Bone is composed of organic proteins, matrix, and cells. The
organic component of bone is 90% collagen type I and provides
the tensile strength. The mineral phase of bone matrix accounts
for 50% of the volume and 65% of the weight of
bone and is composed of highly structured hydroxyapatite crystals
and amorphous calcium phosphates. Bone cells account for only 3% of bone
volume and include osteoblasts, osteoclasts, and osteocytes. Bone
remodeling is ongoing throughout life and occurs predominantly at
the trabecular part of the skeleton. Wolff’s law of adaptation
states that mechanical remodeling of bone occurs in response to
deforming strain. Both osteoblasts (responsible for erosion of existing
bone) and osteoclasts (responsible for repair and remodeling of
erosions) are involved. The exact mechanism of how mechanical strain
activates osteocytes to initiate remodeling is still unknown, but
both chemical messengers (dependent on the prostaglandins PGI2 and
PGE2, IGF-1, and parathyroid hormone) and piezoelectric
effects are believed to be involved.1
High levels of physical activity and stress loading in athletes
increase bone density. The degree of increase in bone density is
proportional to the level of stress loading accomplished in the
athletic activity. For example, the bone mineral density (BMD) of
the distal femur is found to be highest in world-class weightlifters
followed by throwers, runners, soccer players, and then swimmers. This
positive effect on BMD from mechanical loading is also observed
in young women skaters and may counter the adverse estrogen-deficient
effects on bone density seen in woman who are thin and amenorrheic.
Studies on both the elderly and young confirm that strength training
at higher loads increases BMD more when compared with endurance
training at low weights with high repetitions.2
Diarthrodial or synovial joints are capable of large degrees
of motion and, under normal circumstances, tolerate high levels
of friction, shear, and wear with little deterioration throughout
a normal life span. A typical knee or hip joint may withstand loads
up to six times body weight on a repetitive basis for up to a million
times a year.3 Synovial fluid and soft connective
tissue are common to all diarthrodial joints. The soft connective
tissue includes the articular cartilage, joint capsule, meniscal
cartilage, and ligaments. The primary load-bearing structure of
the joint is the articular cartilage. Cartilage is primarily made
up of type II collagen with up to 150 proteoglycan (PG) monomers
linked to a central core of hyaluronic acid (Fig. 43-1). The link
between PG and hyaluronic acid is essential for the structural integrity
of cartilage. These macromolecules are highly hydrophylic, but,
because they are confined in the semirigid collagen matrix, reach
only 20% of their theoretical swell volume. The swelling
pressure caused by the embedded PG is resisted by the tension that
develops in the collagen matrix, and it is this balance of forces
that is essential for modulating the compressibility of the structure
under various loads.
(A) Schematic depiction of the molecular arrangement of
the PG monomer. (B) The PG aggregates along a hyaluronate chain.
(From Zimmerman JR, et al. In: Downey JA, Myers SJ, et al, eds.
The Physiological Basis of Rehabilitation Medicine. 2nd ed. Boston,
Mass: Butterworth-Heinemann, 1994.)
Immobilization of a joint for prolonged periods causes significant
loss of PGs in the cartilage, which in turn causes a loss of resistance
to compression. In the recovery process after injury, both joint
range of motion and stress loading is necessary to reverse the above
Tendons and ligaments are made up of highly organized collagen
fibers (predominantly type I) arranged in a linear fashion. Tendons
transmit the force generated by muscle actions to bones and generate
movement about a joint. Ligaments are capsular if they extend off
of the joint capsule, or accessory when extending between bones.
In contrast to tendons, ligaments prevent excessive movement and
contribute to joint stability. Both tendons and ligaments are made
up of collagen fascicles that spiral on each other with successive
folds or crimps that permit stretch and buffer elongation. The blood
supply to tendons and ligaments is sparse when compared with joints,
muscle, and bone. For example, avascular regions are found in the
central region of the anterior cruciate ligament of the knee and
the supraspinatus tendon of the shoulder.
Tendons are often surrounded by synovial sheaths when there is
a significant pulley action present (e.g., the digit flexor tendons
of the hand). At the junction with the bone, or enthesis, small
synovial bursa are often present to prevent friction (e.g., greater
trochanter bursa, retrocalcaneal bursa, and subacromial bursa).
Golgi and Pancinian organs lie at the myotendinous junction and
transmit information to the central nervous system about muscle
tension and pressure. Tendons demonstrate nonlinear deformation
in response to stress. In the first phase, collagen fibers straighten
and elastic fibers elongate. The second phase requires much greater
force, and is characterized by breaking of collagen cross-links
and disruption of smaller collagen fibers. Finally, increased forces
will result in tendon rupture and failure occurs when a tendon is
stretched 5% to 8% beyond its resting length (Fig.
Load-deformation (strain) curve for ligaments and tendons.
The “toe” region of the curve is within the normal
physiologic range. Greater than 4% strain causes tissue
damage. (From Oakes BW. Tendon/ligament basic science.
In: Harries M, Williams C, et al. Oxford Textbook of Sports Medicine.
2nd ed. Oxford, England: Oxford University Press, 1998.)
Changes in activity significantly affect tendons and ligaments.
Physical training increases the weight and size of tendons and ligaments
and increases the cross-links between collagen fibers. Immobilization
decreases these cross-links and thus diminishes the tensile strength.
Skeletal muscle makes up approximately 40% to 45% of
the total body weight. There are two major types of muscle fibers
(type I and II), which were originally identified with basic histochemical
staining techniques (Fig. 43-3). These staining differences correlate
with underlying differences in structural, contractile, and biochemical
properties. Subtypes of type I and II have been characterized as
well, and Table 43-1 summarizes the differences among fiber types.
Photomicrograph of vastus lateralis from a 21-year-old
man stained for ATPase at pH 4.6 showing type I, type IIA, and type
IIB fibers. (From Lieberman JS, et al. Skeletal muscle: structure, chemistry,
and function. In: Downey JA, Myers SJ, et al, eds. The Physiological
Basis of Rehabilitation Medicine. 2nd ed. Boston, Mass: Butterworth-Heinemann,
Table 43-1 Muscle Fiber
Type Classification ||Download (.pdf)
Table 43-1 Muscle Fiber
|Type I||Type IIA||Type IIB|
The response of muscle to changes in levels of physical activity
can be profound. There are two basic forms of muscle actions: static
(or isometric), in which there is no joint movement, and dynamic
in which there is a change in the length of the muscle and joint
movement occurs. Dynamic actions can be further divided into concentric,
in which the muscle shortens during the increased load (triceps
in a shotput hurl), and eccentric, in which the muscle lengthens
during the increased load (quadriceps when landing from a jump).
Eccentric actions have lower energy requirements but carry an increased
risk of muscle damage and tearing due to higher forces.
Increases in muscle mass with resistance training are primarily
brought about by type II fiber hypertrophy (with a contribution
from type I hypertrophy) rather than by muscle fiber proliferation.
It has been found in animal models that repetitive stretching of
muscle fibers alone is sufficient to cause massive increases in
gene expression of contractile proteins causing muscle hypertrophy.
The resistance to fatigue that develops with endurance training
results from a number of factors including increases in capillary
supply and mitochondrial content (i.e., increase in oxidative capacity)
of the muscle fibers and metabolic adaptations favoring fat metabolism
and glycogen sparing. It is still a contested question whether transformation
of fiber types contributes to the adaptation of muscle to various
training stimuli. The predominance of type I fibers in distance
runners probably results from genetic influences, environmental
factors such as training, and the interaction between the two. Some
studies have shown changes in type IIB to type I with high-intensity
interval training, but others did not show such changes or have
only shown a shift from type IIB to type IIA with endurance training.
In disuse atrophy, the reduction of muscle bulk can be profound,
with up to 30% reduction in cross-sectional area after
1 month of immobilization. Both type I and II fibers are reduced
in size to varying degrees depending on the individual.4
Aging alone has been thought to lead to the loss of muscle mass
and strength. There is a loss of both cross-sectional area and total
number of muscle fibers with age, predominantly affecting type II.
This loss in muscle mass coincides with loss of bone density. However,
recent studies have supported that many of the changes seen are
not inevitable but are the result of decreased activity. The positive
training effects seen on muscles in the young also occur in the
elderly. Even in the 10th decade of life, an elderly person can
make significant increases in muscle mass and strength if given
a progressive resistance-training program. Similar positive changes
in muscle respiratory capacity seen in the young can occur with
endurance training in the elderly.5
Finally, the central nervous system also changes with training.
This is evidenced by the marked improvement in performance that
can occur with training in a specific activity over time, with much
less dramatic changes in peripheral muscle strength. For example,
during a 12-week period of training that included lifting boxes
from the floor to the waist by knee extension, a 200% increase
in weight was achieved with only a 15% increase in absolute
isometric strength of the quadriceps muscle group. Also, the untrained
contralateral limb will show an improvement in performance when
the ipsilateral limb is repetitively trained, suggesting that the
central mechanism plays a role. These changes are felt to result
from neural adaptations including synchronization of motor units
in the trained activity with a more advantageous balance of agonist
versus antagonist muscle activation.2