Front Matter

128 Canine Sports Medicine and Rehabilitation

the elbow. Therefore, moving the shoulder
into flexion and the elbow into extension tests
biceps flexibility (Figure  6.7). Documentation
of abnormal flexibility can be noted as mini­
mally, moderately, or severely restricted or can
be measured with a goniometer.

Treatment of decreased flexibility

Increasing muscle extensibility is accomplished
by stretching the tight muscle. Stretching can be
performed passively, in combination with soft
tissue mobilization or actively with specific
exercises. Similar to the muscle flexibility
assessment position, a passive stretch is per­
formed with the limbs placed in a position that
is opposite to the actions of the muscle.
Typically, the origin of the muscle is stabilized
and the insertion is moved away from the
origin.
The stretch should be moderate (palpable
muscle tension) and within the patient’s com­
fort range. The stretch must be effective but
not painful. If pain is produced, the patient
will splint (involuntary rigid contraction of
the muscles in response to pain), resulting in
a  shortening of the muscle fibers. Human
research has shown that carryover is more
effective with a 30‐second passive, static stretch
than a 15‐second stretch. Gains with an addi­
tional 30 seconds (60 seconds total) were shown
to be minimal (Bandy & Irion, 1994). For added
effectiveness, the stretch can be combined with

soft tissue mobilization of the muscle being

stretched. A muscle can also be stretched

dynamically. This is performed by instructing

the patient to actively move into a position that

stretches the muscle. Dynamic stretching may

not be as effective as static stretching in increas­

ing flexibility (O’Sullivan et al., 2009) but may

be more effective in increasing athletic perfor­

mance (McMillian et al., 2006).

Joint mobilization

Attention to the intrinsic movement of joints

reaches back to the days of Hippocrates

(460–370 bc). Joint manipulation, referred to

as bone setting, spread in Europe between the

seventeenth and early twentieth centuries;

however, no formal training was established

until Andrew Still founded the first school of

osteopathy in 1874. Physical therapists began

studying joint mobilization and manipulation

in manual therapy programs established by

leaders in the field, Freddy Kaltenborn,

Geoffrey Maitland, and Stanly Paris in the early

1960s. Research has demonstrated both biome­

chanical and neurophysiological effects of

joint mobilization; however, the mechanism

of change is still under scrutiny (Brantingham

et al., 2009; Zusman, 2010).

Joint play (or joint mobility) is passive, invol­

untary arthrokinematic motion that occurs

between two joint surfaces during movement.

It is required for normal osteokinematic motion.

Joint play consists of two passive movements:

traction/separation and translatoric gliding,

both of which are required to prevent compres­

sion and/or subluxation of a joint (Kaltenborn

et al., 1999). Loss of joint play may be the result

of capsular tightness that blocks the normal

arthrokinematic gliding within the joint.

Capsular tightness can be identified by assess­

ing the end‐feel during PROM and by assessing

joint play.

The goals of joint mobilization are to increase

arthrokinematic range of motion, improve joint

alignment and tracking, decrease pain, and

reduce muscle spasm by stimulating articular

sensory receptors (Maitland, 1977). Joint mobi­

lization has been shown to have mechanical

effects on the joint capsule (i.e., stretch the

capsule) that correspond with improved ROM

Figure 6.7 Biceps brachii muscle stretch. Moving the
shoulder into flexion and the elbow into extension tests
biceps flexibility.