MNS activation and waking

Ok - back to what I was INITIALLY thinking about this morning : neuroendocrinology of transitions between sleep and waking.

PRE-READING

Observed :

• 1. at initial waking, low conscious data rate, low motor reaction times
• 2. hypoxia ( O2 constrained by beddings etc. ) associated increased wakefulness and stress
• 3. excessive heat ( due to insulation ) associated increased wakefulness and stress
• 4. intentional activation of motor units ( any muscle activity, but commonly seen as clenching, curling, or stretching in the morning ) associated with increased wakefulness but not necessarily stress

Inferred :

• 5. seems that (2,3) are via cortisol, so that makes sense
• 6. seems that (4) is doing something complicated, and I am now reading about neural signal voltages and frequencies

READING yields ...

• 7. "Recruitment" refers to the number of motor units activated. This increases from zero load, and "rate coding" only kicks in more after 80% of recruitment.
• 8. Recruitment of fibres by twitch-type* (Henneman Size Principle) :
• - slow, 1* : lowest activation threshold, "playful"
• - fast, 2a : mid-stage
• - fast, 2b : last-stage, largest motor units, "powerful" 
• 9. Motor neural "rate coding" frequencies :
• - 150 to 200 Hz in elite, trained athletes
• - 60 to 120 Hz in normal, initiation of heavily loaded movement
• - 30 to 60 Hz for sustained, heavy loads
• - 15 to 20 Hz under conditions of fatigue, to protect muscles
• 10a. The system adjacent to, but underlying the triple-network, is ARAS / the Ascending reticular activating system ( add pointer to RAS <- a candidate for consciousness functionality). Conscious MNS activity may originate here.
• 10b. Nerves in muscle spindles and Golgi tendon organs : send proprioceptive feedback back to the CNS, causing stimulation. 
• 10c. High-frequency rate-coding utilises monoaminergic (neurotransmitter) pathways : effects spill over into the cerebral cortex. 

Muscle adaptation notes

TANGENT : ... Mechanotransduction ...

90a. Endurance training -> thyroid etc. hormones -> AMPK-SIRT1-PGC-1a (protein) axis -> mitochondrial biogenesis -> adaptation towards slow, type-1 fibres

90b. Power training -> androgens ( testosterone etc. ) -> hypertrophy of existing fast, type-2a/2b fibres

90c. localised myostatin suppression -> hypertrophy in all of type-1/2a/2b fibres

91a. AMPK-SIRT1-PGC-1a Triggers :

• - AMP/ATP ratio increases (during ATP consumption)
• - cytosolic calcium increases (Ca released from SR)
• - ROS increases (pollution from burning)

91b. Activated PGC-1a moves to the nucleus, where it coordinates BOTH nuclear and mitochondrial genomes!

92a. Hypertrophy Triggers :

• - [ titin, filamin-C, BAG3 proteins are mechanosensory complexes, at the (Z-disc) edges of sarcomeres; sarcomeres are intra-cellular structures ] -> [ cell membrane enzyme activation ] -> mTORC1 activation -> [ mRNA builds more actin and myosin; ribosome biogenesis increases ]

92b. satellite cell fusion

• - day 0 to 1 : sarcolemma ( cell membrane ) damage,  satellite cell activation
• - day 1 to 5 : satellite cell proliferation, differentiation
• - day 4 to 10 : fusion into more nuclei per muscle cell to facilitate control over larger cells
• - day 14 to 28 : maturation, and full functional repair

ASMR & general "open-minded"ness

ASMR* : in terms of brain-networks, neurotransmitters, and endocrine response.

( I was reading up on motor neural voltages, between sleep and non-sleep states, and ended up at ASMR. )

Perhaps this is relevant to my preferred state of mind, as a generalist, whereby I allow myself all-dimensional reactions to stimuli. 

ASMR apparently reflects a "higher than usual" synchrony between the CEN* and DMN*. The SN* is characteristically less-engaged, whereas it is usually responsible for flagging issues, and raising them into priorities, which then interruptively switches between CEN-dominance and DMN-dominance. 

Generally : this appears to be a risk-off state ( see : dACC* ), where sensory inputs of ambiguous risk are not interpreted immediately as threats, but are instead allowed to be contemplated as amusements ( see : NAc, VTA* ). The states of threatened and amused, each involve separate neuroendocrinal cascades, which are available for further reading.

I reflect also on how interoception is often referred to as "subjective feelings" in the literature - whereas I find that subjective feelings may all be quantified in terms of concrete sensory data types.

*

• - Autonomous sensory meridian response
• - Central executive network ( motor task oriented )
• - Default-mode network ( internal imagination oriented )
• - Salient network
• - Dorsal anterior cingulate cortex
• - Nucleus accumbens
• - Ventral tegmental area ( mesolimbic and mesocortical pathways )

Yeah, one of the things putting me off neuro studies for so long was the word soup.