[Postnatal maturation of the diaphragm muscle: ultrastructural and functional aspects]

In the diaphragm muscle, postnatal maturation is associated with major histological and biochemical modifications, as well as a progressive development of the sarcoplasmic reticulum (SR), which in turn are responsible for the progressive postnatal improvement in diaphragmatic contractility. However, the mechanisms by which postnatal maturation induces this improvement in diaphragmatic contractility remain poorly understood and controversial. The aim of this review is to analyze the data from the literature regarding the process involved in the postnatal improvement in diaphragmatic contractility.

References obtained from Pubmed((R)) databank using keywords (diaphragm muscle, postnatal maturation, contractility, muscular fatigue, cross-bridge).

From a cytological point of view, the postnatal development of the diaphragm muscle is processed in two successive generations of fiber types, corresponding to the progressive adaptation of the diaphragm muscle to its physiological function. Indeed, the proportion in type I (slow, aerobic) and type IIB fibers (fast, anaerobic) progressively increases with postnatal maturation, while the proportion in type IIA fibers (fast, intermediate) progressively decreases. The histochemical classification of the type of fiber corresponds to the expression of the different isoforms of myosin heavy chains (MHC). Two types of MHC: MHC embryologic (MCH-emb) and MHC neonatal (MCH-neo), and one type of myosin light chains (MLC) are expressed in the foetal skeletal muscles, then are progressively eliminated during postnatal maturation. For many authors, this progressive transition from immature MHC (MCH-emb and neo) to adult MHC (by chronological order of appearance: MHC-2A, MHC-lente, MHC-2X, MHC-2B) could be responsible for the progressive improvement in postnatal diaphragmatic contractility. This transition could be modulated by external factors, mainly including neural and hormonal stimuli. For others, this transition in MHC expression do not play a major role, and other factors, including the postnatal maturation of the ryanodine receptor (RyR) or developmental changes in cross-bridges (CB) properties should play a central role. The most recent hypotheses proposed included the possibility of a postnatal transition in the expression of structural proteins, which are playing a major role in the maintenance of the stability of the sarcomer, and therefore in force generation.