Two factors that may contribute to this metabolic fatigue:
 1. Build-up of lactic acid – when lactic acid builds up faster than it can be removed from the muscle, it can lead to muscle fatigue (Westerblad, Allen & Lannergren, 2002). 

 

2. Substrate Shortage - Anaerobic glycolysis uses up a large amount of glucose to make relatively small amounts of ATP. Depletion of required glycogen within a muscle results in fatigue as the body is not able to generate adequate energy needed to power the lift (Tesch, Colliander & Kaiser, 1986). 

2. Contraction period: Takes between 10 to 100 milliseconds – Calcium binds to troponin, the myosin-binding site is exposed and sarcomeres actively shorten to the point of peak tension (Tortora et al., 2019). 

3. Relaxation period: Also takes between 10 to 100 milliseconds and is where there is active transport of calcium back into the sarcoplasmic reticulum and muscle fibres return to their resting state (Tortora et al., 2019). 

2.     Isotonic contractions – a concentric contraction will be performed when ben lowers the weight towards his chest, causing the muscle to shorten and an eccentric contraction will occur when he pushes the weight back up away from his chest causing the muscle to lengthen (Tortora, 2019). 

4. The damage to Maria’s brain has resulted in her inability to move her R) arm. Which specific neuron in the neural circuits that make up the somatic motor pathways has been affected in this case? Give a rationale for the answer. (3 marks) (max. 50 words)
The first-order upper motor neurons responsible for carrying electrical impulses to initiate and regulate voluntary movement have been damaged.
Thus, preventing electrical impulses from entering the pyramidal tract, meeting with a lower motor neuron and reaching the effector. Which, ultimately causes deficits in movement of Maria’s right hand. (Emos, M. C & Agarwal, S. 2018).

5. The axons of the neuron identified above extend from the brain via two types of somatic motor pathways - the direct and indirect motor pathways. Which specific pathway is affected? Using this pathway as an example, explain why damage to the L) side of Maria’s brain has affected the movements in Maria’s R) hand. (3 marks) (max. 75 words)
In Maria’s circumstance the direct motor pathway is affected. Via this pathway, from the motor cortex, neurons controlling voluntary movement descend to the medulla where most fibres of the corticospinal tract cross over to the opposite side of the body.
They then synapse with the lower motor neurons, directly supplying the ability to move hand muscles.
Due to crossing over, the neurons on the left side of the body control movement of Maria’s right side (Premkumar, K. 2004).

Primary sources:
Yu, Z., Prado, R., Quinlan, E. B., Cramer, S., & Ombao, H. (2016). Understanding the Impact of Stroke on Brain Motor Function: A Hierarchical Bayesian Approach. US National Library of Medicine: National Institutes of Health, 111 (514), para. 66. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5270649/

 

 

Fridriksson, J., Fillmore, P., Guo, D., Rorden, C. (2014). Chronic Broca’s Aphasia is Caused by Damage to Broca’s and Wernicke’s Areas. Oxford Journals, 25 (12), para. 2. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4669036/ 

Secondary sources:
Tortora, G. J., Derrickson, B. H., Burkett, B., Peoples, G., Dye, Cooke. J., … Mellifont, R. (2018). Principles of anatomy and physiology (2^nd ed.). Milton, QLD: John Wiley & Sons Australia Ltd.

 

Huebner, E. A., Strittmatter, S. A. (2010). Axon Regeneration in the Peripheral and Central Nervous Systems. US National Library of Medicine: National Institutes of Health, 48, para. 2. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2846285/

 

Emos, M. C & Agarwal, S. (2018). Neuroanatomy, Upper Motor Neuron Lesion. NCBI, para. 2. https://www.ncbi.nlm.nih.gov/books/NBK537305/ 

 

Premkumar, K. (2004). The Massage Connection: Anatomy & Physiology (2^nd ed.). Maryland, US: Lippincott Williams & Wilkins 

The zone of proliferating of cartilage is composed of chondrocytes. 

The zone of hypertrophic cartilage is composed of large chondrocytes arranged in columns.

And finally, the zone of calcified cartilage is composed of dead chondrocytes; osteoclasts and osteoblasts.

Phase 2: The reparative phase, lasts days to weeks. The fracture haematoma (the clot) is replaced by a thick layer of soft callus around the bone ends, which is then remodelled into hard callus. This soft callus is achieved by fibroblasts producing the collagen fibres, chondroblasts producing the fibrocartilage. The hard callus is achieved by osteoprogenitor cells developing into osteoblasts and spongy bone trabeculae produced. 

Phase 3: Remodelling occurs over months and years. Dead external callus fragments are resorbed by osteoclasts. Compact bone replaces the spongy bone. The fracture area is shaped/smoothed until it looks normal.

For the growth plate to repair, the area needs a good blood supply.  It is essential to make sure that there is no neurovascular compression with the leg immobilisation.

Preventing further damage or a second trauma is critical to help repair/growth. As a soccer player Tom should protect his knee with a compression sleeve (The Royal Children’s Hospital Melbourne, n.d).

The Pancreas acts as an exocrine and endocrine gland, consisting of pancreatic islets (islets of Langherans) for its endocrine function.
The islets secrete glucagon via the Alpha cells when blood glucose levels are low. They secrete insulin via the Beta cells when blood glucose levels are too high to maintain glucose homeostasis.

 

 2.  Samantha’s blood sugar levels are high. Describe the negative feedback regulation of the hormone involved in hyperglycaemia. (3 marks) (max. 75 words) 

Once in a Hyperglycaemic state the pancreas begins the ‘negative feedback regulation’ to reduce the blood glucose level. First, the Beta cells of the pancreatic islets detect an excess amount of glucose, initiating the excretion of insulin. The insulin targets tissue cells to diffuse the glucose. Then transforms the glucose into glycogen. Next, it speeds up the absorption of amino acids and stimulates both protein and fatty acid synthesis.
This reduces the blood glucose level.

 

Once in a Hypoglycaemic state the pancreas begins the ‘negative feedback regulation’ to raise the blood glucose level. 
First, the Alpha cells of the pancreatic islets detect the low glucose level, initiating the excretion of glucagon. 
The glucagon targets the liver cells to transform glycogen into glucose and stimulate glucose production via lactic acid and amino acids.
This results in an increase of glucose being released into the blood via the liver cells (hepatocytes).

 

Epinephrine (adrenaline) is another hormone that contributes to an elevation in blood glucose levels through the fight or flight mechanism.
Epinephrine is released when the body is affected by stressors such as exercise and stressful situations, in turn increasing the production of glucose via the liver. 
The liver transforms the glucose from glycogen in order to raise blood glucose levels and provide an instant form of energy. 

 

Epinephrine (adrenaline) is secreted via the chromaffin cells which are found within the adrenal medulla of the adrenal gland. Norepinephrine is another hormone that is released at the same time as epinephrine in order to maintain a balance between the two, with 80% being epinephrine and 20% norepinephrine.

 

Bai, D, Zhang. Y, Shen. M, Sun. Y, Xia. Q, Zhang . Y, Liu . X, Wang. H, Yuan. L (2016). Hyperglycemia and hyperlipidemia blunts the Insulin-Inpp5f negative feedback loop in the diabetic heart. Sci Rep. 2016; 6: 22068.

Published online 2016 Feb 24. doi: 10.1038/srep22068

 

Via https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4764951/

 

 

Tortora, J. G., Derrickson, B., Burkett, B., People, G., Dye, D., Cooke, J., … Mellifont, R. (2019). Principles of anatomy and physiology (2nd Asia-Pacific ed.). Milton, QLD: John Wiley & Sons.

 

Sherwin, R. S, and Sacca, L (1984). Effect of Epinephrine on Glucose Metabolism in Humans: Contribution to the Liver. American Journal of Physiology, Vol. 247, Issue 2. Pages E157-E165