load in a constant position or attempts to move an otherwise
supported load that is greater than the tension developed by
the muscle. A contraction in which the muscle changes length,
while the load on the muscle remains constant, is
Depending on the relative magnitudes of muscle tension
and the opposing load, isotonic contractions can be associated
with either shortening or lengthening of a muscle. When ten-
sion exceeds the load, shortening occurs and it is referred to as
On the other hand, if an unsupported
load is greater than the tension generated by cross-bridges, the
result is a
In this situation, the load pulls the muscle to a longer length in
spite of the opposing force produced by the cross-bridges. Such
lengthening contractions occur when an object being supported
by muscle contraction is lowered, as when the knee extensors in
your thighs are used to lower you to a seat from a standing posi-
tion. It must be emphasized that in these situations the length-
ening of muscle ﬁ
bers is not an active process produced by the
contractile proteins, but a consequence of the external forces
being applied to the muscle. In the absence of external lengthen-
ing forces, a ﬁ
ber will only
when stimulated; it will never
lengthen. All three types of contractions—isometric, concentric,
eccentric —occur in the natural course of everyday activities.
During each type of contraction, the cross-bridges
repeatedly go through the four steps of the cross-bridge cycle
illustrated in Figure 9–8. During step 2 of a concentric iso-
tonic contraction, the cross-bridges bound to actin rotate
through their power stroke, causing shortening of the sar-
comeres. In contrast, during an isometric contraction, the
Sequence of Events Between a Motor Neuron Action Potential and Skeletal Muscle Fiber Contraction
1. Action potential is initiated and propagates to motor neuron axon terminals.
2. Calcium enters axon terminals through voltage-gated calcium channels.
3. Calcium entry triggers release of ACh from axon terminals.
4. ACh diffuses from axon terminals to motor end plate in muscle ﬁ ber.
5. ACh binds to nicotinic receptors on motor end plate, increasing their permeability to Na
6. More Na
moves into the ﬁ ber at the motor end plate than K
moves out, depolarizing the membrane and producing the end plate
7. Local currents depolarize the adjacent muscle cell plasma membrane to its threshold potential, generating an action potential that
propagates over the muscle ﬁ ber surface and into the ﬁ ber along the T-tubules.
8. Action potential in T-tubules induces DHP receptors to pull open ryanodine receptor channels, allowing release of Ca
sacs of sarcoplasmic reticulum.
binds to troponin on the thin ﬁ laments, causing tropomyosin to move away from its blocking position, thereby uncovering
cross-bridge binding sites on actin.
10. Energized myosin cross-bridges on the thick ﬁ laments bind to actin:
A + M · ADP · P
A · M · ADP · P
11. Cross-bridge binding triggers release of ATP hydrolysis products from myosin, producing an angular movement of each cross-bridge:
A · M · ADP · P
A · M + ADP + P
12. ATP binds to myosin, breaking linkage between actin and myosin and thereby allowing cross-bridges to dissociate from actin:
A · M + ATP
A + M · ATP
13. ATP bound to myosin is split, energizing the myosin cross-bridge:
M · ATP
M · ADP · P
14. Cross-bridges repeat steps 10 to 13, producing movement (sliding) of thin ﬁ laments past thick ﬁ laments. Cycles of cross-bridge
movement continue as long as Ca
remains bound to troponin.
15. Cytosolic Ca
concentration decreases as Ca
-ATPase actively transports Ca
into sarcoplasmic reticulum.
16. Removal of Ca
from troponin restores blocking action of tropomyosin, the cross-bridge cycle ceases, and the muscle ﬁ ber relaxes.