IV. Maximum isometric tetanic tension is produced at the optimal
sarcomere length L
. Stretching a ﬁ ber beyond its optimal
length or decreasing the ﬁ ber length below L
V. The velocity of muscle ﬁ ber shortening decreases with increases
in load. Maximum velocity occurs at zero load.
Skeletal Muscle Energy Metabolism
I. Muscle ﬁ bers form ATP by the transfer of phosphate from
creatine phosphate to ADP, by oxidative phosphorylation of
ADP in mitochondria, and by substrate-level phosphorylation
of ADP in the glycolytic pathway.
II. At the beginning of exercise, muscle glycogen is the major
fuel consumed. As the exercise proceeds, glucose and fatty
acids from the blood provide most of the fuel, and fatty acids
become progressively more important during prolonged
exercise. When the intensity of exercise exceeds about 70
percent of maximum, glycolysis begins to contribute an
increasing fraction of the total ATP generated.
III. A variety of factors cause muscle fatigue, including internal
changes in acidity, cross-bridge inhibition, glycogen
depletion, and excitation-contraction coupling failure, but
not a lack of ATP.
Types of Skeletal Muscle Fibers
I. Three types of skeletal muscle ﬁ bers can be distinguished
by their maximal shortening velocities and the predominate
pathway they use to form ATP: slow-oxidative, fast-oxidative-
glycolytic, and fast-glycolytic ﬁ bers.
a. Differences in maximal shortening velocities are due
to different myosin enzymes with high or low ATPase
activities, giving rise to fast and slow ﬁ bers.
b. Fast-glycolytic ﬁ bers have a larger average diameter than
oxidative ﬁ bers and therefore produce greater tension, but
they also fatigue more rapidly.
II. All the muscle ﬁ bers in a single motor unit belong to the same
ﬁ ber type, and most muscles contain all three types.
III. Table 9–3 summarizes the characteristics of the three types of
skeletal muscle ﬁ bers.
I. The tension produced by whole-muscle contraction depends on
the amount of tension each ﬁ ber develops and the number of
active ﬁ bers in the muscle (Table 9–4).
II. Muscles that produce delicate movements have a small number
of ﬁ bers per motor unit, whereas large powerful muscles have
much larger motor units.
III. Fast-glycolytic motor units not only have large-diameter ﬁ bers
but also tend to have large numbers of ﬁ bers per motor unit.
IV. Increases in muscle tension are controlled primarily by
increasing the number of active motor units in a muscle, a
process known as recruitment. Slow-oxidative motor units are
recruited ﬁ rst during weak contractions, then fast-oxidative-
glycolytic motor units, and ﬁ nally fast-glycolytic motor units
during very strong contractions.
V. Increasing motor-unit recruitment increases the velocity at
which a muscle will move a given load.
VI. Exercise can alter a muscle’s strength and susceptibility to
a. Long-duration, low-intensity exercise increases a ﬁ ber’s
capacity for oxidative ATP production by increasing the
number of mitochondria and blood vessels in the muscle,
resulting in increased endurance.
b. Short-duration, high-intensity exercise increases ﬁ ber
diameter as a result of increased synthesis of actin and
myosin, resulting in increased strength.
VII. Movement around a joint requires two antagonistic groups
of muscles: one ﬂ exes the limb at the joint and the other
extends the limb.
VIII. The lever system of muscles and bones requires muscle
tension far greater than the load in order to sustain a load
in an isometric contraction, but the lever system produces a
shortening velocity at the end of the lever arm that is greater
than the muscle-shortening velocity.
Additional Clinical Examples
I. Muscle cramps are involuntary tetanic contractions occurring
when overexercise and dehydration cause electrolyte
imbalances in the ﬂ uid surrounding muscle and nerve ﬁ bers.
II. When extracellular calcium falls below normal, sodium
channels of nerve and muscle open spontaneously, which
causes the excessive muscle contractions of hypocalcemic
III. Muscular dystrophies, the most commonly occurring genetic
disorders, result from defects of a muscle membrane-stabilizing
protein known as dystrophin. Muscles of individuals with this
condition progressively degenerate with use.
IV. Myasthenia gravis is an autoimmune disorder in which
destruction of ACh receptors of the motor end plate causes
progressive loss of the ability to activate skeletal muscles.
SECTION A KEY TERMS
central command fatigue
end-plate potential (EPP)
fast ﬁ ber
fast-glycolytic ﬁ ber
glycolytic ﬁ ber