Proceedings of The Physiological Society

King's College London (2009) Proc Physiol Soc 14, PC15

Poster Communications

Skeletal muscle fibre size and function of the myostatin null mouse in response to exercise

A. Matsakas1, A. Otto1, R. Macharia2, K. Patel1

1. School of Biological Sciences, University of Reading, Reading, United Kingdom. 2. Royal Veterinary College, London, United Kingdom.

  • Table 1. Myosin heavy chain isoform profile of the EDL muscle given in percentage Cells with the same symbol (a b c d) differ at the p≤0.05 level n=4-6 animals per group mean±SD

  • Figure. Myofibre cross sectional area of the extensor digitorum longus muscle

Myostatin is a potent inhibitor of skeletal muscle development. Absence of myostatin results in an hypermuscular phenotype through a combination of fibre hypertrophy and hyperplasia. However, the myostatin null mouse has been shown to be weaker than wild-type animals with a compromised capacity to generate force (Amthor et al. 2007). The aim of this study was to determine the response of myostatin null muscle to chronic exercise, assessed through physiological, histological and morphological analysis of the extensor digitorum longus muscle (EDL). Two different exercise regimes were used; compulsory swim activity or spontaneous running activity for 5 weeks. Both exercise regimes undertaken by the animals in this study resulted in an increase in specific force in the null group but no differences were induced in the wild type. The two groups responded independently to exercise in terms of fibre composition. In the trained wild type mice a bidirectional shift was detected, from either type I or IIX/B towards IIA (Table 1). In contrast the myostatin nulls displayed a slight general glycolytic to oxidative transition. Trained animals responded in changes to fibre size dependent on genotype and exercise regime (Figure). Morphometric analysis showed that the IIB fibres of the wild type EDL displayed a remarkable decrease in area of 43% in response to spontaneous running activity, while the myostatin nulls showed only a reduction of 22%. Swim training resulted in 34% and 26% smaller cross sectional areas in the null and wild type groups respectively. In addition, elevated nuclear to cytoplasmic ratio was obeserved in both genotypes following exercise training, with more pronounced changes in the wild type animals. These data provide novel evidence that the myostatin null muscle is generally less plastic that the wild type muscle with regard to long term muscle activity and less prone to changes in myofibre phenotype.

Where applicable, experiments conform with Society ethical requirements