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Cardiovascular system
Cardiovascular system anatomy and physiology
Lymphatic system anatomy and physiology
Coronary circulation
Blood pressure, blood flow, and resistance
Pressures in the cardiovascular system
Laminar flow and Reynolds number
Resistance to blood flow
Compliance of blood vessels
Control of blood flow circulation
Microcirculation and Starling forces
Measuring cardiac output (Fick principle)
Stroke volume, ejection fraction, and cardiac output
Cardiac contractility
Frank-Starling relationship
Cardiac preload
Cardiac afterload
Law of Laplace
Cardiac and vascular function curves
Altering cardiac and vascular function curves
Cardiac cycle
Cardiac work
Pressure-volume loops
Changes in pressure-volume loops
Physiological changes during exercise
Cardiovascular changes during hemorrhage
Cardiovascular changes during postural change
Normal heart sounds
Abnormal heart sounds
Action potentials in myocytes
Action potentials in pacemaker cells
Excitability and refractory periods
Cardiac excitation-contraction coupling
Electrical conduction in the heart
Cardiac conduction velocity
ECG basics
ECG normal sinus rhythm
ECG intervals
ECG QRS transition
ECG axis
ECG rate and rhythm
ECG cardiac infarction and ischemia
ECG cardiac hypertrophy and enlargement
Baroreceptors
Chemoreceptors
Renin-angiotensin-aldosterone system
Physiological changes during exercise
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Jennifer Montague, PhD
Jung Hee Lee, MScBMC
Evode Iradufasha, MD
Rachel Yancey
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.
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