Hearing and Balance: Ear Anatomy, Function — Hearing and Balance: Ear Anatomy and Function - Anatomy and Physiology

SECTION 1

Historical Context & Motivation

The study of hearing and balance has captivated scientists and physicians for centuries, driven by the fundamental question of how a delicate, fluid-filled organ can transform invisible pressure waves into the rich tapestry of sound perception while simultaneously monitoring the body's orientation in three-dimensional space. Early anatomists recognized the ear as far more than a simple collector of sound; dissections revealed intricate chambers, tiny bones, and coiled structures whose functions remained mysterious for generations. The mechanotransduction framework that ultimately explained auditory and vestibular function emerged only through the convergence of anatomy, physics, and neuroscience — a convergence that continues to inform modern cochlear implant design, vestibular rehabilitation, and our understanding of sensory processing at the cortical level.

1561 • Fallopius Describes the Cochlea

Gabriele Falloppio, in his Observationes Anatomicae, provided the first detailed description of the cochlea and semicircular canals, establishing the foundational anatomy of the inner ear for subsequent investigators.

1851 • Corti Identifies the Organ of Hearing

Alfonso Corti used improved microscopy to describe the sensory epithelium within the cochlea — the organ of Corti — containing the hair cells responsible for transducing mechanical vibrations into neural impulses.

1863 • Helmholtz's Place Theory

Hermann von Helmholtz proposed the place theory of hearing, suggesting that different regions of the basilar membrane respond to different frequencies, analogous to piano strings of varying length and tension.

1961 • von Békésy Wins Nobel Prize

Georg von Békésy received the Nobel Prize in Physiology or Medicine for demonstrating the traveling wave pattern along the basilar membrane, experimentally validating and refining Helmholtz's theory through direct observation in cadaveric cochleae.

2018 • Molecular Basis of Mechanotransduction

Researchers identified TMC1 and TMC2 as the principal mechanotransduction channel proteins in hair cells, resolving a decades-long search for the molecular identity of the channels that convert stereocilia deflection into electrical signals.

This lesson addresses the central questions that drove these discoveries: How does the ear partition sound into its component frequencies? How do hair cells convert nanometer-scale mechanical displacements into graded receptor potentials? And how does the vestibular apparatus encode both linear acceleration and rotational movement so that the brain can maintain posture, stabilize gaze, and navigate through space? Understanding these mechanisms requires a thorough appreciation of ear anatomy — from the external pinna to the deepest recesses of the petrous temporal bone.

SECTION 2

Core Principles & Definitions

The ear is conventionally divided into three anatomical regions — the external (outer) ear, the middle ear, and the inner ear — each performing distinct physical and physiological operations on the acoustic signal. Several overarching principles govern how these regions cooperate to produce hearing and balance.

Impedance Matching

Sound travels efficiently in air but encounters resistance at the fluid-filled cochlea. The middle ear ossicles amplify pressure approximately 22-fold through lever action and area ratio differences between the tympanic membrane and oval window, overcoming the impedance mismatch between air and perilymph.

Tonotopic Organization

The basilar membrane is mechanically tuned along its length: the narrow, stiff base resonates at high frequencies (~20,000 Hz) while the wide, flexible apex responds to low frequencies (~20 Hz). This tonotopic map is preserved throughout the auditory pathway to the cortex.

Mechanotransduction

Hair cells convert mechanical energy into electrical signals. Deflection of stereocilia toward the tallest row opens tip-link–gated ion channels, admitting K⁺ and Ca²⁺, which depolarizes the cell and triggers neurotransmitter release onto afferent neurons.

Endolymph Ionic Gradient

The endolymph bathing stereocilia tips is uniquely high in K⁺ (~150 mM) and maintained at a positive endocochlear potential (+80 mV) by the stria vascularis, creating a ~150 mV driving force for K⁺ influx when channels open.

Vestibular Dual Detection

The vestibular apparatus employs two complementary sensor types: the semicircular canals detect angular acceleration via endolymph inertia, while the otolith organs (utricle and saccule) detect linear acceleration and head tilt via calcium carbonate crystals.

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KEY TAKEAWAY

Think of the ear as a sophisticated signal-processing chain, analogous to a recording studio. The external ear acts as a directional microphone collecting sound; the middle ear functions as a preamplifier boosting the signal to overcome a medium change (air to fluid); the cochlea serves as a spectrum analyzer that decomposes the complex waveform into individual frequency components; and the auditory nerve transmits the digitized output to the brain's mixing console — the auditory cortex. Meanwhile, the vestibular system operates like an inertial measurement unit (IMU) in an aircraft, combining gyroscopes (semicircular canals) with accelerometers (otolith organs) to provide continuous orientation data.

SECTION 3

Visual Explanation — Ear Anatomy Overview

Cross-sectional overview of the three ear divisions. The external ear (pinna and external acoustic meatus) funnels sound to the middle ear where three ossicles (malleus, incus, stapes) amplify vibrations. The inner ear houses the cochlea for hearing, the semicircular canals for rotational balance, and the otolith organs (utricle and saccule) for linear acceleration detection. CN VIII carries both auditory and vestibular signals to the brainstem.

The diagram above illustrates the spatial relationships among the ear's three divisions, all housed within or adjacent to the petrous portion of the temporal bone. Sound waves collected by the pinna travel through the external acoustic meatus (approximately 2.5 cm in adults) and strike the tympanic membrane, setting it into vibration. These vibrations are mechanically coupled through the ossicular chain — the smallest bones in the human body — to the oval window of the cochlea. The stapes footplate acts like a piston, generating pressure waves in the perilymph-filled scala vestibuli. Note the round window at the base of the scala tympani: because fluid is incompressible, this compliant membrane bulges outward to accommodate the inward displacement at the oval window, permitting fluid movement and basilar membrane oscillation.

The vestibular apparatus shares the bony labyrinth with the cochlea but serves an entirely different sensory modality. The three semicircular canals are oriented in roughly orthogonal planes (anterior, posterior, and lateral), enabling detection of head rotation in any direction. At the base of each canal sits an enlarged ampulla containing a crista ampullaris with hair cells embedded in a gelatinous cupula. The otolith organs — utricle and saccule — detect linear acceleration and static head position using a different mechanism: hair cells project into a gelatinous layer studded with dense calcium carbonate crystals called otoconia, whose inertia bends the stereocilia when the head accelerates or tilts relative to gravity.

SECTION 4

Mechanism of Hearing — Sound Transduction

The conversion of airborne sound to neural signals involves a remarkable chain of energy transformations. Sound begins as pressure fluctuations in air (acoustic energy), is converted to mechanical vibrations by the tympanic membrane and ossicles, transformed into hydraulic pressure waves in cochlear fluids, and finally transduced into bioelectric signals by hair cells. Understanding the quantitative aspects of these transformations clarifies why each stage is physiologically necessary.

Middle Ear Amplification

PRESSURE AMPLIFICATION RATIO

Pressure Gain = (A_TM / A_OW) × Lever Ratio ≈ (55 mm² / 3.2 mm²) × 1.3 ≈ 22×

Where A_TM = effective area of the tympanic membrane (~55 mm²), A_OW = area of the oval window (~3.2 mm²), and the lever ratio (~1.3) arises from the length difference between the malleus and incus handles. This ~22× amplification corresponds to approximately 25–27 dB of gain, sufficient to overcome the ~30 dB loss at the air–fluid interface.

Sound Intensity and Decibel Scale

SOUND INTENSITY LEVEL

β = 10 × log₁₀(I / I₀) dB

Where β = sound intensity level in decibels, I = measured intensity (W/m²), and I₀ = threshold of hearing (1 × 10⁻¹² W/m²). The human ear spans an enormous dynamic range from 0 dB (threshold) to ~120 dB (pain threshold), representing a 10¹² range of intensities.

Hair Cell Transduction

Within the organ of Corti, the basilar membrane's traveling wave causes the inner hair cells (IHCs, ~3,500 per cochlea) and outer hair cells (OHCs, ~12,000 per cochlea) to respond differently. IHCs are the primary sensory receptors, providing ~95% of the afferent innervation to the brain via spiral ganglion neurons. OHCs function as cochlear amplifiers: their unique motor protein prestin enables rapid changes in cell length (electromotility), locally boosting basilar membrane vibration by 40–60 dB at low sound intensities and thereby sharpening frequency selectivity.

DRIVING FORCE FOR TRANSDUCTION

V_driving = E_endocochlear − V_hair cell ≈ (+80 mV) − (−70 mV) = +150 mV

The endocochlear potential (+80 mV, generated by the stria vascularis) combined with the hair cell's resting membrane potential (−70 mV) creates an unusually large electrochemical driving force of ~150 mV for K⁺ entry through mechanically gated tip-link channels. This large gradient ensures rapid depolarization with minimal channel opening.

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Clinical Note — Ototoxicity

Aminoglycoside antibiotics (gentamicin, streptomycin) and platinum-based chemotherapeutics (cisplatin) are selectively toxic to outer hair cells, particularly at the cochlear base (high-frequency region). Loss of OHC electromotility results in reduced cochlear amplification and elevated hearing thresholds — manifesting clinically as sensorineural hearing loss that initially affects high frequencies. Because mammalian hair cells do not regenerate, this damage is typically permanent.

SECTION 5

Cochlear Cross-Section & Tonotopic Organization

Upper panel: cross-section through the cochlear duct showing the three fluid-filled scalae separated by Reissner's membrane and the basilar membrane. The organ of Corti sits on the basilar membrane with one row of inner hair cells (IHCs) and three rows of outer hair cells (OHCs). The stria vascularis on the lateral wall generates the endocochlear potential. Lower panel: tonotopic gradient from base (high frequency) to apex (low frequency).

The cochlea is effectively a tube coiled 2.5 turns, but when conceptually unrolled, its internal partitioning becomes clear. The scala vestibuli (above) and scala tympani (below) contain perilymph, an extracellular-like fluid rich in Na⁺. Sandwiched between them is the scala media (cochlear duct), filled with endolymph. Reissner's membrane separates the scala vestibuli from the scala media and is thin enough to be acoustically transparent, meaning pressure waves effectively pass through it. The basilar membrane, however, is the critical vibrating structure upon which the organ of Corti rests.

The graded mechanical properties of the basilar membrane underlie tonotopic organization. At the base, the membrane is approximately 0.04 mm wide and very stiff — optimal for vibrating at high frequencies. At the apex, it widens to approximately 0.5 mm and becomes much more compliant, resonating at low frequencies. When a complex sound enters the cochlea, each frequency component causes maximal displacement at a specific position along the basilar membrane. The traveling wave initiated at the base propagates apically, growing in amplitude until reaching its characteristic frequency location, after which it rapidly decays. The tectorial membrane overlying the organ of Corti is coupled to OHC stereocilia, so that relative shearing motion between the tectorial and basilar membranes deflects the stereocilia bundles and triggers mechanotransduction.

Feature	Cochlear Base	Cochlear Apex
Basilar membrane width	~0.04 mm (narrow)	~0.5 mm (wide)
Stiffness	High (100× stiffer than apex)	Low (compliant)
Best frequency	~20,000 Hz	~20 Hz
Damage susceptibility	Most vulnerable to noise/ototoxins	More resistant
Clinical relevance	Presbycusis starts here	Low-frequency hearing preserved longest

Comparison of basilar membrane properties at the base versus apex of the cochlea

SECTION 6

Worked Example — Sound Transduction Pathway

The following worked example traces a 1,000 Hz tone at 60 dB through the entire auditory pathway, integrating anatomical knowledge with quantitative reasoning about sound processing at each stage.

Tracing a 1,000 Hz Tone from Pinna to Auditory Cortex

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Step 1 — External Ear Collection and Resonance

A 1,000 Hz tone (wavelength ≈ 0.34 m in air) enters the pinna, which provides modest directional cues via spectral shaping. The external acoustic meatus, approximately 2.5 cm long, acts as a quarter-wavelength resonator with a resonant frequency near 3,000–4,000 Hz, so our 1,000 Hz tone receives relatively little resonance boost (~2–5 dB). The sound pressure at the tympanic membrane is therefore approximately 60 + 3 = 63 dB SPL.

Sound at tympanic membrane: ~63 dB SPL
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Step 2 — Middle Ear Impedance Matching

The tympanic membrane vibrates and transfers energy to the malleus. The ossicular chain provides a pressure amplification of approximately 22×, equivalent to about 27 dB. At 1,000 Hz, the ossicular chain operates near peak efficiency. However, some energy is lost to friction and the acoustic reflex is not engaged at 60 dB. Net effective gain reaching the oval window: ~25 dB. Effective pressure at oval window: 63 + 25 = 88 dB SPL equivalent in fluid.

Pressure at oval window: ~88 dB SPL equivalent
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Step 3 — Basilar Membrane Traveling Wave

The stapes footplate creates a pressure wave in the scala vestibuli perilymph. This traveling wave propagates from base to apex, reaching maximal displacement approximately 20 mm from the base — the characteristic place for 1,000 Hz. At this location, basilar membrane displacement peaks while the wave rapidly attenuates further apically. Outer hair cell electromotility sharpens the peak, improving frequency selectivity by an estimated 40 dB.

Peak displacement at ~20 mm from base (1,000 Hz characteristic place)
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Step 4 — Hair Cell Mechanotransduction

At the point of maximal basilar membrane displacement, the shearing motion between the basilar and tectorial membranes deflects inner hair cell stereocilia toward the tallest row. Tip-link channels open, allowing K⁺ influx driven by the ~150 mV electrochemical gradient (E_endocochlear − V_rest = +80 − (−70) = +150 mV). The resulting depolarization opens voltage-gated Ca²⁺ channels at the basolateral surface, triggering glutamate release onto Type I spiral ganglion afferents.

IHC depolarization → glutamate release → spiral ganglion neuron firing
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Step 5 — Auditory Pathway to Cortex

Action potentials travel via the cochlear branch of CN VIII to the cochlear nuclei in the medulla. From there, signals ascend through the superior olivary complex (where binaural comparisons begin), lateral lemniscus, inferior colliculus, and medial geniculate nucleus of the thalamus before reaching the primary auditory cortex (Brodmann areas 41/42) in the superior temporal gyrus. The tonotopic map is preserved at each relay, so neurons responding to 1,000 Hz are located in a specific cortical band.

Conscious perception of a 1,000 Hz tone at conversational loudness, processed in ~10 ms

SECTION 7

Comparing Auditory and Vestibular Systems

Although the auditory and vestibular systems share a common embryological origin, reside within the same bony labyrinth, and rely on fundamentally similar hair cell mechanotransduction, they differ substantially in their stimuli, accessory structures, and neural projections. The following comparison highlights both the elegant unity and the functional divergence of these two sensory systems.

Feature	Auditory System (Cochlea)	Vestibular System
Adequate stimulus	Sound pressure waves (20–20,000 Hz)	Angular acceleration (canals); linear acceleration & gravity (otoliths)
Receptor organ	Organ of Corti (on basilar membrane)	Cristae ampullares (canals); maculae (utricle/saccule)
Accessory structure	Tectorial membrane	Cupula (canals); otolithic membrane with otoconia (otoliths)
Hair cell type	IHCs (sensory) and OHCs (amplifier)	Type I (calyx synapse) and Type II (bouton synapse)
Tonic vs. phasic	Primarily phasic (responds to changing stimuli)	Both tonic (otoliths sense gravity constantly) and phasic (canals sense acceleration changes)
Central projections	Cochlear nuclei → superior olivary complex → inferior colliculus → MGN → auditory cortex	Vestibular nuclei → cerebellum, oculomotor nuclei (VOR), spinal cord (VSR), cortex
Conscious perception	Yes — sound perception, speech recognition	Mostly subconscious — becomes conscious mainly during dysfunction (vertigo)

Comparison of auditory and vestibular systems within the inner ear

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KEY TAKEAWAY

The auditory and vestibular systems are like two specialized instruments built on the same platform — much as an accelerometer and a gyroscope in a smartphone both use microelectromechanical (MEMS) technology but measure different physical quantities. Both ear sensors rely on deflecting hair cell stereocilia to open mechanically gated ion channels, but their accessory structures (basilar membrane vs. cupula vs. otolithic membrane) tune them to completely different types of mechanical stimuli. Recognizing this shared transduction mechanism helps explain why diseases affecting the inner ear — such as Ménière's disease — often impair both hearing and balance simultaneously.

SECTION 8

Clinical Connections & Advanced Concepts

Understanding normal ear anatomy and physiology provides the essential foundation for interpreting pathological states, diagnostic tests, and therapeutic interventions. This section connects the mechanisms discussed above to clinical scenarios and previews advanced topics encountered in audiology, otolaryngology, and neuroscience courses.

Concept	Foundational (This Lesson)	Advanced / Clinical Extension
Conductive vs. sensorineural hearing loss	External/middle ear transmit sound mechanically; inner ear transduces via hair cells	Weber and Rinne tuning fork tests distinguish conductive from sensorineural loss; audiometry quantifies thresholds by frequency
Vestibulo-ocular reflex (VOR)	Semicircular canals detect head rotation; signals reach vestibular nuclei	VOR generates compensatory eye movements at ~10 ms latency; caloric testing and video head impulse test (vHIT) assess canal function
Otolith disorders	Otoconia in utricle/saccule sense linear acceleration and gravity	Displaced otoconia cause benign paroxysmal positional vertigo (BPPV); Epley maneuver repositions crystals
Cochlear implants	Tonotopic organization maps frequency to place along basilar membrane	Electrode arrays inserted into scala tympani directly stimulate spiral ganglion neurons at frequency-specific locations, bypassing damaged hair cells
Hair cell regeneration	Mammalian hair cells do not regenerate after damage	Research into Atoh1 transcription factor and Notch signaling aims to reprogram supporting cells into functional hair cells — a potential future cure for sensorineural deafness

Bridging foundational ear anatomy/physiology to clinical and advanced topics

The clinical significance of ear anatomy extends far beyond audiology. The vestibulo-ocular reflex (VOR) exemplifies one of the fastest neural circuits in the body — a three-neuron arc from semicircular canal hair cells through the vestibular nuclei to the extraocular motor nuclei, enabling gaze stabilization during head movement with a latency of only 10–15 milliseconds. Damage to any component of this arc (vestibular nerve, nuclei, or cerebellum) produces nystagmus and oscillopsia, making VOR testing a cornerstone of the neurological examination. Students pursuing neuroscience or clinical medicine will encounter these pathways repeatedly in the study of brainstem lesions, cerebellar disorders, and neuro-ophthalmology.

SECTION 9

Practice Problems

Question 1: CONCEPTUAL

Explain why the middle ear is necessary for efficient hearing. What would happen to hearing sensitivity if the ossicular chain were absent and sound waves in air directly contacted the oval window?

Show answer

Without the middle ear ossicles, approximately 99.9% of sound energy would be reflected at the air–fluid interface due to the impedance mismatch between air and the perilymph of the cochlea. This corresponds to roughly a 30 dB loss. The middle ear overcomes this mismatch primarily through two mechanisms: (1) the area ratio between the tympanic membrane (~55 mm²) and the oval window (~3.2 mm²), which concentrates force over a smaller area and increases pressure by a factor of ~17; and (2) the lever advantage of the ossicular chain (~1.3×). Together, these produce approximately 22× pressure amplification (~25–27 dB gain), nearly compensating for the impedance mismatch. Without these mechanisms, a person would experience severe conductive hearing loss, retaining only bone-conducted hearing.

Question 2: BASIC CALCULATION

A sound has an intensity of 1 × 10⁻⁶ W/m². Calculate its intensity level in decibels using the formula β = 10 × log₁₀(I/I₀), where I₀ = 1 × 10⁻¹² W/m².

Show answer

Substituting the values: β = 10 × log₁₀(1 × 10⁻⁶ / 1 × 10⁻¹²) = 10 × log₁₀(10⁶) = 10 × 6 = 60 dB. This intensity level corresponds roughly to normal conversational speech at one meter. The logarithmic decibel scale compresses the enormous range of audible intensities (10⁻¹² to 10⁰ W/m²) into a manageable 0–120 dB range, reflecting the logarithmic nature of human loudness perception.

Question 3: INTERMEDIATE

A patient presents with hearing loss. Weber testing (a vibrating tuning fork placed on the vertex of the skull) lateralizes to the left ear, and Rinne testing shows bone conduction greater than air conduction in the left ear. (a) What type of hearing loss does the left ear have? (b) Which anatomical structures are most likely affected? (c) Name two possible etiologies.

Show answer

(a) The left ear has conductive hearing loss. Weber lateralizes to the affected ear in conductive loss because ambient masking noise is reduced on that side, making the bone-conducted signal relatively louder. Rinne is negative (BC > AC) because the air conduction pathway is impaired. (b) The pathology lies in the external or middle ear — structures such as the external acoustic meatus (e.g., cerumen impaction, foreign body), tympanic membrane (perforation), or ossicular chain (fixation or discontinuity). (c) Two possible etiologies include otosclerosis (abnormal bone growth fixing the stapes footplate to the oval window) and chronic otitis media with effusion (fluid accumulation in the middle ear cavity dampening ossicular vibration). In both cases, inner ear hair cells remain intact, which is why bone conduction is preserved.

Question 4: APPLIED

A cochlear implant surgeon plans to insert a 24-electrode array into the scala tympani. The array spans from approximately 5 mm to 25 mm from the round window. Based on the tonotopic organization of the basilar membrane, estimate the frequency range this electrode array would cover and explain why electrode placement depth matters for speech perception outcomes.

Show answer

The human basilar membrane is approximately 33–35 mm long. Greenwood's frequency-position function estimates that 5 mm from the base corresponds to approximately 8,000–10,000 Hz, while 25 mm corresponds to approximately 300–500 Hz. Therefore, the 24-electrode array would cover roughly the 500 Hz to 10,000 Hz range — which encompasses the most critical frequencies for speech intelligibility (the 'speech banana' on an audiogram spans approximately 250–6,000 Hz). Deeper insertion toward the apex allows stimulation of lower-frequency regions, improving perception of vowel formants and tonal language pitch. However, deeper insertion risks trauma to the basilar membrane and residual hair cells. The tonotopic mapping must be respected so that each electrode stimulates spiral ganglion neurons tuned to the intended frequency, enabling the brain's existing tonotopic cortical maps to interpret the electrical signals as meaningful sound.

Question 5: CRITICAL THINKING

The endocochlear potential (+80 mV) is metabolically expensive, maintained by the stria vascularis through active K⁺ transport. Propose a hypothesis for why this large positive potential evolved, rather than simply relying on the hair cell's own resting membrane potential for transduction. Consider the trade-offs between sensitivity, speed, and metabolic cost in your analysis.

Show answer

The endocochlear potential effectively doubles the electrochemical driving force for K⁺ entry through mechanotransduction channels (from ~70 mV to ~150 mV), enabling hair cells to generate large receptor potentials even with minimal channel opening. This confers at least three evolutionary advantages. First, sensitivity: the amplified driving force allows detection of basilar membrane displacements as small as 0.3 nm — roughly the diameter of a hydrogen atom — making the ear sensitive enough to detect sounds near the thermal noise floor. Second, speed: a larger driving force means faster depolarization with fewer channels, enabling the temporal precision needed for phase-locking at frequencies up to ~4,000 Hz, which is critical for sound localization and pitch perception. Third, using K⁺ rather than Na⁺ as the charge carrier is energetically efficient at the cellular level — K⁺ exits hair cells down its concentration gradient through basolateral channels without requiring ATP-dependent pumping at the hair cell itself. The metabolic cost is instead borne centrally by the stria vascularis, which has one of the highest metabolic rates of any epithelium. The trade-off is that conditions reducing strial blood flow (e.g., cardiovascular disease, aging) rapidly compromise the endocochlear potential, contributing to presbycusis. Thus, the system sacrifices metabolic robustness for extraordinary sensitivity and speed.

SUMMARY

Lesson Summary

Summary

The human ear accomplishes two critical sensory functions through a shared mechanotransduction platform housed in the temporal bone. For hearing, the external ear collects and funnels sound waves to the tympanic membrane, the middle ear ossicles (malleus, incus, stapes) provide ~22× impedance matching amplification to overcome the air–fluid barrier, and the cochlea performs spectral analysis through its tonotopic basilar membrane, where inner hair cells transduce mechanical vibration into glutamatergic signals on CN VIII afferents, driven by a remarkable ~150 mV endocochlear potential, while outer hair cells actively amplify weak sounds via prestin-mediated electromotility.

For balance, the three semicircular canals detect angular acceleration through endolymph inertia deflecting the cupula, while the otolith organs (utricle and saccule) sense linear acceleration and gravity via dense otoconia overlying macular hair cells. Vestibular output drives the vestibulo-ocular reflex for gaze stabilization and vestibulospinal reflexes for postural control, with signals processed largely below conscious awareness. Clinically, distinguishing conductive from sensorineural hearing loss depends on localizing pathology to the external/middle ear versus the inner ear and CN VIII — a distinction made possible by thorough knowledge of the anatomy and physiology covered in this lesson.