NASM essentials of sports performance training
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NASM essentials of sports performance training

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tissue stiffness, and tissue dehydration (Table 4.3). The major
physical change in the body that affects its flexibility is a loss of muscle protein from atrophy or
sarcopenia (1). Atrophy is the loss in muscle fiber size, while sarcopenia is a decrease in muscle
fiber numbers. This loss in fiber quantity and quality is often replaced by fibrous, fatty connec-
tive tissue.
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The aging process causes muscle and neural atrophy and varies from person to person. The re-
duction of neural cells has been blamed for the general decline in motor control skills in adults.
As activity levels decrease, myofascial and neural atrophy increases. Less extensible, fibrous con-
nective tissue atrophies at a slower rate than muscle (1), meaning greater concentrations of fi-
brous, fatty connective tissues are present with aging. The reduction of neural and muscular cells
leads to decreased neuromuscular efficiency, which further restricts functional mobility (45).
Soft-tissue dehydration is a natural process of aging. Tissue studies have shown that the wa-
ter content in infant tendons is 85% and decreases to 70% in adults (1). Atrophy (muscular and
neural), soft-tissue dehydration, and the other physical changes attributed to aging can be de-
layed with a properly designed integrated training program and by following the integrated flex-
ibility continuum (1).
Immobilization has varying effects on tissues (Table 4.4). Studies have demonstrated that a mus-
cle\u2019s resting length and its length-tension properties will change if the muscle is immobilized in
a lengthened or shortened position for an extended period of time (28,46\u201353). When a muscle
is immobilized in a shortened position there is a reduction in fiber length (due to a 40% reduc-
tion in sarcomere concentration) and an increase in the proportion of connective tissue
(48,50,51), resulting in reduced tissue extensibility and a loss of joint range of motion that leads
to altered length-tension relationships, force-couple relationships, joint arthrokinematics, and
abnormal movement patterns (19). The reduction in muscle protein occurs quickly at a half-time
of 4 to 6 days (54). Conversely, when muscle is immobilized in a lengthened state, sarcomere
concentration increased by as much as 20% with a corresponding increase in force output despite
being immobilized (28,50,55). Remember that sarcomeres (the contractile element) atrophy at
a faster rate than noncontractile connective tissue.
Effects of Immobilization
1. Altered length-tension relationships
2. Altered force-couple relationships
3. Altered arthrokinematics
4. Altered neuromuscular control
5. Cartilage degeneration
6. Loss of ground substance
Results of Loss of Ground Substance
1. Decreased connective tissue lubrication
2. Decreased connective tissue interfiber distance
3. Decreased nutrient diffusion
4. Decreased mechanical barrier against bacteria
Immobilization also results in cartilage degeneration (56,57). Articular cartilage is highly
specialized connective tissue with high tensile strength (56) and needs stress to stay healthy.
Movement is necessary to remodel tissue along the lines of stress (30,53,58). If appropriate
weight bearing does not occur over the entire surface area of the cartilage, the tissue will weaken
and atrophy (56) while the areas being overstressed will wear away prematurely. 
Immobilization also results in loss of ground substance (Table 4.5) (46,47,57), a connective
tissue matrix that houses tissues and cells (glycosaminoglycans and mucopolysaccharides) that,
in articular cartilage, functions to lubricate the connective tissues, providing a critical interfiber
distance that aids in the diffusion of nutrients while acting as a mechanical barrier against bacte-
ria (46,47,50,57). Immobilization decreases the ground substance, which significantly affects the
normal function of the soft-tissue complex.
Soft-Tissue Biomechanics 
Soft tissue demonstrates several unique properties (Table 4.6) (29,30). Elasticity is the spring-like
behavior of connective tissue that enables the tissue to return to its original shape or size when
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forces are removed (1,29,30). The soft tissue of the human movement system demonstrates an
elastic limit. The elastic limit is the smallest value of stress required to produce permanent strain
in the tissue. Below this elastic limit, the soft tissue returns to its original length when the de-
forming forces are removed. However, the result of applying a force beyond the elastic limit is that
the soft tissue does not return to its original length when the deforming forces are removed. The
unrecoverable or permanent elongation in the soft tissue is called plasticity (1,29,30). When stress
is applied beyond the elastic limit, deformation and force are no longer linearly proportional.
The fluid-like property of connective tissue that allows slow deformation with an imperfect re-
covery after the deforming forces are removed is viscoelasticity (1,29,30,59,60). Recovery is due
to the elastic property of the connective tissue, but a lack of full recovery back to normal length
is due to the viscous property of the connective tissue. The viscosity of the soft tissue is time-de-
pendent (59,60). The faster one tries to move, the greater the resistance to elongation. Proper
warm-up and flexibility training reduces tissue viscosity and consequently improves the extensi-
bility of the soft tissue (61). When subjected to loads for prolonged periods of time, the soft tis-
sue adapts with plastic deformation (22,27,28,49,62).
When soft tissue permanently deforms in response to loading it is said to have undergone plastic
deformation (27,29,30). Consequently, there is no tendency for elastic recoil or recovery. Plasticity
is also referred to as the residual or permanent change in connective tissue length due to tissue elon-
gation (as in flexibility training). Integrated flexibility training increases elongation of the intersti-
tial collagenous interfiber matrix, allowing a plastic deformation of the connective tissue. There
needs to be an increase of approximately 3 to 5% in tissue length to elicit a plastic deformation in
the soft tissue (29,30). Tissue overload and microfailure occur at approximately 6 to 10% of tissue
deformation (29,30). When forces exceed the tissue\u2019s adaptive potential, tissue microfailure occurs
and this microfailure contributes to the development of the cumulative injury cycle (Fig. 4.2).
One aspect of the cumulative injury cycle (30) is the development of proinflammatory com-
pounds, which stimulate nociceptors leading to pain and the development of protective muscle
spasm. The chemical changes also lead to the development of fibrotic adhesions in the soft tissue
within only 3 to 5 days following connective tissue insult. These fibrotic adhesions form a weak
inelastic matrix in the connective tissue bundles, decreasing the normal tissue extensibility. This
results in alterations of the normal-length tension relationships and the development of com-
mon muscle imbalances (19).
The nature of soft-tissue remodeling follows Davis\u2019s Law that states soft tissue models along
the lines of stress; the soft-tissue equivalent of Wolff\u2019s Law for bone. If soft tissue has an inelastic
collagen matrix that forms in a random fashion, then alterations in normal tissue extensibility
can result (30). The Sports Performance Professional must follow the integrated flexibility con-
tinuum to restore the normal extensibility of the entire soft-tissue complex (29,30).
The fluid-like property
of connective tissue that allows