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78 Cards in this Set

  • Front
  • Back
3 types of connective tissue in skeletal muscle
Endomysium
Perimysium
Epimysium
Endomysium
surrounds muscle fibers
Perimysium
surrounds fascicles
Epimysium
surrounds whole muscle
What is a motor unit?
one motor neuron plus all the muscle fibers that it innervates
Motor Unit Summation
The muscle fibers in one motor unit are spread out in the muscle. As increased force is required, more motor units are recruited.
Sarcolemma
cell membrane of muscle fiber
Muscle Twitch
one action potential on a muscle fiber - a quick weak contraction
Latent Period
delay between action potential on sarcolemma and initiation of contraction
Twitch summation
if frequency of stimulation is high enough, twitches add together to create more force
Isotonic
muscle allowed to shorten as it contracts
Isometric
Muscle not allowed to shorten. Tension developed measured
Concentric
Force overcomes load; muscle shortens as it contracts. (lifting something, for example)
Eccentric
Force insufficient to overcome load; muscle lengthens as it contracts (lowering something gently, for example)
Type I Muscle Fiber
slow twitch muscle,
oxidative phosphorylation,
high fatigue resistance,
red in color,
high mitochondria content,
used primarily in maintaining posture and walking,
first type of muscle recruited in sedentary individuals.
Type IIa Muscle Fiber
fast twitch
oxidative phosphorylation, intermediate fatigue resistance,
red in color,
high mitochondria content, recruited second
used mostly for endurance activities like walking and jogging.
Type IIx Muscle Fiber
fast twitch
glycolysis,
low fatigue resistance,
white in color,
low mitochondria content, recruited last in the body
only recruited during exercise that requires maximum effort like sprinting.
endurance training and muscular inactivity may result in small changes in the percentage of... _____
IIa and IIx fibers
aging results change of percentage _____ to ____
Fast twitch --> slow twitch
Trained muscles delay fatigue by:
*Making ATP faster
*drawing on fat instead of glycogen
*increasing mitochondria levels
*forming less lactate due to more ATP
mTOR
the "mammalian target of rapamycin"
-regulates cell: growth, proliferation, motility, survival
-regulates protein synthesis and transcription
-major regulator of muscle mass
3 ways increasing mitochondrial production improves endurance
-increased ATP production (most important)
-greater contribution of fat
-decreased protein synthesis
AMPK
(just acronym)
activated protein kinase
What roles do AMPK play?
*increases the mitochondrial content of the muscle
*inhibits mTOR and blocks protein synthesis,
*increases beta oxidation,
*increases glucose levels in the muscle
LKB1
(acronym and function)
Liver Kinase B1
-activates and phosphorylates AMPK
What do gap junctions do?
Connect the cells in the heart so that ions from action potentials spread from one cell to next, causing all cells to contract
Pulmonary Circulation
*right side of heart
*carries blood between heart and lungs
Systemic Circulation
*left side of heart
*carries blood between heart and rest of body
SA node
the pacemaker of the heart, composed of P-cells,
don't have normal resting potential
AV node
Slowly conducting fibers,
delay at the AV-node allows ventricles to fill before contraction occurs there
Bundle of His
Rapidly conducting fibers,
transmit electrical impulses from AV-node to the point of the apex of the fascicular branches
Perkinje Fibers
Rapidly conducting fibers, uses the electrical impulses from the bundle of his to innervate the ventricles causing the cardiac muscle to contract at a paced interval
ECG
electrocardiogram
-used to measure heart beat
-used when electrical impulses are conducted to body surface and measured
Diastole
relaxation
isovolumetric relaxation, ventricular filling
Systole
contraction
isovolumetric contraction, ventricular ejection
Tachycardia
> 100 beats/min
Bradycardia
<60 beats/min
atrial fibrillation
rapid, irregular, uncoordinated depolarizations of the atria with no definite P waves
Ventricular fibrillation
uncoordinated contractions of ventricles, much more serious than atrial fibrillation
Myocardial ischemia
insufficient blood supply to a region of the heart
Lub
closing of atrial valves
Dub
closing of aortic/pulmonary valves
stenotic valve
stiff, narrowed valve that does not open completely
insufficient valve
valve that cannot close completely due to scarred edges
Hypertrophic Cardiomyopathy
abnormal enlargement of the heart muscle.
caused by genetic disorder
often the first symptom among young athletes is sudden death
What are SV, EDV, ESV, CO (or Q)?
How do you calculate CO and SV?
SV: stroke volume

EDV: end diastolic volume is the volume of blood in ventricle before contraction
ESV: end systolic volume is the volume of blood in ventricle after contraction

CO: cardiac output is the total volume of blood pumped by the ventricle per minute

SV= EDV - ESV

CO= HR x SV
Frank-Starling law
the greater the filling, the stronger the contraction, the smaller the end systolic volume
How does sympathetic stimulation affect the Frank-Starling curve?
NE (Sympathetic Nervous System) increases strength of contraction at any given initial fiber length by increasing the rate of sarcoplasmic calcium accumulation. This leads to a more rapid ejection of blood from the ventricles and a decrease in end systolic volume. This increases the stroke volume and moves the Frank-Starling curve up and to the left on the graph.
How is cardiac output regulated?
By regulating heart rate and regulating stroke volume
atherosclerosis:
condition in which an artery wall thickens as the result of a build-up of fatty materials such as cholesterol
arteriosclerosis
any hardening (and loss of elasticity) of medium or large arteries, stiffening of the arteries
Thromboembolism
the formation of a blood clot inside a blood vessel, obstructing the flow of blood
Factors that affect resistance to blood flow:
viscosity of fluid,
length of the vessel,
radius of the vessel <---
How is resistance affected by decreasing the diameter of the vessel?
Decreasing the size of the vessel by one half increases the resistance by a factor of 16. If you decrease the size of the vessel by half you times the blood flow by 1/16
equation to find Flow
Flow = Pressure Gradient/Resistance
5 major types of blood vessels
Arteries
Arterioles
Capillaries
Venules
Veins
Arteries
Rapid transport
low resistance
large diameter
designed to withstand high pressure.
act as pressure reservoirs
Arterioles
resistance vessels,
have smooth muscle rings that regulate radius and resistance,
Capillaries
place of nutrient exchange
Venules
collect blood from capillaries
Veins
thin-walled;
contain smooth muscle
can contract or dilate to serve as blood reservoirs
Two ways of measuring blood pressure:
-Using a cannula connected to a manometer
-auscultatory method
Mean arterial pressure
(systolic + 2(diastolic))/3
Pulse Pressure
the difference between systolic and diastolic blood pressure
Erythrocytes
Red blood cells that carry oxygen
Leukocytes
White blood cells that defend against disease.
albumin
maintains oncotic pressure
Globulin
plays a role in blood clotting, immunodefense, and other functions
Fibrinogen
Plays a role in blood clotting.
Oncotic Pressure
Osmotic pressure developed across the capillary membranes due to the plasma proteins in the blood
3 major steps of hemostasis
vasoconstriction or vasculure spasm,
formation of platelet plug,
formation of fibrin mesh
Intrinsic pathway of fibrin mesh formation
7 steps, all chemicals necessary for this pathway are found in the blood, it gets stronger as it goes down each step
Extrinsic pathway of fibrin mesh formation
4 steps, chemical released by damaged tissue initiates a shortcut, it is faster than intrinsic but not as strong.
Anemia:
a deficiency of Red Blood Cells (leads to decreased oxygen-carrying capacity of blood.)
<40 in men and <37 in women.
Types of Anemia
-hemorrhagic: loss of blood.
-Pernicious: nutritional deficiency; not enough vitamin B12.
-Sickle-cell: abnormal hemoglobin,
-Renal: kidney disease leads to decreased erthropoitin production.
-Aplastic: bone marrow cells destroyed by radiation/drugs.
Polycythemia
Too many red-blood cells
types of polycythemia
primary (polycythemia vera): bone-marrow tumor,
secondary:
chronic hypoxia (high altitude), blood doping: inject red blood cells or erthropoietin.
Hemophilia
Genetic deficiency of one of the clotting factors (usually VIII)