EXERCISE PHYSIOLOGY VERTICAL AND LONG JUMP TESTS
Skeletal muscles in the body require energy in order to work. This energy is present in various forms. There are three major forms of metabolic systems which provide energy for muscle contraction. This includes the aerobic system, the glycogen-lactic acid system, and the phosphagen energy system. In the performance of tasks such as vertical and long jumps, the main form of energy used is the phosphocreatinine-creatinine system (phosphagen).
Phosphocreatinine contains a high-energy phosphate bond which can decompose to creatinine and phosphate ion (Guyton Hall, 2006). Because the amount of ATP in muscle cells is not enough to last for a long time (just between 5 to 6 seconds), the body has to source for alternate sources of ATP that can last continuously, such as the phosphagen system. This system can recycle ADP through the use of its high-energy phosphate bond. With this system, ATP can be produced to last for about 10 to 15 seconds more for muscle activity (Muscle Energetics, 2009).
Power is an important indicator of fitness in several areas including sports physiology. It can determine success in any sport. It can be said or defined as rate at which work is done and can be calculated per unit time. Anaerobic power is defined as the bodys ability to produce ATP in the absence of oxygen for short periods. This experiment tries to evaluate the peak anaerobic power output through the use of two test protocols vertical and long jump tests.
Results
Below are the results for the two experiments, vertical and long jump tests.
1. Vertical jump
Age 32 Gender Male Height 58 Weight 160
Vertical jump height 26.8inches
Vertical jump height (cm) 26.8 x 2.54 68.072
Using the equation below
PAP (Watts) (60.7 VJ cm) (45.3 BM kg) 20556.12
Where PAP Peak anaerobic power, VJ vertical jump height, and BM body mass
The average peak power output measured with this vertical jump protocol averages 4620.2 (SD_822.5) W for males and 2993.7
2. Long jump test
Age 32 Gender Male Height 58 Weight 160
Trial 1 84 inches (213.36 cm)
Trial 2 84 inches (213.36 cm)
Trial 3 90 inches (228.6 cm)
Average 218.44cm
Discussion
The experiment which yielded the above results has fulfilled the criterion for measuring muscle power. It has employed a quantitative formulation which is consistent with the correct definition of power, that is, the rate at which work is done.
Comparing the results of the long jump with normal results as given by Top End Sports, the average of the three results, that is, 218.44 centimeters falls below average (Wilson, 2009). According to this normative data shown in Table 1, an average should be between 221 and 230 centimeters. A very good result starts from 241 centimeters.
Also, using the normative results derived from tests (Table 2) conducted with world class athletes, an average male adult (20 years and above) would have an average vertical jump height of 55cm (Sargent Jump Test, 2010). This implies that the result of the subject in this experiment is above average. The result can be said to be excellent.
Both results are indicative of the peak anaerobic power output. They imply that the anaerobic capacity is above average and that phosphagen energy system needed for short energy explosive bursts is functioning correctly.
Directive Questions
Motor signals are transmitted directly from the cortex to the spinal cord through the corticospinal tract and indirectly through multiple accessory pathways that involve the basal ganglia, cerebellum, and various nuclei of the brainstem (Guyton Hall, 2006). The motor cortex is itself divided into the premotor area, the primary motor cortex and the supplementary motor area.
When commands are received by the fibers of the spinal cord, they are relayed through anterior motor neurons in the anterior horns of the gray matter of the spinal cord. The anterior motor neurons give rise to the nerve fibers that eventually innervate skeletal muscles. Each of these nerve fibers has endings on the skeletal muscle fibers. Most of these nerve fibers are large and myelinated. A junction exists between each nerve fiber and the muscle called the neuromuscular junction. When a nerve impulse is sent to the neuromuscular junction, there is the release of a neurotransmitter, acetylcholine, which stimulates the acetylcholine-gated ion channels on the postsynaptic membrane (skeletal muscle) to open, allowing the passage of the important positive ions sodium, potassium and calcium. The influx of large amounts of sodium ions into the interior of the muscle fiber creates a local positive potential charge within the fiber (end-plate potential). This then initiates an action potential that spreads all over the muscle, causing contraction.
The sliding filament theory of muscular contraction is initiated by the spread of the action potential through the muscle. The actin filaments slide inward among the myosin filaments as a result of forces generated by the interaction of the cross-bridges formed by the myosin filaments with the actin filaments (Guyton Hall, 2006). Also, there is the release of large amounts of calcium ions which also induce the forces between the actin and myosin filaments, causing contraction. The source of energy for this process is from high-energy bonds within the ATP molecule which is broken down to ADP, liberating the energy possessed within.
It has been discovered that following exercise, the muscles become sore. Several hypotheses have been propounded as regards the cause of muscle soreness immediately following an exercise, especially that featuring resistance training. One major hypothesis has linked the production of lactic acid to muscle soreness. During high intensity exercise, the muscles get energy from the phosphagen system for maximum short bursts of power. In this system, stored glycogen in the muscle is split in to glucose, and glucose is metabolized by the exercising muscles. As a result of anaerobic metabolism, large amounts of lactic acid are produced which then diffuses out of the muscle cells into the interstitial fluid and blood. It is then assumed that lactic acid stimulates the pain receptors in the muscle, causing pain, and ultimately causes fatigue (Guyton Hall, 2006).
The major form of exercise that causes muscle soreness is that involving eccentric muscular contraction. Examples include push ups, shoulder press, bench press, etc. During exercise, there is disruption of the microarchitecture of the myofibrils. This is due to active stretching and lengthening of the myofibrils during eccentric muscular contraction. It is this muscle damage that causes the delayed onset muscle soreness (DOMS). In most situations, DOMS does not appear until about eight hours after the exercise and peaks in 24-48 hours. Inflammation and tissue repair causes the physical signs of this condition. There is tenderness, swelling, reduced function, and tremor.
Muscle damage causes the elaboration of some agents which can be used as markers in the study of delayed onset muscle soreness. These markers include creatinine kinase, myoglobin, fibrinogen, albumin, and some electrolytes such as potassium. These agents are normally sequestered within the muscle cells, but as a result of membrane damage, they are released into the bloodstream. In most cases, the elaboration of these substances in the bloodstream is reversible, but in extreme situations can cause medical complications such as rhabdomyolysis. In rhabdomyolysis, accumulation of muscle proteins in the kidneys predispose to renal failure, and also to cardiac arrhythmias.
The sarcoplasmic reticulum is a membrane-bound organelle that surrounds the myofibrils of each muscle fiber. It is important in the organization of muscle contraction.
The current DOMS model ascribes that muscle soreness appears about one to two days after performance of the heavy exercise and peaks 2448 hours after the exercise. According to Clarkson Hubal (2002), the degree of soreness differs from one type of exercise to another, roughly depending on the amount of damage induced. For example, exercises that do not produce profound muscle damage, such as downhill running or isokinetic eccentric knee extension, produce soreness values of about 4 or 5 on a scale of 1 (no soreness) to 10 (very sore), whereas maximal eccentric contractions of the elbow flexors produce soreness values of about 78. The end results include a dull ache which is usually combined with muscular tenderness, stiffness and weakness. The current model explains that DOMS is caused by structural muscular damage resulting from eccentric contractions. It also concludes that the damage resulting from eccentric contractions due to a mechanical insult and not related to metabolic fatigue. This has been attributed to the fact that, as muscle lengthens, the ability to generate tension increases and a higher load is distributed among the same number of fibers, resulting in a higher load per fiber ratio (Clarkson Hubal, 2002). However, another major factor has been pointed to as a promoter of the muscle damage. Inflammation is known to be responsible for the continued damage, and is also responsible for consequent regeneration and repair.
Appendix
Table 1. Normal standing long jump results. Source Wilson, G. (2009)
RatingsMales (cm)Females (cm)Excellent250200Very good241 250191 200Above average231 240181 190Average221 230171 180Below average211 220161 170Poor191 210141 160Very poor191141
Table 2. Normal vertical jump test results. Source Sargent Jump Test, 2010
RatingMales (inches)Males (cm)Females (inches)Females (cm)Excellent 28 70 24 60Very good24 2861 7020 2451 60Above average20 2451 6016 2041 50Average16 2041 5012 1631 40Below average12 1631 408 1221 30Poor8 1221 304 811 20Very poor 8 21 4 11
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