Automated Methods for the Analysis of Skeletal Muscle Fiber Size and Metabolic Type - International Review of Cell and Molecular Biology - page 273

Type I (slow-twitch) or Type II (fast-twitch) ( Schiaffino and Reggiani,
2011 ). Additionally, Type I and Type II fibers vary in their fatigue charac-
teristics and metabolic profile: Type I fibers generally have greater endur-
ance, whereas Type II fibers generally fatigue relatively rapidly (Type II
fibers are further divided into Type IIA, IIB, and IIX). Rarely a muscle
can contain almost pure population of one fiber type (examples include
the soleus muscle in mouse, which has predominantly slow-type fibers,
and the breast meat of a chicken, which contains primarily fast-type fibers;
Edman et al., 1988a ), but more commonly, particularly for humans, a
mixture of both fiber types ( Fig. 7.1 B). The specialized nature of the differ-
ent fiber types has intrigued muscle researchers for decades and much effort
has been directed to understanding the origins and consequences of these
differences, particularly with regard to metabolism.
2. RELEVANCE OF SKELETAL MUSCLE
TO HUMAN HEALTH
Certain areas, which illustrate the wide variety of contexts in which
skeletal muscle is relevant to health and disease are briefly reviewed below.
In all of these research areas, muscle tissue is sampled and assayed for the
expression of Type I and Type II fibers and additionally for biomarkers that
are relevant to the particular subject area.
2.1. Hormonal control of muscle mass
Skeletal muscle mass is directly correlated with testosterone levels through-
out the human life cycle ( Giannoulis et al., 2012 ) and “androgen abuse” in
which anabolic steroids are used by athletes to increase muscle mass and
strength is of concern to society ( Basaria, 2010 ). Components of the
response include increased differentiation of progenitor cells to the muscle
phenotype, increased protein synthesis, and increased cross-sectional area of
both Type I and Type II fibers ( Herbst and Bhasin, 2004 ). Interestingly, the
mechanisms responsible for the effects of testosterone on muscle have
proven elusive. An emerging theme is that testosterone may increase muscle
mass by mechanisms involving inhibition of the effects of myostatin ( Gentile
et al., 2010; Mosler et al., 2012 ), a member of the transforming growth
factor-beta superfamily ( Argiles et al., 2007 ). The knockout of myostatin
in mice and mutation of myostatin in cattle lead to highly muscular pheno-
types, which resemble human body builders and anabolic steroid users
( Grobet et al., 1997; McPherron et al., 1997 ), indicating that myostatin,