When a muscle is stimulated, do all motor units fire? Why, or why not?
Not all motor units fire when a muscle is activated. This is because in the reflex, not all motor units are activated (Brown et al, 2006).
1b). Explain how the force of contraction changes with recruitment.
The force of contraction depends on the activation of muscle fibers. When more motor fibers are recruited, a greater contraction force results (Zatsiorsky & Kraemer, 2006). The stimulation of the smallest muscles such as the slow twitch fibers result from the recruitment of the smallest motor nerves which, occurs first (Zatsiorsky & Kraemer, 2006).
1c). with continues recruitment, is there a point at which there is no further increase in force? If so, when is there no further increase in the amount of force the muscle generates? Why?
Yes, the muscle reaches a state when there is no more increase in force. The transmission of neural signal frequency causes muscle contraction and when it levels off once it generates maximum contraction. When the muscles reach the physiological limit, there will be no further increase in force.
2a). what is active force? If you were to increase voltage to a muscle, what do you think would happen to active force? What would happen to active force as you decrease the voltage? Why?
Active force refers to the force which eliminates the negative effects of stretching processes. Increasing the voltage beyond the threshold, the force in the whole muscle increases increasing the active force (Kimura, 2001). Decreasing the voltage decreases the active force because the stimulus voltage is reduced.
2b). If you were to increase the rate of stimulation to a muscle, what would happen to active force? What if you decreased stimulation? Explain why.
Increasing the rate of stimulation increases the rate of active force. Increasing the stimulation decreases the active force (Brinckmann, Frobin & Leivseth, 2002). When the voltage rises, and is distributed to the entire muscle, more fibers get activated and results into total force generated by the muscles to increase. Decreasing stimulation results in decreasing the active force (Brinckmann, Frobin & Leivseth, 2002).
in the human body, what is the equivalent to voltage? How does it vary during muscle contraction?
Adenosine triphosphate (ATP) is the same as voltage in human body. ATP is broken down during muscle contraction.
What is the human body’s equivalent to rate of stimulation? How does it vary during muscle contraction?
Action potential in the human body is equivalent to stimulation. Its intensity increases during muscle contraction (MacIntosh, Gardiner & McComas, 2006).
2e). Putting it all together, what two things does the human body adjust to maintain a smooth contraction as the weight it bears varies?
Ion balance and ATP.
3a) what specific event(s) is (are) occurring within the muscle during the lag, or latent, period? Include all events. Be specific!
Lag phase:
Action potential is initiated to the motor neuron’s presynatic terminal causing an increase in the permeability of the presynaptic terminal. Calcium ions move to the presynaptic terminal resulting into the release of acetylcholine in the synaptic cleft and binds to acetylcholine receptor molecules after diffusing across the membrane. This leads to opening of the ligand-gated Na+ leading to an increased permeability of postsynaptic membrane allowing the sodium ions to flow into the muscle fiber (Behrens & Beinert, 2014). When the polarization surpasses the threshold it leads to the action potential. The acetylcholine is degraded faster to its constituents reducing its binding time to the receptor. The action potential created in the muscle fiber is transmitted to the T tubules. The Ca+ channels of the sarcoplasmic reticulum membrane gets open due to the increased permeability. The ions then move to the sarcoplasm and eventually bind the troponin (Behrens & Beinert, 2014).
Latent phase:
The acetylcholine is released in the action potential and upon reaching the neuromuscular junction the neuron releases the acetylcholine that moves across the synaptic cleft. The action potential is released in the motor end plate and the entire T tubules before moving throughout the tubules (Behrens & Beinert, 2014). The sarcoplasmic reticulum secretes Ca 2+ due to the action potential. The Ca 2+ released then bind to troponin constituents on the actin helix triggering the tropomyosin molecules to uncover binding locations for myosin cross‐bridge creation. Then the muscle contraction begins if the energy is available (Behrens & Beinert, 2014).
4a) how does active force change when shortening a muscle from its optimum length?
What about when lengthening past optimum length? Why does this happen?
The active force increases when shortening the muscle from its actual size and decreases when lengthening the muscle past its optimal length (Behrens & Beinert, 2014). This is because the muscle will tend to maintain their resting length and resist the stretching because the elastic proteins such as titin that provides the passive resting force (Behrens & Beinert, 2014).
4b). what is passive force? How does passive force change with shortening and lengthening a muscle away from optimum length? Why does this occur?
Passive force is a form of force stretching whereby an external force is applied upon the limb so As to move it to a different position (Millis, 2012). The passive force decreases when shortening the muscle from its optimal size and increases when lengthening the muscle past its optimal length. This is because the muscle will tend to maintain their normal length and resist the stretching due to the elastic proteins which provide the resting force (Millis, 2012).
4c. Define total force, and explain how it is determined. How would total force change when shortening and lengthening a muscle?
Total force is the combination of both the passive and active forces of the muscles at any length. Total force is changed by starting resting length. Lengthening the muscles increase the total force whilst shortening the muscle decreases the total force (Feher, 2012).
References
Behrens, B., & Beinert, H. (2014). Physical Agents: Theory and Practice. Philadelphia: F.A. Davis Company.
Brinckmann, P., Frobin, W., & Leivseth, G. (2002). Musculoskeletal biomechanics. (959669620.) Stuttgart: Thieme.
Brown, S. P., Miller, W. C., & Eason, J. M. (2006). Exercise physiology: Basis of human movement in health and disease. Philadelphia: Lippincott Williams & Wilkins.
Feher, J. J. (2012). Quantitative human physiology: An introduction. New York: McGraw Hill
Kimura, J. (2001). Electrodiagnosis in Diseases of Nerve and Muscle: Principles and Practice. New York: Oxford University Press.
MacIntosh, B. R., Gardiner, P. F., & McComas, A. J. (2006). Skeletal muscle: Form and function. Champaign, Ill: Human Kinetics.
Millis, D. L., & Levine, D. (2012). Canine rehabilitation & physical therapy. Philadelphia, Pa: Saunders.
Zatsiorsky, V. M., & Kraemer, W. J. (2006). Science and practice of strength training. Champaign, IL: Human Kinetics.
