The resting length is a feature of skeletal muscles. The resting length refers to the distance at which muscular contraction is optimized after stimulation in the body. The skeletal muscles and bones are connected through the connective tendon organs. At rest, muscles are not contracted. At this point, the stretching of the muscles refers to the resting length (Winters et al., 2011). Critically, the resting length of the skeletal muscles significantly affects the ability of contraction. In a situation where the resting range is not ideal, the contraction capacity of the muscles cannot be optimized. It is from this perspective that the length-tension relationship can be explored as the impact of the resting fiber length during the contraction of a muscle.
The isometric length-tension curve is essential in explaining the length-tension relationship in muscles. The curve is a reflection of the force generated by a muscle at different lengths. Correspondingly, the power caused by the muscle at different lengths produces different tension levels in various instances that can be plotted as a graph to showcase the relationship (Winters et al., 2014). Critically, the length-tension link depicts that the isometric tension produced by a skeletal muscle is a derivative from the force generated at the myosin and actin filaments. However, it is worth noting that other fundamental variables affect the length-tension relationship at skeletal muscles, such as the type of muscle. The following picture is a depiction of the muscle length-tension relationship:
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Figure 1: Muscle length-tension relationship. Retrieved from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3003754/
Alternative pathways for forming ATP for skeletal muscles
Three distinct pathways can be used for the formation of ATP at the skeletal muscles. The first path is the ATP-CP system. In the path, there is a breakdown of Creatine Phosphate. As a result, there is the production of a phosphate molecule essential during ATP production. It is worth noting that Creatine Phosphate is a limited chemical found in skeletal muscles (Frontera and Ochala, 2015). Distinctively, the limited supply of the chemical bond compound translates to the energy pathway being used for a short period such as a 100m race. Notably, the system does not break down carbohydrates or fats during ATP generation.
The lactic acid system is the second pathway used in ATP generation. Notably, the system is an alternative to the ATP-CP system and does not utilize oxygen. In the process, there are anaerobic reactions that lead to the production of ATP (Frontera and Ochala, 2015). Glucose molecules are derived from the blood and glycogen. Hence, the breakdown of glucose leads to the formation of ATP and pyruvic acid. The system is used just after the end of the ATP-CP system in high-intensity situations such as a race.
The third pathway involves aerobic cellular respiration and is the primary pathway used for ATP production in extended periods. In this pathway, fat and carbohydrate are used as fuel sources (Frontera and Ochala, 2015). The distinct difference in the aerobic cellular respiration pathway is the breakdown of glucose during non-intensive activities to prevent lactic acid build-up. The pathway is ideal for long term activities as it does not lead to immediate ATP production.
Figure 2: ATP-PC System. Retrieved from https://www.pinterest.com/pin/614530311623459017/?lp=true
Figure 3: Lactic Acid System. Retrieved from https://www.pdhpe.net/factors-affecting-performance/how-does-training-affect-performance/energy-systems/lactic-acid-energy-system/
Figure 4: Aerobic Cellular Respiration. Retrieved from https://allinonehighschool.com/aerobic-cellular-respiration/
Compare and contrast the skeletal muscle fiber types
The human muscle fibers are classified based on metabolic types, reaction to neural inputs, and the rate of movement. There are two types of skeletal muscle fibers based on these features, type 1 (slow-twitch) and type 2 (fast-twitch) (Talbot & Maves, 2016). Type 1 fibers use aerobic respiration during muscle contraction and can contract for extended periods (Talbot & Maves, 2016). They are primarily used in endurance activities such as running a marathon and in maintaining posture such as ensuring the head stays upright. The type 1 fiber is located in the red muscles where myoglobin concentration is high to offer a continuous oxygen supply (Talbot & Maves, 2016). ATP in red muscles emerges through oxidative phosphorylation. While glycolysis is faster than oxidative phosphorylation, the latter is efficient, making type 1 muscles resistant to fatigue. Muscle regulation occurs at slow rates for type 1 fiber due to the presence of less sarcoplasmic reticulum that enhances slow calcium release (Talbot & Maves, 2016).
Type 2 fibers obtain energy through glycolysis and contract fast for short periods. Type 2 fibers are in the white muscles with less myoglobin due to the use of anaerobic respiration for power (Talbot & Maves, 2016). Glycolysis is faster but inefficient in ATP production. While type 2 fibers are efficient for short speed bursts than type 1 fibers, they tire quickly due to the creation of lactic acid and the use of the glycogen cycle (Talbot & Maves, 2016).
The two fibers are similar since exercises that focus on the use of specific muscle fiber over other tissues leads to muscle hypertrophy that improves the ability of a person to perform related physical activities. Figure 5 depicts the features of each muscle type while figure 6 demonstrates the location of each muscle type.
Figure 5 Skeletal muscle fiber types ( https://www.just-fly-sports.com/muscle-type-athletic-performance/ )
Figure 5: Slow twitch and fast twitch muscle fibers ( http://histology.med.yale.edu/muscle/muscle_reading.php )
Actions of Vasopressin and Oxytocin
The hypothalamus produces vasopressin and oxytocin within the neurosecretory cells (Baribeau & Anagnostou, 2015). The osmoreceptors in the hypothalamus determine the action of vasopressin as they increase vasopressin secretion after detecting an increase in the osmotic pressure of blood (290 mmol/kg). Vasopressin activity also occurs as a reaction to baroreceptor stimulation. Low blood pressure stimulates increased vasopressin secretion. Upon release, vasopressin acts on the kidney tubule cells for renal collection to activate adenyl cyclase. Adenyl cyclase activates the production of adenosine monophosphate, which then activates intracellular kinases. The kinases cause the kidney’s intracellular water pathways to fuse with the tubule lumen membrane, which enables water from the luminal fluid to flow freely within the cell. The water then moves quickly to the renal medulla’s hyperosmolar extracellular fluid. Vasopressin can also constrict the walls of blood vessels to increase blood pressure when required (Baribeau & Anagnostou, 2015).
Oxytocin is involved in two main activities, which are uterus contraction during birth and lactation. During preterm labor and late pregnancy, progesterone levels decrease while the number of oxytocin receptors raises. The sensitivity of the uterus to oxytocin also increases during this period. Oxytocin then binds to oxytocin receptors on the smooth muscle cells and cause cervix dilation and increase in pain. The reflex increase oxytocin release through the production of prostaglandins, which further increases cervix dilation that leads to parturition.
Oxytocin receptors are also available on myoepithelial cells of the mammary gland. During lactation, the sensitization of the breast nipples through sucking leads to oxytocin release. Oxytocin then causes the alveoli apparatus of the breast to contract, which leads to milk letdown (Baribeau & Anagnostou, 2015)
Figure 7: Vasopressin and oxytocin (red) secretion by the parvocellular neorons (yellow) (Baribeau & Anagnostou, 2015)
Actions of Thyroid Releasing Hormone and Thyroid Stimulating Hormone
Thyroid-stimulating hormone (TSH) modulates the thyroid releasing hormone (TRH). TSH is also the primary stimulator of the synthesis of thyroid hormone. TSH binds to receptors on thyroid epithelial cells to facilitate all the required processes for synthesizing thyroid hormones, which entails thyroglobulin, thyroid peroxidase, and iodide transporter synthesis. The release of TSH is regulated by the hypothalamic-pituitary axis (Pirahanchi, 2019). After being released by the hypothalamus, the TRH stimulates the secretion of TSH through the anterior pituitary’s thyrotrophs. The increase in the level of thyroid hormones in the blood inhibits both TRH and TSH, which causes the thyroid epithelial cells to close (Pirahanchi, 2019). The system starts again when thyroid hormone levels decay and the negative signal fades. TSH stimulates the production of thyroxine, triiodothyronine, and T4 (80 percent), or T3 (20 percent) through the thyroid follicular cells when released. Through de-iodination, T4 can be converted to T3 in which both T4 and T3 act on TSH levels through negative feedback from the anterior pituitary to either decrease TSH levels through increasing their levels or increase TSH through decreasing their levels. TSH levels also determine the endocytosis of colloid rate in which high TSH levels increase the rate of endocytosis, which releases thyroid hormone into the circulation while low TSH levels lead to decreased synthesis and release of thyroid hormone (Pirahanchi, 2019). The primary TSH secretion inhibitor is T3. TSH secretion is also sensitive to minor changes in serum-free T4 through the negative loop. The T4/T3 is linearly related to TSH in which small thyroid hormone changes lead to significant TSH changes. Figure 8 and 9 depict TSH and TRH activity, and the negative feedback loop.
Figure 8: TSH and TRH activity ( http://www.vivo.colostate.edu/hbooks/pathphys/endocrine/thyroid/control.html )
Figure 9: The negative feedback loop ( http://www.vivo.colostate.edu/hbooks/pathphys/endocrine/thyroid/control.html )
Actions of Corticotropin-Releasing Hormone and Adrenocorticotropic hormone
Corticotropin-releasing hormone (CRH) stimulates both the secretion and synthesis of adrenocorticotropic hormone (ACTH) in the anterior pituitary gland’s corticotrophs. After being released from the hypothalamus, CRH stimulates the release of ACTH through the anterior pituitary (Allen, 2019). ACTH stimulates the production of androgens and cortisol through the adrenal cortex by stimulating glucocorticoid secretion like cortisol. High cortisol levels offer a negative feedback system that reduces CRH levels. CRH has one chain consisting of 41 amino acids, and different hormonal and neuronal factors determine its secretion and regulation. CRH is the last part that controls the reaction of the body to different kinds of stress such as internal and external stresses, and emotional and physical stresses (Allen, 2019). The circadian rhythm leads to the secretion of ACTH and affects the secretion of cortisol. Variations in CRH secretion by the hypothalamus and changes in the levels of serum cortisol cause variations in ACTH secretion. A high serum cortisol level inhibits both ACTH and CRH secretion while low serum cortisol levels lead to high levels of both ACTH and CRH. The variations restore the normal levels of cortisol in serum (Allen, 2019).
Excessive CRH secretion causes the number and size of corticotrophs in the pituitary gland to increase. In turn, this leads to the formation of a corticotroph tumor that releases excessive ACTH levels causing the overstimulation of adrenal cortex and abnormal increase of adrenal androgens and cortisol. Excessive cortisol secretion leads to Cushing syndrome that causes muscle and skin atrophy and bone loss. Reducing ACTH secretion leads to low CRH levels, which lead to low levels of adrenocortical (Allen, 2019)
Figure 10: CRH and ACTH action ( http://www.vivo.colostate.edu/hbooks/pathphys/endocrine/hypopit/acth.html )
References
Allen, M. J. (2019, March 3). Physiology, Adrenocorticotropic Hormone (ACTH). Retrieved 25, 2019 from https://www.ncbi.nlm.nih.gov/books/NBK500031/
Baribeau, D. A., & Anagnostou, E. (2015). Oxytocin and vasopressin: linking pituitary neuropeptides and their receptors to social neurocircuits. Frontiers in neuroscience , 9 , 335. doi: 10.3389/fnins.2015.00335
Frontera, W. R., & Ochala, J. (2015). Skeletal muscle: a brief review of structure and function. Calcified tissue international , 96 (3), 183-195. https://doi.org/ 10.1007/s00223-014-9915-y .
Pirahanchi, Y. (2019, April 25). Physiology, Thyroid Stimulating Hormone (TSH). Retrieved 25, 2019 from https://www.ncbi.nlm.nih.gov/books/NBK499850/
Talbot, J., & Maves, L. (2016). Skeletal muscle fiber type: using insights from muscle developmental biology to dissect targets for susceptibility and resistance to muscle disease. Wiley Interdisciplinary Reviews: Developmental Biology , 5 (4), 518-534. doi: 10.1002/wdev.230
Winters, T. M., Takahashi, M., Lieber, R. L., & Ward, S. R. (2011). Whole muscle length-tension relationships are accurately modeled as scaled sarcomeres in rabbit hindlimb muscles. Journal of biomechanics , 44 (1), 109-115. https://doi.org/ 10.1016/j.jbiomech.2010.08.033
