Craniofacial Muscles

222 A. Sokoloff and T. Burkholder
Compared to appendicular muscles, many cranial muscles have relatively high
capillarization and mitochondrial content (Stal and Lindman 2000 ; Kjellgren et al.
2004 ) . Human intrinsic tongue muscle fi bers also have relatively high capillarization
with values similar to extraocular and jaw-closing muscles but two times greater
than appendicular muscles (Granberg et al. 2010 ) . Human intrinsic tongue muscles
also have a moderate to high mitochondrial enzyme activity as do most tongue
muscle fi bers in the cat and rat (Hellstrand 1980 ; Sato et al. 1990 ) .
Interestingly, high capillarization and high mitochondrial enzyme activity in
human tongue muscles are present in fi bers of slow and fast MyHC, suggesting that
tongue muscle fi bers generally are refractive to fatigue. These characteristics accord
with measures of high resistance to fatigue following CNXII branch and hypoglossal
nucleus motoneuron stimulation in the rat (Gilliam and Goldberg 1995 ) . The
high oxidative capacity of human tongue muscle fi bers may support two features of
the tongue motor system that differ from the appendicular system, the constitutive
activity of some tongue motor units (Tsuiki et al. 2000 ; Saboisky et al. 2006 ; Bailey
et al. 2007a ) and the relatively high fi ring rates of motor units activated during
respiration or voluntary tasks (Bailey et al. 2007b ) .
12.6 Aging of Tongue Muscle
Age-related loss of muscle mass and muscle function (i.e., sarcopenia, Cruz-Jentoft
et al. 2010 ) occurs in many motor systems. Features of sarcopenia vary extensively
by muscle but often include decrease in muscle fi ber number and size (especially of
“fast” fi bers). Aging is also associated with changes in MyHC prevalence, increased
hybridization of different MyHC in single fi bers, and increased expression of developmental
MyHC (Andersen 2003 ; Snow et al. 2005 ) . Most motor systems lose
motoneurons with age, and the resultant denervation/reinnervation remodeling of
muscle fi bers may account for some of the above-mentioned anatomical and molecular
changes (Delbono 2003 ; Snow et al. 2005 ) .
Tongue muscles appear spared from many age-related changes typical of motor systems.
Although studies of aging of mammal tongue musculature are few, there is little
evidence of fi ber atrophy, expression of developmental MyHC, change in fi ber type
prevalence/MyHC composition (Connor et al. 2009 ; Sokoloff et al. 2010 ; Rother et al.
2002 ; but see Nakayama 1991 ) , and evidence for only minimal change in neuromuscular
junction morphology (Hodges et al. 2004 ) . Interestingly, hypoglossal nucleus
motoneuron number is preserved with age (Sturrock 1991 ; Gai et al. 1992 ) , which protects
tongue muscles from cell-loss-induced denervation/reinnervation remodeling.
The bases for the apparent protection of tongue muscles from typical age-related
neuromuscular pathology are not known. As noted, some GG motor units are constitutively
active indicating a high duty cycle of some tongue motor units. Tongue
motor units typically have high rates of activation. During swallowing high tongue
pressures are generated in normal swallows, although this can be increased in effortful
swallows (Hind et al. 2001 ) . In appendicular muscles, resistance exercise can delay