Exam III Phys

How is a skeletal muscle fiber different from a typical cell?

• Long, cylindrical, striated, and multinucleated.

• Sarcomeres contain actin and myosin for contraction.

• T-tubules conduct electrical signals.

• Sarcoplasmic reticulum (SR) stores Ca²⁺

What are the three functional states of thin filaments?

• Blocked: Tropomyosin prevents myosin binding.

• Closed: Ca²⁺ binds TnC, allowing weak myosin binding.

• Open: Strong myosin binding shifts tropomyosin further, promoting contraction.

What are the three myosin crossbridge states, and how does ATP regulate them?

• Detached: ATP binds myosin, causing detachment.

• Weakly bound: Energized myosin attaches to actin.

• Strongly bound: Pi release promotes the power stroke.

• ATP hydrolysis energizes the myosin head for the next cycle.

What are the steps of skeletal muscle excitation-contraction coupling and relaxation?

• Contraction: ACh → Muscle AP → T-tubules → DHPR → RyR → SR releases Ca²⁺ → TnC → Contraction.

• Relaxation: SERCA uses ATP to return Ca²⁺ to the SR, allowing tropomyosin to block actin.

Why does rigor mortis eventually progress to secondary flaccidity?

• ATP depletion prevents SERCA function and myosin detachment.

• Persistent actin-myosin binding produces rigor mortis.

• Proteolytic degradation of muscle proteins produces secondary flaccidity.

How do skeletal, cardiac, and smooth muscle differ structurally and functionally?

• Skeletal: Striated, multinucleated, voluntary, somatic motor control.

• Cardiac: Branched, striated, involuntary, intercalated discs, ANS modulation.

• Smooth: Spindle-shaped, non-striated, involuntary, autonomic and hormonal control.

How do gap junctions create a functional syncytium?

Gap junctions allow electrical current to pass between adjacent cardiac or single-unit smooth muscle cells, synchronizing depolarization and contraction.

Where does contraction-triggering Ca²⁺ come from in each muscle type?

• Skeletal: SR through DHPR-RyR coupling.

• Cardiac: Extracellular Ca²⁺ triggers SR release (CICR).

• Smooth: Extracellular Ca²⁺ influx and IP₃-mediated intracellular release.

How does Ca²⁺ regulation differ between striated and smooth muscle?

• Striated: Ca²⁺ binds troponin C → Tropomyosin shifts → Contraction.

• Smooth: Ca²⁺ binds calmodulin → MLCK activates → Myosin phosphorylation → Contraction.

• Relaxation in smooth muscle: MLCP dephosphorylates myosin.

How do concentric, eccentric, and isometric contractions differ?

• Concentric: Muscle shortens (lifting a dumbbell).

• Eccentric: Muscle lengthens while resisting a load (lowering a dumbbell).

• Isometric: Muscle generates tension without changing overall length (holding a dumbbell).

Why do muscles use different fuels depending on exercise intensity and duration?

• Brief/explosive: Stored ATP and creatine phosphate.

• High intensity: Anaerobic glycolysis using glucose/glycogen.

• Prolonged/low intensity: Aerobic metabolism using carbohydrates and fats.

What do respiratory quotient (RQ) values of 1.0, 0.8, and 0.7 indicate?

• RQ = 1.0: Carbohydrate oxidation.

• RQ ≈ 0.8: Mixed fuel use or protein oxidation; often associated with rest.

• RQ = 0.7: Fat oxidation.

How do slow, intermediate, and fast muscle fibers differ?

• Slow (Type I): Aerobic, high myoglobin, fatigue-resistant.

• Intermediate (Type IIa): Oxidative and glycolytic, balanced endurance and power.

• Fast glycolytic (Type IIx): Rapid, powerful contractions; fatigue quickly.

How do motor unit recruitment, rate coding, and twitch summation increase muscle force?

• Recruitment: Activates more motor units.

• Rate coding: Increases motor neuron firing frequency.

• Twitch summation: Repeated stimulation before relaxation increases total tension.

How does the length-tension relationship differ between skeletal and cardiac muscle?

• Skeletal: Operates near the plateau → Relatively stable force.

• Cardiac: Operates on the ascending limb → Greater stretch increases force (Frank-Starling mechanism).

How is skeletal muscle force regulation different from cardiac output regulation?

• Skeletal: Motor unit recruitment and firing frequency.

• Cardiac: Heart rate, stroke volume, Ca²⁺ signaling, ventricular filling, and ANS regulation.

Cardiac output = Heart rate × Stroke volume.

What pathway does blood follow through the heart and major blood vessels?

• Pulmonary circuit: Venae cavae → Right atrium → Tricuspid valve → Right ventricle → Pulmonary valve → Pulmonary arteries → Lungs.

• Systemic circuit: Pulmonary veins → Left atrium → Mitral valve → Left ventricle → Aortic valve → Aorta → Body.

What are the three layers of the heart wall and their functions?

• Epicardium: Outer protective layer.

• Myocardium: Contracting cardiac muscle that generates pumping pressure.

• Endocardium: Inner endothelial lining.

How do desmosomes and gap junctions coordinate cardiac contractions?

• Desmosomes: Mechanically attach cardiomyocytes and prevent separation.

• Gap junctions: Allow electrical signals to spread between cells, coordinating contractions.

Which ion channels produce the action potential in cardiac pacemaker cells?

• HCN channels: Contribute to spontaneous pacemaker depolarization.

• Ca²⁺ channels: Produce the action potential upstroke.

• K⁺ channels: Produce repolarization.

Which ion channels produce the action potential in cardiac contractile cells?

• Na⁺ influx: Rapid depolarization.

• Ca²⁺ influx: Plateau phase.

• K⁺ efflux: Repolarization.

What is the cardiac conduction pathway?

SA node → Atria → AV node → Bundle of His → Right/left bundle branches → Purkinje fibers → Ventricles.

The AV node delays conduction to allow atrial contraction before ventricular contraction.

How does calcium-induced calcium release (CICR) produce cardiac contraction?

• Depolarization opens L-type Ca²⁺ channels.

• Incoming Ca²⁺ activates RyR on the SR.

• SR releases additional Ca²⁺.

• Ca²⁺ binds troponin C → Contraction.

Why can cardiac muscle not undergo tetanus?

Its prolonged absolute refractory period overlaps most of the contraction, preventing twitch summation and allowing the heart to relax and refill.

What do the P wave, QRS complex, and T wave represent on an EKG?

• P wave: Atrial depolarization.

• QRS complex: Ventricular depolarization.

• T wave: Ventricular repolarization.

Electrical activity precedes mechanical activity.

What is the sequence of mechanical phases during the cardiac cycle?

1. Atrial systole → Completes ventricular filling.

2. Isovolumetric contraction → Pressure increases.

3. Ventricular ejection → Blood exits ventricles.

4. Isovolumetric relaxation → Pressure decreases.

5. Passive ventricular filling → Ventricular volume increases.

How do pressure changes control the opening and closing of heart valves?

• AV valves open: Atrial pressure exceeds ventricular pressure.

• Semilunar valves open: Ventricular pressure exceeds arterial pressure.

• Valves close: Pressure gradients reverse, preventing backflow.

How do ventricular pressure, aortic pressure, and ventricular volume change in a Wiggers diagram?

• Filling: Ventricular volume increases.

• Isovolumetric contraction: Ventricular pressure increases; volume unchanged.

• Ejection: Ventricular volume decreases; aortic pressure initially rises.

• Isovolumetric relaxation: Ventricular pressure decreases; volume unchanged.

What are the four phases of a cardiac pressure-volume loop?

1. Ventricular filling: Volume increases.

2. Isovolumetric contraction: Pressure increases; volume constant.

3. Ventricular ejection: Volume decreases.

4. Isovolumetric relaxation: Pressure decreases; volume constant.

What do preload, afterload, and contractility represent on a pressure-volume loop?

• Preload: Ventricular filling/stretch; related to end-diastolic volume (EDV).

• Afterload: Pressure opposing ventricular ejection.

• Contractility: Ability to generate force, reflected by the end-systolic pressure-volume relationship.

How do venous return and preload affect stroke volume?

Increased venous return → Increased EDV/preload → Greater sarcomere stretch → Stronger contraction → Increased stroke volume (Frank-Starling mechanism).

How do heart rate and stroke volume determine cardiac output?

Cardiac output (CO) = Heart rate (HR) × Stroke volume (SV). Increasing either variable increases CO if the other remains constant.

How does the autonomic nervous system regulate pacemaker firing frequency?

• Sympathetic: NE → β₁/Gs → cAMP ↑ → HCN/Ca²⁺ activity ↑ → HR ↑.

• Parasympathetic: ACh → M₂/Gi → cAMP ↓ and K⁺ efflux ↑ → Hyperpolarization → HR ↓.

How do arteries, capillaries, and veins differ in their wall structures?

• Arteries: Thick tunica media containing smooth muscle.

• Capillaries: Thin endothelium and basement membrane.

• Veins: Thinner walls, larger lumens, and valves.

How does capillary structure promote nutrient and gas exchange?

Thin simple squamous endothelium and basement membranes minimize diffusion distance, allowing efficient exchange. Fenestrations increase permeability in certain capillaries.

How do vessel radius, viscosity, and length affect vascular resistance?

• Radius ↑: Resistance decreases substantially.

• Viscosity ↑: Resistance increases.

• Vessel length ↑: Resistance increases.

Resistance is proportional to 1/r⁴. Halving radius increases resistance approximately 16-fold.

How does blood vessel branching affect blood pressure, velocity, and resistance?

• Capillaries: Greatest total cross-sectional area and slowest velocity.

• Arterioles: Greatest adjustable resistance and major pressure drop.

• Veins: Blood velocity increases as total cross-sectional area decreases.

What are the major components of blood and their proportions?

• Plasma (55%): Mostly water, proteins, and solutes.

• Formed elements (45%): RBCs, WBCs, and platelets.

• Hematocrit: Percentage of blood volume occupied by RBCs.

How do RBCs, WBCs, and platelets differ in structure and function?

• RBCs: Biconcave, no nucleus; transport O₂ using hemoglobin.

• WBCs: Defend against pathogens and regulate immune responses.

• Platelets: Megakaryocyte-derived fragments involved in clotting.

How do different organs coordinate RBC production and heme recycling?

• Kidneys: Release erythropoietin (EPO).

• Bone marrow: Produces RBCs.

• Spleen: Macrophages remove aging RBCs and recycle iron.

• Liver: Processes bilirubin from heme breakdown and excretes it into bile.

How does regulation of RBC production differ from WBC production?

• RBCs: Kidney-derived EPO stimulates erythropoiesis during low oxygen.

• WBCs: Colony-stimulating factors regulate production.

• G-CSF: Granulocytes.

• M-CSF: Monocytes.

• GM-CSF: Granulocytes and monocytes.

• Multi-CSF: Multiple blood cell lineages.

How does the lymphatic system return excess interstitial fluid to the bloodstream?

Interstitial fluid → Lymphatic capillaries → Lymphatic vessels → Lymph nodes → Thoracic/right lymphatic duct → Venous circulation.

Skeletal muscle movement and breathing help propel lymph.

How do primary and secondary lymphoid organs differ?

• Primary: Lymphocyte maturation. Bone marrow (B cells), thymus (T cells).

• Secondary: Lymphocyte activation. Lymph nodes, spleen, tonsils, and MALT.

What are cytokines, CD molecules, PAMPs, and DAMPs?

• Cytokines: Immune signaling proteins (IL-2).

• CD molecules: Cell identification/signaling markers (CD4, CD8).

• PAMPs: Pathogen-associated patterns (bacterial LPS).

• DAMPs: Cellular injury signals (extracellular ATP).

How do innate and adaptive immunity differ, and which cells participate?

• Innate: Rapid, broad defense; neutrophils, macrophages, mast cells, dendritic cells.

• Adaptive: Antigen-specific defense; B cells, CD4 helper T cells, CD8 cytotoxic T cells.

How do innate immune responses differ between bacterial and viral infections?

• Bacterial: PAMP/DAMP detection → Inflammation → Neutrophil recruitment → Phagocytosis.

• Viral: Type I interferons establish an antiviral state; CD8 T cells later kill infected cells presenting viral antigens on MHC I.

What causes the four cardinal signs of inflammation?

• Redness: Vasodilation.

• Heat: Increased local blood flow.

• Swelling: Increased vascular permeability.

• Pain: Tissue injury and inflammatory stimulation of nociceptors.

How do innate and adaptive defenses differ in timing and specificity?

• Innate: Immediate, broad recognition; barriers, phagocytes, inflammation, interferons.

• Adaptive: Slower during first exposure, antigen-specific; B/T cells and immunological memory.

How do CD4 helper T cells and CD8 cytotoxic T cells differ in activation?

• CD4: Recognizes antigens presented on MHC II; helps coordinate immune responses.

• CD8: Recognizes antigens presented on MHC I; kills infected cells.

• Both: Require B7-CD28 co-stimulation and undergo clonal expansion.

How do memory B and T cells provide long-term protection?

• Memory B cells: Support faster antibody responses upon re-exposure.

• Memory T cells: Support faster antigen-specific cellular immune responses.

• Both produce a faster secondary immune response.

How does antibody structure determine its function?

• Two heavy + two light chains: Form a Y-shaped antibody.

• Variable regions: Bind specific antigens.

• Constant/Fc region: Interacts with immune cells, promoting pathogen clearance.