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Metabolic Control
- CNS effects immediate and short lived (ANS)
- Endocrine responds slowly but lasts
(inc) or (dec) refers to the effect of exercise on the hormone:
Anterior pituitary
Posterior pituitary
Parathyroid
GH (inc)
ADH
PTH
TSH
Oxytocin
*released if low blood Ca2+
ACTH
Prolactin
FSH
LH
Adrenal Medulla
Epinephrine (inc)
Norepinephrine (inc)
Adrenal Cortex
Mineralocorticoids (inc)
Corticosteroids
Androgen/Estrogen
Pancreas
Insulin (dec)
Glucagon (inc)
Somatostatin
Steroids are soluble in lipids
1. Enter cell
2. Bind to recptor in cytoplasm/nucleus
3. Activate DNA  forms RNA
4. mRNA directs PROTEIN SYNTHESIS
non-steroid: not lipid soluble
1. bind to receptor on cell membrane
2. activates cascade that causes cellular changes
Post-exercise: epinephrine decreases in a few minutes
Norepinephrine takes hours to decrease
ADH: change permeability of kidney’s ducts
Aldosterone: renal reabsorption of Na+
Principles of muscle contraction
Muscle is 60% protein, 40% water
Sarcolemma: plasmalemma + basement membrane
T-tubules: transmit action potential
Sarcoplasmic reticulum: stores, releases, reuptakes Ca2+
Actin: thin fiber
Myosin: thick fiber
I band: just thIn filaments
H band: just tHick filaments
A band: where they All cross
1. action potential goes down T tubule
2. calcium released from sarcoplasmic reticulum
3. calcium binds to troponin (removes blocking action of tropomyosin)
Thyroid
T3 (inc)
T4 (inc)
Calcitonin (?)
Kidney
Renin
Erythropoetin
Titan: largest protein in the body and anchors myosin
Nebulin: specifies length of thin filament
Actin is the little balls on the tropomyosin strand
Tropomyosin: strand
Troponin: tiny heads in balls that attach to calcium
TnT: binds troponin to tropomyosin
TnC: binds troponin to calcium
TnI: inhibitory when no calcium
They hydrolysis of ATP “cocks” myosin head
- attaches to actin and movment occurs
- cross bridge attachment requires new ATP
Muscle fibers:
1. slow oxidative
2. fast oxidative glycolytic (IIA)
3. fast glycolytic (IIB)
*specialization is due to alpha motor neuron innervating mm.
*smaller fibers are recruited first (type II)
*endurance training increases the oxygen capacity of all 3 types
Neural Control
Diencephalon: thalamus, hypothalamus
Cerebral cortex: motor, sensory, association
Thalamus: sensory except smell , regulates slee/alert, motor control, relays to cerebral cortex
Hypothalamus:
homeostasis
- ANS control center
- Limbic system
Epithalamus: melatonin (pineal gland)
Cerebellum: processes data from motor cortex, proprioceptors, visual/equilibrium paths, coordination
Brain stem: respirator and cardiovascular control, pain control
Medulla: vomiting, hiccupping, swallowing, coughing, sneezing
Neurons need a lot of glucose
Absolute refractory period: the sodium channels are still open (AP occurring)
Relative refractory period: potassium channels open; in process of repolarization
2 major neurotransmittors in regulating physical response to exercise:
1. Acetylcholine (mm movement)
2. Norepinephrine (wakefulness, arousal)
EPSPs and IPSPs are related to sodium permeability
Force generation:
Recruitment: recruit more and more motor units
Rate coding: motor unit firing rate; tiny muscles use this method
Proprioception:
Muscle spindles:
1. Monitor length changes
2. Speed of length changes
3. These are parallel to muscle fibers
Golgi tendon organ:
1. Monitor tension (within the tendon)
Energy expenditure
RER = respiratory exchange ratio
RER = VCO2/VO2
Carb: 1.0
Fatty acid: .7
VO2: volume of O2 consumed
VCO2: volume of CO2 produced
**at SUBMAX the trained individual will use less O2. At MAX the trained individual has increased VO2 max so they use
more O2
Lactate threshold = anaerobic threshold
This is the point at which production > clearance
EPOC: excess post-exercise oxygen consumption
Not necessarily correlated with lactate
- Much more of a deficit when exercising at VO2 max
- Deficit of O2 during exercise: ATP-Cr, glycolysis, stored O2
The trained individual is better at lactate removal
Exercise/Stroke and Mm Adaptation
- stroke severely deconditions people
- VO2 max needs to be 15 mL * kg^-1 * min^-1 for ADLs
- If you stop using certain motor units, the body might stop sending blood there
- Exercise prescription: 20-60 min, 3-5 days/week, 40-70% VO2 max
Type I: oxidative
Type IIA: oxidative glycolytic
Type IIB: glycolytic
Type I takes more effort to produce force
SAID: specific adaptions to imposed demands
DOMS: delayed onset muscle soreness