The action potential produced at the end-plate (as a result of neuromuscular transmission) travels along the length of the muscle fibre (in both directions) with a conduction velocity of 1 to 5 m/sec. The mechanisms by which this muscle action potential triggers contraction of the muscle fibre is known as excitation-contraction coupling and involves a number of distinct steps:
A. The action potential travelling along the muscle fibre meets the T-tubules and flows down the T-tubules into the middle of the muscle fibre.
B. The presence of the action potential within the T-tubules triggers the opening of voltage-gated Ca2+ channels in the walls of the sarcoplasmic reticulum.
C. The opening of Ca2+ channels in the sarcoplasmic reticulum enables Ca2+ to run down its concentration gradient into the sarcoplasm and causes the sarcoplasmic Ca2+ concentration to increase from its resting level of 10-7M to around 10-4M.
D. The dramatic increase in sarcoplasm Ca2+ concentration triggers the molecular processes which cause the myofibril to shorten.
E. The myofibrils shorten virtually simultaneously which results in the contraction of the whole muscle fibre.
F. When action potentials stop flowing down the T-tubules, a calcium pump in the membrane of the sarcoplasmic reticulum pumps calcium out of the sarcoplasm and back into the sarcoplsmic reticulum.
G. The Ca2+ concentration within the sarcoplasmic reticulum then returns to resting levels, and myofibrils return to their normal length.
H. The muscle fibre relaxes.
The temoral relationship between the events outlined above is illustrated in the diagram opposite. This shows the results of an experiment performed on a single isolated skeletal muscle fibre in which the muscle fibre action potential (blue) is recorded at the same time as the tension is measured (orange) and the sarcoplasmic Ca2+ concentration monitored (purple) using technique known as calcium imaging.
As you can see, there is a significant delay between the end of the action potential and the beginning of the contraction of the muscle fibre (as indicated by the increase in tension).
This delay reflects the time required for the Ca2+ channels to open, the Ca2+ to enter the sarcoplasm, and the molecular events which lead to myofibril shortening to be initiated. All this adds up to a significant delay between the action potential and the peak force being generated.
One initiated, the mechanical activity within the muscle fibre may last 100 ms or more. Similarly, there is a gradual decline in tension after the peak as the Ca2+ is pumped out of the sarcoplasm, and the myofibrils return to their resting length.