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129 Cards in this Set

  • Front
  • Back
What are the energy foods and what functions do they fuel?
Carbs, Fats & Proteins

muscle activity
secretion by glands
maintenance of membrane potentials
synthesis of substances in cells
absoption of food in GI tract
What is the role of glucose in carbohydrate metabolism?
Glucose is the final common pathway to transport carbs to tissues

fructose and galactose are converted to glucose in the liver
How is glucose transported?
Cannot diffuse across cell membrane bc it is too large
-Transported through facilitated diffusion by carrier molecules

Insulin present in blood helps metabolize glucose to increase transport
Phosphorylation
Once glucose enters the cell it combines with a phosphate radical which is facilitated by the enzyme Glucokinase. Once this happens glucose cannot diffuse back out of the cell. Glucose becomes Glucose-6-Phosphate
-Krebs cycle begins
Glycogenesis
Once glucose enters the cell it can be converted to glycogen and stored for energy (in liver and muscle cells)
Glycogenolysis
Breakdown of the cell's glycogen to form glucose
-catalyzed by the enzyme phosphorylase
Phosphorylase
the enzyme that catalyzes glycogenolysis

-activated by epinephrine & glucagon
Glycolysis
The splitting of glucose to yield pyruvate. The energy from this process is used to form ATP.

occurs in the cytoplasm of the cell
can occur either anaerobically or aerobically

4 molecules of ATP formed, but
Net gain: 2 ATP (2 needed for reaction to occur)
2 NADH + H+
2 pyruvate
Formation of Acetyl CoA
2 pyruvic acid molecules from glycolysis are converted to 2 molecules of Acetyl CoA

What is formed:
2 molecules of Acetyl CoA
2 molecules of CO2
4 H atoms
*NO ATP formed (6 molecules of ATP will be formed when the 4 H atoms are oxidized)
Citric Acid Cycle (Krebs Cycle)
Occurs in the mitochondria
-operates only under aerobic conditions

Oxaloacetic Acid combines with Acetyl CoA
-CoA is released to be used to form more acetyl coa when combined with pyruvic acid from glycolysis
-Acetyl group used in reaction to eventually form oxaloacetic acid which fuels the cycle to continue

Net gain:
2 molecules of ATP
4 CO2
16 H
2 CoA
Dehydrogenase
enzyme that releases H atoms during glycolysis & Krebs cycle

20/24 H atoms released combine with NAD+ to make NAD + H+
Oxidative Phosphorylation
H atoms from glycolysis and Krebs enter the mitochondrial membrane
-each H atom is split into H ion and an electron
-electrons combine w/water to form hydroxyl ions
-hydroxyl ions and H combine to form water

20/24 H atoms are oxidized, yielding 3 ATP for every 2 H atoms= (30 ATP)
-remaining 4 H are released to give off 4 more ATP

Net: 34 ATP
Electron Transport Chain
Part of Oxidative Phosphorylation
-occurs in the inner membrane of the mitochondria

-energy released from electron mvmt pumps H ions from inner matrix (neg electrical potential) to outer matrix (positive charge)
-ions flow through ATP synthase complex
-energy from ion flow used to convert ADP to ATP
What is facilitated diffusion?
the transfer of a molecule in or out of a cell through transport proteins

-the transfer of ATP back to the cytoplasm
-how glucose enters the cell for metabolism
Summary of ATP Formation in Carb metabolism
Glycolysis --> 2 ATP

Krebs Cycle --> 2 ATP

Oxidative Phosphorylation --> 34 ATP

38 ATP TOTAL
Functions of the liver
-degrade fatty acids for energy
- synthesize triglycerides from carbohydrates
-synthesize other lipids from fatty acids (esp. cholesterol & phospholipids)
-detox
Synthesis of Triglycerides
excess carbs are converted to these to be stored in the form of fatty acids to be used for energy in the future

-Conversion of carbs to acetyl CoA
How are triglycerides used?
they are hydrolized into fatty acids and glycerol
-transported in blood to active tissues where they will be oxidized for energy
-only brain cells and red blood cells cannot use fatty acids for energy
-glycerol is converted to glycerol-3-phosphate which enters glycolytic pathway for glucose breakdown
Beta Oxidation of Fatty Acids
the oxidation of fatty acids that occurs only in the mitochondria
-fatty acid molecule oxidized to yield acetyl coA --> Krebs cycle --> electron transport chain
-produces 5x the APT of carbs

*yields 9 ATP from krebs
*yields 139 ATP from oxidation of H
-2 ATP used
=NET: 146 ATP
Oxidation of Acetyl CoA in fat metabolism
acetyl CoA molecules made by beta oxidation of fatty acids enter Krebs cycle
-combine with oxaloacetic acid to form citric acid (degraded into CO2 and H atoms)
-H atoms are then oxidized
Formation of ATP from oxidation of 1 molecule of fatty acid
Net gain is 146 molecules of ATP

-104 H atoms released by degradation of 1 fatty acid molecule
-34 H removed b flavoproteins (yield 34 ATP)
-70 removed by NAD+ (yield 105 ATP)
-both group oxidized in mitochondria

---> TOTAL of 139 ATP from oxidation of H atoms of fatty acid
-9 ATP from Krebs cycle
-HOWEVER- 2 ATP used to start cycle again= 146 net
Importance of fat synthesis
give us the ability to store carbohydrates since glycogen is minimal in the body

fat stores 150 times the energy carbs can store
Proteins
composed of amino acids
-each amino acid has an acidic group (COOH) and an amino group (NH2)

-there are 10 essential amino acids that the body needs that must be obtained from food- CANNOT BE SYNTHESIZED BY THE BODY
Deamination
the breakdown of amino acids
-occurs in the liver
-mainly by transamination
-also by oxidative deamination
-during this process AMMONIA is released
-resulting keto acids can be oxidized to release energy though the krebs cycle (used the same way acetyl coA is degraded by this cycle in carb & lipid metabolism)
Urea
ammonia that is released during deamination of amino acids is removed from the blood and converted to this
-occurs in the liver
-ammonia is toxic to the body and must be removed this way by the liver
Oxidation of deaminated amino acids
removal of amino group NH2
-ammonia is released
-keto acid formed
-enters Krebs cycle
Transamination
MAIN reaction by which an amino group is removed in order for an amino acid to metabolized
-amino group is transfered to a keto acid
Peptide/Protein Hormones
-hormones of the anterior and posterior pituitary gland, pancreas (insulin & glucagon) and parathyroid gland (PTH- parathyroid hormone)
-synthesized in the rough endoplasmic reticulum of cell
-then transfered to the golgi apparatus for packaging into secretory vesicles
-vesicles stored in cytoplasm
-hormones released when vesicles fuse with cell membrane and are released by exocytosis
Steroid Hormones
-hormones of the adrenal cortex (cortisol & aldosterone), ovaries and testes and placenta
-usually synthesized from cholesterol
-not stored in vesicles (don't need to be bc they are highly lipid soluble)
-when needed, they can easily diffuse through cell membrane to enter interstitial fluid, then blood
Amine Hormones
-hormones that are made in the glands themselves
-ie: thyroid hormones (T3, T4) slow acting bc receptor is in cell nucleus
-adrenal medulla (epinephrine and norepiniephrine) fast acting bc receptor is in/or cell surface
Negative Feedback Loop
when the output of the system causes an opposite change in the variable
-constitutes over 99% of the loops that occur in our body
Positive Feedback Loops
when the output of the system causes a change in the variable which reinforces the original stimulus
ie: labor, blood clotting
*1% of all loops that occur
Cholesterol
-a lipid
-present in cellular membranes
-made up of hydrocarbons
-used to make steroids like cortisol, progesterone, estrogen & testosterone
What hormones does the hypothalamus secrete?
1. TRH (thyroid releasing hormone)
2. CRH (corticotropic releasing hormone)
3. GnRH (gonadotropic releasing hormone)
4. PIH (prolactin inhibiting hormone)
5. GHIH (growth hormone inhibiting hormone)
6. GHRH (growth hormone releasing hormone)
What hormones does the anterior pituitary secrete?
in response to hypothalamic releasing hormones,

-Growth Hormone (GH)
-TSH (thyroid stimulating hormone)
-ACTH (adrenocorticotropic hormone)
-FSH & LH (follicle stimulating hormone and luteinizing hormone)
-Prolactin
What neurohormones does the posterior pituitary secrete?
-ADH (antidiretic hormone) retains water in body, 1. affects kidney 2. raises blood pressure by contricting arterioles

-Oxytocin (stimulates contraction of smooth muscle in uterus & breasts during childbirth and nursing
Adrenal Glands
located superior to kidneys
-adrenal medulla- catecholamines - epinephrine and norepinephrine
-adrenal cortex- corticosteroids- cortisol and aldosterone
Adrenal Medulla
the middle gland
**secretes epinephine & norepinephrine (adrenaline)
Hormones of the Pancreas
-regulate blood glucose levels
*glucagon (increase blood glucose levels)
*insulin (decreases blood glucose levels)
Parathyroid
located on the posterior surface of the thyroid gland
-secretes PTH (increases blood calcium levels by stimulating osteoclasts to break down bone and release calcium)
Insulin
peptide hormone secreted into circulation during absorptive state in response to an increase in blood glucose levels
-causes a decrease in blood glucose levels
-stimulated glycogenesis
Glycogenesis
occurs mainly in the liver
-the enzymatic conversion of glucose itno gylcogen for storage
-occurs in response to the release of insulin during absorptive state
Glucagon
-comes from the pancreas
-peptide (protein) hormone secreted into circulation during postabsorptive state in response to a decrease in blood glucose levels
- causes an increase in blood glucose levels
-stimulated gluconeogenesis
Gluconeogenesis
occurs mainly in the liver
-enzymatic synthesis of glucose from noncarbohydrate molecules
-occurs in response to the release of glucagon during postabsorptive state
Hyperglycemia
-high blood sugar
-a sympton of diabetes mellitus
-caused by the inability of insulin to function properly
Hyooglycemia
-low blood sugar
-caused by hypersecretion of insulin
Aldosterone
secreted from the cortex of the adrenal gland
-causes an increase in reabsorption of Na+ and water
-causes increase in bp
-decreases levels of K+ in blood
Clearance of Hormones
two factors influence the amt of hormone in the blood

1. rate of hormone secretion
2. rate of hormone removal
- hormones cleared from plasma by destruction by tissues, binding with tissues, excretion by liver, excretion by kidneys
Locations for hormone receptors
-in or on the cell membrane (peptide, protein, catecholamines)
-in the cytoplasm (steroid)
-in the cell nucleus (thyroid hormones)
Down/Up Regulation
*number of receptors on a target tissue is not constant

ie: increase in hormone concentration and increased binding with target cell receptors may cause number of receptors to decrease

-or-

stimulating hormone will produce greater number of receptors
Hormone-receptor complex
Once a hormone binds with a receptor on the target tissue, the hormone forms this

examples are: Ion channel-linked receptors
G protein-linked receptors
Enzyme-linked protein receptors
Ion Channel-Linked Receptors
***all neurotransmitters (Norepinephrine, acetylcholine)
-change the structure of the receptor
-opens or closes channels for ions to pass
-mvmt of ions causes effects on postsynaptic cells
*few hormones work this way
G Protein-Linked Hormone Receptors
a hormone binds with a receptor that indirectly links with an ion channel or enzyme
-hormone can increase or decrease activity of intracellular enzymes bc hormone can be linked to a stimulatory or inhibitory G-protein
Enzyme-Linked Hormone Receptors
-have hormone binding sites on outside of cell membrane and catalytic or enzyme binding site on inside
-hormone binds to extracellular part and an enzyme is immediately activated on the inside of cell membrane
Pituitary Gland
-aka Hypophysis
-connected to Hypothalamus by hypophysial stalk
-anterior pituitary: adenohypophysis (6 peptide hormones)
-posterior pituitary: neurohypophysis (2 peptide hormones)
Diureses
state when too much water is lost
Diabetes Insipidus
-not enough ADH
-urinate frequently
-constantly thirsty
Control of Pituitary gland
-secretion from posterior pituitary is controlled by nerve signals that originate in the hyporthalamus
-secretion from anterior pituitary is controlled by hypothalamic releasing hormones
What are the hypothalamic releasing and inhibitory hormones?
1. TRH- thyrotropin-releasing hormone cause release of TSH- thyroid stimulating hormone
2. CRH- Corticotropin-releasing hormone cause release of ACTH- adrenocorticotropin hormone
3. GHRH- growth hormone-releasing hormone cause release of GH - growth hormone
4. GHIH- growth hormone-inhibitory hormone inhibits GH
5. GnRH- Gonadatropin-releasing hormone: release of LH and FSH
6. PIH- prolactin-inhibitory hormone: inhibits prolactin
Functions of the hormones of the Anterior Pituitary Hormones
GH- Growth Hormone: increases metabolism of fatty acids, decreases glucose utilization, increases rate of production of chondrocytic and osteogenic cells
ACTH- adrenocorticotropin hormone: stimulates production of glucocoricoids and androgens from adrenal cortex

FSH- stimulates development of ovarian follicles

LH- stimulates ovulation and production of sex hormones

Prolactin- milk production & secretion

TSH- thyroid stimulating hormone: production of thyroid hormones
Growth Hormone
secreted by the anterior pitiuitary after stimulation from GHRH from hypothalamus

-unlike all other anterior pituitary hormones, GH affects on almost all tissues of body, not just one target tissue

-increases metabolism of fatty acids
-decreases glucose utilization
-increases rate of production of chrondroycitic and osteogenic cells
Effects of Growth Hormone
-increases reproduction of chondrocytic & osteogenic cells (cartilage & bone)
-promotes conversion of chondrocytic cells to osteogenic cells
-increases protein deposit to these cells
-increased glucose production in liver
-increase of insulin
-decrease of glucose uptake in tissues (glucose is being stored)
-increased rate of protein synthesis in most cells
-mobilization of fatty acids from adipose tissue
-deceased rate of glucose utilization
*GH increases during first 2 hours of sleep
*GH stimulated by exercise, excitement, trauma, hypoglycemia, acute starvation
Thyroid Gland
located below larynx
-secretes *Thyroxine (T4)* and Triiodothyronine (T3)
**93% T4, but 1/2 T4 is converted to T3 which is the hormone that goes to tissue
-controlled by TSH of anterior pituitary gland
Transport of T3/T4
-combines with plasma proteins when it enters the blood (released slowly into tissues due to bond with plasma proteins)
-slow onset but long duration of action
-reglated by negative feedback loops
Effects of Thyroid hormones
*increase metabolism
-increase number and activity of mitochondria
-increase active transport of ions through cell membrane
-stimulation of fat & carbohydrate metabolism
-increases secretion rates of most other glands
-increase need for PTH (stimulates osteoclasts to break down dead bone)
Hyperthyroidism
Overactive thyroid
-excitability
-increased sweating
-weight loss
-muscle weakness
-inability to sleep
-nervousness tremor
Hypothyroidism
Underactive thyroid
-lethargy
-slowed heart rate
-weight gain
-decreased cardiac output
Adrenal cortex
secretes corticosteroids (derived from the steroid cholesterol)
has 3 distinct layers:
-zona glomerulosa: secretes aldosterone- controlled by angiotensin II
-zona fasciculata: secretes cortisol- controlled by ACTH
-zona reticularis: secretes adrenal adrogens
Aldosterone
Secreted by Adrenal Cortex (zona glomerulosa)
*increases blood pressure*

-increases renal sodium reabsorption
-increases potassium secretion
-increases H+ ion secretion
Regulation of Aldosterone
1. increased potassium concentration causes increased secretion of aldosterone

2. increased activity of ***renin-angiotensin system*** increases secretion of aldosterone
Coristol
-A Glucocorticoid
-secreted by the Adrenal Cortex (zona fasciculata)

-resists stress (counteracts insulin)
-slows infammation
-stimulates gluconeogenesis (increase in glycogen storage in liver, decrease in rate of glucose ultilization)
-stimulates breakdown of fats and proteins
Diaphysis
Shaft of long bone
-purpose: to withstand strong forces w/o breaking
-compact bone with thin layer of spongy bone lining inside surface
-medullary cavity in center that contains bone marrow
Metaphysis
Between growth plates and diaphysis where growth occurs
Epiphysis
End of bone
-purpose: to articulate with another bone and form joint
-composed mainly of spongy bone containing red marrow
-articular surface covered with articular cartilage
Articular Cartilage
Covers the articular surface of the epiphysis
-Purpose: shock absorption, cushioning
-composed of hyaline cartilage (most abundant cart. in body)
-very poor blood supply
-Cart damage will not heal on its own, no nerve supply to cartilage- sometimes requires microfracture surgery
Periosteum
Lines outer surface of bone except articular cartilage
-function: site of attachment for ligaments and tendons
-houses cells for bone repair
-highly innervated with nerve fibers
Medullary Cavity
Cavity located w/in Diaphysis of a long bone
-houses bone marrow- red and yellow (red: produces blood cells)
Hematopoiesis
production of blood cells in red bone marrow located in the medullary cavity
Endosteum
Thin membrane that lines the inner surface of bone w/in medullary cavity
-contains cells important in forming and repairing bone
Osteoclasts
Break down bone tissue in the matrix of the bone
-stimulated by PTH
Osteoblasts
Build up bone by secreting in the matrix tissue of bone
Osteocytes
Mature osteoblasts
-when osteoblasts are fully surrounded by matrix of the bone in small chambers called lacunae
Matrix
Collagen fibers & Osteoid tissue add resiliency and prevent bone from becoming dry

Hydroxyapatite crystals (calcium-phosphate salts) give bone its rigidity
Compact Bone
Diaphysis of long bones
Outer surfaces of epiphyses (cortex)

-Composed of osteons, which are composed of haversian canals
-Volkmann's canals connect blood vessels from one haversian canal to another
-Lacunae (which house osteocytes) are connected by canals called canaliculi
Spongy Bone
Epiphysis of long bones
Center of all bones

-Trabeculae- branches in spongy bone that border spaces
-No need for canals since spaces allow for diffusion
Endochondral Ossification
Occurs within a cartilage model
*occurs in most bones of the human body
-primarily in diaphysis (medullary cavity), secondary in epiphysis (epiphyseal plate)
Intramembranous Ossification
Occurs within a membrane
ie: flat bones of the skull
Wolf's Law
Calcium is laid down in bone in response to stress
-clinically: has a piezoelectric effect where osteoclasts cannot break down this bone= osteophyte (bone spur)
Osteoporosis
Most common bone disease
-decease in total bone mass
-primarily affects spongy bone bc it is softer
-primarily affects postmenopausal women
Tissue components of Skeletal Muscle
*Skeletal Muscle Tissue- responsible for contracting
*Fibrous Fascia- connective tissue that gives support and shape to muscle tissue
Components of Skeletal Muscle
From Large to Small:
-Muscle
-Fascicles
-Muscle fibers
-Myofibril
-Sarcomere
Endomysium
Fascia that surrounds each individual muscle fiber
Perimysium
Fascia that surrounds a group of muscle fibers **creates fascicle**
Epimysium
Fascia that surrounds entire muscle
Sarcomere
Make up Myofibrils that make up muscle fiber
-runs from one z-line to the next z-line
-functional unit of skeletal muscle- makes muscle contract
-contain actin (thin) & myosin (thick w/myosin heads)
Sliding Filament Mechanism
*requires energy from ATP
*how the sarcomere shortens are actin & myosin filaments slide along each other

1. Message from nervous system
2. sarcoplasmic reticulum releases calcium into sarcoplasm
3. Calcium ions attach to actin forming binding sites
4. Myosin heads attach to binding sites creating cross-bridges
5. Myosin heads bend to pull actin towards center
6. Cross-bridges break, reattach to next binding site and pull towards center
Energy Source for Sliding Filament Mechanism, where does it come from?
Energy from ATP to furnish cross-bridging and reuptake of Calcium into sarcoplasmic reticulum

ATP comes from
1. Stored ATP
2. Stored Creatine Phosphate (short acting)
3. Gylcolysis (anaerobic, relatively short acting)
4. Krebs cycle, oxidative phosphorylation (aerobic- longer lasting bc of oxygen)
Nervous System Control of Muscle Contraction
Motor neuron reaches muscle at the Neuromuscular junction- synaptic cleft
-binding of neurotransmitters to motor end plate initiates electrical signal along the sarcolema (mvmt along membrane, not in cell)
-signal reaches interior of muscle fiber via transverse tubules (T tubules)
-Once signal reaches interior of muscle fiber, sliding filament mechanism begins
-As long as the motor neuron is stimulating the muscle fiber, contraction will continue
Sarcoplasm
cytoplasm of muscle fiber
Sarcoplasmic Reticulum
endoplasmic reticulum of muscle fiber
Sarcolemma
cell membrane of muscle fiber
Motor Unit
*One motor neuron and all of the muscle fibers that it controls*
-small motor units produce fine mvmts
-large motor units produce gross mvmts
*there can be multiple motor units within one muscle
PTH
Parathyroid hormone- secreted by the parathyroid
-increases blood calcium by stimulating osteoclasts
Fracture & Healing of bone
after a fracture, bone goes through process of:

Hematoma: bleeding from blood vessels

Callus Formation: fibrocartilagenous tissue forms over fracture

Remodeled Bone: fibrocartilaenous tissue is replaced by bone
What two steps of the sliding filament mechanism require energy?
1. to furnish formation of cross bridges
2. for reuptake of calcium back into sarcoplasmic reticulum
All or None Response Law
* When a muscle fiber contracts, it contracts 100%
Sarcomere Structure
A-Band: dark band contains myosin & actin in the center of sarcomere

H-Band: contains ONLY myosin
M-Line: w/i the H-Band, at center of mysoin (vertically)

I-Band: light band, contains ONLY actin (btw sarcomeres)
Z-Line: borders of the sarcomere
Myosin Filament in Detail
each myosin filament looks like a golf club--> myosin protein head and myosin tail

myosin molecules are positioned so that the heads stick out at each end

many myosin filaments are bound together in one sarcomere
Actin in Detail
made up of 3 separate protein molecules

-Actin: contains binding sites for myosin
-Troponin: ability to move tropomyosin so actin binding sites are exposed
-Tropomyosin: block binding sites of actin

*actin binding sites are not normally exposed- only when sliding filament mechanism occurs
Types of Muscle Fibers
Fast Fatiguable Fibers (FF)

Fast Fatigue-Resistant Fibers (FR)

Slow Fibers (SO)
Fast Fatiguable Fibers
Large axonal connections
multiple fibers innervated by each axon
Large fiber diameters
Very fast twitch time
Extremely high tension develops (quads)
Unable to maintain constant tension w/o rest

-High ATP-ase activity (breaking down of ATP)
-High levels of glycolytic enzymes
-Low levels of oxidative enzymes
Fast Fatigue-Resistant Fibers
Moderate sized axonal connections
Multiple fibers innervated by each axon
Moderate fiber diameters
Fast twitch time
High tension development
Maintain tension, but reduces over time w/o rest

-High ATP-ase activity
-High levels of glycolytic enzymes
-High levels of oxidative enzymes
Slow Fibers
SO

Small sized axonal connections
Few fibers innervated by each axon
Small fiber diameters
Delayed twitch time
Limited tension development
Maintain constant tension w/numerous contractions w/o rest

-Low ATP-ase activity
-Low levels of glycolytic enzymes
-High levels of oxidative enzymes

ie: soleus- constantly firing while we stand
Longitudinal Muscle
Muscle w/fibers that run longitudinally
types:
Fusiform
Strap
Rectangular
Rhomboidal
Trianglar (fan)
Pennate Muscle
Muscle w/fibers arranged in a feather-like manner

-Unipennate: central tendon w/fibers running diagonally off side of tendon

-Bipennate: central tendon w/fibers running diagonally off both sides of tendon

-Multipennate: more than one central tendon w/fibers running diagonally off one or both sides of tendon
Difference btwn Longitudinal Muslce & Pennate Muscle
Longitudinal Muscle-
*Long muscle fibers, but less
*Fibers oriented along entire length of muscle
*Results in more force on tendon

Pennate Muscle
*Short muscle fibers, but many
*Fibers oriented at oblique angle (pennation angle) to the length of muscle
*Pennation angle results in less force on tendon
Active Tension
Muscle Tension created by sliding filament mechanism
Passive Tension
Muscle tension created by fascia
Total tension
Active & Passive Muscle Tension combined
What does the strength of a muscle's contraction depend on?
The number of cross bridges formed
What is Active Insufficiency?
Muscle weakness secondary to a decrease in the number of cross bridges

-Due to muscle being too short of too long (ie: complete wrist flexion of extension prevents tight grip)
When is muscle tension the greatest?
At the muscle's resting length- allows for maximal cross bridge interaction
What does isometric force do?
Provides stability to joints
Explain the Force Velocity Curve for Concentric/Eccentric/Isometric Conraction
Concentric: As load increases, velocity of shortening decreases

Eccentric: As load increases, velocity of lengthening increases

Isometric: No velocity
Muscle Spidles
Sensory receptors w/in the belly of the muscle
-detect lengthening
-causes spinal cord to initiate reflex contraction to prevent tearing
Plyometric training
exercise training designed to produce fast, powerful mvmts, typically for athletes
Gamma Motor System
Sets the sensitivity of a muscle spindle
*Sets resting tone of muscle
-gamma LMN travels from spinal cord and synapses with intrafusal fibers of the muscle spindle
-gamma LMN can contract the muscle spindle to make it more taut and therefore more sensitive to stretch
-
Alpha Motor System
Directs actual muscle contraction by stimulating contraction of extrafusal fibers of muscle
Golgi Tendon Organs
Located w/in the tendon
-prevents tendon from being torn
-attached between sensory neuron and muscle fibers
-sensitive to pulling forces on tendon