Download - MCB 135E Discussion
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MCB 135E Discussion
GSI: Jason LowryDec. 9, 2004
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Topics
• Muscle Growth and Plasticity• Nutrition• Eating Disorders• Homeostasis• Hormesis
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Muscle Growth and Plasticity
1. What are the major components of muscle?2. From what embryologic layer are muscles
derived?3. Which kinds of muscles are under autonomic
control? Which are under voluntary control?4. What kind of neuron innervates muscle and
causes it to contract?5. What specialized oxygen-carrying molecule is
found in muscle?
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Embryology
• All muscles derive from the MESODERM of the GASTRULARemember? Morula then Blastula then Gastrula
• From its mesoderm layer:A) striated or voluntary musclesB) cardiac muscle or scalariformC) smooth muscle (of GI tract, Urinary, etc)
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Importance of the Nervous System
• Autonomic nervous system controlssmooth and cardiac muscles
• Central nervous system controlsthe voluntary muscles
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Histology
Each fiber being a multinucleated cell
consists of myofibrils in bundles with a
large number of mitochondria and a
myoglobin (pigmented protein)
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Muscle Growth and Plasticity
1. What are the main proteins of the myofibril unit?
2. Know the characteristics of the two main muscle fiber types.
3. What is myoplasticity?4. From what molecule does muscle obtain ATP
for contraction? Under what conditions might lactate be produced? Under what conditions is the TCA cycle used to produce ATP?
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Contractility
Secondary to the sliding characteristic of the 2 main proteins of the myofibrils:
MYOSIN
ACTIN (thinner)
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Steps in Contraction1. Discharge of motor-neuron at the myo-neural plate with release of
the neurotransmitter acetylcholine (Ach)
2. The binding of Ach to its receptors increases Na+ and K+ conductance, generating an action potential
3. The sarcoplasmic reticulum releases Ca++, activating the enzyme troponin, which uncovers the myosin binding sites allowing cross-linkages between actin and myosin to form
Steps in RelaxationCa++ pumped back in the sarcoplasmic reticulum, and the release of Ca++ from the troponin induces cessation of interaction between actin and myosin.
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THE FUEL
GLUCOSE, 6 carbon (C) compound, enters the muscle +/- insulin
Broken into 3C compound: Lactate and Pyruvate
Lactate to pyruvate and/or back to circulation for gluconeogenesis
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Muscle Growth and Plasticity
1. How does muscle change after development? Do we make new muscle cells? If not, then how do our muscles become bigger with use?
2. What kinds of exercise lead to an increase in cross-sectional area of muscle fibers? What kinds of exercise increase the level of oxidative metabolism?
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TYPES of FIBERS
Type 1: reddish Slow Oxidative (SO)
Type 2: pale and divided intoFast Oxidative Glycolytic (FOG)Fast Glycolytic (FG)
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The number and type of fibers is dictated by genetic determinants but
……..ALAS!!!
Appropriate stimulations may induce an almost complete change
Hence…..
MYOPLASTICITY
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Myoplasticity: ConceptAbility of the muscle to alter the quantity and the type of
its proteins in response to stimulations
Modalities of stimulations: 1) Physical activities leading to an increase in its cross-
sectional area2) Increase in the muscular mass with changes in the
myosin typeMuscle plasticity may involve:
• Change in the amount of protein• Change in the type of protein
• Combination of both
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Myoplasticity Due to Exercise
• Endurance exercise increases the oxidative metabolism of the muscle
• Resistance training increases the cross-sectional area due to true hypertrophy of the single cells
• Inactivity induces rapid regression
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Muscle Fiber Number Virtually Fixed at Birth
• The increase in mass (hypertrophy, sometimes as much as 50%) is due to increase in length and in the cross-sectional area of the muscle fibers.
This is due to an increase in the number of myofibrils (from 75 to over 1000)
• The capacity for regeneration and plasticity is a response to neural, hormonal and nutritional differences
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Nutrition
1. What are the stimulators of appetite?2. What the depressors of appetite?3. What is the sense of satiety? What are its
inducers?4. Why does it make sense for high insulin levels
to stimulate hunger?5. What kind of cell secretes leptin? Why does it
make sense for this cell type to secrete a depressor of hunger?
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Nutrition
1. What is the basal requirement of nutrients for an very active adolescent or adult?
2. How many Kcal are there in 1 gm of fat? in 1 gm of protein? in 1 gm of carbohydrate?
3. What features of our intestinal tract point towards our being omnivores?
4. Why is it that water is so important?5. What form must carbohydrates be in to be
absorbed through the intestinal wall?
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Supply of Calories• From ATP = 1 kcal (walk 10 meters)• From CP = 10 kcal (walk 100 meters)
• From blood glucose = 80 kcal• From liver glycogen = 400 kcal
• From muscle glycogen = 1600 kcal All of the above enough for a marathon!
• Lipids only a very slow turnover to energy• Proteins a very very slow turnover to energy
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Caloric production
• FATS : 1 gm = 9 kcal• PROTEINS : 1 gm = 4 kcal• CHO : 1 gm = 4 kcal
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The Caloric Requirement
1. The calorie and the kilocalorie
2. The basal requirement = 1600 kcal
3. Requirements for moderately active adult1800 2200 kcal
4. For a very active adolescent or adult: 3000 kcal or more
5. Memo the THYROID EFFECT !!!!
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Nutrition
1. What is the minimum safe percentage of protein in an adult diet? Why is it dangerous to take in less?
2. What two vitamin levels should be checked with frequency in a vegan diet to ensure adequate intake?
3. What kinds of fat are best for us to take in? What is one solid fat that is good for us?
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The Macronutrients: Lipids
• Saturated, no double bonds, usually solid
• Trans-fats, from liquid to solid format (usually commercial only)
• Mono-unsaturated, like olive oil
• Poly-unsaturated, like most other oils
• OMEGA 3, fatty acids, like many fish oils
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The Macronutrients: Proteins
• Protein intake at least 11-12% of the total
• Intakes below 8.7% carry severe risk of serious deficits
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Nutrition
1. What are the micronutrients?2. Why do we need fiber in our diets?3. Has caffeine been shown to be bad for the
average person?
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The Micronutrients• Salt, Na+ (<5 mg/day) and K+ (deficits, excesses,
need)
• Ca+ (1800 mg/day), P and Fl (bone metabolism)
• Fe++ (deficit and excess), Cu, Mn, and Mg
• Other metals: Cr, Se, Zn and the Metalloid I
• Memo the hidden aspects of hypothyroidism
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RDA/ day(for some components)
Ca++ : 1800 mg or more
P : 1200 mg
Fe++ : 10-12 mg
I : 150 g
Se : 45-50 g
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The Macronutrients: Fibers
• High risk for the “vegans”
• Benefits and risk of the fibers
• The good and the not so good vegetables
• CONCLUSION: long live the Mediterranean diet but….with some cracks!!!
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Addicting Substances
Coffee and Tea (caffeine and teine)Memo: aminophylline and brochospasm
ALCOHOLIC BEVERAGES!!!The benefits and the…….
Disasters!!!!
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Stress: Homeostasis
1. What does the term "homestasis" mean?2. What does the term "allostasis" mean?3. What is the General Adaptation Syndrome?
How might the ideas of the adaptation syndrome be applied to developmental periods?
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Stress, Homeostasis, and Allostasis
An organism must vary all parameters of its internal milieu and match them appropriately to environmental demands through:
Homeostasis: steady state and optimal set-points are achieved; it is obtained by repeated fluctuation s of various physiological systems (allostasis) and/or long-term exposure to elevated levels of physiologic activity
Allostasis: emphasis is on optimal operating ranges of physiologic systems; it represents stability obtained through change
Allostatic load: the cumulative, multi-system view of physiologic toll that may be exacted on the body through attempts at adaptation
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Stress: Hormesis
1. What types of physical stress affect cortisol secretion? What types of psychological stress?
2. What role does stress play in longevity3. Why do we get sick when we are stressed?
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Hormesis• Hormesis: the beneficial action (s) resulting from
the response of an organism to a low-intensity stressor
• The term “Hormesis” was first utilized by T. D. Luckey in 1991 in a book entitled Radiation Hormesis.
• High doses of radiation increase mortality and shorten life; small doses of radiation prolong life (as compared to the non-irradiated animals).
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Hormesis & Chaperones• The beneficial effects of moderate stress on the
resistance to extreme and prolonged stresses, and the promotion of longevity, may be due to their action in stimulating the production of “heat-shock proteins” (HSP) (also known as “stress proteins”).
• HSP are a type of “chaperone” protein – Chaperones ubiquitin, glucose related proteins,
endoplasmic reticulum chaperones.
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Hormesis & Chaperones
• During stress, HSP level increases and protects the normal assembly of proteins by promoting their appropriate folding
• In C. Elegans it has been shown that upon stress, there is increase levels of HSP together with a longer life.
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However, there is no such thing as a “free meal”
Increased longevity is associated with unwanted effects on growth, fertility, length of development, metabolic rate, etc.
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Stress1. What is the difference between a specific and a
nonspecific response to stress? Give an example of each.
2. Know the features of the fight/flight response. 3. What bodily functions are inhibited by stress?
Stimulated?4. What happens to the immune system during
prolonged stress?
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Some Characteristics of StressStress induces defense mechanisms for maintenance of homeostasis in response to environmental challenges
Types of stress known to stimulate the HPA axis*:
Physical Stress:hypoglycemia, trauma, exposure to extreme temperatures, infections, heavy exercise
Psychological Stress: Acute anxiety, Anticipation of stressful situations, Novel situations, Chronic anxiety
Exposure to stress generates:
Specific responses: varying with the stimulus and generating different responses with each stimulus
Non-Specific responses:always the same, regardless of the stimulus and mediated through stimulation of neural, endocrine & immune axes
*HPA axis = hypothalamo-pituitary-adrenal axis
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“Fright, Flight, or Fight” Responses to Stress•Increased blood pressure•Increased heart rate•Increased force of heart contraction•Increased heart conduction velocity•Shift of blood flow distribution
•Away from the skin and splachnic regions•And more to heart, skeletal muscle, and brain
•Contraction of spleen capsule•Increased depth and rate of respiration•Mobilization of liver glycogen to glucose (glycogenolysis)•Mobilization of free fatty acids from adipose tissue (lipolysis)•Mydriasis (widening of pupil)•Accommodation for far vision (relaxation of ciliary muscle)•Widening of palpebral fissure (eyelids wide open)•Piloerection•Inhibition of gastrointestinal motility and secretion, contraction of sphincters•Sweating (cold sweats as skin blood vessels are constricted).
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Pathophysiologic Responses During and After StressDuring Stress
Energy storage ceases because:Sympathetic activity
Parasympathetic activityInsulin secretion
Access to energy storage is facilitated & energy storage steps are reversed:glucocorticoid secretion
Epinephrine/norepinephrine secretionGlucagon secretion
After StressIf physiologic responses are insufficient and adaptation is incomplete, symptoms
of poor health are registered (e.g. loss of energy when freeing energy from storage and returning to storage)
Examples of consequences:
Muscle wasting, Diabetes (Type 2), ulcers, colitis, diarrhea
Inhibition of growth (in childhood), Osteoporosis (in old age)
LHRH, testosterone