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Physiological changes during exercise

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Biochemistry and nutrition

Biochemistry

Biochemistry and metabolism
Metabolic disorders
High Yield Notes
6 pages
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Content Reviewers:

Viviana Popa, MD

During physical exercise, our organs and tissues are working hard to keep us moving; or, technically speaking, for our musculoskeletal system to do its job.

Now it’s fairly obvious that during exercise, skeletal muscles work, or contract, harder and faster than when we’re at rest, so they use a lot of energy in a short time, so they need a lot more blood and oxygen to keep going.

So organ systems like the cardiovascular and respiratory system have to make some quick physiological adjustments, to meet the skeletal muscles demand.

Moreover, the endocrine system also kicks things into high gear, by secreting hormones like cortisol and adrenaline, that speed up intracellular processes to keep us going.

But before we delve into the specifics of that, let’s remember how muscle contraction works on a microscopic level.

So, skeletal muscles are made up of muscle fibers which are actually the skeletal muscle cells.

We just call them “fibers” because they are long, multinucleated cells, meaning they have more than one nucleus.

Their structure also differs from other cells because their cytoplasm, sometimes also called sarcoplasm, is filled with stacks of long filaments called myofibrils, which are made up of contractile units called sarcomeres.

And finally, sarcomeres are made up of the thick myosin filaments, and thin actin filaments, which can slide over one another, shortening the sarcomeres.

So when all the sarcomeres in a muscle fiber do that in sync, that results in shortening of the muscle as a whole, or muscle contraction.

And this process is powered by energy in the shape of ATP molecules, where adenosine-triphosphate.

The three phosphates in the molecule are linked in a chain, and between two adjacent phosphate molecules, there are high-energy phosphate bonds.

ATP molecules attach to a part of the myosin filament called the myosin head.

The myosin head is actually an ATPase, or an enzyme that can cleave an ATP molecule into ADP and phosphate ion, releasing the energy stored in the bonds.

After the energy is released, ADP detaches from the myosin head, so myosin can bind to actin filaments, forming cross-bridges that result in shortening of the muscle fiber.

Now, ATP molecules come from two sources: first, there’s a small stash spread out between myofibrils, which is just about enough to sustain muscle contraction for a single bout of exercise - like hitting a tennis ball with a racket.

But these ATP stores get depleted quickly, so if you want to keep playing tennis after the serve, muscle cells need to generate some more ATP.

ATP can be generated through a number of biochemical pathways.

First one is substrate phosphorylation - which means a phosphate is added to a molecule, in this case, the leftover ADP. In muscles, the phosphate comes from creatine phosphate, which splits into phosphate and creatine under the action of an enzyme called creatine phosphokinase.

Unfortunately, creatine phosphate also runs out rather quickly.

So 10 to 30 seconds after the onset of exercise, ATP needs to be generated through anaerobic glycolysis, or the breakdown of glucose into pyruvate and lactic acid.

This process happens in the cytoplasm, and it doesn’t require oxygen but it only yields about 2 ATP molecules per molecule of glucose.

What’s more, in the absence of oxygen, pyruvate is converted to lactic acid in the cytoplasm, so this causes a buildup of lactic acid, which causes muscle fatigue after about 1 minute of intense exercise.

Lactic acid can also spill into the bloodstream, making blood PH take a dip.

This is detected by peripheral chemoreceptors, which are specialized neurons located in the walls of the carotid arteries and the aortic arch.

When they register that blood PH dropped, these neurons fire more impulses, notifying the respiratory centers in the brainstem that they have to increase the respiratory rate and depth of breathing, all together called hyperventilation.

So more air, and, in turn, more oxygen reaches the alveoli, which are the tiny air sacs where gas exchange occurs.

More oxygen in the alveoli leads to pulmonary vasodilation, meaning these tiny vessels of the pulmonary capillary bed start to widen, reducing the pulmonary vascular resistance, so more blood flows through.

A decrease in pulmonary vascular resistance and an increase in pulmonary blood flow in all three zones the lungs; the upper, the middle and the lower ones, allow blood to reach all of these zones almost equally.

As a result, we get a more even distribution of pulmonary perfusion, and the physiological dead space, or the number of alveoli that were not actively used for gas exchange, also decreases.

This increases efficiency in gas exchange between the alveoli and the pulmonary capillaries, so more oxygen gets in the blood, and more carbon dioxide leaves the blood.

At the same time, when chemoreceptor firing rate increases, it also notifies the cardiac centers in the nucleus tractus solitarius located in the medulla oblongata, which signal the brain to turning down the parasympathetic stimulation to the heart, while increasing sympathetic stimulation - aka the fight or flight response.

Part of the fight or flight response is that brain signals the adrenal glands above the kidneys to release epinephrine, and when epinephrine gets to the heart, it binds to the adrenergic receptors of the heart muscle, making heart rate and contractility increase.

This means heart muscle fibers contract faster and stronger and the amount of blood the heart pumps out in a minute, increases as well.

Finally, epinephrine also causes systemic vasoconstriction, which means visceral blood vessels contract, so there’s reduced blood flow to the kidneys, liver and the gastrointestinal system.

Sources
  1. "Medical Physiology" Elsevier (2016)
  2. "Physiology" Elsevier (2017)
  3. "Principles of Anatomy and Physiology" Wiley (2014)
  4. "Effects of exercise on hematological parameters, circulating side population cells, and cytokines" Experimental Hematology (2008)
  5. "Cardiovascular Physiology Concepts" Lippincott Williams & Wilkins (2011)
  6. "Glucose-sensing mechanisms in pancreatic β-cells" Philosophical Transactions of the Royal Society B: Biological Sciences (2005)
  7. "Human Anatomy & Physiology" Pearson (2018)