Developmental Programming of Fetal Skeletal Muscle and Adipose Tissue Development

Abstract

All important developmental milestones are accomplished during the fetal stage, and nutrient fluctuation during this stage produces lasting effects on offspring health, so called fetal programming or developmental programming. The fetal stage is critical for skeletal muscle development, as well as adipose and connective tissue development. Maternal under-nutrition at this stage affects the proliferation of myogenic precursor cells and reduces the number of muscle fibers formed. Maternal over-nutrition results in impaired myogenesis and elevated adipogenesis. Because myocytes, adipocytes and fibrocytes are all derived from mesenchymal stem cells, molecular events which regulate the commitment of stem cells to different lineages directly impact fetal muscle and adipose tissue development. Recent studies indicate that microRNA is intensively involved in myogenic and adipogenic differentiation from mesenchymal stem cells, and epigenetic changes such as DNA methylation are expected to alter cell lineage commitment during fetal muscle and adipose tissue development.

Developmental programming of type 2 diabetes

“…Alterations in the differentiation potential of adipocytes have been proposed to be associated with the metabolic programming effects of suboptimal nutrition in early life [23][24][25]. The impact of maternal obesity during gestation on adipocyte commitment and differentiation via epigenetic mechanisms in the offspring was recently investigated [26].…”

Position statement on youth resistance training: the 2014 International Consensus

“…Further increases in muscle cross-sectional area, muscle pennation angle and continued motor unit differentiation will typically enable adolescents to express greater levels of force, and partly explain the age-related differences in strength between children, adolescents and adults 50. The number of muscle fibres that an individual will possess is determined as a result of prenatal myogenesis,51 and therefore it should be noted that postnatal increases in muscle cross-sectional area will be largely governed by increases in muscle fibre size, not an increase in the number of muscle fibres 51 52…”

The Childhood Obesity Epidemic as a Result of Nongenetic Evolution: The Maternal Resources Hypothesis

“…Because osteocytes, myocytes, and adipocytes share a common pool of progenitor cells, reduced PA leads to a reduction in the physiological resources (e.g., muscle development, strength, coordination) necessary for lifelong PA, and every kilocalorie of energy that is not used to build muscle and bone may be used to further increase adipocyte size and/or number. 121,153 As such, the predisposition to obesity would be instantiated via accelerated hyperplastic adiposity, inactivity, decrements in the physiological resources necessary for movement (e.g., strength, coordination), and the initiation of a positive feedback loop that negatively alters health trajectories over successive generations via mother-daughter transmission.…”