1st year medical school physiology essay:
Describe the effects between the action potential arriving at the axon terminal and skeletal muscle contraction.
Muscle spindles are proprioceptors that consist of intrafusal muscle fibers enclosed in a sheath (spindle). They run parallel to the extrafusal muscle fibers and act as receptors that provide information on muscle length and the rate of change in muscle length. The spindles are stretched when the muscle lengthens. This stretch causes the sensory neuron in the spindle to transmit an impulse to the spinal cord, where it synapses with alpha motor neurons. This causes activation of motor neurons that innervate the muscle. The muscle spindles determine the amount of contraction necessary to overcome a given resistance. When the resistance increases, the muscle is stretched further, and this causes spindle fibers to activate a greater muscle contraction.
Contraction of muscles takes place with relativity between Actin and Myosin Filaments. Here, Ach. regards to acetylchloine. Interaction between Actin and myosin will bring contraction in muscle.
Muscles is a contractile tissue which brings about movement.
Muscle cell responsible for our movement both visible and invisible, example walking, talking, bowel movement ,urination, breathing, heartbeats, the dilation and constriction of the pupils of our eyes and many other.
When we are still sitting or standing muscle cells keep us erect.
CONT...Muscles can be regarded as motors of the body.Muscles comprises about 40% to 50% (approximate) of body weight.There are approximate 650 muscles in body.Alternating contraction and relaxation of cells
1st year medical school physiology essay:
Describe the effects between the action potential arriving at the axon terminal and skeletal muscle contraction.
Muscle spindles are proprioceptors that consist of intrafusal muscle fibers enclosed in a sheath (spindle). They run parallel to the extrafusal muscle fibers and act as receptors that provide information on muscle length and the rate of change in muscle length. The spindles are stretched when the muscle lengthens. This stretch causes the sensory neuron in the spindle to transmit an impulse to the spinal cord, where it synapses with alpha motor neurons. This causes activation of motor neurons that innervate the muscle. The muscle spindles determine the amount of contraction necessary to overcome a given resistance. When the resistance increases, the muscle is stretched further, and this causes spindle fibers to activate a greater muscle contraction.
Contraction of muscles takes place with relativity between Actin and Myosin Filaments. Here, Ach. regards to acetylchloine. Interaction between Actin and myosin will bring contraction in muscle.
Muscles is a contractile tissue which brings about movement.
Muscle cell responsible for our movement both visible and invisible, example walking, talking, bowel movement ,urination, breathing, heartbeats, the dilation and constriction of the pupils of our eyes and many other.
When we are still sitting or standing muscle cells keep us erect.
CONT...Muscles can be regarded as motors of the body.Muscles comprises about 40% to 50% (approximate) of body weight.There are approximate 650 muscles in body.Alternating contraction and relaxation of cells
New Directions in Targeted Therapeutic Approaches for Older Adults With Mantl...i3 Health
i3 Health is pleased to make the speaker slides from this activity available for use as a non-accredited self-study or teaching resource.
This slide deck presented by Dr. Kami Maddocks, Professor-Clinical in the Division of Hematology and
Associate Division Director for Ambulatory Operations
The Ohio State University Comprehensive Cancer Center, will provide insight into new directions in targeted therapeutic approaches for older adults with mantle cell lymphoma.
STATEMENT OF NEED
Mantle cell lymphoma (MCL) is a rare, aggressive B-cell non-Hodgkin lymphoma (NHL) accounting for 5% to 7% of all lymphomas. Its prognosis ranges from indolent disease that does not require treatment for years to very aggressive disease, which is associated with poor survival (Silkenstedt et al, 2021). Typically, MCL is diagnosed at advanced stage and in older patients who cannot tolerate intensive therapy (NCCN, 2022). Although recent advances have slightly increased remission rates, recurrence and relapse remain very common, leading to a median overall survival between 3 and 6 years (LLS, 2021). Though there are several effective options, progress is still needed towards establishing an accepted frontline approach for MCL (Castellino et al, 2022). Treatment selection and management of MCL are complicated by the heterogeneity of prognosis, advanced age and comorbidities of patients, and lack of an established standard approach for treatment, making it vital that clinicians be familiar with the latest research and advances in this area. In this activity chaired by Michael Wang, MD, Professor in the Department of Lymphoma & Myeloma at MD Anderson Cancer Center, expert faculty will discuss prognostic factors informing treatment, the promising results of recent trials in new therapeutic approaches, and the implications of treatment resistance in therapeutic selection for MCL.
Target Audience
Hematology/oncology fellows, attending faculty, and other health care professionals involved in the treatment of patients with mantle cell lymphoma (MCL).
Learning Objectives
1.) Identify clinical and biological prognostic factors that can guide treatment decision making for older adults with MCL
2.) Evaluate emerging data on targeted therapeutic approaches for treatment-naive and relapsed/refractory MCL and their applicability to older adults
3.) Assess mechanisms of resistance to targeted therapies for MCL and their implications for treatment selection
Report Back from SGO 2024: What’s the Latest in Cervical Cancer?bkling
Are you curious about what’s new in cervical cancer research or unsure what the findings mean? Join Dr. Emily Ko, a gynecologic oncologist at Penn Medicine, to learn about the latest updates from the Society of Gynecologic Oncology (SGO) 2024 Annual Meeting on Women’s Cancer. Dr. Ko will discuss what the research presented at the conference means for you and answer your questions about the new developments.
Anti ulcer drugs and their Advance pharmacology ||
Anti-ulcer drugs are medications used to prevent and treat ulcers in the stomach and upper part of the small intestine (duodenal ulcers). These ulcers are often caused by an imbalance between stomach acid and the mucosal lining, which protects the stomach lining.
||Scope: Overview of various classes of anti-ulcer drugs, their mechanisms of action, indications, side effects, and clinical considerations.
The prostate is an exocrine gland of the male mammalian reproductive system
It is a walnut-sized gland that forms part of the male reproductive system and is located in front of the rectum and just below the urinary bladder
Function is to store and secrete a clear, slightly alkaline fluid that constitutes 10-30% of the volume of the seminal fluid that along with the spermatozoa, constitutes semen
A healthy human prostate measures (4cm-vertical, by 3cm-horizontal, 2cm ant-post ).
It surrounds the urethra just below the urinary bladder. It has anterior, median, posterior and two lateral lobes
It’s work is regulated by androgens which are responsible for male sex characteristics
Generalised disease of the prostate due to hormonal derangement which leads to non malignant enlargement of the gland (increase in the number of epithelial cells and stromal tissue)to cause compression of the urethra leading to symptoms (LUTS
micro teaching on communication m.sc nursing.pdfAnurag Sharma
Microteaching is a unique model of practice teaching. It is a viable instrument for the. desired change in the teaching behavior or the behavior potential which, in specified types of real. classroom situations, tends to facilitate the achievement of specified types of objectives.
Flu Vaccine Alert in Bangalore Karnatakaaddon Scans
As flu season approaches, health officials in Bangalore, Karnataka, are urging residents to get their flu vaccinations. The seasonal flu, while common, can lead to severe health complications, particularly for vulnerable populations such as young children, the elderly, and those with underlying health conditions.
Dr. Vidisha Kumari, a leading epidemiologist in Bangalore, emphasizes the importance of getting vaccinated. "The flu vaccine is our best defense against the influenza virus. It not only protects individuals but also helps prevent the spread of the virus in our communities," he says.
This year, the flu season is expected to coincide with a potential increase in other respiratory illnesses. The Karnataka Health Department has launched an awareness campaign highlighting the significance of flu vaccinations. They have set up multiple vaccination centers across Bangalore, making it convenient for residents to receive their shots.
To encourage widespread vaccination, the government is also collaborating with local schools, workplaces, and community centers to facilitate vaccination drives. Special attention is being given to ensuring that the vaccine is accessible to all, including marginalized communities who may have limited access to healthcare.
Residents are reminded that the flu vaccine is safe and effective. Common side effects are mild and may include soreness at the injection site, mild fever, or muscle aches. These side effects are generally short-lived and far less severe than the flu itself.
Healthcare providers are also stressing the importance of continuing COVID-19 precautions. Wearing masks, practicing good hand hygiene, and maintaining social distancing are still crucial, especially in crowded places.
Protect yourself and your loved ones by getting vaccinated. Together, we can help keep Bangalore healthy and safe this flu season. For more information on vaccination centers and schedules, residents can visit the Karnataka Health Department’s official website or follow their social media pages.
Stay informed, stay safe, and get your flu shot today!
These lecture slides, by Dr Sidra Arshad, offer a quick overview of physiological basis of a normal electrocardiogram.
Learning objectives:
1. Define an electrocardiogram (ECG) and electrocardiography
2. Describe how dipoles generated by the heart produce the waveforms of the ECG
3. Describe the components of a normal electrocardiogram of a typical bipolar leads (limb II)
4. Differentiate between intervals and segments
5. Enlist some common indications for obtaining an ECG
Study Resources:
1. Chapter 11, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 9, Human Physiology - From Cells to Systems, Lauralee Sherwood, 9th edition
3. Chapter 29, Ganong’s Review of Medical Physiology, 26th edition
4. Electrocardiogram, StatPearls - https://www.ncbi.nlm.nih.gov/books/NBK549803/
5. ECG in Medical Practice by ABM Abdullah, 4th edition
6. ECG Basics, http://www.nataliescasebook.com/tag/e-c-g-basics
Explore natural remedies for syphilis treatment in Singapore. Discover alternative therapies, herbal remedies, and lifestyle changes that may complement conventional treatments. Learn about holistic approaches to managing syphilis symptoms and supporting overall health.
Lung Cancer: Artificial Intelligence, Synergetics, Complex System Analysis, S...Oleg Kshivets
RESULTS: Overall life span (LS) was 2252.1±1742.5 days and cumulative 5-year survival (5YS) reached 73.2%, 10 years – 64.8%, 20 years – 42.5%. 513 LCP lived more than 5 years (LS=3124.6±1525.6 days), 148 LCP – more than 10 years (LS=5054.4±1504.1 days).199 LCP died because of LC (LS=562.7±374.5 days). 5YS of LCP after bi/lobectomies was significantly superior in comparison with LCP after pneumonectomies (78.1% vs.63.7%, P=0.00001 by log-rank test). AT significantly improved 5YS (66.3% vs. 34.8%) (P=0.00000 by log-rank test) only for LCP with N1-2. Cox modeling displayed that 5YS of LCP significantly depended on: phase transition (PT) early-invasive LC in terms of synergetics, PT N0—N12, cell ratio factors (ratio between cancer cells- CC and blood cells subpopulations), G1-3, histology, glucose, AT, blood cell circuit, prothrombin index, heparin tolerance, recalcification time (P=0.000-0.038). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and PT early-invasive LC (rank=1), PT N0—N12 (rank=2), thrombocytes/CC (3), erythrocytes/CC (4), eosinophils/CC (5), healthy cells/CC (6), lymphocytes/CC (7), segmented neutrophils/CC (8), stick neutrophils/CC (9), monocytes/CC (10); leucocytes/CC (11). Correct prediction of 5YS was 100% by neural networks computing (area under ROC curve=1.0; error=0.0).
CONCLUSIONS: 5YS of LCP after radical procedures significantly depended on: 1) PT early-invasive cancer; 2) PT N0--N12; 3) cell ratio factors; 4) blood cell circuit; 5) biochemical factors; 6) hemostasis system; 7) AT; 8) LC characteristics; 9) LC cell dynamics; 10) surgery type: lobectomy/pneumonectomy; 11) anthropometric data. Optimal diagnosis and treatment strategies for LC are: 1) screening and early detection of LC; 2) availability of experienced thoracic surgeons because of complexity of radical procedures; 3) aggressive en block surgery and adequate lymph node dissection for completeness; 4) precise prediction; 5) adjuvant chemoimmunoradiotherapy for LCP with unfavorable prognosis.
ARTIFICIAL INTELLIGENCE IN HEALTHCARE.pdfAnujkumaranit
Artificial intelligence (AI) refers to the simulation of human intelligence processes by machines, especially computer systems. It encompasses tasks such as learning, reasoning, problem-solving, perception, and language understanding. AI technologies are revolutionizing various fields, from healthcare to finance, by enabling machines to perform tasks that typically require human intelligence.
Title: Sense of Smell
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the primary categories of smells and the concept of odor blindness.
Explain the structure and location of the olfactory membrane and mucosa, including the types and roles of cells involved in olfaction.
Describe the pathway and mechanisms of olfactory signal transmission from the olfactory receptors to the brain.
Illustrate the biochemical cascade triggered by odorant binding to olfactory receptors, including the role of G-proteins and second messengers in generating an action potential.
Identify different types of olfactory disorders such as anosmia, hyposmia, hyperosmia, and dysosmia, including their potential causes.
Key Topics:
Olfactory Genes:
3% of the human genome accounts for olfactory genes.
400 genes for odorant receptors.
Olfactory Membrane:
Located in the superior part of the nasal cavity.
Medially: Folds downward along the superior septum.
Laterally: Folds over the superior turbinate and upper surface of the middle turbinate.
Total surface area: 5-10 square centimeters.
Olfactory Mucosa:
Olfactory Cells: Bipolar nerve cells derived from the CNS (100 million), with 4-25 olfactory cilia per cell.
Sustentacular Cells: Produce mucus and maintain ionic and molecular environment.
Basal Cells: Replace worn-out olfactory cells with an average lifespan of 1-2 months.
Bowman’s Gland: Secretes mucus.
Stimulation of Olfactory Cells:
Odorant dissolves in mucus and attaches to receptors on olfactory cilia.
Involves a cascade effect through G-proteins and second messengers, leading to depolarization and action potential generation in the olfactory nerve.
Quality of a Good Odorant:
Small (3-20 Carbon atoms), volatile, water-soluble, and lipid-soluble.
Facilitated by odorant-binding proteins in mucus.
Membrane Potential and Action Potential:
Resting membrane potential: -55mV.
Action potential frequency in the olfactory nerve increases with odorant strength.
Adaptation Towards the Sense of Smell:
Rapid adaptation within the first second, with further slow adaptation.
Psychological adaptation greater than receptor adaptation, involving feedback inhibition from the central nervous system.
Primary Sensations of Smell:
Camphoraceous, Musky, Floral, Pepperminty, Ethereal, Pungent, Putrid.
Odor Detection Threshold:
Examples: Hydrogen sulfide (0.0005 ppm), Methyl-mercaptan (0.002 ppm).
Some toxic substances are odorless at lethal concentrations.
Characteristics of Smell:
Odor blindness for single substances due to lack of appropriate receptor protein.
Behavioral and emotional influences of smell.
Transmission of Olfactory Signals:
From olfactory cells to glomeruli in the olfactory bulb, involving lateral inhibition.
Primitive, less old, and new olfactory systems with different path
These simplified slides by Dr. Sidra Arshad present an overview of the non-respiratory functions of the respiratory tract.
Learning objectives:
1. Enlist the non-respiratory functions of the respiratory tract
2. Briefly explain how these functions are carried out
3. Discuss the significance of dead space
4. Differentiate between minute ventilation and alveolar ventilation
5. Describe the cough and sneeze reflexes
Study Resources:
1. Chapter 39, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 34, Ganong’s Review of Medical Physiology, 26th edition
3. Chapter 17, Human Physiology by Lauralee Sherwood, 9th edition
4. Non-respiratory functions of the lungs https://academic.oup.com/bjaed/article/13/3/98/278874
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Unit Three - Excitable Tissues (Muscle).ppt
1. MUSCLES
MUSCULAR TISSUE & HOMEOSTASIS
• Muscular tissue contributes to homeostasis by producing body
movements, moving substances through the body, &
producing heat to maintain normal body temperature.
• Although bones provide leverage & form the framework of the
body, they cannot move body parts by themselves.
• Motion results from alternating contraction & relaxation of
muscles.
• Muscles make up 40 - 50% of total adult body weight. 1
2. MUSCLES, cont’d
• Your muscular strength reflects the primary function of muscle
– transformation of chemical energy into mechanical energy
to generate force, perform work & produce movement.
• In addition, muscle tissues stabilize body position, regulate
organ volume, generate heat, and propel fluids & food matter
through various body systems.
• Functions OF Muscle Tissue
− Through sustained contraction or alternating contraction and
relaxation, muscular tissue has four key functions:
2
3. Muscle Functions
1. Producing body movements
– Movements of the whole body such as walking & running, and
localized movements (grasping a pencil or nodding of head).
2. Stabilizing body positions
– Skeletal muscle contractions stabilize joints & help maintain
body positions, such as standing or sitting.
3. Storing & moving substances within the body
– Food storage of in stomach or urine in urinary bladder.
– Cardiac muscle contraction to pump blood & moves in blood
vessels, bile storage in the gall bladder.
4. Generating heat
– As muscular tissue contracts, it produces heat, a process
known as thermogenesis.
– This important to maintain normal body temperature.
3
4. Types of Muscle Tissue
4
• There are 3 types of muscle tissue
5. Skeletal/Voluntary muscles
• Are attached to bones & moves the skeleton
• Are elongated, cylindrical & multinucleated cells
• Are striated (alternating light & dark bands) muscles
• Are voluntary muscles, controlled by somatic NS
Cardiac muscles
– Are muscles of the heart - used to pump blood through circulatory
system.
– Are striated, uni- or binucleated
– Has sarcomeres & T-tubules
– Are involuntary, controlled by ANS, drugs & hormones
• Have the property of autorhythmicity & syncytium
– Cardiac muscle cells are joined by structures called intercalated
discs.
Types of Muscle Tissue
5
6. Types of Muscle, cont’d
Smooth muscles
− Are involuntary, non-striated muscle tissue, and controlled by
ANS, drugs & hormones.
– Located in the wall of hallow organs (GIT, blood vessels,
uterus, u-bladder & iris).
– Have non-striated appearance, mononucleated cells
– Involuntary muscles
– Have the property of autorhythmicity & syncytium.
• Syncytium – is a cell made from the fusion of many others.
6
7. Skeletal muscle
cell
Cardiac muscle
cell
Smooth muscle cell
Elongated Cells Branching Cells Spindle-Shaped Cell
Multiple
Peripheral Nuclei
Single Central
Nucleus
Single Central
Nucleus
Visible Striations Visible Striations Lack Visible
Striations
Voluntary Involuntary Involuntary
7
Comparison of Skeletal, Cardiac & Smooth Muscle Cells
8. Properties of Muscle Tissue
• Muscular tissue has four special properties that enable it to
function & contribute to homeostasis:
1. Excitability
• The ability to receive & respond to a stimulus
2. Contractility
− The ability of muscular tissue to contract forcefully when
stimulated by an action potential.
3. Extensibility
− The ability of muscular tissue to stretch
4. Elasticity
− The ability of muscular tissue to return to its original length &
shape after contraction or extension.
8
9. • Each of our skeletal muscles is a separate organ composed
of hundreds to thousands of cells, which are called muscle
fibers b/c of their elongated shapes.
• Thus, muscle cell & muscle fiber are two terms for the
same structure.
• Skeletal muscle also contains connective tissues
surrounding the muscle fibers & the whole muscles, and
blood vessels & nerves.
9
Skeletal Muscle Tissue
11. • Skeletal muscles are attached to bones via tendons.
• Skeletal muscles are composed of connective tissue and
contractile cells.
Three connective tissue layers of the muscle are endomysium,
perimysium & epimysium:
– Bind the muscle cells together and
– Provide strength & support to the entire muscle.
• Connective tissue surrounding the entire muscle is epimysium.
• Bundles of muscle cells are called fascicles.
• Connective tissue surrounding fascicles is called perimysium.
Connective tissue surrounding the individual muscle cells is
endomysium:
– Function to electrically insulate muscle cells from one another.
Whole Skeletal Muscle
11
13. • Muscle fibers: alternative name for skeletal muscle cells.
Nucleus: contains the genetic material.
Sarcolemma: plasma membrane of skeletal muscle cells.
Sarcoplasm: muscle fiber cytoplasm.
– contains a lot of mitochondria, glycogen (provide energy),
myoglobin & creatine-PK, as well as myofibrils & SR.
Sarcoplasmic reticulum (SR): interconnecting tubules of ER
that surround each myofibril.
A skeletal muscle cell has two tubular structures:
a. Transverse tubules (T-tubules). Function: conduction of
depolarization.
b. Longitudinal tubules (sER). Function: Ca2+ storage.
13
Fine structures of the skeletal muscle
15. Fine structures, cont’d
Terminal cisternae: sac-like regions of SR that contain Ca2+ ions.
T-tubules: invaginations of the sarcolemma that project deep into
the cell.
Triad: a group of one T-tubule lying b/n two adjacent terminal
cisternae.
Cytosol: intracellular fluid
Mitochondria: sites of ATP synthesis
Myofibril: contains contractile filaments within skeletal muscle.
– Myofibril is made of myofilaments called thin filaments (actin)
and thick filaments (myosin)
15
16. • Muscle fiber plasma
membrane is known as
sarcolemma
• Muscle fiber cytoplasm
is known as
sarcoplasm
• Sarcoplasm has lots of mitochondria, lots of glycogen granules (to
provide glucose for energy needs) as well as myofibrils &
sarcoplasmic reticuli
• Sarcolemma has invaginations that penetrate through the cell
called transverse tubules or T tubules
16
17. Sarcoplasmic Reticulum
• Muscle cell version
of the smooth ER.
• Function: calcium
storage depot in
muscle cells.
• Loose network of
this membrane
bound organelle
surrounds all the
myofibrils in a
muscle fiber.
17
18. Myofibrils
• Each muscle fiber contains rod-like structures called myofibrils
that extend the length of the cell.
• Are basically long bundles of protein structures called
myofilaments & their actions give muscle the ability to contract.
• Myofilaments are classified as thick filaments & thin filaments.
18
19. Myofilaments
• 2 types of myofilaments (thick & thin) make up myofibrils.
• Thick myofilaments are made the protein myosin.
A single myosin protein
resembles 2 golf clubs whose
shafts have been twisted
about one another
About 300 of these myosin
molecules are joined together
to form a single thick
filament.
19
20. • Each thin filament is made up of 3 different types of protein: actin,
tropomyosin & troponin.
• Each thin filament consists of a long helical double strand.
• Actin is globular protein & on each actin subunit, there is a myosin
binding site.
• Loosely wrapped around actin helix & covering the myosin binding
site is the filamentous protein, called tropomyosin.
• Bound to both actin & tropomyosin is a triad of proteins collectively
known as troponin.
20
21. • Each myofibril is made up 1000’s of repeating individual
units known as sarcomeres.
• Each sarcomere is an ordered arrangement of thick & thin
filaments. Notice that it has:
regions of thin filaments by themselves.
a region of thick filaments by themselves.
regions of thick filaments & thin filaments overlapping.
Myofibrils
21
22. • The sarcomere is flanked by 2 protein structures known as Z
lines (discs).
• The figure below shows you structure of the bands in terms of
major proteins, actin & myosin:
In the A band 2 proteins are overlap.
The I band contains only the actin protein.
An H zone which contains only thick filaments.
22
Sarcomere
23. • The portion of the
sarcomere which does
not contain any thick
filament is known as I
band.
• The I band contains
only thin filament & is
light under the
microscope.
– One I band is actually
part of 2 sarcomeres.
In the middle of the H zone is a structure
called the M line w/c functions to hold
the thick filaments to one another.
Sarcomere, cont’d
23
24. Each muscle fiber
has many T-tubules.
– Typically each
myofibril has a
branch of a T-tubule
encircling it at each
A-I junction
At each A-I junction,
the SR will expand
& form a dilated sac
(terminal cisterna)
Each T-tubule will be flanked by a
terminal cisterna. This forms a so-
called triad consisting of 2 terminal
cisternae & one T-tubule branch.
T-Tubules & SR
24
25. Place your right palm on the back of your left hand. Now slide your
right palm toward your left elbow.
– What happened to the distance between your elbows?
It got shorter!
– This is how muscle contraction occurs.
– The thin filaments slide over the thick filaments. This pulls the Z
discs closer together. When all the sarcomeres in a fiber do this,
the entire fiber gets shorter which pulls on the endomysium,
perimysium, epimysium & attached tendon & then pulls on the
bone. So, that is why we have movement.
Muscle Contraction:
The Sliding Filament Hypothesis
25
26. Here is what happens
as the filaments slide
& the sarcomere & the
muscle fiber shortens.
In the process of
contraction, what
happens to the:
1. Distance b/n Z discs
2. Length of the A band
3. Length of the H zone
4. Length of the I band
26
27. • Hanson & Haxley proposed that skeletal muscle shorten
during contraction because the thick & thin myofilaments
slid past one another. Their model is known as the sliding
filament mechanism of muscle contraction.
27
Muscle Contraction: Sliding Filament Hypothesis
28. All the sarcomeres in a fiber will contract together. This
contracts the fiber itself. The number of fibers contracting
will determine the force of contraction of the whole
muscle.
The process of the whole muscle contraction divided into
four steps:
– Excitation
– Excitation-contraction coupling
– Contraction
– Relaxation
28
Sliding Filaments
29. • All cells have a voltage difference across their plasma
membrane. This is the result of several things:
1. The ECF is very high in [Na+] while the ICF is very high in
[K+]. The plasma membrane is impermeable to Na+ but slightly
permeable to [K+]. As a result, K+ is constantly leaking out of
the cell. In other words, positive charge is constantly leaking
out of the cell.
29
Excitation
30. Excitation, cont’d
2. The Na+/K+ pump is constantly pumping 3Na+ ions out & 2K+
ions in for every ATP used. Thus, more positive charge is leaving
than entering.
3. There are protein anions (i.e., negatively charged proteins) within
the ICF that cannot travel through the plasma.
What this adds up to is fact that the inside of the cell is negative
with respect to the outside. The interior of the cell has less
positive charge than the exterior.
30
31. Excitation, cont’d
• This charge separation is known as a membrane potential
(abbreviated Vm).
• The value for Vm in inactive muscle cells is –90 mV.
• Cells that exhibit a Vm are said to be polarized.
• Vm can be changed by influx or efflux of charge.
31
32. Excitation, cont’d
• The plasma membrane has integral proteins that act as gated
ion channels.
• These are channels that are normally closed, but in response
to a certain signal, they will open & allow specific ions to
pass through them.
• Ion channels may be:
– Ligand-gated the binding of an extracellular molecule (e.g.,
hormone, NT) causes these channels to open.
– Voltage-gated Vm causes these channels to open.
– Mechanically-gated stretch or mechanical pressure opens
these channels.
• When a channel is open, its specific ion(s) will enter or exit
depending on their electrochemical gradient.
32
33. Excitation, cont’d
In general each muscle is
served by one nerve – a
bundle of axons carrying
signals from spinal cord to
muscle.
Within the muscle, each axon
will go its own way &
eventually branch into multiple
small extensions called
telodendria. Each
telodendrium ends in a bulbous
swelling known as the
synaptic end bulb.
The site of interaction b/n a neuron & any other cell is known
as a synapse. The synapse b/n a neuron & a muscle is known as
the neuromuscular junction (NMJ).
33
34. The minute space b/n the synaptic end bulb & sarcolemma is
known as the synaptic cleft.
There is a depression in the sarcolemma at the synaptic cleft known
as the motor end plate.
The synaptic end
bulb is filled with
vesicles that contain
the neurotransmitter,
acetylcholine (ACh).
The motor end plate
is secure full of ACh
receptors (nicotinic).
34
Neuromuscular Junction (NMJ)
35. • Transmission is unidirectional.
• There is a single NMJ per muscle fiber.
• The neurotransmitter is always acetylcholine
Synthesis: Choline + Acetyl-COA = ACh by the action of
choline acetyl-COA transferase
Storage: ACh form a complex with ATP, packed in vesicles.
Release: Released by Ca-dependent exocytosis.
Metabolism: Metabolized by the action of ACh-Esterase
• The post junctional receptor is always nicotinic receptor.
• The effect of ACh on nicotinic receptor is always excitatory
producing EPSP/EPP.
• It is fatigable due to depletion of ATP & NT storage. 35
Characteristics of Neuromuscular Junction
36. Excitation, cont’d
1. A nerve signal will arrive at the synaptic end bulb & this will
cause the ACh-containing vesicles to undergo exocytosis.
2. ACh will diffuse across the synaptic cleft & bind to the ACh
receptors. These receptors are actually ligand-gated Na+
channels. The binding of ACh causes them to open.
3. Na+ will rush into the cell, making the local cell interior more
positive. This is known as depolarization. It is a local event!
36
37. Excitation, cont’d
• Adjacent to the motor end plate, the sarcolemma contains voltage-
gated ion channels. In order for these channels to open, the Vm
must depolarize from its resting value of –90 mV to approximately
–50 mV. This is the threshold. The Vm must become this positive
for the voltage-gated channels to open.
• The degree of depolarization depends on how much Na+ influx
occurred which in turn depends on how many Na+ channels were
opened by binding ACh.
• If the Vm fails to depolarize to threshold, nothing will happen. The
Vm will soon return to normal & no muscle contraction will occur.
• If the Vm does reach the threshold, two types of voltage-gated ion
channels will open:
– Fast Na+ channels
– Slow K+ channels
37
38. Excitation, cont’d
• If Vm reaches threshold, fast Na+ channels open & Na+ rushes in
causing the Vm to depolarize to +30mV. The depolarization stops
when the Na+ channels become inactivated.
• At this point, slow K+ channels have opened & K+ efflux occurs.
This returns Vm back to its resting level. This is repolarization.
• If we were to graph this change in Vm over time, it would look
somewhat like the animation below.
• This is known as an action potential.
38
39. Excitation, cont’d
39
• An AP can propagate itself across the surface of the plasma
membrane.
• The depolarization caused by the Na+ influx in one particular
area of the sarcolemma causes voltage-gated channels in the
adjacent membrane to open.
• The resulting ionic influx then causes voltage-gated channels
to open in the next patch of membrane & so on. Thus, AP
propagates itself.
40. • When a muscle fibre membrane is depolarized, contraction of
the fibre follows. The process by which depolarization initiates
contraction is called excitation-contraction coupling.
• It has several steps as follow:
1. AP initiated & propagated along the motor nerve fibre & arrives
at the end feet.
2. Opening of voltage-gated Ca-channels & influx of Ca2+ to
trigger release of Ach.
3. Ach released by Ca-dependent exocytosis & diffuse through the
synaptic cleft & binds to the nicotinic receptors on
postjunctional membrane.
4. Opening of ligand gated Na-channels & influx of Na+ to produce
EPP. 40
Mechanism of muscle contraction
(Excitation-contraction coupling)
41. Excitation-contraction coupling, cont’d
5. Spread of depolarization through the sarcolemma & T-tubules.
6. Depolarization of the T-tubules stimulate SR to release Ca2+ ions
into the sarcoplasm.
7. Then Ca2+ binds to troponin-C.
8. Ca2+ & troponin-C combination detaches troponin-I from the active
sites of actin.
9. The detachment of troponin-I from actin displaces tropomyocin,
uncovering the active sites of actin filaments.
10. When the active site of actin is exposed, the heads of myosin
connect to the actin, making cross-bridges.
11. The ATPase enzyme on the myosin heads hydrolysis ATP into ADP
+ -P plus energy.
12. The released energy causes the movement of myosin head (power
stroke) towards the centre.
13. Then, head of myosin is charged with a new molecule of ATP &
detached from actin leading to muscle relaxation. 41
42. Mechanism of Muscle Relaxation
• Has the following steps:
1. Following muscle contraction, Ca2+ is re-uptake back into SR
by Ca-pump requiring ATP.
2. Ca2+ in sarcoplasm → Ca2+ detaches from troponin-C →
Tropomyosin covers the active sites of the actin.
3. Head of myosin charged with ATP & detached from the actin.
• Muscle relaxation is an active process requiring energy.
• Therefore, a large amount of energy (ATP) consumed during
muscular performance for the following activities:
1. To move the head of myosin (power stroke), Myosin ATPase.
2. For active pump of Ca2+ from the sarcoplasm to SR, Ca-ATPase.
3. For Na-K pump in the membrane, Na-K ATPase.
4. For muscle relaxation
42
44. Types of Skeletal Muscle Fibers
• Based on the velocity of shortening, major pathways used to form
ATP, & fatigability, muscle fibers are classified into two types:
Fast/glycolytic fibers, have:
– Myosin with high ATPase activities
– Few mitochondria
– High content of glycolytic enzymes
– Large storage of glycogen
– Little myoglobin contents
Slow oxidative fibers, have:
– Myosin with low ATPase activities
– Numerous mitochondria
– High capacity of oxidative phosphorylation
– Rich in arterial blood supply, high BF
– Large amount of myoglobin contents
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45. Atrophy
• Reduction in size of a cell, tissue, or organ
Often caused by disuse. E.g. Astronauts or
As result of a nerve injury.
Hypertrophy
• Increase in size of a cell, tissue or an organ.
In muscles, hypertrophy of the organ is always due to
cellular hypertrophy (increase in cell size) rather than
cellular hyperplasia (increase in cell number)
Muscle hypertrophy occurs due to the synthesis of more
myofibrils & synthesis of larger myofibrils.
As a result, there is an increase in the force & strength of
contraction, decrease in fatigability.
Muscle Atrophy & Hypertrophy
45