Brain-derived neurotrophic factor is associated with human muscle satellite cell differentiation in response to muscle-damaging exercise.

Muscle satellite cell (SC) regulation is a complex process involving many key signalling molecules. Recently, the neurotrophinbrain-derived neurotropic factor (BDNF) has implicated in SC regulation in animals. To date, little is known regarding the roleof BDNF in human SC function in vivo. Twenty-nine males (age, 21 ± 0.5 years) participated in the study. Muscle biopsies from thethigh were obtained prior to a bout of 300 maximal eccentric contractions (Pre), and at 6 h, 24 h, 72 h, and 96 h postexercise.BDNF was not detected in any quiescent (Pax7+/MyoD−) SCs across the time-course. BDNF colocalized to 39% ± 5% of proliferating(Pax7+/MyoD+) cells at Pre, which increased to 84% ± 3% by 96 h (P < 0.05). BDNF was only detected in 13% ± 5% of differentiating(Pax7−/MyoD+) cells at Pre, which increased to 67% ± 4% by 96 h (P < 0.05). The number of myogenin+ cells increased 95% from Pre(1.6 ± 0.2 cells/100 myofibres (MF)) at 24 h (3.1 ± 0.3 cells/100 MF) and remained elevated until 96 h (cells/100 MF), P < 0.05. Theproportion of BDNF+/myogenin+ cells was 26% ± 0.3% at Pre, peaking at 24 h (49% ± 3%, P < 0.05) and remained elevated at 96 h(P < 0.05). These data are the first to demonstrate an association between SC proliferation and differentiation and BDNFexpression in humans in vivo, with BDNF colocalization to SCs increasing during the later stages of proliferation and earlydifferentiation. [ABSTRACT FROM AUTHOR]