exphys exam 1 dr b

5 functions of CV system

Deliver o2 & substrates, remove metabolic waste, thermoregulation, immune function, acid-base balance

SA Node function

Depolarization. Internal pacemaker of the heart

AV Node function

Signal release, “quick delay” allows for ventricular filling

Heart murmur and cause

Abnormal sounds. Caused by stenosis or prolapse

Atherosclerosis

Narrowing of coronary artery due to formation of plaque

Myocardium composition (fiber type)

Type I fibers (highly resistant to fatigue)

Myocardium is rich in what cell structure

Very high in capillaries and mitochondrial density

Desmosomes in cardiac muscle

Anchor individual cells and gap junctions to maintain structural identity

Autonomic Neural Hypothesis

One mechanism behind exercise induced reductions in HR. ANH: shift from sympathetic to parasympathetic activity dominance (increase in vagal tone)

Intrinsic Rate Hypothesis

one mechanism behind exercise induced reductions in HR. Change in inherent pacemaker rate (rate of spontaneous depolarization of SA node)

p wave

Atrial depolarization

qrs complex

Ventricular depolarization

t wave

Ventricular repolarization

arrhythmia

Irregular heartbeat

A-Fib

Depolarization at 200-400 bpm. Does not allow for atrial kick

PVC

Premature Ventricular Contraction. Normal when training, but not in succession.

Ventricular Tachycardia

Rapid, abnormal heart rhythm originating in the ventricles. Bc ventricles are beating faster than the heart can fill, this results in a lack of oxygenated blood to the body

V-fib

Severe heart rhythm disorder when the ventricles quiver instead of contracting, resulting in no blood being pumped to brain or body

Atrial kick (70/30)

Active contraction of the atria forces the leftover blood into the ventricles before they pump blood out. Roughly 70% of the blood flows passively while the heart is resting and relaxed. Other 30% is the atrial kick, essentially just the contraction of the atria that forces the remaining blood into the ventricles

Ejection fraction

How much blood is left over in comparison to the amount that was originally there

Frank-Starling Mechanism

Force of contraction is a result of fiber lengths. Increased ventricular filling is equal to higher contraction force. Increased EDV causes greater fiber stretch and results in a more forceful contraction. May also lead to ejection volume

Torsional Contraction

A more efficient way to get blood out of the heart. Aids in ventricular ejectiIon

3 primary factors that blood flow resistance thru vessels are dependent on

Vessel size, blood viscosity, vessel length

Increased blood flow occurs via which two potential mechanisms

Increasing pressure gradient (heart is pumping harder and faster = increase Q, which raises P at the beginning of the arterial system) OR decreasing vascular resistance (vasodilation)

Vasomotor tone

Moderate vessel constriction to maintain BP = tonic vasoconstriction

Functional Sympatholysis

Endothelial Derived Hyper Polarizing Factor is released which prevents arterioles from vasoconstrictions, allowing more o2 delivered to working tissues (prevents fight or flight response)

How is compensatory vasodilation caused

Hypoxia (lack of O2 to tissues)

What are the 3 most abundant MHC isoforms?

MHC - Myosin-Heavy Chain. Type I, Type IIa, and Type IIx

What is the difference between a phenotype and isoform

Isoform is the genetic representation, whereas phenotype is the physical representation of what muscle fiber does

What type of phenotype does most exercise promote

Slow-twitch phenotype, but must have specific programming to also target higher threshold phenotypes

Sliding filament theory does not explain…

Mechanics of active muscle lengthening

Winding Filament Theory

Modern mod of sliding filament theory. Explains how muscles produce so much force, especially when lengthening under tension. Explains eccentric contraction → think of stretching a slinky then releasing it

Properties of active muscles mimic the actions of

A spring. Can store and return elastic potential energy. Greater tensile force when stretched and less tensile force when shortened proportionate to their change in length. Think: hamstring and rubber band example from class

If muscles can shorten against either a max load or lighter load at ~MVC, please explain the differences in energy recovery versus storage

Shortening slow→ energy storage dominant, stored thru thin filament rotation, PEVK wind around actin

Bc muscle contraction is so slow, elastic energy recovered from, PEVK segment is very small

Shortening fast → energy recovery dominant, thin filament translation

Bc muscle contraction is so fast, active release and recovery of energy from PEVK segment exceeds that of storage via thin filament rotation

3 roles of Titin in the muscle

• myosin stabilizer

• Prevents overstretching of sarccomere

• Acts as a spring to increase low-cost eccentric force generation

Steps of muscle contraction

Action potential reaches motor neuron → AP travels to axon terminal, Ach is released to transmit potential across synapse to muscle → AP causes sodium to enter cell membrane (depolarization), AP signal to T-tubules to SR which causes a release of calcium into sarcoplasm → CAlcium binds to troponin on actin heads, shifts tropomyosin off actin heads and allows for myosin binding → Myosin head finds actin, cross bridge formed, myosin TILTS and PULLS (power stroke) actin in to generate force → many power strokes occur during contraction (sliding filament theory) → continued contraction until myosin reaches z lines, or when calcium retreats to SR → muscle returns to relaxed state, tropomyosin covers actin binding site

Type I Muscle fiber

Aerobic form, slower contraction speed, recruited most frequently, has small motor neuron size, slow conduction speed (110ms). Has low glycolytic ability, and is fatigue resistant.

Type II muscle fibers

Anaerobic, faster contraction speed, 50 ms conduction time.

Type II has greater power capacity due to:

larger fiber size

more innervations in their motor units

more effective SR for calcium release

can reach peak tension faster

Type IIa has a good glycolytic ability, but IIx is even greater

IIa had moderate fatigue resistance, where IIx has very little resistance

What are two primary factors that increase the contraction force of a muscle?

Increased motor unit recruitment and frequency of stimulation

Rate coding

Increasing rate of motor unit firing

Force velocity relationship

Concentric→ ability for muscle to generate force decrease as speed of movement increase, ie relationship is inversely proportional

Ecc → ability to generate force increases as speed of movement increases, in other words: relationship is proportional

Length-Tension relationship

How muscle force is produced is dependent on starting length of the muscle.

Active force at longer lengths is decreased (reduction in the amount of cross bridges formed)

Active force = peak at resting

The more stretched, the more passive tension dominates

Active force = # of cross b’s

Passive force = degree of stretch

Relationship between thoracic volume and lung pressure

During inspiration, increased thoracic volume results in a pressure decrease (boyle’s law states in inversely proportional relationship between volume and pressure)

Tidal volume

Amt of air that moves in/our of lungs during normal respirations

Think rolling in/out with the tides, very relaxed (like normal breathing)

Total lung capacity

The volume of air that lungs can hold after a very deep inspiration

Residual volume

The air that remains in lungs even after exhaling as hard as possible. Like, cannot forcibly exhale this trapped air under any circumstances

Vital capacity

Amount of air exhaled after maximum inhalation

ERV

Expiratory Reserve Volume. Amount of air you can forcibly exhale after normal exhale

ERV

Expiratory Reserve Volume. Amount of air you can forcibly exhale after normal exhale

FRC

Functional Residual Capacity. Volume of air left over in the lung after normal exhalation

Why is pulmonary pressure is lower than arterial pressure

Pressure = flow * resistance.

Blood flow to lungs is equal volume to systemic circulation

Lungs offer less resistance to blood flow; located right next to the heart. Short distance and highly elastic vessel network allow teh same volume of blood to circulate with far less force needed to pump blood to the rest of the body

PO2 and PCO2 at atmosphere for arterial and venous blood

A→100 mmHg PO2 and 40 mmHg PCO2 (leaving lungs)

V→ 40 mmHg PO2 and 46 mmHg PCO2 (returning to heart/lungs)

What type of pressure gradient across the membrane will result in greater/faster diffusion? What advantage in diffusion does CO2 have over O2 and why it matters?

Steeper pressure gradient results in faster diffusion. Fick’s law states gas exchange is proportional to the diff in partial pressure btwn 2 sides of a membrane. CO2 has a far greater advantage because it is 20x more solvable in body tissues, which allows it to diffuse rapidly, despite having a smaller pressure gradient. It matters because this means your body can easily and quickly clear toxic CO2 waste

Reasons why the graph might shift right in O2 dissociation

Increased temp, increased PCO2, increased 2,3 BPG/DPG, decreased pH

Decreased hemoglobin affinity for O2 AKA easily releases O2 to tissues

Reasons the graph might shift left in O2 dissociation

Decreased temp, lower pH, decreased PCO2, presence of fetal hemoglobin, carbon monoxide binding

Increased Hb affinity for O2, facilitating more O2 to lungs instead of surrounding tissue

g of Hb/100mL is avg for a human. How about the difference btwn men and women

~15g of Hb avg

~12-16g Hb for women

~~14-18g Hb for men

Bohr and Haldane effect

Bohr - O2 dump in tissues. Helpful in high intensity exercise

→ increased CO2 and H ions will decrease Hb affinity for O2, forcing it to unload O2 in working tissues where waste products are high

Haldane - CO2 dump in lungs.

→ deoxyHb has higher affinity for CO2 compared to oxyHb. Increased O2 and PCO2 in lungs cause decreased affinity of Hb for CO2. CO2 released in lungs for expiration

Ways CO2 is expelled

Bicarbonate (CO2 to lungs, majority is done this way)

Bound to Hb (Carbaminohemoglobin) globin of Hb

Dissolved in blood plasma

How does low PO2 in the mitochondria and PCO2 difference between muscles and capillaries facilitate O2 and CO2 transfer between tissues?

Incredibly low po2 in mitochondria creates a steeeep pressure gradient that pulls O2 out of capillaries and into the cells where it is consumed

Working muscles produce high levels of CO2 creating a steep pressure gradient that forces CO2 out of the muscle cells and into the low pressure capillary blood for removal

How does high PO2 in the lungs and low PCO2 in the alveoli facilitate reoxygenation of blood and expiration of CO2.

High PO2 in the lungs creates a pressure gradient that drives O2 from the alveoli across respiratory membrane and into the lower-oxygen deoxygenated blood.

LOW PCO2 in the alveoli creates a gradient that forces higher pressure CO2 carried by the blood to rapidly diffuse out into the air sacs so it can be exhaled

Where is 2,3-diphosphoglycerate found and why it is important to O2 delivery?

Found in Red Blood Cells. 2,3 DPG loosely binds to Hb, reducing its affinity for O2, allowing for more O2 to release in tissue, given a PO2 decrease (important when in areas with high altitude AKA low PO2)