Bio 211- Anatomy and Physiology I

Bio 211- Anatomy and Physiology I • Today’s topics • Muscular system

Organization of muscles and the muscular system • Muscle function: • Movement – • Generate force to move bones • Generate force to move body contents • Stability – • Muscle tone resists force of gravity and helps stabilize some joints • Posture • Communication – • Speaking, writing, facial expressions, etc… • Control of body openings – • SPHINCTER muscles control openings of eyes, mouth, digestive system, urethra, anus • Heat production - • Muscles generate a lot of heat when contracting (85% of body heat) • Keeps body around 98.6 degrees – important for enzyme function! These functions may be carried out by skeletal, smooth, or cardiac muscle, but we’ll mostly focus on skeletal muscle

Connective tissues of a muscle • A muscle (biceps brachii, pectoralis, etc..) is an organ made up of 1,000s of individual muscle cells (MUSCLE FIBERS) that work together to generate force • Muscles contain a great deal of connective tissue • Keeps muscle fibers organized • Allows attachment to bone/other structures

Connective tissues of a muscle Innermost Thinnest • ENDOMYSIUM : areolar connective tissue that surrounds EACH muscle fiber • Muscle fibers are grouped together in bundles called FASCICLES • PERIMYSIUM : Thicker connective tissue that surrounds EACH FASCICLE • Fascicles can be seen with the naked eye as “grains” – like on a piece of steak • EPIMYSIUM : Thicker connective tissue that surrounds the ENTIRE MUSCLE • Keeps fascicles bundled together • FASCIA : Connective tissue that surrounds and separates muscles from other tissues • DEEP FASCIA – separates layers of muscles from one another • SUPERFICIAL FASCIA – contains adipose tissue and separates muscles from overlying skin Outermost Thickest

Connective tissues of a muscle Attachment of muscle to bones • DIRECT : connective tissue surrounding muscle (epimysium) fuses directly with the periosteum of the bone • Intercostal and some facial muscles attach this way • INDIRECT : Epimysium and deep facia transitions into a tendon which then inserts into the periosteum of a bone • Very common, creates a physical gap between muscle and bone • APONEUROSIS : Broad, sheet-like tendon that fuses muscle to bone (abdominal muscles) Aponeurosis of external oblique

Muscle anatomy terminology Most muscles of the body are attached to different bones on either end. The contraction of the muscle causes the movement of one of the bones • ORIGIN – the stationary attachment point of a muscle to a bone – this bone does not move when muscle is contracted • INSERTION : the moveable attachment point of a muscle to a bone – this bone moves when the muscle contracts

Actions of groups of muscles Very often, two or more muscles act together (or against each other) to produce movement at a joint • AGONIST : muscle that produces the most force during a particular movement • SYNERGIST : muscle that aids the agonist in producing a given movement • Usually insertion is different than that of the agonist – helps ensure a stable joint and prevent damage to a muscle or joint • ANTAGONIST : muscle that opposes the agonist – creates movement in a joint that is in the opposite direction of the agonist • FIXATOR : a muscle that prevents movement of a bone – Ex.: rhomboids prevent movement of the scapula when the biceps brachii contracts • Instrinsic muscles have an origin and insertion in the SAME region (tongue, back muscles, etc..) • Extrinsic muscles have an origin and insertion in DIFFERENT regions • Flexor digitorumsuperficialis originates on humerus and proximal radius (elbow and forearm) but inserts on the phalanges

Skeletal muscle histology • Reminder – generally, skeletal muscle is VOLUNTARY, while all smooth and cardiac muscle is INVOLUNTARY • There are a few exceptions like the muscles of the diaphragm which are skeletal AND involuntary (more than one, located near plasma membrane) (long and cylindrical) (thin C.T. that surrounds EACH muscle fiber) (due to overlapping of actin and myosin) • Muscle fibers have several nuclei because they come from the fusion of several MYOBLASTS • Occurs during embryonic development • Undifferentiated myoblasts exist in adults as SATELLITE CELLS (a form of stem cell)

Microscopic anatomy of a muscle fiber • Like all cells, muscle cells have a nucleus, plasma membrane, cytoplasm, etc… • In muscle cells these structures have special names: • Plasma membrane = SARCOLEMMA • Cytoplasm = SARCOPLASM • Endoplasmic reticulum = SARCOPLASMIC RETICULUM • - VERY important to muscle fiber function because it acts as the internal storage site of Ca2+ (needed for muscle contraction) NOTE: this is ONE individual muscle fiber

Microscopic anatomy of a muscle fiber • The vast majority of space inside a cell is occupied by the protein filaments neededto contract – bundles of filaments (called MYOFILAMENTS) combine to form MYOFIBRILS • Larger muscle fibers will contain more myofibrils • Other essential organelles (mitochondria, ER, etc…) are packed in between the myofibrils • The sarcoplasmic reticulum forms a network around each myofibril (allows rapid and even distribution of Ca2+ ions) • Dilations of the S.R. are known as TERMINAL CISTERNAE (contain a great deal of Ca2+) Myofilaments (Thick/thin/elastic filaments) Myofibrils Muscle Fibers Muscle Tissue

Microscopic anatomy of a muscle fiber • TRANSVERSE TUBULES (T-tubules) small tubes that are created by the infolding of the sarcolemma • The T-tubule has two terminal cisternae on either side to form a TRIAD • The T-tubule carries electrical signals (nerve impulses) to the interior of the cell and triggers the release of Ca2+ from the SR and terminal cisternae (needed for contraction) Nerve impulse

Molecular structure of myofibrils • Each MYOFIBRIL consists of a bundle of long, parallel myofilaments : Thick filaments, thin filaments, elastic filaments • Thick Filaments – • Made up of hundreds of protein molecules called MYOSIN – shaped like a golf club • Myosin molecules are arranged end-to-end in a spiral fashion with the “heads” facing outward • Thin filaments – • Made up of long winding strands of the protein ACTIN • Every molecule of actin has an ACTIVE SITE that can potentially bind to the myosin head • When a muscle is relaxed, the active sites of actin are covered up by two proteins called TROPOMYOSIN and TROPONIN – myosin can’t bind to actin and cause contraction • Elastic filaments – • Smallest of the filaments – made up of protein called TITIN • A stretchy filament that anchors the thick filaments in place

Molecular structure of myofibrils • Myosin and actin are considered CONTRACTILE PROTEINS since they are responsible for the actual shortening of the muscle fiber (contraction) • Tropomyosin and troponin are considered REGULATORY PROTEINS since their job is to regulate when and if a muscle cell will contract • There are also a number of accessory proteins that also play a role in muscle fiber contraction • DYSTROPHIN – a HUGE protein that anchors actin filaments to the endomysium • Links the shortening of myofilaments to sarcolemma and external CT • This protein is mutated and non-functional in the disease MUSCULAR DYSTROPHY – patients exhibit progressive loss of skeletal muscle function

Organization of filaments in a myofibril • The thick, thin, and elastic filaments are arranged in a VERY specific, ordered fashion that allows contraction to occur efficiently • Z-DISK is a large protein that the thin filaments and elastic filaments are attached to • Z-disk is also attached to sarcolemma – helps translate contraction of myofibrils to contraction of muscle fiber • Thick filaments are suspended between the thin filaments by elastic filaments • Two Z-disks with the associated myofilaments in between is called a SARCOMERE – the functional unit of contraction in a myofibril • Muscle cell stimulation brings the Z-disks closer together, shortening the length of the sarcomere = CONTRACTION!!

Organization of filaments in a myofibril • Remember that skeletal muscle contains STRIATIONS – alternating bands of light and dark • The I-band (light band) of the sarcomere contains only elastic filaments and thin filaments – more light passes through when looking under microscope • The A-band (dark band) contains overlapping thin, thick, and elastic filaments • LIGHT = I -band DARK = A-band • The H-band is the region in the middle where there are only thick filaments since the thin filaments do not extend that far

Organization and association of sarcomere elements with linking proteins, sarcolemma, and endomysium • Linking proteins such as dystrophin allows muscle cell to translate shortening of sarcomere into shortening of muscle cell and shortening of muscle tissue

Role of the nervous system in muscle contraction • A stimulus from the nervous system is needed to “excite” each muscle fiber to contract • Specialized neurons that trigger muscle contraction are known as MOTOR NEURONS • As the axon of a motor neuron approaches the muscle it branches out into hundreds of smaller fibers – allows one neuron to stimulate MANY different muscle fibers • This arrangement helps coordinate the timing of the contractions of the 1000s of muscle fibers found in a muscle • Although each neuron can stimulate 100s of muscle fibers, one muscle fiber only receives input from one neuron– prevents the muscle fiber from getting “mixed signals”

Role of the nervous system in muscle contraction • When a motor neuron sends an impulse, ALL of the muscle fibers associated with it contract at the same time – this group of muscle fibers is called a MOTOR UNIT • Large muscles may have 100s of different motor units • Overall strength of muscle contraction depends on # of motor units stimulated • The muscle fibers of a motor unit are spread out over a large area • This allows a muscle to contract uniformly during a weak contraction – don’t only want one little area to contract (very inefficient) • The process of adding more motor units during a strong contraction = RECRUITMENT • Ability to vary # of motor units AND size of motor units allows us to vary force of contraction!!!

Role of the nervous system in muscle contraction • Having many motor units is important for repeated or sustained muscle contractions • Eventually, some motor units fatigue and others will take over (like shift work) • Not all motor units contain the same # of muscle fibers • Activation of smaller motor units allow for weaker muscle contractions • Activation of larger motor units lead to strong contractions • Weak nerve impulse = fewer and smaller motor units → weak contraction, fine movement • Strong nerve impulses = more, larger motor units → strong contraction, large movements

The neuromuscular junction How does a nerve “tell” a muscle when and how to contract??? • Neurons “talk” to muscle fibers via the NUEROMUSCULAR JUNCTION • Interaction between a motor neuron and a muscle fiber is a SYNAPSE • Nerves don’t physically contact muscle fibers – separated by a very small gap called the SYNAPTIC CLEFT • Neurons communicate with muscle cells using a NEUROTRANSMITTER: • ACETYLCHOLINE (Ach) • Acts like a chemical messenger that carries the signal from the neuron to the muscle cell

The neuromuscular junction • Motor nerves contain an large bulb at their ends called a SYNAPTIC BULB • This bulb contains vesicles filled with ACh • Region of the sarcolemma that contains ACh receptors is called MOTOR END PLATE • Arrival of a nerve impulse at the synaptic bulb trigger the exocytosis of ACh • ACh travels across the synaptic cleft and binds to ACh receptors on the sarcolemma • The binding of ACh to receptors on the muscle fiber initiates events that cause contraction (more later) • After the ACh binds to receptors on the muscle fiber it is rapidly degraded by ACETYLCHOLINESTERASE – prevents the muscle from constant stimulation (allows it to relax)

Excitation of cells of the muscular system • Motor neurons and muscle fibers are both known as ELECTRICALLY EXCITABLE • The voltage across the cell membrane changes when the cell is stimulated • Normally, a resting cell contains a negative charge INSIDE the cell as compared to the positive charge OUTSIDE • Negatively charged ions, proteins, and DNA inside, lots of Na+ outside • There is SOME K+ inside the cell but not enough to neutralize the negative charge • When there is a charge difference across the cell membrane, the cell is said to be POLARIZED • Negative = iNside , pOsitive = Outside Na+ Na+ Na+ _ _ DNA, protein, phosphate K+ _ _ Na+ K+ K+ _ _ Na+ _ Na+ Na+ • The electrochemical Na+ gradient (more outside, less inside) is maintained by the Na+/K+ ATPase

Excitation of cells of the muscular system • Stimulation of a muscle cell leads to DEPOLARIZATION of the cell membrane • Stimulus causes Na+ ion channels to open • Na+ rushes in (down conc. gradient) • For a BRIEF period the inside of the cell becomes positively charged • Depolarization causes Na+ channels to close and K+ channels to open • K+ rushes out (down its conc. gradient) • Loss of (+) charged K+ allows inside of cell to regain negative charge • Return of membrane charge (− inside, + outside) is called REPOLARIZATION • The change of the cell interior from (–) to (+) and then back to (-) is known as an ACTION POTENTIAL Na+ Na+ Na+ Na+ Na+ Na+ _ _ _ _ DNA, protein, phosphate DNA, protein, phosphate K+ K+ _ _ _ _ Na+ Na+ K+ K+ K+ K+ _ _ _ _ Na+ Na+ Na+ Na+ Na+ Na+ DEPOLARIZED _ _ _ _ Na+ Na+ DNA, protein, phosphate K+ Na+ _ Na+ POLARIZED Na+ K+ K+ REPOLARIZED Na+ Na+ _ _

Localization of an action potential • An action potential is a LOCAL occurrence at a specific region of the cell membrane • Only a small part of the muscle cell membrane is depolarized at a given time • Think of “The Wave” at a sports event DEPOLARIZATION NERVE OR MUSCLE FIBER DEPOLARIZATION NERVE OR MUSCLE FIBER DEPOLARIZATION REPOLARIZATION NERVE OR MUSCLE FIBER • Depolarization of a region is IMMEDIATELY followed by repolarization • Necessary to allow a nerve or muscle cell to be restimulated • Depolarization of one region triggers the depolarization of a region next to it • Allows action potentials to be self-propagating REPOLARIZATION

Excitation of skeletal muscle Motor end plate • Nerve impulse arrives at synaptic bulb • Entrance of Ca2+ into synaptic bulb triggers exocytosis of ACh-containing vesicles • ACh travels across synaptic cleft and binds to ACh receptors on sarcolemma • The region of the muscle fiber where ACh binds is called the MOTOR END PLATE-the muscle part of the neuromuscular junction

Excitation of skeletal muscle • The ACh receptors actually play two roles : ACh receptor AND ion channel • LIGAND-GATED ION CHANNEL – opens up when ACh binds to it • Binding of ACh (ligand) to its receptor causes conformational change that “opens” up the ion channel • Na+ ions rush IN, causing voltage across membrane to reverse (depolarize) • This LOCAL fluctuation of membrane voltage (at the motor end plate) leads to the activation of VOLTAGE-GATED ion channels on the REST of the muscle fiber

Ligand-gated -vs- Voltage gated ion channels Motor end plate The rest of the muscle cell Na+ Na+ OUTSIDE (+) Ligand Ligand INSIDE (-) Na+ Na+ • Ligand gated ion channels are ion channels that open up in response to a ligand (ACh) binding to them • These channels will only be found at the motor end plate of a muscle cell • When ACh binds to the channel it opens up letting Na+ enter the cell • Voltage gated ion channels are ion channels that require a change in membrane voltage to open and cause depolarization • These channels sense changes in membrane voltage (a nearby depolarization) that triggers them to open up and let Na+ enter the cell • Found over the rest of the muscle cell (but not at motor end plate) • These channels are responsible for propagating the action potential over the surface of a muscle cell

Excitation/Contraction coupling This is the process by which we translate the action potential on the sarcolemma to the contraction of myofilaments inside the muscle cell • Action potentials that leave the motor end plate spread out over the entire surface of the sarcolemma and travel down T-tubules • Dependent on voltage gated ion channels • These action potentials trigger the opening of Ca2+ channels in the SR allowing Ca2+ to exit the SR and enter the sarcoplasm (where the myofilaments are located)

Excitation/Contraction coupling • Ca2+ released from the SR binds to troponin on the thin filaments and causes troponin to change shape and expose active sites on actin molecules • The exposure of the active sites on actin (thin filaments) makes them available to bind to the heads of the myosin molecules (thick filaments)

Contraction This is the process by which the muscle fiber generates tension (force) and is capable of contraction Sliding filament theory States that during contraction, myofilaments (thick and thin) slide past each other thereby generating tension and pulling the Z-disks closer to each other → shortening of the sarcomere

Contraction • In the 1st step of contraction, the myosin head binds one molecule of ATP • The enzyme MYOSIN ATPase hydrolyzes ATP, releasing energy (ATP→ADP+P +ENERGY) • This energy is used to activate the myosin head • The myosin head “reaches” out to bind to the active site of actin • In the 2nd step, the myosin head binds to the exposed active site of actin, creating a CROSS-BRIDGE

Contraction • After binding to actin, the myosin head releases the ADP+ P causing it to return to its original conformation • This pulls on the thin filament, bringing the Z-disks closer • Binding of a new molecule of ATP causes the myosin head to release the actin molecule • Hydrolysis of another ATP then allows the myosin head to “reach” out to another actin molecule farther down the thin filament • Each “ratcheting” of the myosin head uses one ATP • Each myosin head ratchets 5X per second • 1000s of myosin heads work together to shorten each muscle fiber – Contraction uses a HUGE amount of ATP!!!

Relaxation • Once the contraction is finished, the motor neuron stops releasing ACh • Remaining ACh bound to the receptors on the sarcolemma is degraded by ACETYLCHOLINESTERASE • This prevents action potentials from being generated at the motor end plate • Without stimulation, Ca2+ is pumped back INTO the SR – active transport (uses ATP) • As Ca2+ diffuses away from troponin, the tropomyosin molecules cover up the active sites of actin again – prevents myosin from binding • Without myosin binding, the thin filaments slide BACK over the thick filaments and the sarcomere lengthens (returns to resting length)

Summary Arrival of action potential at synaptic bulb of motor neuron causes release of ACh across synaptic cleft (process requires Ca2+) Binding of ACh to sarcolemma at motor endplate creates local action potential (dependent on the availability of ACh from motor neuron) Action potential at motor end plate spreads out over sarcolemma and down T-tubule to SR (these action potentials are generated by voltage gated ion channels and are dependent on the initial ACh-dependent action potential) Release of Ca2+ from SR allows active sites of actin to be bound by myosin heads “Ratcheting” of the myosin heads is dependent on the energy released from ATP hydrolysis “Ratcheting” of myosin causes thin filaments to slide over the thick filaments – brings Z-disks closer to each other (sarcomere shortening) End of motor neuron stimulation causes Ca2+ to be pumped back into SR (diffuses away from troponin) – active transport of Ca2+ requires ATP Myosin releases actin and allows thin filaments to slide back over thick filaments and return to resting position (sarcomere lengthens) Be sure to understand and remember which steps in the entire process require ATP, ACh, or Ca2+ !!!!!!

Action potential and muscle physiology animations Action potential at Neuromuscular junction Action potentials and muscle contraction Crossbridge formation and contraction contraction of the sarcomere ALSO BE SURE TO LOOK AT ANIMATIONS ON APRevealed!!!

What factors are needed and when??? Ca2+ ACh ATP • ACh release: • Ca2+ triggers exocytosis of ACh from synaptic bulb • Crossbridge formation: • Ca2+ binds to troponin causing tropomyosin to shift positions and expose active sites of actin • Maintenance of cell polarization: • Na+/K+ ATPase requires ATP to maintain Na+ gradient thereby keeping interior of cell negatively charged • Muscle fiber contraction: • Myosin heads use ATP to “reach” out and attach to active sites of actin • Muscle fiber relaxation: • Ca2+ pumps use active transport to pump Ca2+ BACK into the SR • Action potential generation: • ACh binds to receptors on sarcolemma of motor end plate causing Na+ channels to open and lead to depolarization of sarcolemma • Without this initial action potential there can be NO MUSCLE CONTRACTION

Length-Tension relationship and muscle tone • The amount of force or tension a muscle can generate is related to how contracted or stretched it was prior to stimulation • If a muscle is overly stretched or contracted before stimulation → weak contraction • A -OPTIMAL RESTING LENGTH the thin filaments are just overlapping with all the myosin heads → maximal contraction • B – When the muscle is overly contracted the thin filaments overlap the thick filaments so much that the thick filaments are nearly butting up against the Z-disk → no room for additional sarcomere shortening • C – When the muscle is overly stretched only a SMALL part of the thin filament overlaps with the thick filaments → myosin heads on thick filaments can’t “get a hold” of thin filaments A B C

Muscle tone • Even at rest, muscles maintain a certain degree of contraction called MUSCLE TONE • This partial contraction is the result of a spinal reflex involving stretch receptors buried within the muscle tissue • This allows the sarcomeres of the muscle fibers to remain at their optimal length • Muscle tone is important for posture, balance, and joint stability • Muscles of the trunk and legs keep us centered and upright WITHOUT conscious effort • Muscle tone in deltoid and biceps brachii helps stabilize shoulder joint Stretch receptor Motor neuron

Whole muscle physiology • In order for a muscle to contract we need a sufficiently strong stimulus that can trigger the contraction of the muscle fibers in a motor unit • An single impulse may not be strong enough to trigger a contraction, requiring REPEATED or STRONGER nerve impulses to reach THRESHOLD (i.e., cause enough Ca2+ release to trigger sarcomere shortening) • The period of time between the initial stimulus and the beginning of muscle contraction is called the LATENT PERIOD (only a few milliseconds) • The cycle of contraction and relaxation is known as a MUSCLE TWITCH

Whole muscle physiology • During the CONTRACTION phase: • Sarcomeres shorten → muscle fibers shorten → whole muscle contracts • This phase is relatively short because the SR rapidly reabsorbs the Ca2+ • This is the phase where the muscle generates tension and force (pulling on tendons or bone of origin and insertion) • During the RELAXATION phase: • Ca2+ is reabsorbed by the SR • Troponin and tropomyosin cover up active sites on actin (no more crossbridges) • Thin filaments slide BACK over thick filaments • Sarcomere lengthens → muscle fiber lengthens → muscle relaxes

Strength of Muscle Twitches • Earlier we talked about how muscle contraction is dependent on: • # of motor units involved • Size of motor units involved • Strength of nerve impulse • We can also alter muscle contraction via strength of muscle fiber contraction • ELECTRICAL STIMULATION (excitation) of the fiber is “all-or-none”, but contraction strength varies with: • Strength of stimulation (nerve impulse or voltage) • Stimulation frequency • Degree of stretch before stimulation • Temperature (warm enhances, but extremes inhibit contraction) • Muscle pH (low pH inhibits contraction-decreases myosin action) • Hydration (proper hydration of cell required for organization of myofibrils) • A strong contraction occurs at maximum sarcomere shortening (more interaction between actin and myosin heads) • A weak contraction occurs when the sarcomere shortens only part way before relaxing (not enough myosin heads pulling on actin to completely shorten sarcomere)

Strength of Muscle Twitches • Note : NEURON = one individual neural cell • NERVE = a bundle of axons from many neurons • Larger nerves contain axons from more neurons • Strength of stimulation • An increase in stimulation strength causes more axons within the motor nerve to be stimulated • Once THRESHOLD is reached : • Greater # of axons stimulated = Greater nerve impulse = Greater # of motor units stimulated • The addition of more motor units involved in a contraction is known as RECRUITMENT • Beyond a certain point, additional stimulation (or voltage) will not increase muscle contraction because all fibers are contracting maximally

Strength of Muscle Twitches • Frequency of stimulation • Repeated, rapid stimulation causes Ca2+ levels to increase in the muscle fiber → stronger muscle fiber contraction (more exposed active sites on actinfor myosin binding) • Rapid stimulation prevents all of the Ca2+ from being reabsorbed by SR→Ca2+ accumulates→stronger contraction (TREPPE EFFECT) • As a muscle twitches rapidly, it generates heat, allowing myosin heads to “ratchet” more efficiently→stronger contraction

Strength of Muscle Twitches • Frequency of stimulation • When stimulation is very rapid (faster than needed for Treppe effect), one muscle contraction begins before the previous one ends – overlapping contractions • As a result, successive nerve impulses stimulate a partially contracted muscle fiber → stronger contraction (INCOMPLETE TETANUS) • If stimulation rate continues to increase, the muscle does not have time to relax at all leading to a sustained, continuous contraction (COMPLETE TENTANUS) – almost never occurs in our bodies though……..

Different types of muscle contractions • Not every muscle contraction results in shortening of the muscle length and movement of a body part • Muscle contraction technically refers to the generation of force and tension within a muscle At this point muscle tension exceeds the load and the muscle is allowed to shorten • Isometric contraction (constant length) – muscle contracts (develops tension) but DOES NOT SHORTEN in length • Isotonic contraction (constant force) – muscle contracts (develops tension) and may either lengthen or shorten depending on force of contraction • Both of these contractions are in play when we lift a weight

Muscle Metabolism • By now we know that ATP is required for at least 3 steps in the contraction of a muscle: • Maintenance of polarized nerve and muscle cells (Na+/K+ ATPase) • Contraction of myofilaments (“ratcheting” of myosin heads) • Relaxation of myofilaments (Active transport of Ca2+ back into SR) • Without a constant supply of ATP muscles CANNOT contract – no other energy source exists • Muscles can generate ATP in two different ways depending on the supply of oxygen • AEROBIC RESPIRATION – when oxygen is available • ANAEROBIC FERMENTATION – when oxygen is NOT available

Aerobic Respiration The Krebs cycle takes place here • Aerobic respiration in muscle tissue typically involves the oxidation of glucose (sugar) or fatty acids (lipids) • Amino acids from protein can be used to synthesize ATP, but is definitely not the preferred source - we’d rather use them to make new proteins!! • This process requires oxygen and has the potential to generate much more ATP than anaerobic fermentation • Waste product is CO2 - easy to get rid of via breathing • The key step in this process is called the KREBS CYCLE (citric acid cycle) • Glucose and fatty acids are converted into ACETYL CoAthat enters the Krebs cycle

Bio 211- Anatomy and Physiology I