Time course of changes in capillarization in hypertrophied rat plantaris muscle

Abstract

The time course of angiogenesis during hypertrophy of the rat plantaris muscle was studied by using a unilateral, synergistic ablation model. Animals (n = 6/group) were euthanized 2, 5, 7, 15, 21, and 30 days postmyectomy. Sections from both the hypertrophied and contralateral muscles were simultaneously stained for capillaries and muscle fiber type. Mean fiber cross-sectional area (FA) and various indexes of capillarity were determined by using a video analysis system. The capillary supply to individual fibers, assessed as the FA supplied per capillary contact, remained unchanged until day 21 (compared with day 2) and exhibited a significant increase at day 30. Analysis of the time course of capillary development on the basis of the number of capillary contacts per fiber, and of hypertrophy on the basis of FA, yielded half-lives of 10.1 and 11.2 days, respectively. It was concluded that angiogenesis during muscle overload is tightly coupled to the changes in FA, which could suggest that the two processes are initiated and/or driven by some common factor(s).

Local capillary supply in muscle is not determined by local oxidative capacity

“…It is striking, however, that the local capillary supply was more tightly related to FCSA than fibre oxidative capacity. Consistent with these observations, fibre hypertrophy and angiogenesis during muscle overload have a similar time course (Plyley et al, 1998), further supporting a coupling between fibre size and local muscle capillarisation. Such a coupling is, in part, explicable by the fact that not only muscle fibres and satellite cells, but also endothelial cells act as mechanotransducers and may secrete factors with reciprocal effects in response to mechanical deformation (Christov et al, 2007).…”

Heat stress inhibits skeletal muscle hypertrophy

“…Since plantaris overload causes both an increased muscle mass as well as increased Type I MHC expression (Noble et al 1983, Locke et al 1994, Plyley et al 1998, Macpherson et al 1999, it was necessary to consider changes in Type I MHC in context to changes in muscle mass. After 1 day of overload, plantaris muscle Type I MHC content remained unchanged from their respective contralateral controls, regardless of whether animals experienced a prior heat stress (no significant differences were observed).…”

“…It is well known that increased muscle fiber size and increased protein content occur following overload (Hubbard et al 1975, Plyley et al 1998, Macpherson et al 1999. During the process of muscle hypertrophy, muscle fibers adapt by increasing the number of sarcomeres, mostly in parallel (peripheral accumulation of sarcomeres) and, to a much lesser extent, in series (elongation of existing fibers).…”

“…A work-induced hypertrophy model, employing the removal of the synergists involved in plantar flexion (synergistic ablation) of the rat hindlimb, is well established; previous studies have documented the biochemical and anthropomorphic changes to the rat plantaris muscle following ablation-induced overload (Noble et al 1983, Locke et al 1994, Plyley et al 1998, Macpherson et al 1999. In particular, these studies consistently reported increased Type I myosin heavy chain (Type I MHC) content in chronically overloaded rat plantaris muscles.…”

Myogenic Akt Signaling Regulates Blood Vessel Recruitment during Myofiber Growth

“…Conversely, myofiber atrophy that occurs with aging, disuse, and myopathic disease is associated with capillary loss (8,28). It has been shown that angiogenesis and compensatory muscle hypertrophy are temporally coupled, suggesting that these two processes may be controlled by common regulatory mechanisms (47). However, nothing is known about the molecular events that coordinate myofiber hypertrophy and the recruitment of new blood vessels.…”