Current concepts of tendinopathy – what are the theories looking at the histology of tendon pathology? Is there an element of inflammation? What happens to the tendon? Do you support the theories? Use evidence to support the histological underpinning of tendonopathy.
Satellite cells are important structures. What effects do they have on tissue hypertrophy, atrophy and aging? Can they be influenced to improve outcomes for hypertrophy, atrophy and age related changes? Use evidence to support your opinion.
Each subject 250 words and 3 sources each .
HEALTH SCIENCES AND NURSING
Tendinopathy usually occurs in sports an in the numerous occupational sectors as well that entail repetitive activity. The human body comprises of around 600 muscle-tendon units. Any tendon in the body can undergo Tendinopathy based on the stress concentration at its insertion. Studies suggest that Tendinopathy tends to arise in the places where there is an increment of a constant volume of load (Rees et al. 2006). (Rees et al. 2006). Other variables that promote Tendinopathy include increased weight, exercise, hereditary factors and progressing in age. When a patient shows tendon discomfort, certain processes determine the occurrences of the pain (Rees et al. 2014). (Rees et al. 2014). The mechanism is analyzed to determine the tissue overload. The etiological hypotheses that determine the mechanisms include vascular, mechanical and neurological ideas.
The mechanical hypothesis determines eventual failure and tendon fatigue owing to repeated loading that that generates physiological stress to the tendon. The neural theory states that excessive stimulation on the nerve ends produces neuronal homeostasis consequently harmful alterations in the tendon matrix (Paavola et al. 2012). (Paavola et al. 2012). The vascular theory maintains that tendons are active tissues that require a blood supply. Affected tendons due to Tendinopathy can encounter insufficient vascular supply with diminished blood perfusion. Chronic tendon problems such as tendinitis cause chronic discomfort and inflammation. Tendonitis creates enlarged tendon nodes with reduced performances. However, during surgical biopsies, the tendons lack inflammatory cells, but in clinical situations, the tendons are characterized by discomfort, poor function, and inflammation.
Satellite cells are activated when single muscle fibers activate. However, the population of the cells can be heterogeneous which impacts the potential of its activation. Mechanically stretching the injured fiber induces a growth factor of the hepatocyte which binds on the satellite cells. The cells convert into fibrogenic lineage from myogenic lineage. In hypertrophy, satellite cells are important for hypertrophic development, muscle repair, and growth. Studies (Schultz et al. 2012) done shows that during muscle growth models the muscle stem cells get activated hence cell activation is a key necessity for muscle hypertrophy. When the skeletal muscle was irradiated, and all satellites cells killed hypertrophic overload was prevented altogether. However, a recent study indicated that satellite cells are not so crucial in muscle hypertrophy. Satellite cells greatly contribute to the creation of new fiber muscles (Snow 2014). (Snow 2014). The cells have chemotactic characteristics that allow the cells to migrate within a fiber thereby regenerating new tissues. The satellite cells begin the process during a mitotic phase that multi generates satellite cells which travel to the cytosol and plasma membrane before aligning and fusing into a myonuclear that develops a muscle fiber. During muscle atrophy, the satellite cells undergo apoptosis which causes a myonuclear loss in the atrophying muscle. Atrophy contrasts the muscular growth process in which the muscle cells undergo union with myofibers and proliferation (Goldberg et al. 2015). (Goldberg et al. 2015). Satellite cells can be produced to improve aging, atrophy, and hypotrophy through toxin induction that retains the regeneration capacity while creating effective muscle tissue repair. Reduction in the number of satellite cells severely impairs the regenerative capacities of the skeletal muscle, notably following injuries or age. The toxins replace satellite cells such as Paz7+ that promotes muscle regeneration and maturation notably in senior people(Goldberg et al. 2015). (Goldberg et al. 2015). Resistance exercise can be utilized to improve hypotrophy by activating muscle cells. However, the process is sluggish and can take weeks or months to recover.
Bibliography
Rees, J.D., Wilson, A.M. and Wolman, R.L., 2006. Current concepts in the management of tendon problems. Rheumatology, 45(5), pp.508-521.
Rees, J.D., Stride, M. and Scott, A., 2014. Tendons–time to review inflammation. Br J Sports Med, 48(21), pp.1553-1557.
Paavola, M., Kannus, P., Järvinen, T.A., Khan, K., Józsa, L. and Järvinen, M., 2012. Achilles tendinopathy. JBJS, 84(11), pp.2062-2076.
Schultz, E. and Lipton, B.H., 2012. Skeletal muscle satellite cells: variations in proliferative potential as a function of age. Mechanisms of ageing and development, 20(4), pp.377-383.
Snow, M.H., 2014. The impact of aging on satellite cells in skeletal muscles of mice and rats. Cell and tissue research, 185(3), pp.399-408.
Goldberg, A.L., Etlinger, J.D., Goldspink, D.F. and Jablecki, C., 2015. Mechanism of work-induced hypertrophy of skeletal muscle. Medicine and science in sports, 7(3), pp.185-198.
