Muscle Fatigue
INTRODUCTION
Muscle fatigue may be defined as the failure of a muscle’s ability to contract and catalyze force. The onset of muscle fatigue may result from intense exertion through oxygen debt. Muscle contraction is very important to human beings. It is by way of muscle contraction that we are able to move. Muscle contraction also fulfills some other important functions in the body, such as posture, joint stability, and heat production. Posture, such as sitting and standing, is maintained as a result of muscle contraction. The skeletal muscles are continually making fine adjustments that hold the body in stationary positions.
Like most functions that occur within the human body, muscle contraction requires energy. The energy to move muscles comes from the molecule ATP (adenosine triphosphate). Energy is released when ATP hydrolyzes to form adenosine diphosphate (ADP) and a phosphate ion (Pi):
Muscles are arranged into motor units, which consist of a nerve and the neuromuscular junctions that connect the nerve to the muscle cells. This organization permits a single nerve cell to fire a signal to all the muscle cells within that unit, resulting in simultaneous contraction of the unit.
A single nerve impulse results in a muscle twitch; the muscle is stimulated and then relaxes quickly before the maximum tension can develop. If the impulses continue in succession, a stronger twitch develops. This cumulative effect results because the muscle does not completely rest between twitches. If the action potential is consistently rendered, without a period of rest for muscle cells, an unbroken muscular contraction develops called a tetanus. In this situation ATP levels are quickly diminished, and muscle fatigue occurs.
Sustained exercise can deplete oxygen levels, resulting in an accumulation of lactic acid. Fatigue may be as a result to the direct effect of heightened lactic acid within muscle.
Lactic acid begins to form once you exceed your anaerobic threshold. Typically, this intensity is 85-90% of your maximum heart rate (MHR). It important to understand how muscles function because without the functioning of muscles we could not exist. Exercise improves lactic acid tolerance by improving oxygen delivery to muscle cells and enhancing performance levels.
The purpose of this lab was to measure the number of times an individual can contract the muscles in their non dominant arm by squeezing a tennis ball firmly before reaching muscle fatigue and tetany. And to compare individual results of the experiment with that of the entire class
HYPOTHESIS
Repeated exertion is one factor that causes muscle fatigue.
There will be a point when an individual’s muscles will no longer be able to continue squeezing the ball with the same force.
The Number of squeezes will decline as time increases
MATERIALS
-Stopwatch
-Tennis ball
PROCEDURE
The experiment group was made of three participants Johanna, Tina and Leonie. Johanna was selected to be the first test subject. The second member, Tina was given the task of time keeping and the third participant Leonie, was responsible for recording the data throughout the experiment. Johanna sat with her elbow resting on the lab table in a similar manner to the arm-wrestling position but with her palm facing down and the ball in her non-dominant hand. When the timekeeper was ready Johanna started squeezing the ball with just enough intensity to contract the muscles of her arm as fast as possible. While she squeezed, Tina alerted the group at 15 seconds intervals for 2 minutes. Leonie then recorded the number of contractions Johanna managed to do during each 15-second period. Johanna took a 1-minute break between trials. The experiment was then repeated for a second and third trial. The roles were interchanged until Leonie and Tina also got a chance to be the test subject.
Results
Table 1: Leonie Smith Trial Data
Trial 1
Trial 2
Trial 3
Time in Seconds
Number of Contractions
Time in Seconds
Number of Contractions
Time in Seconds
Number of Contractions
0-15
37
0-15
35
0-15
39
15-30
39
15-30
36
15-30
37
30-45
38
30-45
35
30-45
40
45-60
39
45-60
35
45-60
34
60-75
36
60-75
36
60-75
38
75-90
37
75-90
34
75-90
36
90-105
36
90-105
35
90-105
36
105-120
35
105-120
34
105-120
35
Table 2: Class Total Trial Data
Trial 1
Trial 2
Trial 3
Time in Seconds
Number of Contractions
Time in Seconds
Number of Contractions
Time in Seconds
Number of Contractions
0-15
26.0625
0-15
27.75
0-15
29.9375
15-30
27.25
15-30
27.4375
15-30
26.875
30-45
26.9375
30-45
26.4375
30-45
27.375
45-60
25.4375
45-60
25.875
45-60
25.50
60-75
25.6875
60-75
26.5
60-75
26.0625
75-90
24.625
75-90
26.875
75-90
26.875
90-105
26
90-105
25.8125
90-105
26.5625
105-120
25.1875
105-120
26.375
105-120
27.125
Table 1 showed the individual trials for Leonie Smith. The number of contractions she managed to do per 15 seconds averaged at 37.125. The highest number of contractions in the first trial was 39 which occurred at both the second (15-30 seconds) and fourth (45-60 seconds) time intervals. The lowest number of contractions in the first trial was 35 which occurred in the eighth (105-120 seconds) and final time slot. For trial number 2 her contractions averaged at 35. The highest number of contractions she managed to do in the second trial was 36 which she did at both intervals 2 (15-30 seconds) and 5 (60-75 seconds). The lowest number of contractions was 34 and took place at time intervals 6 (75 -90 seconds) and 8 (105 -120 seconds). In her third attempt she averaged 36.875. The highest number of contractions she managed to do in the third trial was 40 which she did at interval 3 (30-45 seconds). The lowest number of contractions was 34 and took place at time interval 4 (45-60 seconds).
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Table 2 illustrates an average of all the trials the students completed. The number of contractions done by the class a whole per 15 seconds averaged at 25. 898 in the first trial. The highest number of contractions in the first trial was 27.25 which occurred at the second (15-30 seconds) time interval. The lowest number of contractions in the first trial was 24.625 which occurred in the sixth (75-90 seconds) time slot. In trial number 2 the total contractions averaged at 26.63The highest number of contractions for the class in the second trial was 27.75 which occurred at interval 1 (0-15 seconds) The lowest number of contractions was 25.8125 and took place at time intervals 7 (90-105 seconds). In the third trial the class averaged 27.04. The highest number of contractions in this trial was 29.9375 which occurred at interval 1(0-15 seconds). The lowest number of contractions was 25.50 and took place at time interval 4 (45-60 seconds).
DISCUSSION
The purpose of this lab was firstly to measure the number of times an individual can contract the muscles in their non dominant arm by squeezing a tennis ball firmly before reaching muscle fatigue and tetany. And secondly to compare individual results of the experiment with that of the class.
The probability of error was very high during this lab. There were many varying factors that could skew the results. These factors included varying strengths of persons involved in the experiment as well as the degree to which the effort exerted upon the tennis ball was equal whether in the same trial or otherwise. The degree to which the instructions were followed exactly as given was also a concern. The individual trial for Leonie Smith decreased from 37.125 to 35 in the second trial when compared to first trial. The average number of trials slightly increased from 35 to 36.875 in the third trial when compared to the second trial. These findings did not support the expectation that the number of contractions would steadily decrease over the period of the three trials. These findings may be because the ball may have been squeezed with varying intensity and speed in the different trials as well as the rest time may have caused the muscles to completely reset and recover. The results for the class average showed an increase. An average of 25.89, 26.63 and 27.04 contractions were recorded for trials 1,2 and 3 respectively. Again, maybe the reason for these results which do not support the hypotheses is that persons performed the exercise at varying speed and intensity and rest time perhaps provided a reset of muscle cells.
Continuous exercise can create oxygen debt in muscle cells resulting in an accumulation of lactic acid. Fatigue may attribute to the high levels of lactic acid inside the muscle fibers.
Lactic acid begins to form when anaerobic threshold is surpassed. The anaerobic threshold intensity is usually 85-90% of your maximum heart rate (MHR).
Despite the unexpected results of this experiment there is sufficient evidence to support the hypotheses that repeated exertion is one factor that causes muscle fatigue and further that after repeated exertion there will be a point when an individual’s muscles will no longer be able to continue squeezing the ball with the same force and therefore the number of squeezes will decline as time increases. There are at least two theories which seek to explain why muscles become fatigued. The muscle may simply run out of energy. ATP is the main energy store inside and outside the muscle. However, when tested even very fatigued muscle though diminished have ample stores of ATP in them. This means that it is unlikely that muscles completely run out of energy at any one time. The second theory is that a build up of waste products for example inorganic phosphate or lactic acid which has always been the assumed cause of fatigue. Maybe these waste products impact the release of calcium for the sarcoplasmic reticulum. Scientists are still not able to provide a full explanation as to why muscle fatigue occurs. It could be a combination of all the theories.
References
10.3 Muscle Fiber Contraction and Relaxation – Anatomy and Physiology. (2013, March 6). Retrieved from https://opentextbc.ca/anatomyandphysiology/chapter/10-3-muscle-fiber-contraction-and-relaxation/
Muscle Fatigue: Why do muscles get tired and weak after exercise? (2017, October 20). Retrieved from https://www.youtube.com/watch?v=ZqwGTso2Wmc
Skeletal muscle fatigue ? regulation of excitation’contraction coupling to avoid metabolic catastrophe. (2012, May 1). Retrieved from https://jcs.biologists.org/content/125/9/2105
Wise, E. (2017). Laboratory Manual for Saladin’s Anatomy & Physiology. New York, NY: McGraw-Hill Education.
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