What can be described as "an overwhelming flow of emotions" often relates to an amygdala hijack. The amygdala is part of the limbic system and present at the lower end of both hemispheres of the brain. It is responsible for the emotional processing of any stimulus. The amygdala is also responsible for the evolutionary fight or flight response - which in early man, was very important, as exposure to physical harm (being attacked by a wild animal, being vulnerable to natural disasters etc.) was more than what it is today. The fight or flight response allows us to decide, when presented with a threat, a suitable reaction. The 'fight or flight' , controlled by the sympathetic nervous system, has a counter known as the 'rest and digest' response, automated by the parasympathetic nervous system. 'These are nicknames for each branch of your autonomic nervous system, which controls bodily processes without your conscious input.'
In today's day and age, the fight for survival is far less due to exponential human advancement. However, our brains have not been given enough time to adjust perfectly to the modern way of life. This results in our fight or flight response remaining as it was and acting up when other forms of threat presents itself. This can have adverse effects as a mechanism originally built to protect us in times of extreme danger now may function in times of inconvenience, sadness, anger, panic, or stress.
This takeover of the amygdala is deep rooted - the thalamus is usually responsible for the sending of stimuli to the prefrontal cortex of our brain for rational analysis. The neocortex is a recently evolved layer that regulates interpretation, comprehension, planning, executive functioning, analysis, and synthesis. However, during an amygdala hijack, the thalamus bypasses this data to the amygdala which interprets it from a unilateral aspect and outputs an emotional response. Here, the frontal lobes play no part as the impulses carrying information regarding the stimuli has not reached them. The neuronal pathway differs from the 'normal' one.
This occurs as the amygdala causes several observable biological changes within the body that are commonly known - goosebumps, pupils being dilated, rapid breathing, butterflies in our stomach etc. These changes stem from an increased concentration of release the hormones adrenaline and cortisol in our blood by the adrenal glands. Adrenaline, also known as epinephrine, causes the dilation of airways to increase oxygen intake and the contraction of arteries to enhance oxygenated blood supply to dominant muscle groups. This is related to us 'feeling butterflies' and 'getting the chills' - i.e. the sudden constriction of blood vessels surrounding the stomach and intestine along with the contraction of our digestive muscles and the contraction of pili muscles present at the base of each of our hair follicles, causing a shallow depression, that results in the surrounding skin seeming elevated. 'The contraction also causes the hair to stand up whenever the body feels cold. In animals with a thick hair coat this rising of hair expands the layer of air that serves as insulation.'Besides heat retention, this also protects several animals by making them seem larger, thus chasing their prey away. A fitting example would be of a porcupine that flares its fur and quills at notice of danger.
However, in humans there is no such function as our hair is not thick / long enough for insulation or protrusion; this demonstrates, again, why the 'fight or flight' response by the amygdala and sympathetic nervous system is not well adapted to the setting of today. Pupil dilation, medically known as mydriasis, is to do with letting in a greater amount of light while a faster heart beat is for efficient circulation of oxygen and nutrients to major muscle groups; this leads to increased blood pressure as well.
An amygdala hijack usually leads to all the above listed symptoms, but to a degree where the body is unable to internalize, rationalize, interpret, analyse and/or react to the threat. Another case may be when there is no real danger present, yet the amygdala and sympathetic nervous system react as through there are. A continued firing of the amygdala is unhealthy and may lead to a person developing anxiety and/or depression along with chronic fatigue, stress, high blood pressure etc. Correlational findings between amygdala activation (and volume) and childhood maltreatment has been found. This basically means that the likelihood of an amygdala hijack in somebody with a traumatic childhood increases tenfold due to a prolonged period of use of the fight or flight response.
Controlling an amygdala hijack can be done with training the mind - for instance, when panicked, practicing taking a deep breath and a walk - alongside other exercises like meditation and yoga.
What happens to our abdominal muscles when we cough? What happens when we do a bicep curl? How do an octopus's tentacles move with such dexterity?
All the above phenomena have to do with muscle contraction - the intricate molecular movements in our muscle fibers that allow us to move freely. The sliding filament theory explains the mechanism of muscle contraction at a molecular level; where proteins responsible for locomotive function within a sarcomere cause the exertion of contractile force. This bundle of proteins is collectively known as a myofibril.
A muscle cell is made up of several stacked, repeating units known as sarcomeres that contract - thus causing the cell, tissue, and muscle to contract in turn. These sarcomeres, within them, have protein filaments that are thick and thin. The thick filaments are called myosin while the thin ones are known as actin; these parallelly overlap to perform their function. The actin filaments, being thin, are able to slide easily towards the thick myosin filaments - that have a chain of myosin heads; these do not shift when the sarcomere contracts. This immobile myosin-rich area of the sarcomere can be represented as an A-Band that has a midline, labeled 'M' at its center. The A-Band has actin dense areas on both sides - these are known as I-Bands. The lateral edges of a sarcomere also have Z-Bands which shorten when muscle contraction occurs. Each of these Z-Bands has Z-Lines passing in a crisscross fashion through them - these structures are where the outmost ends of the actin filaments are connected to the Z-Band. This complex unit can be simply understood by looking at Image 1 where 'a)' shows us a sarcomere when the muscle is relaxed and 'b)' when it is contacted.
After understanding the structure of a sarcomere, it is necessary to understand how these filaments slide to generate tension and contract. This can be easily understood in steps -
The myosin heads have an S1 region that consists of are globular structures nearest to the actin - this 'has multiple hinged segments, which can bend and facilitate contraction.'
The S1 region binds to the actin and then contracts, bringing the actin closer towards the A-Band.
The contraction of the S1 region occurs by an angular change and is known as a power stroke as it requires the hydrolysis of ATP (which releases energy by breaking an energy-rich phosphate bond).
This formation of the S1 region of myosin bound to the actin is known as a cross-bridge, sown in Image 2.
Then, the actin is released by the S1 region to undergo binding by the next S1 region.
'The slimmer and typically longer "tail" region of myosin (S2) also exhibits flexibility, and it rotates in concert with the S1 contraction.'
It is in this way that myosin and actin form a cycle. The myosin continues to bind, contract, and release actin - pushing it closer to the A-Band until there is a maximal overlap of myosin and actin, with the Z-lines close to the M-line.
The regulation of muscle contraction is performed by 2 other proteins known as troponin and tropomyosin, along with the cofactors (non-proteins in enzymes) calcium and ATP. ATP is needed for the provision of energy during the power stroke while calcium allows the cross-bridge formation of myosin and actin to occur. This is as the S1 regions on the myosin filaments are covered by tropomyosin - only when these are moved is myosin exposed and able to perform its function. Calcium aids in this process as it binds to troponin (the smaller protein) causing a conformational change that then moves tropomyosin away from the myosin binding sites. The calcium ions for this are released from the sarcoplasmic reticulum - an organelle similar to the endoplasmic reticulum in other cells.
It is in this manner that muscle contraction takes place - with the closeness of each M-line in a sarcomere increasing as the myofibrils go on to perform their respective functions.