7 questions — Aligned to EAP objectives — Martini Chapter 7
Q1MC
The root "sarco-" means flesh. Which term correctly uses this root to name a structure of a muscle fiber?
Sarcolemma — the plasma membrane of a muscle fiber
Myosin — the thick protein filament of a sarcomere
Endomysium — the deepest connective tissue wrapping
Perimysium — the connective tissue surrounding a fascicle
Correct — sarco- = flesh. Sarcolemma (lemma = sheath) = plasma membrane of a muscle fiber. Also: sarcoplasm, sarcoplasmic reticulum, sarcomere. Myosin derives from mys (muscle). Epimysium, perimysium, endomysium all derive from mys.
Incorrect — sarco- = flesh. Sarcolemma is the plasma membrane; sarcoplasm is the cytoplasm. Myosin = mys (muscle). The -mysium terms all derive from mys, not sarcos.
Q2MC
The prefix "epi-" means on or over. Based on this, the epimysium is the connective tissue layer that:
Surrounds individual muscle fibers within a fascicle
The root "meros" means part. This root appears in which muscle anatomy term?
Myosin — the thick filament protein
Perimysium — the fascicle connective tissue wrap
Sarcomere — the repeating contractile unit of a myofibril
Isometric — constant-length contraction
Correct — meros = part. Sarcomere = sarco (flesh) + meros (part) = the repeating contractile unit of a myofibril, bounded by Z lines. It is the "flesh part" — the fundamental unit of contraction.
Incorrect — meros = part → sarcomere (sarco = flesh + meros = part). Myosin from mys. Perimysium from peri + mys. Isometric from iso (equal) + metron (measure).
Q4FITB
A bundle of muscle fibers wrapped together by the perimysium is called a ___.
Correct — fascicle (fasciculus = little bundle). Each muscle is divided into fascicles, each wrapped by perimysium, which also carries blood vessels and nerves to the fibers within.
Incorrect — fascicle. From fasciculus = little bundle. Wrapped by perimysium. Whole muscle = epimysium. Individual fibers = endomysium.
Q5MC
The root "tetanos" means stiff or rigid. In a physiological context, tetanus refers to:
A single brief contraction-relaxation cycle in response to one action potential
Progressive increase in twitch force from repeated identical stimuli
A sustained maximal contraction from very rapid repeated stimulation
The resting state of a muscle maintaining baseline tone
Correct — tetanos = stiff/rigid. Physiological tetanus = sustained maximal contraction from rapid stimuli that prevent relaxation. Calcium never fully returns to the SR; the muscle stays contracted. Same root as the disease caused by Clostridium tetani.
Incorrect — tetanos = stiff → tetanus = sustained maximal contraction. Single twitch = one stimulus. Progressive increase = treppe. Baseline tone = muscle tone.
Q6MC
The root "-trophy" means nourishment or development. Which statement correctly applies this root?
Atrophy means increased muscle fiber size from resistance training
Hypertrophy means above-normal development — individual fibers enlarge
Dystrophy means normal development in a well-trained athlete
Tetanus means sustained muscle stiffness from rapid stimulation
Incorrect — hypertrophy = hyper + trophy = above-normal development. Atrophy = without nourishment = wasting. Dystrophy = bad development = disease. Tetanus = tetanos root, not trophy.
Q7MC
The roots "syn-" (together) and "ergon" (work) combine to form synergist. A synergist muscle is one that:
Directly opposes the prime mover to limit range of motion
Assists the prime mover and reduces unnecessary movement
Converts chemical energy to mechanical energy at the molecular level
Serves as the primary muscle generating force for a movement
Correct — syn (together) + ergon (work) = works together. Synergists assist the prime mover and often stabilize joints against unnecessary movement. Antagonists oppose the prime mover; agonists (prime movers) generate the primary force.
Incorrect — syn + ergon = works together = assists the prime mover. Opposing = antagonist. Primary mover = agonist/prime mover. Synergist assists.
2624 — Functions of Skeletal Muscle
7 questions — Aligned to EAP objectives — Martini Chapter 7
Q8MC
The human body contains approximately how many skeletal muscles?
About 100
About 350
About 700
About 1,500
Correct — approximately 700 skeletal muscles. Each is an organ composed of muscle tissue, connective tissue, nerves, and blood vessels. They range from the tiny stapedius in the ear to the large gluteus maximus.
Incorrect — approximately 700. The exact count varies slightly by source but 700 is the Martini textbook figure.
Q9MC
The abdominal wall and pelvic floor muscles prevent visceral organs from dropping downward. This represents which function of skeletal muscle?
Maintaining posture and body position
Guarding body entrances and exits
Supporting soft tissues
Maintaining body temperature
Correct — supporting soft tissues. The muscles of the abdominal wall and pelvic floor support visceral organs against gravity, preventing prolapse. This is distinct from posture (maintaining body orientation) and guarding (sphincter control).
Incorrect — supporting soft tissues. Abdominal/pelvic floor muscles prevent organ prolapse. Posture = maintaining body orientation. Guarding = sphincter control at body openings.
Q10MC
Skeletal muscle contributes to temperature maintenance primarily by:
Absorbing heat from blood and releasing it through the skin
Generating heat as a byproduct of metabolic reactions, both at rest and during activity
Contracting only during extreme cold to directly warm circulating blood
Directing blood flow from the core to the skin for heat dissipation
Correct — muscle metabolism generates heat continuously. At peak activity, skeletal muscles generate up to 40× the resting heat output. Shivering is a specialized form — rapid contractions specifically for heat production during cold exposure.
Incorrect — all muscle metabolism generates heat. At peak activity = 40× resting heat output. Shivering = rapid contractions specifically for heat production. Heat generation is continuous, not only during cold.
Q11MC
Because muscles can only pull (shorten) and cannot push, movement in opposite directions at a joint requires:
Tendon recoil after muscle relaxation
Antagonistic muscle pairs that pull in opposite directions
A single large muscle with two distinct attachment points
Cartilaginous springs at joint surfaces
Correct — antagonistic pairs. Muscles can only shorten (pull). Moving in opposite directions = one pair of antagonists. Example: biceps brachii flexes; triceps brachii extends. One contracts while the other relaxes.
Incorrect — antagonistic pairs. Muscles can only pull. Two directions = two muscles pulling in opposite directions. One contracts, one relaxes.
Q12SATA
Select ALL five major functions of skeletal muscle as listed in the Martini textbook.
Correct — all five are the functions of skeletal muscle. Know them in order: (1) skeletal movement, (2) posture maintenance, (3) soft tissue support, (4) guarding entrances/exits, (5) temperature maintenance.
Incorrect — all five are correct and must be selected: skeletal movement, posture, soft tissue support, guarding entrances/exits, temperature maintenance.
Q13MC
The external urethral and anal sphincters are skeletal muscles that guard body openings. Their voluntary control is provided by:
The autonomic nervous system acting on smooth muscle sphincters
Cardiac pacemaker signals coordinating sphincter timing with heart rate
The somatic nervous system — these are voluntary skeletal muscles
Hormonal signals that open and close the sphincters automatically
Correct — external sphincters = skeletal muscle = voluntary somatic control. Internal sphincters = smooth muscle = involuntary autonomic control. The ability to consciously defer urination/defecation comes from voluntary control of the skeletal external sphincters.
Incorrect — external sphincters = skeletal muscle = voluntary somatic control. Internal sphincters = smooth muscle = autonomic. The voluntary aspect of elimination is the skeletal sphincter's function.
Q14MC
Each skeletal muscle functions as an organ. Which combination of tissues makes up a typical skeletal muscle organ?
Muscle tissue and nervous tissue only
Muscle tissue, connective tissue, blood vessels, and nerves
Muscle tissue and connective tissue only, with no direct nerve supply
Muscle tissue, cartilage, and bone at the tendon attachments
Correct — skeletal muscles are organs composed of muscle tissue plus connective tissue, blood vessels, and nerves. This is the textbook definition of a skeletal muscle as an organ. The connective tissue components (epimysium, perimysium, endomysium) also contribute collagen to the tendons.
Incorrect — skeletal muscles as organs = muscle tissue + connective tissue + blood vessels + nerves. All four components are present and required. Cartilage and bone are not part of the muscle organ itself.
2625 — Organization of Skeletal Muscle
8 questions — Aligned to EAP objectives — Martini Chapter 7
Q15MC
The connective tissue layers of a skeletal muscle from outermost to innermost are:
Endomysium → perimysium → epimysium
Perimysium → epimysium → endomysium
Epimysium → perimysium → endomysium
Epimysium → endomysium → perimysium
Correct — epimysium (outer, whole muscle), perimysium (middle, fascicle), endomysium (inner, individual fiber). Epi = on, peri = around, endo = within. All three contribute collagen fibers to the tendons at each end.
Incorrect — epi (outer) → peri (middle) → endo (inner). The prefix meanings give you the order: on/over → around → within.
Q16FITB
The outermost connective tissue layer that wraps an entire skeletal muscle and blends with its tendons is the ___.
Correct — epimysium. Epi- = on/over + mys = muscle. The outermost connective tissue wrap. Its collagen fibers extend into the tendons at both muscle ends.
Incorrect — epimysium. Epi- = on/over. Outermost wrap of the whole muscle. Perimysium wraps fascicles. Endomysium wraps individual fibers.
Q17MC
Transverse tubules (T tubules) are:
Modified collagen fibers transmitting tension from myofibrils to tendons
Channels connecting terminal cisternae to the sarcoplasmic reticulum lumen
Extensions of the sarcolemma that conduct action potentials deep into the fiber interior
Protein bridges connecting thick and thin filaments in the zone of overlap
Correct — T tubules = invaginations of the sarcolemma (plasma membrane) that carry action potentials from the cell surface deep into the fiber, ensuring all sarcomeres receive the signal simultaneously.
Incorrect — T tubules = sarcolemma extensions that conduct action potentials into the fiber interior. NOT collagen, NOT SR channels, NOT cross-bridges.
Q18MC
A triad is the functional unit for excitation-contraction coupling. It consists of:
Three myofibrils wrapped by a single loop of sarcoplasmic reticulum
One T tubule flanked on each side by a terminal cisterna
Three sarcomeres connected by a shared Z line
Two T tubules surrounding one terminal cisterna
Correct — triad = 1 T tubule + 2 terminal cisternae (one on each side). The T tubule carries the electrical signal; the cisternae store and release calcium. The "tri" = three components: cisterna-tubule-cisterna.
Incorrect — triad = 1 T tubule flanked by 2 terminal cisternae. Not three myofibrils, not three sarcomeres, not two T tubules flanking one cisterna.
Q19MC
The terminal cisternae of the sarcoplasmic reticulum store and release:
Glucose for immediate ATP synthesis during contraction
Pre-energized myosin heads ready to form cross-bridges
Calcium ions (Ca²⁺) that trigger contraction when released
ATP reserves that fuel the cross-bridge cycle directly
Correct — terminal cisternae store Ca²⁺. T tubule action potential → cisternae release Ca²⁺ into sarcoplasm → Ca²⁺ binds troponin → tropomyosin moves → active sites exposed → cross-bridges form.
Incorrect — terminal cisternae store Ca²⁺. Calcium release is the trigger coupling electrical signals to mechanical contraction. Not glucose, not myosin heads, not ATP.
Q20MC
The sarcolemma of a muscle fiber is:
The cytoplasm of a muscle fiber containing organelles and myofibrils
The plasma membrane of a muscle fiber
The connective tissue wrapping around each individual muscle fiber
The specialized smooth ER network storing calcium ions
Correct — sarcolemma = sarco (flesh) + lemma (sheath) = the plasma membrane of a muscle fiber. Compare: sarcoplasm = cytoplasm, sarcoplasmic reticulum = specialized ER, endomysium = connective tissue wrap.
The sarcoplasm of a muscle fiber differs from typical cytoplasm in that it contains large amounts of:
Hemoglobin for oxygen transport to neighboring fibers
Glycogen granules and myoglobin in addition to normal cytoplasmic contents
Only water and dissolved proteins, lacking organelles
No mitochondria — skeletal muscle relies entirely on anaerobic energy
Correct — sarcoplasm contains glycogen granules (stored fuel) and myoglobin (oxygen-storage protein) in addition to normal contents. Myoglobin stores O₂ within the fiber — unlike hemoglobin, which transports O₂ in blood. Skeletal muscle has abundant mitochondria.
Incorrect — sarcoplasm contains glycogen (fuel) and myoglobin (O₂ storage). Hemoglobin is in red blood cells, not muscle fibers. Skeletal muscle has abundant mitochondria for aerobic metabolism.
Q22MC
Satellite cells are stem cells found in the endomysium. Their primary function is to:
Produce the collagen fibers of the endomysium
Secrete hormones that regulate muscle hypertrophy systemically
Divide and differentiate to repair or replace damaged muscle fibers
Store glycogen reserves adjacent to myofibrils
Correct — satellite cells are muscle stem cells in the endomysium that activate when muscle is damaged. They divide and differentiate into new muscle fibers. Resistance training also activates them, contributing to hypertrophy.
Incorrect — satellite cells = muscle stem cells in the endomysium that repair damaged fibers. Not collagen producers, not hormone secretors, not glycogen stores.
2626 — Sarcomere Structure
8 questions — Aligned to EAP objectives — Martini Chapter 7
Q23MC
The A band of a sarcomere is defined by the length of the thick (myosin) filaments. During muscle contraction, the A band:
Narrows as thick filaments shorten during the power stroke
Disappears completely at maximal contraction
Remains constant in width because myosin filament length never changes
Widens as thin filaments are drawn deeper into the thick filament array
Correct — the A band corresponds to thick filament length, which never changes. A band width = CONSTANT during contraction. The I band and H band both narrow. Remembering that A = Always constant is the classic exam trick.
Incorrect — A band = CONSTANT (A = Always constant). Thick filaments don't shorten. I band narrows. H band narrows. A band stays the same.
Q24MC
The I band (the thin-filament-only zone at each end of the sarcomere) during contraction:
Widens as thin filaments are pulled apart during the power stroke
Stays constant in width like the A band
Narrows as thin filaments slide toward the M line
Disappears immediately at the onset of any contraction
Correct — I band narrows. The I band is the thin-filament-only zone. As thin filaments slide toward the center during contraction, this zone shrinks. It does NOT disappear in normal contractions — only extreme shortening would eliminate it.
Incorrect — I band narrows (thin filaments slide toward M line). It doesn't stay constant (A band stays constant, not I). It doesn't disappear in normal contractions.
Q25FITB
The boundary structures that define each sarcomere — the protein discs where thin filaments are anchored — are the ___ lines.
Correct — Z lines (Z discs). Each sarcomere runs from Z to Z. Z lines anchor thin filaments and move closer together as the sarcomere shortens. M line = center, anchoring thick filaments. Z = boundary, M = midpoint.
Incorrect — Z lines. Each sarcomere = Z to Z. Z lines anchor thin filaments. M line is at the center anchoring thick filaments. Z = boundary, M = middle.
Q26MC
In a resting muscle, tropomyosin's role is to:
Connect myosin heads to actin in preparation for contraction
Anchor thin filaments to the Z lines
Cover the active sites on actin, blocking myosin cross-bridge formation
Store calcium ions until an action potential triggers their release
Correct — tropomyosin physically covers the active sites on actin at rest, blocking myosin attachment. Troponin holds tropomyosin in this blocking position. When Ca²⁺ binds troponin, the tropomyosin shifts, exposing the sites.
Incorrect — tropomyosin blocks actin active sites at rest. Troponin HOLDS it in the blocking position. Calcium is stored in the SR, not by tropomyosin.
Q27MC
When calcium ions (Ca²⁺) bind to troponin, the result is:
Immediate ATP hydrolysis to energize the myosin heads
Cross-bridge formation between myosin and the Z line proteins
A conformational change that moves tropomyosin away from the actin active sites
Calcium directly attaches to myosin heads, enabling them to bind actin
Incorrect — Ca²⁺ binds troponin → tropomyosin shifts → active sites on actin exposed. ATP energizes myosin separately. Calcium binds troponin, not myosin heads.
Q28MC
The H band is:
The thin-filament-only zone at each end of the sarcomere
The protein disc at the center of the A band that anchors thick filaments
The thick-filament-only zone in the center of the A band where no thin filaments overlap
The region where thick and thin filaments overlap to form cross-bridges
Correct — H band = thick-filament-only zone in the center of the A band. The M line bisects it. During contraction, thin filaments slide INTO the H band, shrinking it. At full contraction the H band can disappear completely.
Incorrect — H band = thick-filament-only zone at the center of the A band. Thin-filament-only = I band. Central protein disc = M line. Zone of overlap = lateral A band areas.
Q29MC
During muscle contraction, the zone of overlap between thick and thin filaments:
Decreases as thick filaments shorten
Stays constant because both bands narrow equally
Disappears in any normal contraction
Increases as thin filaments slide deeper into the thick filament array
Correct — zone of overlap INCREASES. Thin filaments slide inward, overlapping more of the thick filament array. More overlap = more potential cross-bridges. This is why resting length (optimal overlap) generates peak isometric force.
Incorrect — zone of overlap INCREASES as thin filaments slide inward. Thick filaments don't shorten — A band is constant. Overlap increases as H band shrinks.
Q30MC
Before contraction begins, myosin heads are in a "cocked" pre-energized state because they are already bound to:
Calcium ions from the terminal cisternae
Actin active sites at the zone of overlap
ADP and inorganic phosphate (Pi), having already hydrolyzed an ATP molecule
Troponin molecules along the thin filament
Correct — myosin heads are pre-energized by ATP hydrolysis: they carry ADP + Pi before contraction begins. When active sites are exposed, the head binds actin and releases Pi, triggering the power stroke. Then a new ATP binds to detach the head.
Incorrect — myosin heads = pre-energized by hydrolyzing ATP to ADP + Pi BEFORE contraction begins. Calcium is not bound to myosin. Myosin binds actin (not troponin). The energy was loaded before the trigger arrives.
2627 — Skeletal Muscle Contraction
10 questions — Aligned to EAP objectives — Martini Chapter 7
Q31MC
Acetylcholine (ACh) is released from the axon terminal into the synaptic cleft by:
Active transport pumps in the axon terminal membrane
Passive diffusion down its concentration gradient
Exocytosis — synaptic vesicles fuse with the membrane and release their contents
Voltage-gated potassium channels opening when the action potential arrives
Correct — ACh is released by exocytosis. The action potential triggers Ca²⁺ influx into the axon terminal → vesicles fuse with the membrane → ACh released into the synaptic cleft.
Incorrect — exocytosis. AP → Ca²⁺ enters terminal → vesicles fuse → ACh released. Not diffusion (passive), not active transport, not K⁺ channels.
Q32MC
Acetylcholinesterase (AChE) breaks down ACh in the synaptic cleft after each stimulus. Without AChE:
No action potential would be generated in the muscle fiber
Calcium would not be released from the sarcoplasmic reticulum
The muscle would be continuously stimulated and unable to relax
The muscle fiber would fail to repolarize after its action potential
Correct — AChE terminates the ACh signal. Without it, ACh keeps binding receptors → continuous action potentials → continuous contraction → unable to relax. This is the mechanism of organophosphate toxicity (nerve agents).
Incorrect — without AChE, ACh persists → continuous stimulation → continuous contraction. The problem is signals cannot be STOPPED, not that they cannot start.
Q33MC
ACh binding to motor end plate receptors increases sodium permeability, causing Na⁺ to rush in. This generates:
Direct cross-bridge formation between myosin and actin
Immediate calcium release from the terminal cisternae
An action potential in the muscle fiber sarcolemma
The power stroke of myosin cross-bridges
Correct — ACh → receptor binding → Na⁺ influx → action potential in the sarcolemma. The AP then spreads across the sarcolemma AND down T tubules to trigger Ca²⁺ release. Na⁺ influx creates the electrical signal; it does not directly cause Ca²⁺ release.
Incorrect — ACh → Na⁺ influx → action potential in the sarcolemma. The AP then travels down T tubules → Ca²⁺ release → cross-bridge formation. Steps happen in sequence.
Q34MC
When the action potential reaches the triads (T tubule + terminal cisternae), the immediate result is:
Cross-bridge formation between myosin heads and actin
ATP hydrolysis to energize the myosin heads
Massive release of Ca²⁺ from the terminal cisternae into the sarcoplasm
Troponin conformational change that moves tropomyosin away from actin
Correct — T tubule action potential → voltage sensors detect it → terminal cisternae release massive Ca²⁺ into sarcoplasm. Ca²⁺ then binds troponin → tropomyosin shifts → cross-bridges form. Calcium release is the immediate event.
Incorrect — T tubule AP → Ca²⁺ release from terminal cisternae. Cross-bridge formation comes AFTER calcium release and troponin binding. ATP hydrolysis occurs BEFORE (myosin pre-loaded state).
Q35MC
After Ca²⁺ exposes the active sites on actin, the pre-energized myosin head binds and then:
Hydrolyzes a new ATP molecule to begin the power stroke
Releases ADP + Pi, completing the power stroke and pulling the thin filament toward the M line
Immediately detaches from actin and waits for a new ATP
Binds calcium directly to confirm the active site is accessible
Correct — the pre-energized myosin head (carrying ADP + Pi) binds the exposed active site → releases ADP + Pi → power stroke occurs → thin filament pulled toward M line. The energy came from the ATP hydrolyzed EARLIER.
Incorrect — power stroke uses energy from releasing ADP + Pi (ATP was hydrolyzed BEFORE binding). Myosin attaches → releases ADP + Pi during stroke → THEN needs new ATP to detach.
Q36FITB
The binding of a new ___ molecule to the myosin head causes cross-bridge detachment from actin.
Correct — ATP. New ATP binds the myosin head → head detaches from actin → ATP is hydrolyzed → head re-cocked for next cycle. Without ATP = cross-bridges cannot detach = rigor mortis.
Incorrect — ATP. New ATP binds myosin → detachment → ATP hydrolyzed → head re-cocked. ATP absence = permanent lock = rigor mortis.
Q37MC
Botulinum toxin causes flaccid paralysis because it:
Prevents ACh release from the axon terminal into the synaptic cleft
Directly prevents calcium from binding to troponin
Correct — botulinum toxin prevents ACh release from the axon terminal. No ACh = no motor end plate stimulation = no action potential in the muscle fiber = flaccid paralysis. It acts at the presynaptic terminal before the receptor level.
Incorrect — botulinum toxin prevents ACh RELEASE from the axon terminal. Blocking receptors = curare (different drug). Destroying AChE = organophosphate toxicity. Botulinum acts presynaptically, upstream of the receptor.
Q38MC
Myasthenia gravis is an autoimmune disease in which the immune system destroys:
Myosin heads of the thick filaments
Acetylcholinesterase enzymes in the synaptic cleft
ACh receptors on the motor end plate
Terminal cisternae of the sarcoplasmic reticulum
Correct — myasthenia gravis = auto-antibodies destroy ACh receptors at the motor end plate. Fewer receptors → weaker, fatigable responses. Treated with AChE inhibitors so surviving ACh lasts longer in the cleft.
Incorrect — myasthenia gravis destroys ACh RECEPTORS on the motor end plate. Not myosin heads, not AChE, not the SR. Antibodies target the post-synaptic membrane specifically.
Q39MC
Rigor mortis occurs after death because:
Calcium floods all cells simultaneously, triggering a final maximal contraction
Acetylcholinesterase remains active and continuously stimulates all muscles
ATP production ceases, so myosin heads cannot detach from actin
Sarcomeres lock at maximum overlap as the cell membrane fails
Correct — rigor mortis = ATP depletion after death. Without ATP, myosin heads cannot detach from actin (ATP binding is required for detachment). All muscles become locked in a semi-contracted state. Begins ~3 hours post-mortem; resolves ~48-60 hours later as proteins decompose.
Incorrect — ATP depletion prevents cross-bridge DETACHMENT. Without ATP, myosin stays locked to actin = rigid muscles = rigor mortis. Cross-bridges can form but cannot release.
Q40SATA
Select ALL steps that are part of initiating a skeletal muscle contraction (from ACh release to the power stroke).
Correct — all five steps are correct and in order. Know the complete sequence: (1) ACh exocytosis, (2) motor end plate AP, (3) T tubule → Ca²⁺ release, (4) troponin-tropomyosin, (5) cross-bridge and power stroke.
Incorrect — all five are correct. Complete sequence: ACh release → end plate AP → T tubule → Ca²⁺ release → troponin/tropomyosin → active site exposure → cross-bridge → power stroke.
2628 — Contraction Types & Motor Units
8 questions — Aligned to EAP objectives — Martini Chapter 7
Q41MC
A muscle twitch is:
The maximum force a motor unit generates over time
A sustained contraction from very rapid stimulation
A single contraction-relaxation cycle in response to one action potential
Progressive increase in twitch force from repeated identical stimuli
Correct — a twitch = single contraction-relaxation cycle from one AP. It has three phases: latent period (AP spreads, Ca²⁺ released — no tension yet), contraction (tension rises), relaxation (Ca²⁺ pumped back, tension falls).
Incorrect — twitch = single contraction-relaxation cycle. Sustained maximal contraction = tetanus. Progressive increase from identical stimuli = treppe.
Q42MC
During the latent period of a muscle twitch, what is happening?
Cross-bridges are rapidly cycling but generating no net force
Calcium is being pumped back into the SR in preparation for relaxation
The action potential is spreading and Ca²⁺ is being released, but no tension has developed yet
Myosin heads are detaching from actin in preparation for the contraction phase
Correct — during the latent period (~2 ms), the AP is sweeping across the sarcolemma and down T tubules, Ca²⁺ is being released, but cross-bridges haven't yet begun generating tension. Tension development begins with the contraction period.
Incorrect — latent period = AP spreading + Ca²⁺ releasing, but no tension yet. Ca²⁺ pumping back = relaxation period. Cross-bridge cycling generates tension during the CONTRACTION period.
Q43MC
When a second stimulus arrives before the muscle fully relaxes from the first twitch, tensions add together. This is called:
Complete tetanus
Treppe
Wave summation
Motor unit recruitment
Correct — wave summation (temporal summation). Second stimulus before relaxation → new contraction adds to residual tension → peak tension higher than a single twitch. Progressively faster stimuli → incomplete then complete tetanus.
Incorrect — wave summation = tensions adding together from rapid stimuli. Complete tetanus = no relaxation, smooth maximal contraction. Treppe = progressive increase from identical-frequency stimuli. Recruitment = more motor units activated.
Q44MC
An isometric contraction differs from an isotonic contraction in that during an isometric contraction:
Concentric shortening occurs against a constant load
No cross-bridge activity takes place
Tension increases but muscle length does not change
The muscle requires less ATP per unit time
Correct — isometric = iso (same) + metron (measure) = constant length. Muscle generates tension but cannot overcome the resistance to shorten. Examples: holding a position, pressing against an immovable wall.
Incorrect — isometric = constant length, variable tension. Isotonic = constant tension, variable length. Cross-bridges cycle in both. Isometric can be very ATP-demanding due to sustained tension.
Q45MC
A concentric isotonic contraction is one in which:
The muscle lengthens under tension while resisting an external load
The muscle generates tension but neither shortens nor lengthens
The muscle shortens while maintaining relatively constant tension
The twitch is too brief to move the attached bone
Correct — concentric = muscle shortens. Eccentric = muscle lengthens under load. Isometric = no length change. Most everyday movements (lifting, walking, throwing) primarily involve concentric contractions of the prime mover.
The muscle shortens while moving a load in the direction of contraction
Multiple motor units are activated simultaneously to increase force
The muscle lengthens while still generating tension to control movement
The muscle is at rest and generating only resting tone
Correct — eccentric = muscle lengthens while generating tension. Example: biceps brachii slowly lowering a weight — it's contracting (generating tension) but being stretched by the load. Eccentric contractions generate more DOMS (delayed onset muscle soreness).
Incorrect — eccentric = lengthening under tension. Shortening under load = concentric. Multiple motor units = recruitment. Resting tone = low-level isometric activity.
Q47MC
Motor unit recruitment increases force production by:
Increasing the rate of stimulation to a single motor unit
Activating additional motor units — small ones first, then progressively larger ones
Increasing the calcium released from the SR per action potential
Lengthening individual muscle fibers to increase their contractile range
Correct — recruitment = activating more motor units. The size principle: small type I motor units are recruited first; large type II units are added as demand increases. This provides fine control at low forces and maximum force when needed.
Incorrect — recruitment = activating more motor units, starting small and adding larger ones. Increasing stimulation rate = temporal summation/tetanus. Ca²⁺ per AP is fixed. Fiber length doesn't increase by recruitment.
Q48MC
A motor unit consists of:
All the motor neurons innervating a single skeletal muscle
A single muscle fiber and all the sarcomeres within it
One motor neuron and all the muscle fibers it innervates
A group of slow and fast fibers that always contract together
Correct — one motor neuron + all the fibers it controls = motor unit. The number of fibers per motor unit varies: eye muscles have very few (precise control), leg muscles have thousands (power). Fibers of one motor unit are scattered throughout the muscle.
Incorrect — motor unit = 1 motor neuron + all its muscle fibers. Not all neurons to one muscle (that's the entire innervation). Not just one fiber. Not a mix of slow and fast fibers.
2629 — Muscle Energy
10 questions — Aligned to EAP objectives — Martini Chapter 7
Q49MC
A resting muscle fiber contains only enough stored ATP for:
About 15 seconds of maximal contraction
About 30 seconds of moderate activity
A few seconds of maximal contraction
About 5 minutes of low-intensity activity
Correct — only a few seconds of directly stored ATP. The fiber must continuously regenerate it from: creatine phosphate (next ~15 seconds), then aerobic metabolism + glycolysis for extended activity.
Incorrect — a few seconds of stored ATP. CP extends this another ~15 seconds. 15-second figure refers to CP reserves, not stored ATP itself.
Q50MC
Creatine phosphate (CP) reserves can regenerate ATP for approximately how long during maximal activity?
5–10 seconds
About 15 seconds
About 2 minutes
About 15 minutes
Correct — creatine phosphate sustains peak activity for about 15 seconds by rapidly transferring its phosphate to ADP → ATP. This is why a 100-meter sprint can be completed almost entirely on ATP + CP stores. After 15 seconds, aerobic and glycolytic pathways dominate.
Incorrect — CP lasts ~15 seconds at peak demand. CPK catalyzes the transfer: CP + ADP → creatine + ATP. This is the fastest energy source but rapidly depleted.
Q51MC
At resting levels of activity, aerobic metabolism provides approximately what percentage of the muscle's ATP?
About 10%
About 40%
About 95%
About 60%
Correct — ~95% of resting ATP comes from aerobic metabolism in the mitochondria. Fatty acids (from circulating lipids) are the primary fuel at rest. Only at peak activity does glycolysis become a major contributor.
Incorrect — ~95% of resting ATP is aerobic. Glycolysis is much less efficient and only becomes dominant at high activity levels when oxygen delivery can't match demand.
Q52MC
Each glucose molecule processed by anaerobic glycolysis alone yields a net of:
36–38 ATP molecules
About 100 ATP molecules
2 ATP molecules
4 ATP molecules gross, 2 ATP net
Correct — glycolysis yields a net of 2 ATP per glucose. The 36-38 figure applies to complete aerobic metabolism. Glycolysis is fast but inefficient — its advantage is speed under anaerobic conditions, not yield.
Incorrect — glycolysis alone = 2 ATP (net) per glucose. 36-38 ATP = complete aerobic metabolism. Glycolysis is fast but inefficient; speed is the advantage, not yield.
Q53MC
During intense exercise, anaerobic glycolysis must supplement aerobic metabolism because:
Aerobic metabolism shuts down completely during strenuous activity
Glycolysis produces more ATP per glucose molecule than aerobic respiration
Aerobic ATP production cannot increase fast enough to meet the full ATP demand of peak activity
Mitochondria are damaged by the heat generated during intense contractions
Correct — at peak activity, ATP demand exceeds what aerobic metabolism can supply. Glycolysis is faster to activate and supplements aerobic output, but produces lactic acid and H⁺ that accumulate and cause fatigue. Aerobic metabolism continues throughout — glycolysis is the supplement, not the replacement.
Incorrect — aerobic metabolism continues during intense exercise but cannot ramp up fast enough to fully meet peak demand. Glycolysis is faster but produces less ATP and generates fatigue-causing H⁺. Mitochondria are not damaged by heat.
Q54FITB
The additional oxygen consumed after exercise ends — used to replenish CP, restore glycogen, and clear lactate — is called the ___ debt.
Correct — oxygen debt (also called EPOC — excess post-exercise oxygen consumption). The elevated post-exercise O₂ consumption restores: CP reserves, muscle glycogen, clears blood lactate, and returns the body to pre-exercise conditions.
Incorrect — oxygen debt. The extra O₂ consumed during recovery to restore pre-exercise conditions. Also called EPOC. The "debt" was incurred during peak activity when aerobic supply fell short.
Q55MC
Muscle fatigue occurs primarily due to:
The motor neuron stopping firing despite adequate ATP in the muscle
Lactic acid directly destroying ATP molecules needed for cross-bridge cycling
Energy reserve depletion combined with pH drop from H⁺ accumulation, impairing contraction
Complete motor unit recruitment having been reached
Correct — fatigue = energy depletion + H⁺ accumulation (from lactate dissociation) lowering intracellular pH → enzyme inhibition → impaired cross-bridge cycling. Fatigue is a protective mechanism that occurs before structural damage in most cases.
Incorrect — fatigue = energy depletion + H⁺ lowering pH. Motor neurons keep firing. Lactate itself isn't directly toxic — H⁺ is the culprit. Reaching maximum recruitment isn't fatigue.
Q56SATA
Select ALL energy sources that contribute to ATP production in skeletal muscle — from fastest but most limited to slowest but most sustained.
Correct — all four contribute to muscle ATP production. In order: stored ATP (seconds) → CP (15 seconds) → glycolysis (minutes, limited by fatigue) → aerobic (hours, limited by fuel). Know all four sources and their relative speed and capacity.
Incorrect — all four are correct energy sources. The sequence is: stored ATP → CP → glycolysis → aerobic. Each is progressively slower to activate but more sustained.
Q57MC
Resting skeletal muscle primarily uses which fuel source for aerobic ATP production?
Glucose from liver glycogen stores
Amino acids from protein breakdown
Fatty acids from circulating lipids
Lactate recycled from previous contractions
Correct — resting muscle primarily oxidizes fatty acids from circulating lipids. The fuel mix shifts toward glucose/pyruvate during activity. This is why sustained low-intensity exercise (aerobic zone) preferentially burns fat.
Incorrect — resting muscle primarily uses fatty acids. Fuel mix shifts to glucose during activity. Protein breakdown for energy = starvation or prolonged exhaustive exercise only.
Q58MC
Lactic acid dissociates into lactate and H⁺ ions. The H⁺ contributes to muscle fatigue by:
Directly destroying ATP molecules needed for cross-bridge cycling
Preventing calcium release from the SR by blocking T tubule function
Lowering intracellular pH, inhibiting enzymes involved in contraction
Blocking ACh receptors at the motor end plate
Correct — H⁺ lowers intracellular pH → enzyme inhibition → impaired cross-bridge cycling → fatigue. The pH drop also affects SR calcium release. Lactate itself can be used as a fuel by the liver and heart.
Incorrect — H⁺ lowers pH → enzyme inhibition → fatigue. H⁺ doesn't destroy ATP. T tubule function is a separate pathway. ACh receptors are on the motor end plate, not inside the fiber.
2630 — Muscle Fiber Types
8 questions — Aligned to EAP objectives — Martini Chapter 7
Q59MC
Fast (type II) muscle fibers reach peak twitch tension in:
About 40–100 milliseconds
10 milliseconds or less
About 3–4 seconds
About 1 second
Correct — fast fibers reach peak twitch tension in ≤10 ms. Slow fibers take ~100 ms. Fast fibers are 2-3× larger in diameter, generate more force per fiber, but fatigue rapidly due to reliance on glycolysis.
Incorrect — fast fibers = ≤10 ms to peak tension. Slow fibers = ~100 ms. 40–100 ms is the slow fiber range. Fast fibers are named for their rapid peak tension development.
Q60MC
Compared to fast (type II) fibers, slow (type I) fibers are:
Larger in diameter and generate more force
Higher in glycolytic enzyme activity and fatigue faster
Smaller in diameter and more resistant to fatigue
Lacking mitochondria and reliant entirely on glycolysis
Correct — slow fibers (type I) are smaller in diameter (~half that of fast fibers) and highly fatigue-resistant. They have abundant mitochondria, high myoglobin, rich capillary supply, and rely on aerobic metabolism — perfect for sustained, low-force activities.
Incorrect — slow fibers are SMALLER in diameter. Fast fibers are larger. Slow fibers are fatigue-RESISTANT. Slow fibers have MORE mitochondria and primarily use aerobic metabolism.
Q61MC
The high fatigue resistance of slow (type I) fibers is supported by:
High glycolytic enzyme activity for rapid ATP production
Large amounts of glycogen stored within each fiber
High myoglobin content, rich capillary supply, and abundant mitochondria
Large diameter and high myosin concentration
Correct — slow fiber fatigue resistance = myoglobin (O₂ storage) + dense capillaries (O₂ delivery) + abundant mitochondria (aerobic ATP). The red color of slow fibers comes from myoglobin and capillary blood.
Incorrect — fatigue resistance in slow fibers = myoglobin + capillaries + mitochondria (aerobic capacity). Glycolysis and large diameter are fast fiber characteristics. Glycogen stores are higher in fast fibers.
Q62MC
A soldier is running a 400-meter sprint at maximum effort. The contracting muscles are primarily utilizing:
Type I slow oxidative fibers
A 50/50 mix of fast and slow fibers
Type II fast glycolytic fibers
Cardiac muscle fibers recruited through the nervous system
Correct — maximum effort, short duration = type II fast fibers. Fast fibers generate high force rapidly using glycolysis. Slow fibers dominate during sustained low-intensity activities. Cardiac muscle is not under voluntary somatic control.
Incorrect — sprint = fast (type II) fibers. Slow fibers for sustained, lower-intensity activity. A mix is used at moderate intensity. Cardiac muscle is involuntary.
Q63MC
Hypertrophy of skeletal muscle refers specifically to:
An increase in the number of muscle fibers from stem cell differentiation
Conversion of slow fibers to fast fibers from high-intensity training
An increase in the diameter of existing individual muscle fibers
Addition of entirely new muscle organ units
Correct — hypertrophy = individual fiber enlargement (more myofibrils, larger diameter per fiber). NOT new fiber formation (hyperplasia). Training stimulates myofibril synthesis. The muscle looks bigger because each fiber is bigger, not because there are more fibers.
Incorrect — hypertrophy = individual fiber ENLARGEMENT. NOT new fiber formation (that's hyperplasia). NOT fiber type conversion. Satellite cells assist but don't add new fibers in normal training.
Q64FITB
The duration of contractions that can be sustained using only glycolysis and ATP/CP — without relying on aerobic metabolism — is called ___ endurance.
Correct — anaerobic endurance. Improved by high-intensity, short-duration training (sprints, heavy resistance). Limited by lactate/H⁺ accumulation. Contrast with aerobic endurance — sustained by oxidative metabolism.
Incorrect — anaerobic endurance. Contractions sustained by glycolysis + ATP/CP = anaerobic. Aerobic endurance = sustained by oxidative metabolism. Different training approaches for each.
Q65MC
Aerobic endurance training (e.g., distance running) improves performance primarily by:
Increasing the diameter of fast fibers to generate more force
Converting fast fibers to slow fibers to resist fatigue
Improving cardiovascular delivery and aerobic metabolic capacity without significant hypertrophy
Increasing the number of motor units available for recruitment
Correct — aerobic training improves cardiovascular function (cardiac output, capillary density), mitochondrial efficiency, and fat oxidation. It does NOT produce significant hypertrophy. Fiber type ratios don't change — metabolic and cardiovascular adaptations drive the improvement.
Incorrect — aerobic training = cardiovascular + metabolic improvements, NOT hypertrophy (that's anaerobic/resistance training). Fiber type conversion doesn't occur. Motor unit number is fixed.
Q66MC
An individual's ratio of slow to fast muscle fibers is:
Determined primarily by training — endurance athletes develop more slow fibers over time
Fixed at birth by genetic factors and does not change with training
Determined by diet — high-protein diets promote fast fiber development
Altered by aging — fast fibers gradually convert to slow fibers after age 40
Correct — fiber type ratio is genetically determined and cannot be changed by training or diet. Training improves fiber performance but cannot convert type I to type II or vice versa. Elite sprinters are born with high fast-fiber percentages; elite marathoners with predominantly slow.
Incorrect — fiber type ratio is GENETICALLY FIXED. Training improves performance within each fiber type. Diet doesn't alter ratios. After 40, fast fibers may atrophy preferentially, but conversion to slow doesn't occur.
2631 — Comparison of Muscle Tissue Types
8 questions — Aligned to EAP objectives — Martini Chapter 7
Q67MC
Cardiac muscle is found exclusively in:
The diaphragm and accessory breathing muscles
The walls of large arteries and veins
The walls of the heart (myocardium)
The sphincters at cardiac junctions of the GI tract
Correct — cardiac muscle = exclusively in the heart wall (myocardium). Diaphragm = skeletal. Blood vessel walls = smooth. GI cardiac sphincters = smooth. "Cardiac" literally means heart — found only there.
Intercalated discs are unique to cardiac muscle. The gap junctions within them:
Anchor the cell to the basement membrane for structural support
Allow calcium to be stored in compartments between adjacent cells
Enable electrical signals to pass directly between adjacent cardiac cells, synchronizing contraction
Prevent action potentials from spreading between cells for independent control
Correct — gap junctions in intercalated discs allow ions to pass between cardiac cells, spreading action potentials. This makes cardiac muscle function as a syncytium — electrically connected cells all contracting together for coordinated pumping.
Incorrect — gap junctions TRANSMIT electrical signals between cardiac cells for coordinated contraction. The opposite of preventing signal spread. Basement membrane anchoring uses hemidesmosomes.
Q69MC
Cardiac muscle exhibits automaticity, meaning it:
Automatically converts to a faster fiber type under high cardiac demand
Can regulate its contraction speed based on local oxygen availability
Can generate action potentials and contract without any neural input
Automatically recruits additional muscle layers when load increases
Correct — automaticity = self-generating action potentials without neural input. The SA node sets the rhythm. The ANS modulates rate but the heart beats without it. This is why transplanted hearts can still function without direct nerve connections.
Incorrect — automaticity = self-generating APs without neural input. The SA node (pacemaker) generates rhythm. ANS modulates but does not initiate. Fiber type conversion doesn't occur with demand changes.
Q70MC
Cardiac muscle cannot undergo tetanic contractions. This is physiologically essential because:
Tetanus would convert cardiac fibers to slow oxidative type
A tetanized heart cannot relax to fill with blood, making effective pumping impossible
Tetanus would exhaust all cardiac glycogen within minutes
Sustained contraction would prevent intercalated discs from opening
Correct — a tetanized heart locks in a contracted state and can never refill with blood → no cardiac output → death. The prolonged cardiac refractory period specifically prevents tetanus. This is life-saving physiology built into the membrane properties.
Incorrect — tetanized heart cannot relax → cannot fill with blood → no pumping → death. Fiber type doesn't change with tetanus. Glycogen depletion is a separate issue. Intercalated discs are structural features, not openings.
Q71MC
Smooth muscle differs from skeletal muscle in that smooth muscle:
Contains sarcomeres and shows cross-striations under a microscope
Uses calcium ions in its contraction mechanism
Lacks sarcomeres and striations — thick filaments are scattered irregularly throughout the cell
Cannot generate sustained force like skeletal muscle
Correct — smooth muscle has NO sarcomeres and NO striations. Thick filaments are scattered throughout the sarcoplasm (not organized into parallel arrays). Thin filaments anchor to dense bodies rather than Z discs. The cell contracts with a corkscrew-twisting motion.
Incorrect — smooth muscle = NO sarcomeres, NO striations. Calcium IS used in all three muscle types. Smooth muscle can sustain force for long periods (e.g., blood vessel tone).
Q72MC
Smooth muscle can contract over a much wider range of lengths than skeletal or cardiac muscle. This is functionally important because:
Smooth muscle must generate more peak force than skeletal muscle
Smooth muscle must contract faster than skeletal muscle
Smooth muscle is under voluntary control requiring a wide range of positions
Correct — wide functional length range = hollow organ adaptation. The bladder, stomach, and uterus change volume dramatically. Sarcomere-organized skeletal muscle has a narrow optimal length range that would be inadequate for these organs.
Incorrect — wide length range = hollow organ adaptation (bladder empty vs. full, stomach fasted vs. fed). Smooth muscle doesn't generate more peak force. Smooth muscle is SLOWER than skeletal. Smooth muscle = involuntary (autonomic) control.
Q73SATA
Select ALL features that are unique to cardiac muscle and NOT shared with skeletal or smooth muscle.
Correct — intercalated discs, automaticity, and inability to tetanize are all unique to cardiac muscle. Calcium use and actin/myosin are found in all three muscle types — do NOT select them.
Incorrect — cardiac-unique features: intercalated discs (gap junctions), automaticity (self-pacing), no tetanus possible. Calcium use and actin/myosin are found in all three muscle types.
Q74MC
In smooth muscle, calcium ions that trigger contraction come primarily from:
The sarcoplasmic reticulum, identical to the mechanism in skeletal muscle
Mitochondria within the smooth muscle cell
The extracellular fluid, entering through the plasma membrane
Glycogen granules that release calcium as they are metabolized
Correct — smooth muscle relies primarily on extracellular Ca²⁺ entering through the plasma membrane, unlike skeletal muscle (SR only) and cardiac muscle (both sources). This difference explains why smooth muscle responds differently to calcium channel blockers.
Incorrect — smooth muscle Ca²⁺ = primarily extracellular fluid entering through plasma membrane. Skeletal = SR exclusively. Cardiac = both. Mitochondria and glycogen do not store calcium for contraction.
2632 — Axial Muscles
10 questions — Aligned to EAP objectives — Martini Chapter 7
Q75MC
The masseter is a primary chewing muscle. Its origin is the:
Mandible
Temporal lines of the skull
Zygomatic arch
Styloid process of the temporal bone
Correct — masseter: origin = zygomatic arch, insertion = mandible, primary action = elevate mandible (close jaw). The temporalis originates from the temporal lines. The pterygoids assist with grinding movements.
Incorrect — masseter origin = zygomatic arch. It inserts on the mandible. Temporal lines = temporalis. Styloid process = stylohyoid and related muscles.
Q76MC
When both sternocleidomastoid (SCM) muscles contract simultaneously, the result is:
Rotation of the head to the right
Extension of the neck, head tilting backward
Flexion of the neck — the chin moves toward the chest
Elevation of the sternum and clavicle
Correct — bilateral SCM = neck flexion (chin toward chest). Each SCM runs from the sternum/clavicle to the mastoid process. Bilateral = equal pull both sides = pure flexion. Extension comes from posterior muscles like splenius capitis.
When only the right sternocleidomastoid muscle contracts, the result is:
Neck flexion with the chin moving directly forward
Extension and rotation of the head to the right
The head tilts toward the right shoulder and the face rotates to the left
Depression of the right clavicle
Correct — unilateral SCM: tilt toward the SAME side (right), face rotates toward the OPPOSITE side (left). Bilateral = pure flexion. The angle of pull creates the tilt-and-rotation pattern at the mastoid process attachment.
Incorrect — right SCM: head tilts right, face rotates left. Same side tilt, opposite face rotation. Bilateral = flexion. SCM does not depress the clavicle.
Q78MC
The external intercostal muscles' primary role during breathing is:
Depressing the ribs to reduce thoracic volume during expiration
Elevating the ribs to expand the thoracic cavity during inspiration
Stabilizing the ribs laterally during coughing
Rotating the trunk by pulling the rib cage toward the pelvis
Correct — external intercostals = elevate ribs = inspiration. Internal intercostals = depress ribs = forced expiration. External = inspiration, internal = expiration is the standard distinction.
Incorrect — diaphragm contraction = flattens + moves down = inspiration. Thoracic compression occurs on relaxation, producing expiration, not on contraction.
Q80MC
Unlike the oblique muscles, the transversus abdominis:
Flexes the vertebral column when both sides contract
Rotates the trunk when one side contracts
Compresses the abdominopelvic cavity without producing rotation
Elevates the ribs during deep inspiration
Correct — transversus abdominis has horizontal fibers — it acts like a girdle to compress the abdomen but cannot rotate the trunk. The obliques can rotate because their fibers run diagonally. The transversus is the deepest abdominal muscle.
Incorrect — transversus = compresses without rotation. Obliques = can rotate. Flexion = rectus abdominis. Rib elevation = intercostals and scalenes.
Q81FITB
The vertical midline band of dense connective tissue separating the left and right rectus abdominis muscles is called the ___ ___.
Correct — linea alba (Latin: white line). Formed by the interlacing aponeuroses of the external oblique, internal oblique, and transversus abdominis. Runs from xiphoid process to pubic symphysis. Relatively avascular — preferred midline surgical incision site.
Incorrect — linea alba. Latin for "white line." The midline aponeurotic band between the rectus abdominis columns, formed by the interlacing aponeuroses of all three lateral abdominal muscles.
Q82MC
Bilateral contraction of the erector spinae group produces:
Lateral flexion of the vertebral column to the same side
Extension of the vertebral column and maintenance of upright posture
Trunk rotation toward the contracting side
Compression of the abdominopelvic cavity
Correct — bilateral erector spinae = spine extension + upright posture. These anti-gravity muscles continuously resist spinal flexion from gravity. The three columns (spinalis, longissimus, iliocostalis) run alongside the spine. Unilateral = lateral flexion to the same side.
Select ALL muscles whose primary actions include compressing the abdominopelvic cavity.
Correct — the three lateral abdominal muscles (external oblique, internal oblique, transversus abdominis) compress the abdominopelvic cavity. Rectus abdominis primarily flexes the spine; erector spinae extends it. Select only the three compressors.
Incorrect — compressors = external oblique + internal oblique + transversus abdominis. Rectus abdominis = spinal flexion. Erector spinae = extension. Only the three lateral abdominal wall muscles compress the cavity.
Q84MC
The external urethral and anal sphincters are skeletal muscles. This means they are under:
Involuntary autonomic control — same as the internal sphincters
Cardiac pacemaker timing to coordinate with abdominal pressure waves
Voluntary somatic control — allowing conscious deferral of urination and defecation
Hormonal control that coordinates with GI peristaltic activity
Correct — external sphincters = skeletal = voluntary somatic control. Internal sphincters = smooth = involuntary autonomic. Voluntary deferral of elimination depends entirely on the voluntary external skeletal sphincters. This is lost in certain spinal cord injuries.
10 questions — Aligned to EAP objectives — Martini Chapter 7
Q85MC
The deltoid originates from the acromion, scapular spine, and lateral clavicle. Its primary action is:
Medial rotation of the humerus
Extension of the shoulder
Abduction of the shoulder
Adduction of the shoulder
Correct — deltoid = shoulder abduction (primary). Anterior fibers assist flexion; posterior fibers assist extension. Inserts on the deltoid tuberosity of the humerus. The middle fibers are the primary abductors.
Incorrect — deltoid = abduction. Medial rotation = subscapularis. Extension = posterior deltoid fibers and latissimus dorsi. Adduction = pectoralis major and latissimus dorsi.
Q86MC
The triceps brachii is notable because it is:
The only muscle capable of shoulder flexion in the upper limb
The strongest supinator of the forearm
The only muscle that extends the elbow
The primary wrist flexor
Correct — triceps brachii is the ONLY elbow extensor. All three heads (long, medial, lateral) insert on the olecranon of the ulna. The long head also crosses the shoulder joint. No other muscle can extend the elbow.
Incorrect — triceps = only elbow extensor. Its three heads all converge on the olecranon. It cannot flex the elbow, supinate, or flex the wrist.
Q87MC
The biceps brachii performs which combination of actions?
Elbow extension and pronation
Shoulder extension and elbow flexion
Elbow flexion and supination of the forearm
Wrist flexion and shoulder abduction
Correct — biceps brachii = elbow flexion + forearm supination. The supination action is powerful — turning a screwdriver forcefully uses the biceps heavily. It also assists shoulder flexion via its proximal scapular origins.
Incorrect — biceps = elbow flexion + supination. Extension = triceps. Pronation = pronator teres/quadratus. Wrist flexion and shoulder abduction are performed by other muscles.
Q88MC
The four muscles of the rotator cuff that stabilize the glenohumeral joint are:
Deltoid, biceps brachii, coracobrachialis, and brachialis
Supraspinatus, infraspinatus, teres minor, and subscapularis
Pectoralis major, latissimus dorsi, teres major, and coracobrachialis
Rhomboid major, rhomboid minor, trapezius, and serratus anterior
Correct — rotator cuff = SITS: Supraspinatus (abduction), Infraspinatus (lateral rotation), Teres minor (lateral rotation), Subscapularis (medial rotation). Their tendons form a cuff reinforcing the shoulder joint capsule. The deltoid is NOT a rotator cuff muscle.
Incorrect — rotator cuff = SITS mnemonic: Supraspinatus, Infraspinatus, Teres minor, Subscapularis. Deltoid is not part of the rotator cuff. The other options are unrelated muscle groups.
Q89MC
All three hamstring muscles (biceps femoris, semitendinosus, semimembranosus) share a proximal origin on the:
Posterior femur (linea aspera)
Anterior superior iliac spine
Ischial tuberosity
Greater trochanter of the femur
Correct — all three hamstrings originate on the ischial tuberosity (the "sit bone"). They insert on the tibia and fibula to perform hip extension and knee flexion. Explosive hip flexion during sprinting commonly strains the proximal hamstring attachment here.
Incorrect — hamstrings = ischial tuberosity. Linea aspera = some hip adductor origins. Anterior superior iliac spine = sartorius and rectus femoris. Greater trochanter = gluteal insertion sites.
Q90MC
Of the four quadriceps muscles, which one also crosses the hip joint?
Vastus lateralis
Vastus medialis
Vastus intermedius
Rectus femoris
Correct — rectus femoris originates on the anterior inferior iliac spine of the pelvis, crossing both the hip and knee joints. The three vastus muscles originate on the femur — they only cross the knee. Rectus femoris therefore also flexes the hip.
Incorrect — rectus femoris originates on the pelvis (AIIS), crossing both hip and knee. The three vastus muscles originate on the femur and only cross the knee.
Q91MC
Both gastrocnemius and soleus plantar flex the foot via the Achilles tendon. However, only the gastrocnemius can also flex the knee because:
The soleus attaches to the fibula only, mechanically excluding knee action
The gastrocnemius has a larger pennation angle enabling multi-joint action
The gastrocnemius originates on the femoral condyles, above the knee joint
The soleus lacks a tendon long enough to reach the knee
Correct — gastrocnemius crosses the knee because its proximal origin is on the femoral condyles, above the knee. Soleus originates below the knee (tibia and fibula) and cannot act on it. A muscle must cross a joint to move it.
Incorrect — gastrocnemius crosses the knee because its origin (femoral condyles) is ABOVE the knee. Soleus origin is below the knee — it cannot act on the knee regardless of tendon length or attachment site.
Q92MC
The gluteus maximus is the largest muscle in the body. Its primary actions are:
Hip abduction and medial rotation
Hip adduction and flexion
Hip extension and lateral rotation
Knee extension and hip abduction
Correct — gluteus maximus = hip extension + lateral rotation. Most active during powerful movements: running, climbing stairs, rising from seated. During level walking, the gluteus medius (abduction + stabilization) is more active.
Incorrect — gluteus maximus = hip extension + lateral rotation. Abduction = gluteus medius. Hip flexion = iliopsoas. Knee extension = quadriceps.
Q93FITB
The three hamstring muscles all originate on the ___ tuberosity of the pelvis.
Correct — ischial tuberosity. The inferior bony prominence of the ischium — the "sit bone." All three hamstrings (biceps femoris long head, semitendinosus, semimembranosus) originate here and insert distally to flex the knee and extend the hip.
Incorrect — ischial tuberosity. The sit bone. All three hamstrings originate here. Sprinting strains commonly occur at this proximal attachment during explosive hip flexion.
Q94MC
The preferred intramuscular injection site in infants and young children is the:
Deltoid — the largest accessible upper limb muscle
Gluteus medius — the standard adult injection site
Rectus femoris — on the anterior thigh
Vastus lateralis — well-developed in infants with minimal adjacent neurovascular structures
Correct — vastus lateralis is preferred in infants because it is large, accessible, and free of major nerves and vessels nearby. The deltoid is too small, and the gluteus medius is underdeveloped until the child has been walking for some time.
Incorrect — vastus lateralis = preferred IM site in infants. Deltoid = too small in infants. Gluteus medius = preferred adult site but underdeveloped in young children. Rectus femoris is an alternative but not first choice.
2634 — Effects of Aging on Skeletal Muscle
4 questions — Aligned to EAP objectives — Martini Chapter 7
Q95MC
With aging, skeletal muscle mass declines (sarcopenia) primarily because:
Fiber type conversion from slow to fast fibers reduces endurance capacity
Motor nerve supply to peripheral muscles is progressively eliminated
Muscle fiber diameter decreases as the number of myofibrils per fiber declines
Glycogen and creatine phosphate stores are permanently depleted
Correct — sarcopenia = fibers shrink because they lose myofibrils. Smaller fibers = fewer myofibrils = less force. Along with fiber shrinkage, reserves of ATP, CP, glycogen, and myoglobin all decline. Fast fibers are most affected.
Incorrect — sarcopenia = fiber diameter decreases due to myofibril loss. Fiber type conversion does not occur. Motor nerve supply declines but fiber myofibril loss is the primary mechanism. Glycogen/CP are not permanently depleted in living fibers.
Q96MC
With aging, fibrosis of skeletal muscle means:
Enlargement of remaining fast fibers to compensate for atrophied slow fibers
Increased satellite cell activity replacing lost fibers
Functional muscle tissue is replaced by fibrous connective tissue
Conversion of aerobic to anaerobic fiber metabolism with aging
Correct — fibrosis = muscle replaced by non-contractile fibrous connective tissue. This reduces force production and increases stiffness. Satellite cell activity declines with age, making replacement less efficient. Fibrosis increases progressively from mid-adulthood.
Incorrect — fibrosis = muscle replaced by fibrous connective tissue. Not fiber enlargement, not satellite cell activation (satellite cells decline with age), not fiber type metabolism conversion.
Q97MC
According to the Martini textbook, the rate of age-related muscle function decline:
Is significantly slower in individuals who exercise regularly
Is faster in males than females due to testosterone-dependent maintenance
Is the same for everyone — exercise builds a higher baseline, not a slower slope
Stops at age 70 when fiber loss reaches a stable plateau
Correct — the rate of decline is the same for all individuals. Exercise cannot alter the rate — it only establishes a higher starting baseline. A well-trained 60-year-old may still perform above an untrained person's peak, but the slope of decline is identical.
Incorrect — rate of decline = same for everyone. Exercise raises the starting peak but does not change the slope. This is why building maximum muscle function early in life matters for maintaining independence in old age.
Q98MC
Elderly individuals are at increased risk for heat-related illness during exertion because:
Myoglobin loss reduces aerobic capacity and increases metabolic heat production
Blood supply to the skin is reduced while sweat gland activity also decreases
Decreased fiber diameter reduces heat generation but paradoxically increases core temperature
Fibrosis impedes blood flow to active muscles, trapping metabolic heat within the fibers
Correct — aging simultaneously reduces dermal blood supply AND sweat gland activity. Both are required for heat dissipation: blood vessels bring metabolic heat to the skin surface; sweat removes it by evaporation. Losing both creates serious thermoregulatory impairment.
Incorrect — heat risk = reduced dermal blood flow + decreased sweating, both at the same time. Myoglobin loss affects endurance, not heat regulation. Fibrosis is not a thermoregulatory issue.
2635 — System Relationships
2 questions — Aligned to EAP objectives — Martini Chapter 7
Q99MC
During sustained skeletal muscle activity, the cardiovascular system responds by:
Constricting vessels in active muscles to prevent excessive blood pressure
Decreasing heart rate to prevent cardiac fatigue
Increasing cardiac output and dilating vessels in active muscles to deliver more O₂
Redistributing all blood from visceral organs to the skin only
Correct — cardiovascular response: increased cardiac output (rate + stroke volume) + vasodilation in active muscles = more O₂ and nutrient delivery + CO₂ removal. Skin vessels dilate for heat dissipation. Visceral flow decreases so blood can be redirected to working muscles.
Incorrect — exercise = increased cardiac output + vasodilation in active muscles. Vasoconstriction would impair O₂ delivery. Heart rate increases. Blood redirects toward muscles and skin — not skin only.
Q100MC
The diaphragm and external intercostal muscles directly link the muscular system to the:
Cardiovascular system — their contractions increase venous return
Digestive system — they increase abdominal pressure during swallowing
Respiratory system — their contractions perform the mechanical work of breathing
Nervous system — the phrenic nerve is the only neural connection involved
Correct — diaphragm and external intercostals ARE the breathing muscles. Their skeletal muscle contractions expand the thorax to create inspiration. This is the primary muscular-respiratory system connection described in the textbook for this chapter.
Incorrect — respiratory system. The diaphragm and external intercostals are skeletal muscles that perform ventilation mechanics. This is the direct muscular-respiratory connection. Increased venous return and abdominal pressure effects are secondary consequences, not the primary link.
SOMAPL17 Practice Test — Complete
The Muscular System — Objectives 2623–2635
-- correct-- incorrect-- total
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SOMAPL17 — The Muscular System
Study guide aligned to objectives 2623–2635. Covers medical vocabulary, skeletal muscle functions, tissue organization, sarcomere structure, contraction mechanics, energy systems, fiber types, muscle tissue comparison, axial and appendicular muscles, aging, and systemic relationships.
13 objectives15 exam questionsObjectives 2623–2635Source: Martini Ch. 7
OBJ Click any card to expandTRAP Exam traps flagged in redTIP Clinical notes in green
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Objectives 2623–2635
2623Medical Vocabulary — Latin/Greek roots►
These word roots from the textbook Vocabulary Development section appear throughout Chapter 7. Knowing them decodes unfamiliar muscular system terms on the exam.
fasciculusbundle → fascicle = bundle of muscle fibers within perimysium
syn- / ergontogether / work → synergist helps a prime mover work efficiently
bi / caputtwo / head → biceps (two tendons of origin)
Note
Tetanus the disease (Clostridium tetani) and tetanus the muscle response share a name but are unrelated mechanisms. The disease suppresses motor neuron inhibition. The muscle response is normal physiology produced by high-frequency stimulation.
2624Functions of Skeletal Muscle Tissue — five primary functions►
Skeletal muscles are organs composed primarily of skeletal muscle tissue but also containing connective tissues, nerves, and blood vessels. The muscular system includes approximately 700 skeletal muscles performing five primary functions.
1. Produce Movement of the Skeleton
Skeletal muscle contractions pull on tendons and thereby move the bones. These contractions may produce a simple motion, such as extending the arm, or the highly coordinated movements of swimming, skiing, or typing.
2. Maintain Posture and Body Position
Continuous muscle contractions maintain body posture. Without this constant action, you could not sit upright without collapsing, or stand without toppling over.
3. Support Soft Tissues
The abdominal wall and floor of the pelvic cavity consist of layers of skeletal muscle. These muscles support the weight of our visceral organs and shield our internal tissues from injury.
4. Guard Entrances and Exits
Skeletal muscles encircle openings of the digestive and urinary tracts. These muscles provide voluntary control over swallowing, defecation, and urination.
5. Maintain Body Temperature
Muscle contractions require energy, and whenever energy is used in the body, some of it is converted to heat. Heat from working muscles keeps body temperature in the range required for normal functioning. Shivering is an extreme example.
Exam Trap
The answer is FIVE functions. Skeletal muscles can only PULL (generate tension) — they cannot push. Movement results from tension transmitted through tendons to bone. The diaphragm is a skeletal muscle that normally functions subconsciously but can be voluntarily controlled.
Clinical
Voluntary control over defecation and urination depends on skeletal muscle sphincters (external urethral and external anal sphincters). Spinal cord injury above sacral level eliminates voluntary external sphincter control even though smooth muscle internal sphincters remain intact.
2625Organization of Muscle at the Tissue Level — layers, fibers, organelles►
Skeletal muscle has a precise hierarchical organization from the whole organ down to the individual protein filament. Three connective tissue layers wrap each level of organization and converge at each end to form the tendon or aponeurosis.
1
EpimysiumLayer of collagen fibers surrounding the entire muscle. Separates the muscle from surrounding tissues and organs. (epi = on)
2
PerimysiumConnective tissue dividing skeletal muscle into compartments. Each compartment contains a bundle of muscle fibers called a fascicle. Contains blood vessels and nerves supplying the fascicles. (peri = around)
Fascicle = fasciculus = a bundle of muscle fibers
3
EndomysiumSurrounds each individual skeletal muscle fiber and ties adjacent fibers together. Contains capillaries, nerve fibers, and stem cells (satellite cells) for repair. (endo = inside)
4
Tendon or AponeurosisAt each end of the muscle, collagen fibers of all three layers converge. A cord = tendon. A flat sheet = aponeurosis. Tendon fibers interweave with bone periosteum. Every contraction pulls on the tendon, which pulls on the bone.
5
Sarcolemma and T TubulesThe plasma membrane of a muscle fiber (sarcolemma) surrounds the cytoplasm (sarcoplasm). Openings across the sarcolemma lead into T tubules (transverse tubules) filled with extracellular fluid. T tubules carry action potentials deep into the fiber, coordinating simultaneous contraction of all sarcomeres.
6
Sarcoplasmic Reticulum and TriadsSpecialized smooth ER forming a tubular network around each myofibril. Stores calcium ions in terminal cisternae. A T tubule sandwiched between two terminal cisternae = a triad. The T tubule signal triggers Ca2+ release from the cisternae to start contraction.
7
Myofibrils and MyofilamentsCylindrical myofibrils (1-2 micrometers diameter, as long as the fiber) responsible for contraction. Each fiber contains hundreds to thousands of myofibrils. Myofibrils contain thick (myosin) and thin (actin) myofilaments organized into sarcomeres. Each muscle fiber is multinucleate (hundreds of nuclei beneath the sarcolemma).
Exam Trap
T tubules do NOT store calcium. The sarcoplasmic reticulum (specifically the terminal cisternae) stores Ca2+. T tubules only carry the electrical signal. A triad = 1 T tubule flanked by 2 terminal cisternae. Confusing T tubules with SR is a classic exam error.
2626Structural Components of a Sarcomere — bands, lines, zones, filaments►
The sarcomere is the smallest functional unit of the muscle fiber. Each myofibril contains approximately 10,000 sarcomeres end to end. Resting length is about 2 micrometers. Differences in size and density of thick and thin filaments account for the banded (striated) appearance.
Structure
Description
Change During Contraction
Z lines
Protein discs marking the boundaries of each sarcomere. Thin (actin) filaments anchor here. Strands extend from Z lines to ends of thick filaments to maintain alignment.
Move CLOSER together
M line
Proteins at center connecting central portions of adjacent thick filaments to each other.
Stays centered
A band
DARK band; spans the full length of the thick (myosin) filaments. Zone of overlap lies within the A band.
Width UNCHANGED
I band
LIGHT band; region of thin filaments only, between two successive A bands, including the Z line.
Gets SMALLER
H band
Lighter central zone of A band; thick filaments only, no overlap with thin filaments.
Gets SMALLER
Zone of overlap
Region within A band where thick and thin filaments interdigitate. Cross-bridges form here during contraction.
Gets LARGER
Each thin filament is a twisted strand of actin molecules, each with an active site capable of binding myosin. In a resting muscle, active sites are covered by tropomyosin strands held in position by troponin bound to the actin strand. Calcium is the key that unlocks active sites: Ca2+ binds troponin, troponin changes shape, tropomyosin swings away, active sites are exposed.
Thick filaments are composed of myosin molecules, each with a tail and globular head. Myosin heads project outward from the M line. In the resting sarcomere each myosin head is already energized (cocked) with ADP and phosphate bound. When active sites are exposed, heads bind to form cross-bridges and pivot toward the M line (power stroke).
Exam Trap
The A band width stays CONSTANT during contraction — it equals the thick filament length and never changes. Everything else changes. A band = dArk = constant. I band = lIght = narrows. H band = Hole in the middle = shrinks. Z lines move closer together. Zone of overlap increases.
2627Key Steps in Muscle Fiber Contraction — NMJ through sliding filament►
Skeletal muscle fibers contract only under nervous system control. Each fiber is controlled by a motor neuron at a neuromuscular junction (NMJ). The axon terminal contains vesicles filled with acetylcholine (ACh). A narrow synaptic cleft separates the axon terminal from the motor end plate on the sarcolemma. Both the cleft and motor end plate contain acetylcholinesterase (AChE) which breaks down ACh.
1
ACh Released at NMJAction potential arrives at axon terminal. Vesicles fuse with the membrane. ACh released by exocytosis into the synaptic cleft.
2
Action Potential Generated in SarcolemmaACh binds to receptors on motor end plate. Na+ permeability increases. Na+ rushes into sarcoplasm. Action potential generated and sweeps across the entire sarcolemma surface.
3
AChE Breaks Down AChAChE quickly breaks down ACh in the synaptic cleft and motor end plate, inactivating the ACh receptors. No further stimulus until the next action potential arrives at the axon terminal.
4
Action Potential Travels Down T TubulesAction potential spreads across sarcolemma and down T tubules deep into the fiber interior, reaching the triads.
5
Calcium Released from SRT tubule signal triggers massive release of Ca2+ from the terminal cisternae of the sarcoplasmic reticulum into the sarcoplasm around the sarcomeres.
6
Active Sites Exposed on ActinCa2+ binds to troponin. Troponin changes shape. Tropomyosin swings away from active sites on actin molecules of the thin filaments.
7
Cross-Bridge FormationEnergized myosin heads (cocked with ADP + Pi bound) bind to exposed active sites, forming cross-bridges.
8
Power StrokeStored energy used to pivot myosin head toward M line. Thin filament pulled toward center of sarcomere. Bound ADP and phosphate group released. Sarcomere shortens.
9
Cross-Bridge Detachment and RecyclingNew ATP binds to the myosin head. Link between head and active site is broken. Free myosin head splits ATP into ADP + Pi. Energy released recocks the head. Cycle repeats as long as Ca2+ and ATP are available.
Relaxation: action potentials stop, AChE eliminates ACh, SR calcium pumps recapture Ca2+, troponin-tropomyosin return to resting positions covering active sites, cross-bridge cycling stops, muscle returns passively to resting length. Contraction is active; elongation is entirely passive.
Exam Traps
Botulism: bacterial toxin prevents ACh RELEASE from axon terminal = flaccid paralysis. Myasthenia gravis: autoimmune destruction of ACh RECEPTORS at motor end plate = progressive weakness. Rigor mortis: ATP depleted after death = SR cannot pump Ca2+ = cross-bridges cannot detach = muscles lock contracted (begins 2-7 hours after death, resolves 1-6 days later). Organophosphates inhibit AChE = ACh accumulates = sustained depolarization = convulsions then paralysis.
2628Types of Muscle Contractions — twitch, tetanus, isotonic, isometric►
A twitch is a single stimulus-contraction-relaxation sequence. A myogram is a graph of tension development during a twitch. Three phases in the gastrocnemius twitch (total ~40 msec): latent period (~2 msec, Ca2+ released, no tension yet); contraction phase (~15 msec, tension rises to peak); relaxation phase (~25 msec, Ca2+ recaptured, tension falls).
INCOMPLETE TETANUS
Second stimulus arrives before relaxation phase ends. Twitches add together (summation). Tension rises to a peak during rapid cycles of contraction and relaxation. Brief relaxation periods still occur.
Virtually all normal muscular contractions involve incomplete tetanus of the participating muscle fibers.
COMPLETE TETANUS
Stimulus rate so high that SR cannot recapture Ca2+. High Ca2+ concentration prolongs contraction making it continuous. Relaxation phase completely eliminated. Maximum tension produced and sustained.
Tension plateaus at maximal levels. Cannot occur in cardiac muscle.
A motor unit = one motor neuron + all the muscle fibers it innervates. Eye muscles: 2-3 fibers per unit (fine control). Leg muscles: up to 2,000 fibers per unit (power). Recruitment = activating progressively more motor units to produce a smooth, steady increase in muscular tension. Motor unit fibers are intermingled with those of other units so pull direction stays constant regardless of which units are active.
Isotonic Contraction
Tension rises, then the skeletal muscle length changes while tension remains constant until relaxation occurs. Lifting an object off a desk, walking, and running involve isotonic contractions. (iso = equal, tonos = tension)
Isometric Contraction
The muscle as a whole does not change length and the tension produced never exceeds the load. Examples: pushing against a closed door, trying to pick up a car. Many everyday reflexive postural contractions opposing gravity are isometric. (metron = measure)
Muscle Tone and Atrophy
Some motor units are always active even when the whole muscle is not contracting. Their contractions do not produce enough tension for gross movement but they tense and firm the muscle. This resting tension = muscle tone. A skeletal muscle not regularly stimulated will atrophy — fibers become smaller and weaker. Initially reversible; dying fibers replaced by fibrous tissue permanently.
Exam Trap
Cardiac muscle CANNOT undergo tetanus — its plasma membrane properties differ from skeletal muscle and the SR cannot stay open long enough. A tetanic heart could not pump blood between beats. Smooth muscle CAN tetanize; skeletal CAN tetanize; cardiac CANNOT.
Muscle contraction requires large amounts of energy. An active skeletal muscle fiber may require 600 trillion ATP molecules per second. A resting fiber contains only enough ATP to sustain a contraction for a few seconds. Three systems generate ATP to meet demand throughout the duration of activity.
ATP + Creatine Phosphate (Immediate)
Fastest; active in the first ~15 seconds
At rest, surplus ATP transfers energy to creatine forming creatine phosphate (CP). During contraction: CP + ADP yields ATP + creatine. Regulated by creatine phosphokinase (CPK/CK). Resting muscle has ~6x more CP than ATP. Elevated blood CPK = muscle cell damage.
Aerobic Metabolism (Mitochondria)
Sustained moderate activity; requires O2
Provides 95% of resting ATP. Citric acid cycle in mitochondria. Each pyruvate yields 17 ATP. Resting muscle burns fatty acids. When activity begins, switches to pyruvate from glycolysis. Limited by O2 delivery: mitochondrial output can increase 40x resting, but peak demand = 120x resting.
Glycolysis (Anaerobic)
Peak activity; occurs in cytoplasm; no O2 needed
Breakdown of glucose to pyruvate in cytoplasm. Glucose from glycogen granules stored in sarcoplasm. Net yield: 2 ATP per glucose (vs. 34 more ATP from aerobic completion). At peak activity: glycolysis provides ~2/3 of ATP; mitochondria ~1/3. By-product: lactic acid = lactate + H+ = pH drop = fatigue.
Fatigue and Recovery
Inability to contract despite continued stimulation
Caused by: (1) exhaustion of energy reserves, (2) pH drop from lactic acid. Recovery: SR pumps Ca2+ back in; liver converts lactate to glucose to glycogen; CP and ATP stores replenished. Extra O2 consumed during recovery above resting = oxygen debt. Explains continued heavy breathing after exercise stops.
Activity Level Summary
Resting: fatty acids oxidized aerobically; surplus ATP builds CP and glycogen. Moderate: aerobic breakdown of glucose and fatty acids; mitochondria meet demand. Peak: glycolysis dominant (~2/3 ATP); lactate accumulates; mitochondria provide only ~1/3.
Clinical
Elevated blood CPK (creatine phosphokinase) indicates muscle cell membrane damage allowing the enzyme to leak into circulation. Used clinically to diagnose rhabdomyolysis, myocardial infarction, and other muscle damage conditions.
2630Muscle Fiber Types and Performance — fast vs. slow, aerobic vs. anaerobic endurance►
Muscle performance = force (maximum tension produced) and endurance (time activity can be sustained). Two major factors: fiber type and physical conditioning. The human body contains two contrasting types of skeletal muscle fibers.
Property
Fast Fibers (Fast-Twitch)
Slow Fibers (Slow-Twitch)
Peak tension time
0.01 sec or less
~3x longer than fast
Diameter
Large
About half of fast fibers
Myofibrils
Densely packed; more power
Less dense
Mitochondria
Few
Many (aerobic capacity)
Glycogen reserves
Large
Smaller
Capillary supply
Standard
Extensive network
Myoglobin
Little — pale/white appearance
Abundant — red appearance
Primary energy
Glycolysis (anaerobic)
Aerobic metabolism
Fatigue rate
Rapid
Resistant to fatigue
Best suited for
Short, powerful bursts
Sustained activity
Most human muscles appear pink (mixed fiber types). Eye and hand muscles: no slow fibers (swift, brief contractions needed). Back and calf muscles: dominated by slow fibers (continuous postural contraction). The percentage of fast vs. slow fibers is genetically determined. Training cannot convert fiber type but can increase fatigue resistance of fast fibers.
ANAEROBIC ENDURANCE
Length of time contractions can be supported by glycolysis + ATP/CP reserves. Involves fast muscle fibers.
Training: frequent, brief, intense workouts. Result: hypertrophy — each fiber increases in diameter. NUMBER of fibers does NOT increase. Examples: sprinting, pole vault, weightlifting.
AEROBIC ENDURANCE
Length of time contractions can be sustained by mitochondrial activities. Determined by substrate availability.
Training: sustained low-level activity (jogging, distance swimming). Aerobic training does NOT produce hypertrophy. Endurance athletes carboload (high-carb diet 3 days before event) to maximize glycogen stores.
Exam Trap
Hypertrophy = individual fibers get LARGER. The NUMBER of muscle fibers does NOT increase with training. Aerobic training does NOT produce hypertrophy. Only anaerobic/resistance training causes hypertrophy. Myoglobin stores O2 within the fiber for use during contraction — it is structurally related to hemoglobin but is NOT the same molecule.
2631Skeletal vs. Cardiac vs. Smooth Muscle — structure and function comparison►
Actin and myosin are present in all three muscle types. However, their internal organization, control mechanisms, calcium sources, and functional properties differ significantly.
Property
Skeletal Muscle Fiber
Cardiac Muscle Cell
Smooth Muscle Cell
Location
Attached to skeleton
Heart only
Walls of most organs
Shape
Long cylinders
Branched cells
Spindle-shaped
Nuclei
Multiple, near sarcolemma
Usually single, central
Single, centrally located
Striations
Yes
Yes
No
Sarcomeres
Yes, along myofibrils
Yes, along myofibrils
No; filaments scattered in sarcoplasm
Special junctions
None
Intercalated discs with gap junctions
Anchoring sites transmit contractile forces
Control
Neural, single NMJ; voluntary
Automaticity (pacemaker cells); involuntary
Automaticity (pacesetter cells); neural or hormonal; involuntary
Ca2+ source
SR only
SR + extracellular fluid
Extracellular fluid + SR
Tetanus possible?
Yes
NO
Yes
Fatigue
Rapid fatigue
Resistant to fatigue
Resistant to fatigue
Energy source
Aerobic (moderate); glycolysis at peak
Aerobic; lipid or carbohydrate
Primarily aerobic
Cardiac unique features: Intercalated discs contain gap junctions allowing action potentials to pass directly cell-to-cell, producing simultaneous contraction of entire chambers. Automaticity = contracts without neural input. Contractions last ~10x longer than skeletal. Cannot tetanize — heart must relax between beats to fill with blood.
Smooth unique features: No sarcomeres, no striations. Thick filaments scattered in sarcoplasm; thin filaments anchored to sarcolemma and cytoplasmic dense bodies. Contraction causes a corkscrew twist. Can contract over a wider range of lengths — critical for hollow organs (bladder, stomach) undergoing large volume changes. Many cells respond to hormones and pacesetter cells without direct motor neuron input. Sphincters = rings of smooth muscle in digestive and urinary systems.
Exam Traps
Cardiac muscle has automaticity AND cannot tetanize — both are unique to cardiac muscle. Smooth muscle CAN tetanize. Skeletal cannot achieve automaticity. Extracellular Ca2+ entry is important for BOTH cardiac AND smooth muscle contraction, but NOT for skeletal muscle.
2632Main Axial Muscles and Their Actions — head, neck, spine, trunk, pelvic floor►
Axial muscles arise on the axial skeleton, position the head and spinal column, and move the rib cage. They encompass roughly 60% of all skeletal muscles and do NOT move the pectoral or pelvic girdles. A prime mover (agonist) is chiefly responsible for a particular movement. Antagonists oppose that movement. Synergists help the prime mover work efficiently. Fixators stabilize the origin of a prime mover.
Exam Trap
Voluntary control of urination and defecation = SKELETAL muscle (external sphincters). Internal sphincters are smooth muscle and are involuntary. Axial muscles do NOT move the pectoral or pelvic girdles — that is the role of the appendicular muscle group.
2633Main Appendicular Muscles and Their Actions — shoulders, upper limbs, pelvic girdle, lower limbs►
Appendicular muscles stabilize or move components of the appendicular skeleton. The pectoral girdle connection to the axial skeleton must act as a shock absorber while allowing upper limb mobility. The pelvic girdle connection transfers weight from the axial to the appendicular skeleton with emphasis on power over mobility.
Muscle
Primary Action(s)
Key Origin / Insertion / Note
Trapezius
Elevates, adducts, depresses, or rotates scapula (depending on active region); can extend/hyperextend neck
Occipital bone and spinous processes of thoracic vertebrae to clavicle and scapula.
Levator scapulae
Elevates scapula (shrugging)
Covered by trapezius; transverse processes of C1-C4.
Rhomboid muscles
Adducts (retracts) scapula toward midline
Spinous processes of lower cervical and upper thoracic vertebrae.
Serratus anterior
Protracts shoulder; abducts and medially rotates scapula
Origin: ribs 1-9; Insertion: vertebral border of scapula.
Pectoralis minor
Depresses and protracts shoulder
Origin: ribs 3-5; Insertion: coracoid process of scapula.
Deltoid
Abduction at shoulder
Major abductor of the arm; IM injection site (2.5 cm distal to acromion).
Pectoralis major
Flexion, adduction, and medial rotation at shoulder
Large anterior chest muscle; cartilages of ribs 2-6, sternum, clavicle to greater tubercle of humerus.
Latissimus dorsi
Extension, adduction, and medial rotation at shoulder
Lower thoracic vertebrae, ribs, lumbar vertebrae to intertubercular groove of humerus.
Supraspinatus*
Abduction at shoulder
*Rotator cuff (SITS). Tendons blend with shoulder joint capsule for support. Common throwing-sport injury site.
Infraspinatus*
Lateral rotation at shoulder
*Rotator cuff. Infraspinous fossa of scapula to greater tubercle.
Teres minor*
Lateral rotation at shoulder
*Rotator cuff. Lateral border of scapula to greater tubercle.
Subscapularis*
Medial rotation at shoulder
*Rotator cuff. Subscapular fossa of scapula to lesser tubercle.
Biceps brachii
Flexion at shoulder and elbow; supination
Short head from coracoid process; long head from supraglenoid tubercle; inserts on radial tuberosity. Strongest when forearm supinated.
Triceps brachii
Extension at elbow
ONLY elbow extensor. Long head from scapula; inserts on olecranon of ulna.
Brachialis
Flexion at elbow
Pure elbow flexor; anterior distal humerus to ulnar tuberosity.
Brachioradialis
Flexion at elbow
Lateral epicondyle of humerus; forms lateral forearm bulge.
Pronator teres
Pronation
Medial epicondyle of humerus to lateral radius. With pronator quadratus.
Supinator
Supination
Works with biceps brachii; lateral epicondyle of humerus.
Flexor carpi radialis
Flexion and abduction at wrist
Medial epicondyle to 2nd and 3rd metacarpal bases.
Flexor carpi ulnaris
Flexion and adduction at wrist
Opposite direction from flexor carpi radialis.
Palmaris longus
Flexion at wrist
Tendinous sheet on the palm.
Extensor carpi radialis
Extension and abduction at wrist
Posterior forearm; distal lateral humerus.
Extensor carpi ulnaris
Extension and adduction at wrist
Lateral epicondyle of humerus and ulna; base of 5th metacarpal.
Gluteus maximus
Extension and lateral rotation at hip
Largest muscle in body; primary power for running and climbing. Iliac crest, sacrum, coccyx to iliotibial tract and gluteal tuberosity.
Gluteus medius
Abduction and medial rotation at hip
Preferred IM injection site (posterior/lateral superior quadrant).
Gluteus minimus
Abduction and medial rotation at hip
Deep to gluteus medius; lateral surface of ilium.
Iliopsoas (Psoas major + Iliacus)
Flexion at hip and/or lumbar intervertebral joints
Largest hip flexor; inserts at lesser trochanter of femur. Two muscles sharing a common insertion.
Adductor group (magnus, longus, brevis, pectineus, gracilis)
Adduction at hip; flexion and medial rotation (varies by muscle)
Strain of one of these = "pulled groin."
Biceps femoris
Flexion at knee; extension and lateral rotation at hip
Hamstring. Origin: ischial tuberosity and linea aspera of femur.
Semitendinosus
Flexion at knee; extension and medial rotation at hip
Hamstring. Origin: ischial tuberosity.
Semimembranosus
Flexion at knee; extension and medial rotation at hip
Hamstring. Origin: ischial tuberosity. Pulled hamstring = strain in one of these three.
Sartorius
Flexion at knee; flexion and lateral rotation at hip
Longest muscle in the body; "tailor's muscle" (crossing-legs position). Anterior superior iliac spine to medial tibia.
Rectus femoris
Extension at knee; flexion at hip
Quadriceps. ONLY quadriceps muscle crossing the hip joint. Anterior inferior iliac spine to tibial tuberosity via patellar ligament.
Vastus lateralis
Extension at knee
Quadriceps. Preferred IM site in infants and young children.
Vastus medialis
Extension at knee
Quadriceps. Entire length of linea aspera of femur.
Vastus intermedius
Extension at knee
Quadriceps. Lies beneath the other three; not visible in surface view.
Popliteus
Rotates tibia medially; flexion at knee
Unlocks the extended/locked knee. Lateral condyle of femur to posterior proximal tibial shaft.
No femoral origin = does NOT cross or flex knee. Head and proximal shaft of fibula to calcaneus via calcaneal tendon.
Tibialis anterior
Dorsiflexion at ankle; inversion of foot
Opposes gastrocnemius. Lateral condyle and proximal shaft of tibia to 1st metatarsal base.
Fibularis (peroneus) muscles
Eversion of foot; plantar flexion at ankle
Fibula and lateral condyle of tibia to metatarsal bases.
Exam Traps
Triceps brachii is the ONLY elbow extensor. Biceps brachii produces supination AND flexion — loses mechanical advantage with forearm pronated. Rectus femoris is the ONLY quadriceps muscle crossing the hip joint. Soleus does NOT flex the knee because it has no femoral origin. Gastrocnemius DOES flex the knee because it originates on the femoral condyles.
Clinical — IM Injection Sites
Gluteus medius (posterior/lateral superior quadrant): large, few vessels and nerves, up to 5 mL. Deltoid (2.5 cm distal to acromion): accessible but limited volume. Vastus lateralis: preferred in infants, young children, and elderly patients with atrophied gluteal and deltoid muscles — thick muscle, no large vessels or nerves encountered.
2634Effects of Aging on Muscle Tissue — four changes and clinical implications►
Aging degrades every aspect of muscular performance. The rate of decline is the same in all people regardless of exercise patterns or lifestyle. To be in good shape late in life, an individual must be in very good shape early in life. Regular exercise helps control body weight, strengthens bones, and generally improves the quality of life at all ages.
1. Skeletal Muscle Fibers Become Smaller in Diameter
Reduction in size reflects a decrease in the number of myofibrils. Fibers contain smaller ATP, CP, and glycogen reserves and less myoglobin. Overall effects: reduced muscle strength, reduced endurance, tendency to fatigue rapidly. Cardiovascular performance also decreases — blood flow to active muscles does not increase with exercise as rapidly as in younger people.
2. Skeletal Muscles Become Less Elastic (Fibrosis)
Aging skeletal muscles develop increasing amounts of fibrous connective tissue — a process called fibrosis. Fibrosis makes the muscle less flexible and less responsive. Collagen fibers restrict movement and circulation.
3. Tolerance for Exercise Decreases
Lower tolerance results from the tendency to tire quickly and from reduced thermoregulatory capacity. Individuals over age 65 cannot eliminate muscle-generated heat as effectively as younger people, leading to risk of overheating during exercise.
4. Ability to Recover from Muscular Injuries Decreases
When an injury occurs, repair capabilities are limited and scar tissue formation is the usual result. Dying muscle fibers are not replaced. In extreme atrophy the functional losses are permanent. This is why physical therapy is critical for patients who are temporarily unable to move normally.
Key Principle
The rate of muscular decline is universal — regular exercise does not slow the rate of decline itself. Exercise preserves function only by maintaining a higher starting point. Extremely demanding exercise in the elderly can damage tendons, bones, and joints. Regular moderate exercise — not extreme exercise — is the goal at all ages.
Clinical
Physical therapy is critical for patients who are temporarily unable to move normally. Muscle atrophy is initially reversible, but dying fibers are not replaced. Early intervention prevents permanent functional loss. Even brief periods of immobilization following injury or surgery require active rehabilitation to prevent significant long-term deficits.
2635Functional Relationships with Other Body Systems — systems integrator►
Even when the body is at rest, the muscular system is interacting with other organ systems. The changes that occur during exercise provide a good example of such interactions. Active muscles consume oxygen and generate carbon dioxide and heat, requiring coordinated responses from every other system.
Integumentary System
Removes excess body heat generated by contracting muscles
Blood vessels dilate and sweat gland secretion increases — promotes evaporation and heat removal from skin surface. Synthesizes vitamin D3 for calcium and phosphate absorption needed by muscle. Skeletal muscles pulling on dermis of face produce facial expressions.
Skeletal System
Provides sites of attachment and the lever system
Provides movement and support. Mechanical stress from tendons maintains bone mass. Muscles stabilize bones and joints. Bone provides mineral reserve (calcium, phosphate) for maintaining normal levels in body fluids required for muscle contraction.
Nervous System
Directs immediate responses; coordinates all systems during exercise
Motor neurons provide mandatory stimulation for skeletal muscle contraction. Directs heart rate, respiratory rate, sweat gland activity, and release of stored energy reserves. Coordinates all organ system responses during exercise.
Endocrine System
Directs long-term changes in response to activity
Hormones adjust metabolic rate and mobilize fuel reserves. Epinephrine mobilizes glucose. Works with nervous system to direct responses of other systems during exercise and recovery.
Cardiovascular System
Delivers O2 and nutrients; removes CO2 and heat
During exercise: blood vessels in active muscles and in the skin dilate, heart rate increases. Speeds O2 delivery and CO2 removal. Brings heat to skin for radiation. Elevated blood CPK indicates skeletal muscle damage.
Respiratory System
Increases O2 delivery; removes excess CO2
Rate and depth of respiration increase during exercise, keeping pace with increased blood flow through the lungs. Diaphragm and intercostals are skeletal muscles that power breathing — voluntarily controllable and automatically rhythmic.
Digestive System
Provides fuel for muscular activity
Provides nutrients: glucose, fatty acids, amino acids. Abdominal wall muscles assist digestion by compressing digestive organs. Smooth muscle in digestive walls performs peristalsis. Skeletal muscle sphincters control defecation.
Urinary System
Eliminates metabolic wastes from muscle activity
Removes excess water, salts, and waste products generated by active skeletal muscles. External urethral sphincter (skeletal muscle) provides voluntary control of urination.
The Big Picture
During vigorous exercise, every organ system responds simultaneously. Cardiovascular: vessels dilate, heart rate increases. Respiratory: rate and depth increase. Integumentary: vessels dilate, sweating increases. Nervous and endocrine: coordinate all responses and release stored energy. The muscular system is the primary driver of these whole-body responses.