Front Matter

54 Canine Sports Medicine and Rehabilitation

Hypertrophy and sarcopenia

Muscle mass is governed by a complex
combination of mediators including insulin,
insulin‐like growth factors, androgens, myosta­
tin, cytokine/myokines, and plasma amino
acids (Solomon & Bouloux, 2006; Spangenburg,
2009). From a veterinary perspective, muscle
hypertrophy has been a desired phenotype in
agriculture and performance arenas. Selective
breeding has perpetuated a genetic mutation
in  the myostatin gene that is associated with
constitutive muscle hypertrophy. Myostatin is a
negative regulator of myofiber differentiation,
satellite cell maturation and muscle biosynthetic
activity, and its inactivation leads to hypertro­
phy (Bradley et  al., 2008). Heterozygotes for
the  myostatin loss‐of‐function mutation have
shown improved racing performance, which
has led to perpetuation of this trait within
the Whippet population (Mosher et al., 2007).
Androgens and other anabolic mediators
such as growth hormone play a role in the con­
trol of muscle mass; however, the effects of these
compounds on musculoskeletal homeostasis
are highly species‐specific. Normal physiologi­
cal concentrations of canine gonadal steroids
may augment the stimulatory effects of exercise
on skeletal myofiber synthesis; however, their
impact on the development and maintenance of

overall muscle mass is less pronounced than in

other species (West & Phillips, 2010). Although

banned within organized canine athletics,

exogenous anabolic steroids and growth hor­

mone can induce supraphysiological muscle

hypertrophy. In combination with appropriate

conditioning, this may confer some perfor­

mance advantage to canine athletes involved in

resistance events such as weight pulling or

sprinting. However, augmentation of muscle

mass is unlikely to be beneficial in canine

endurance activities.

Sarcopenia refers to the progressive decrease

in muscle mass and strength that occurs with

aging. Sarcopenia reflects loss of myofibers due

to apoptosis, as well as decreases in myofiber

size. Overall muscle circumference is often

maintained during early sarcopenia, as lost

myofibers are replaced with adipose and

fibrous tissue (Freeman, 2012). Declining per­

formance may be the only early clinical indica­

tor of this condition. Muscle loss becomes

measurable as sarcopenia progresses and is

common in the geriatric population. Until

recently, this phenomenon had not been

documented in dogs, but recent biochemical

assessment of aging canine muscle has con­

firmed that the upregulation of autophagy is

occurring in elderly dogs leading to myofiber

Tr opomyosin

Tr oponin C

Tr oponin I Ca++

Ca++

Myosin

Sarcoplasmic

reticulum

α-actin

Figure 3.8 Calcium released from the sarcoplasmic reticulum binds to troponin C, triggering myosin–actin interaction
through conformational changes in tropomyosin. Source: Used with permission from Hand et al., 2010.