Muscle and Cardiovascular Physiology: Study Guide (Chapters 12–15)

Skeletal Muscle Physiology

Skeletal Muscles

Skeletal muscles are voluntary muscles attached to bones and responsible for body movement. They are composed of long, multinucleated fibers with a striated appearance due to the arrangement of contractile proteins.

• Structure: Muscle fibers, myofibrils, sarcomeres (functional units), and connective tissue sheaths.

• Function: Produce movement, maintain posture, stabilize joints, and generate heat.

Sarcomere Structure (Bands)

The sarcomere is the basic contractile unit of muscle fiber, defined by the area between two Z-discs.

• A band: Dark region containing thick (myosin) filaments; includes overlap with thin (actin) filaments.

• I band: Light region containing only thin (actin) filaments.

• H zone: Central region of A band with only thick filaments.

• M line: Center of the H zone; holds thick filaments together.

• Z disc: Boundary of the sarcomere; anchors thin filaments.

Transverse Tubules (T-Tubules) and D1/HP Receptor

T-tubules are invaginations of the muscle cell membrane that transmit action potentials into the muscle fiber. The DHP receptor (dihydropyridine receptor) acts as a voltage sensor in the T-tubule membrane, triggering calcium release from the sarcoplasmic reticulum via the ryanodine receptor.

Steps of Muscle Contraction (Excitation-Contraction Coupling)

1. Action potential travels down motor neuron to neuromuscular junction.

2. Acetylcholine (ACh) is released, binding to receptors on the muscle fiber.

3. Muscle fiber depolarizes; action potential travels along sarcolemma and T-tubules.

4. DHP receptor senses voltage change, activates ryanodine receptor, releasing Ca2+ from sarcoplasmic reticulum.

5. Ca2+ binds to troponin, shifting tropomyosin and exposing myosin-binding sites on actin.

6. Myosin heads bind to actin, initiating the contraction cycle (sliding filament theory).

7. Ca2+ is pumped back into the sarcoplasmic reticulum for relaxation.

Sliding Filament Theory (Contraction Cycle)

• Myosin heads attach to actin, forming cross-bridges.

• Power stroke: Myosin head pivots, pulling actin filament toward the center of the sarcomere.

• ATP binds to myosin, causing detachment from actin.

• ATP hydrolysis re-cocks the myosin head for another cycle.

Isotonic vs. Isometric Muscle Contraction

• Isotonic contraction: Muscle changes length (shortens or lengthens) while tension remains constant (e.g., lifting a weight).

• Isometric contraction: Muscle develops tension without changing length (e.g., holding a weight steady).

Muscle Fatigue (Causes)

• Depletion of energy reserves (ATP, glycogen).

• Accumulation of metabolic byproducts (lactic acid, inorganic phosphate).

• Impaired excitation-contraction coupling.

Latent Period

The brief delay between the muscle action potential and the onset of contraction, representing the time required for excitation-contraction coupling.

Motor Units

A motor unit consists of a single motor neuron and all the muscle fibers it innervates. The size of the motor unit determines the precision of muscle control.

Comparison: Smooth vs. Skeletal Muscle Contraction

• Skeletal muscle: Voluntary, striated, fast contraction, uses troponin-tropomyosin regulation.

• Smooth muscle: Involuntary, non-striated, slower contraction, uses calmodulin-mediated regulation.

Types of Muscle Tissue

Feature	Skeletal	Cardiac	Smooth
Striations	Yes	Yes	No
Control	Voluntary	Involuntary	Involuntary
Nuclei	Multinucleated	1-2 per cell	Single
Location	Attached to bones	Heart	Walls of hollow organs

Reflexes and Motor Control

Effectors in a Reflex

Effectors are muscles or glands that carry out the response to a stimulus in a reflex arc.

Reflex Arc and Integration Centers

• Reflex arc: Pathway involving receptor, sensory neuron, integration center (CNS), motor neuron, and effector.

• Integration center: Usually the spinal cord or brainstem where sensory input is processed and response is initiated.

Crossed Extensor Reflex

A polysynaptic reflex that maintains balance by activating extensor muscles on the side opposite to the stimulus (e.g., stepping on a sharp object).

Autonomic vs. Somatic Reflexes

• Somatic reflexes: Involve skeletal muscles; usually conscious control.

• Autonomic reflexes: Involve smooth muscle, cardiac muscle, or glands; involuntary control.

Cardiac Muscle and Cardiovascular System

Intercalated Discs

Specialized connections between cardiac muscle cells containing gap junctions and desmosomes, allowing synchronized contraction and electrical coupling.

Electrical Conduction System of the Heart

• Sinoatrial (SA) node: Pacemaker of the heart; initiates action potentials.

• Atrioventricular (AV) node: Delays impulse before passing to ventricles.

• Bundle of His, bundle branches, Purkinje fibers: Distribute impulse through ventricles.

Phases of Action Potentials in Myocardial Contractile Cells

• Rapid depolarization: Due to Na+ influx (voltage-gated Na+ channels open).

• Plateau phase: Due to Ca2+ influx (L-type Ca2+ channels open) and K+ efflux (some K+ channels closed).

• Repolarization: Due to K+ efflux (K+ channels open, Ca2+ channels close).

• Long refractory period: Prevents tetanus in cardiac muscle.

Phases of the Cardiac Cycle

1. Atrial systole (contraction)

2. Isovolumic ventricular contraction

3. Ventricular ejection

4. Isovolumic ventricular relaxation

5. Ventricular filling

Events During Isovolumic Contraction and Ventricular Ejection

• Isovolumic contraction: Ventricles contract with all valves closed; pressure rises but no blood ejected.

• Ventricular ejection: Semilunar valves open; blood is pumped into arteries.

Valves of the Heart

• Atrioventricular (AV) valves: Tricuspid (right), bicuspid/mitral (left).

• Semilunar valves: Pulmonary (right ventricle to pulmonary artery), aortic (left ventricle to aorta).

Heart Sounds

• First sound (S1): Closure of AV valves (beginning of ventricular systole).

• Second sound (S2): Closure of semilunar valves (end of ventricular systole).

The Three Waves of ECG and Cardiac Cycle Events

• P wave: Atrial depolarization.

• QRS complex: Ventricular depolarization (and atrial repolarization).

• T wave: Ventricular repolarization.

Preload, Afterload, EDV, ESV, Stroke Volume, Cardiac Output

• Preload: Degree of stretch of cardiac muscle before contraction (related to EDV).

• Afterload: Resistance the ventricles must overcome to eject blood.

• End-diastolic volume (EDV): Volume of blood in ventricle at end of diastole.

• End-systolic volume (ESV): Volume of blood in ventricle at end of systole.

• Stroke Volume (SV): Amount of blood ejected per beat.

• Cardiac Output (CO): Volume of blood pumped per minute.

Formulas:

• $SV = EDV - ESV$

• $CO = SV \times HR$

Starling's Law of the Heart

The force of ventricular contraction increases with increased EDV (preload), ensuring that the heart pumps out all the blood returned to it.

Factors Affecting Heart Rate

• Autonomic nervous system (sympathetic increases, parasympathetic decreases HR)

• Hormones (e.g., epinephrine)

• Body temperature, fitness level, age

Compensation for Decreased Blood Volume

• Increased heart rate

• Vasoconstriction

• Hormonal responses (ADH, aldosterone)

Blood Vessels and Hemodynamics

Metarterioles

Short vessels that link arterioles and capillaries; regulate blood flow into capillary beds.

Angiogenesis

The formation of new blood vessels from pre-existing vessels; important in growth, development, and wound healing.

Blood Pressure: Definition and Measurement

• Blood pressure (BP): The force exerted by blood against vessel walls.

• Measured as: Systolic/diastolic (e.g., 120/80 mmHg).

Mean Arterial Pressure (MAP) and Pulse Pressure

• MAP: Average pressure in arteries during one cardiac cycle.

• Pulse pressure: Difference between systolic and diastolic pressure.

Formulas:

• $Pulse\ Pressure = Systolic\ BP - Diastolic\ BP$

• $MAP = Diastolic\ BP + \frac{1}{3}(Systolic\ BP - Diastolic\ BP)$

Osmotic, Oncotic, and Colloid Pressure

• Osmotic pressure: Pressure exerted by solutes drawing water across a membrane.

• Oncotic (colloid osmotic) pressure: Osmotic pressure due to plasma proteins (mainly albumin) in blood.

Baroreceptors (Cardiac Reflexes)

Stretch-sensitive receptors in the carotid sinus and aortic arch that detect changes in blood pressure and initiate reflexes to maintain homeostasis.

Peripheral Resistance

The opposition to blood flow due to friction between blood and vessel walls; mainly determined by vessel diameter, blood viscosity, and vessel length.

Relationship Between Blood Volume, Cardiac Output, Vessel Diameter, Blood Flow, and Blood Pressure

• Increased blood volume or cardiac output raises blood pressure.

• Decreased vessel diameter (vasoconstriction) increases resistance and blood pressure.

• Blood flow is directly proportional to pressure difference and inversely proportional to resistance.

Formula:

• $Flow = \frac{\Delta P}{R}$

Relationship Between Pressure, Flow, and Resistance

• Blood flow ($Q$) is determined by the pressure gradient ($\Delta P$) divided by resistance ($R$):

$Q = \frac{\Delta P}{R}$

Local Vasodilators and Vasoconstrictors

• Vasodilators: Nitric oxide, adenosine, low O2, high CO2, histamine.

• Vasoconstrictors: Endothelin, vasopressin, high O2, sympathetic stimulation.

Active vs. Reactive Hyperemia

• Active hyperemia: Increased blood flow in response to increased metabolic activity.

• Reactive hyperemia: Increased blood flow following a period of reduced blood supply.

Additional Key Concepts

• Excitation-contraction coupling: The process linking muscle fiber excitation to contraction via Ca2+ release.

• Pacemaker of the heart: The SA node.

Additional info: For more detailed mechanisms, refer to textbook figures and diagrams illustrating the cardiac cycle, muscle contraction, and vascular regulation.