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Review |
Normal mammalian skeletal muscle and its phenotypic plasticity
Department of Anatomy, University of Bern, Bühlstrasse 26, CH-3000 Bern 9, Switzerland
* e-mail: hoppeler{at}ana.unibe.ch
Accepted 13 May 2002
Since muscle mass makes up such a high proportion of total body mass, there
must have been considerable selective pressure to minimize the cost of
maintenance and to maximize the functionality of muscle tissue for all
species. Phenotypic plasticity of muscle tissue allows the species blueprint
of muscle tissue to be modified to accommodate specific demands experienced by
animals over their lifetime. In this review, we report the scaling of muscle
structural compartments in a set of mammals spanning five orders of magnitude
(17 g woodmice to 450 kg horses and steers). Muscle mass, muscle myofibrillar
volume and sarcoplasmic space were found to represent similar relative
quantities in all species studies (scaling factor close to unity).
Mitochondrial volumes were found to be systematically smaller in larger
animals (scaling factor 0.91) and closely related to the scaling of
O2max (0.92) and
were tracked by the scaling of total capillary length (0.95). In this set of
species, we therefore found that maximal metabolic rate and supporting
structures did not scale to the 0.75 power of body mass as generally
suggested. Muscle phenotypic plasticity is reasonably well characterized on a
structural and functional basis, but we still know little about the signals
that cause the changes in gene expression necessary for phenotypic changes in
muscle. The molecular responses of human m. vastus lateralis to endurance
exercise indicate that a single bout of exercise causes specific transient
transcriptional adaptations that may gradually accumulate after their
translation into the (structural) modifications seen with phenotypic
plasticity. Metabolic and mechanical factors are recognized candidate factors
for the control of exercise-induced gene transcription in muscle. Distinct
protein kinases and transcription factors emerge as possible interfaces that
integrate the mechanical (MAPKs and jun/fos) and metabolic (AMPK, HIF-1
and PPAR) stimuli into enhanced gene transcription in skeletal
muscle.
Key words: scaling, morphometry, mRNA, O2max, muscle, phenotype, plasticity
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