle and improved endurance capacity. Apelin, an exerkine, is elevated due to ME, and maternal apelin administration mirrors the effect of ME on mitochondrial biogenesis in fetal muscle.

Exercise prevents the adverse effects of maternal obesity on placental vascularization and fetal growth.

Key Points: Maternal exercise improves the metabolic health of maternal mice challenged with a high-fat diet. Exercise intervention of obese mothers prevents fetal overgrowth. Exercise intervention reverses impaired placental vascularization in obese mice.

Plasma apelin levels in overweight/obese adults following a single bout of exhaustive exercise: A preliminary cross-sectional study.

Introduction: Physical activity is beneficial for preventing metabolic diseases. Here, the circulatory level of apelin, one of the myokines, was assessed in patients with obesity to examine the effects of body composition, metabolic parameters, and physical fitness on apelin secretion following an exercise program.

Methods: A total 60 subjects [34 women (21 lean and 13 overweight/obese) and 26 men (8 lean and 18 overweight/obese)], age 30-59 years, with body mass index (BMI) of 18-30kg/m were recruited based on the guidelines for Korean obesity therapy in a clinical trial.

Exercise-induced myokines: a brief review of controversial issues of this decade.

Introduction: Myokines, known to mediate metabolism, inflammation, and other pathophysiological conditions, have been widely investigated, including myokines induced by exercise. However, among published literature, there is substantial inconsistency in the quantification of exercise-induced myokines. Here, we summarized and compared published data regarding the effects of exercise on commonly studied myokines including apelin, Brain-derived neurotrophic factor (BDNF), Interleukin-15 (IL-15), irisin, and Secreted protein acidic and rich in cysteine (SPARC) during the last decade and discussed possible reasons for discrepancy in these reports.

Effects of exercise-induced apelin levels on skeletal muscle and their capillarization in type 2 diabetic rats.

Introduction: Exercise-induced apelin as a myokine is believed to play a role in the improvement of type 2 diabetes mellitus (T2DM) and capillarization. In this study, we evaluated the association between exercise-induced apelin and muscle capillarization.

Methods: Zucker rats underwent a treadmill exercise program.