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Need help with College level Physiology question - I need a thorough explanation because I need...

Need help with College level Physiology question - I need a thorough explanation because I need to understand these questions in full please

During exercise – as compared to rest – what are aspects of blood transport that can be modified to increase oxygen delivery to the exercising muscles? (I would like to see a minimum of 4 modifications addressed). Be sure to be explicit about how each modification increases oxygen delivery.

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Exercise requires more energy as muscle contraction uses more energy i the form of ATP. For ATP generation more amount of oxygen is used. So during exercise large amount of oxygen is required by the muscle tissue.

Accordingly the blood flow has to be altered to supply the oxygen required by the exercising muscle. Various mechanism are used to increase the blood flow to the muscle in order to ensure that more oxygen is supplied.

Resting blood flow to muscle is usually 2–4 ml/100 g muscle/min, but might increase to nearly 100 ml/100 g muscle/min during maximal exercise.

This due to the action of vasodilatory metabolites such as AMP, adenosine, H+, K+ and phosphate acting on pre-capillary sphincters and increase the blood flow.

In addition, decreased pH and increased temperature shift the oxygen dissociation curve for haemoglobin to the right in exercising muscle. This assists in unloading more oxygen from the blood into the muscle.

During muscular contraction, blood flow is restricted briefly but overall it is enhanced by the pumping action of the muscle. Whilst muscle and coronary blood flow increase, cerebral blood flow is maintained constant and splanchnic flow is reduced.

The increase in blood flow to muscles requires an increase in the cardiac output, which is in direct proportion to the increase in oxygen consumption.

The cardiac output is increased by rise in the heart rate and the stroke volume that empties the heart completely by a forcible systolic contraction.

These chronotropic and inotropic effects on the heart are brought about by stimulation from the noradrenergic sympathetic nervous system. The increase in heart rate is also mediated by vagal inhibition and is sustained by autonomic sympathetic responses and carbon dioxide acting on the medulla.

Stretching of the walls of the arterioles and vasodilatation takes place, which decreases the peripheral vascular resistance to allow more blood flow.

In this way increased oxygen delivery is acheived by modification in the blood flow.

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