Midterm 1 Content Flashcards
Lecture 1:
What are 3 types of Muscle Tissue?
1.) Skeletal Muscle
2.) Cardiac Muscle
3.) Smooth Muscle
Lecture 1:
What is Skeletal Muscle?
Generates force production to move limbs & is under voluntary control & has striated muscle fibres
main focus of the course
Lecture 1:
What is Cardiac Muscle?
Striated muscle proteins but not under voluntary control as muscle generates own rhythm
Lecture 1:
What is Smooth Muscle?
Muscle fibres contract involuntarily
- vessels constrict/dilate to regulate blood flow
Lecture 1:
What are Myofibrils?
Muscle proteins that are the smallest unit of the muscle (muscle —> fasciculi—>muscle fibre —> myofibril)
Hundreds of thousands of them per muscle fibre
Lecture 1:
What are Sarcomeres?
The basic contractile element of skeletal muscle & go end to end for full myofibril length
The individual functional units of a muscle fibre with the power stroke cross bridge cycling that shortens the muscle
Lecture 1:
When discussing Sarcomeres, what are the different bands/zones that cause the striations (striped appearance)?
A-bands - dark stripes (contain both actin & myosin)
I-bands - light stripes (only actin here when relaxed)
H-zone - middle of A-band
M-line - middle of H-zone (where myosin group together)
Lecture 1:
What are the 2 types of Protein Filaments in Sarcomeres?
- describe each & what zone/band they are
1.) Actin (thin filaments)
- lighter under microscope & form the I-band
- composed of globular proteins joined together to make a chain
2.) Myosin (thick filaments)
- darker under microscope & forms the H-zone
*A-band contains both actin & myosin filaments
Lecture 1:
What does Myosin look like?
2 intertwined filaments with globular heads 360degs out of the thick filament axis & interact with actin for contraction
Lecture 1:
What are the 3 proteins that actin is composed of?
1.) Actin - contains myosin-binding site
2.) Tropomyosin - covers active site (for myosin head) at rest
3.) Troponin (anchored to actin) - moves tropomyosin when muscle is ready for muscle contraction
Lecture 1:
What is Titan & a few points on it
Third myofilament that acts like a spring (tension increases with muscle activation & force)
- attaches myosin to the Z-disk of actin
- Calcium binds to titan to increase muscle force when stretched
- stabilizes sarcomeres, centers myosin, & prevents overstretching
Lecture 1:
What is a Motor Unit?
Consists of a single motor neuron & all fibres it innervates (the nerve & the muscle fibres)
- more operating motor units = more contractile force
Lecture 1:
What is the Neuromuscular Junction?
Consists of the synapse between a motor neuron & muscle fibre (between nerve & motor unit connection)
- site of communication between a neuron & muscle
Lecture 1:
When discussing Muscle fibre contraction, What is Excitation-Contraction Coupling?
The combined process of turning a nerve on (exciting it) to the contraction of proteins in a muscle fibre
Lecture 1:
What are the 6 main steps of Excitation-Contraction Coupling?
1.) Action Potential (AP) develops in the brain
2.) AP arrives at the axon terminal & releases Acetylcholine (ACh)
3.) ACh crosses the synapse & binds to ACh receptors on plasmalemma
4.) AP travels down Plasmalemma & T-tubules
5.) triggers release of Ca2+ from sarcoplasmic reticulum (SR)
6.) Ca2+ enables actin-myosin contraction & muscle movement occurs
Lecture 1:
What is the role of Calcium in Muscle Fibres?
Calcium is an ion that causes muscle contraction as it signals muscle proteins to contract
- Calcium is released into SR & bind to troponin on thin filament to move tropomyosin and reveal the sites on actin for myosin heads to binds to
Lecture 1:
In the sliding filament theory, What happens in relaxed vs contracted states?
1.) Relaxed State - no actin-myosin interaction occurs at binding sites & myofilaments only overlap a little
- no calcium as binding sites covered by troponin
2.)Contracted State - myosin head pulls actin towards sarcomere center (power stroke) & filaments slide past eachother
- sarcomeres, myofibrils, & muscle fiber all shorten
Lecture 1:
In the sliding filament theory, what happens after the power stroke ends?
After power stroke ends, myosin detaches from active sites & myosin head rotates back to original position
- myosin attaches to another active site farther down
Lecture 1:
What causes the sliding filament theory to end?
Either the Z-disk reaches myosin filaments or AP stops & Calcium is pumped back into sarcoplasmic reticulum
Lecture 1:
What is the energy source for muscle contractions?
Adenosine Triphosphate (ATP) is necessary for muscle contraction
- it binds to the myosin head & ATP becomes ADP + Pi + energy
Lecture 1:
What are the 3 main types of muscle fibres?
1.) Type I
2.) Type IIa
3.) Type IIx
Lecture 1:
What percentage of muscle fibres does type I make & what is its peak tension?
- type of twitch?
Approx 50% of fibres in an average muscle & peak tension is 110ms
- slow twitch fibres as take a long time to reach peak force production (slow oxidative fibres)
Lecture 1:
What percentage of muscle fibres does type II make & what is its peak tension?
- type of twitch?
Type IIa & IIx both make up approx 25% of fibres in average muscle & peak muscle tension is 50ms
- fast twitch muscle fibres as they are fast to contract but quicker to fatigue
- IIa = fast oxidative fibre & IIx = fast glycolytic fibre
Lecture 1:
What are Gel Electrophoresis?
Type I & II fibres have different types of myosin so this process separates types of myosin by size
Lecture 1:
What is the difference in the Sarcoplasm Reticulum’s of Type I vs Type II fibres?
Type II fibres have a more highly developed SR & the calcium release is faster & Vo is 3-5times faster
Lecture 1:
What is the difference in motor units in Type I vs Type II muscle fibres?
Type I motor units have smaller neurons with <300 fibres & type II motor units have larger neurons with >300 fibres
- more units in type II, meaning more connections to the brain
Lecture 1:
How are fibre types distributed?
Each person has a unique ratio that is mostly based on genetics
- arm & leg ratios are similar in one person
- typically more type I in endurance athletes & more type II in power athletes
Lecture 1:
What is the only muscle in the body that is 100% type I fibres in everyone?
The Soleus is type I in everyone
Lecture 1:
What happens to Type I muscle fibres during exercise?
The possess high aerobic endurance & maintain prolonged exercise
- require oxygen for ATP production
- recruited for low-intensity aerobic exercise & DPA
- ATP efficiently produced from fat & carbs
Lecture 1:
What happens to Type II muscle fibres during exercise?
- in general, Type IIa, & type IIx
In general, they fatigue quickly as poor aerobic endurance & produce ATP anaerobically
- Type IIa: produce more force & fatigue slower than I
- Type IIx: seldom used for everyday activities
Lecture 1:
When are Type IIa vs Type IIx muscle fibres used?
IIa - used for short, intense endurance (1,600m run)
IIx - used for short, explosive sprints (100m)
Lecture 1:
What are 2 main determinants of fibre type?
- explain each
1.) Genetics - determine which motor neurons innervate fibres & differentiate based on neuron
2.) Training - differentiate endurance, strength, & detraining. Training can induce small fibre type changes (10%)
Lecture 1:
What effect does aging have on muscle fibre type?
Aging causes a loss of type II motor units as they begin behaving like type I fibres
Lecture 1:
What is Motor Unit Recruitment?
- what order are units recruited in?
A method used for altering force production
- recruitment order = Type I, Type IIa, Type IIx
Lecture 1:
When discussing motor unit recruitment, how is force production altered?
- less force production = fewer/smaller motor units
- more force production = more/larger motor units
- type I units are smaller than type II
Lecture 1:
What are the 2 main types of Muscle Contraction?
1.) Static (isometric)
2.) Dynamic
Lecture 1:
What is Static Muscle Contraction?
Isometric contraction where muscle produces force but doesn’t change length
- joint angle doesn’t change & myosin cross-bridges form & recycle with no sliding
Lecture 1:
What is Dynamic Muscle Contraction?
Muscle produces force & changes length
- joint movement is produced. Muscle lengthens/shortens
Lecture 1:
What are the 2 types of Dynamic Muscle Contractions?
1.) Concentric (most common) - muscle shortens as sarcomere shortens & filaments slide towards eachother
2.) Eccentric - muscle lengthens as cross-bridges form but sarcomere lengthens (eg; lowering heavy weight)
Lecture 2:
What are Substrates?
Fuel sources we make energy from (eg; adenosine triphosphate ATP)
Macronutrients absorbed from the diet - carbs, proteins, & fat (lipids)
Lecture 2:
What is Bioenergetics?
The process that converts substrates into energy
- a cellular-level process
Lecture 2:
What is Metabolism?
Chemical reactions that occur in the body
Lecture 2:
How is energy release measured?
Calculated from heat production
- calculated in calories — 1cal = heat energy req’d to raise 1g of water from 14.5 degrees to 15.5
Lecture 2:
what is 1,000 calories equal to?
1,000 cal = 1 kcal = 1 Calorie (dietary)
Lecture 2:
What are the 3 main substrates used as fuel for exercise?
- what are the key organic molecules they have?
1.) Carbohydrates
2.) Fat
3.) Protein
- all contain carbon, hydrogen, oxygen, &/or nitrogen
Lecture 2:
What type of substrate is used for short exercise? Which for long exercise?
Short = more carbohydrate
Long = carbohydrate & fat
Lecture 2:
What are Carbs converted into to be used as energy?
All carbs are converted to glucose & yield about 4.1kcal/g
Lecture 2:
Approximately how many kcals of glucose are stored in the body?
~2,500kcal
Lecture 2:
Where is extra glucose stored in the body & what is it stored as?
Extra glucose is stored as glycogen in the liver & muscles
- glycogen converted back to glucose when needed to make more ATP
Lecture 2:
How much energy does fat yield?
Fat yields almost double the amount of energy as carbs as it makes 9.4kcal/g
- yields high net ATP but slow ATP production
Lecture 2:
How much fat substrate can be stored in the body?
70,000+ kcal of fat stored in the body
Lecture 2:
What does fat get broken down into when used for energy?
Broken down into free fatty acids (FFAs) & glycerol
**only FFAs are used to make ATP
Lecture 2:
When is protein used for energy?
- how much energy does it yield?
Used for energy during starvation & yields 4.1kcal/g
Lecture 2:
How are proteins broken down & what are they broken down into?
Need to be broken down into individual amino acids & then into glucose in order to be used.
- convert into FFAs through lipogenesis for energy storage and cellular energy substrate
Lecture 2:
How is energy rate production controlled?
Energy is released at a controlled rate based on availability of primary substrate
Lecture 2:
What is the Mass Action Effect when discussing rate of energy production?
Explain how substrate availability affects metabolic rate
- more substrate available = higher pathway activity
- excess of given substrate = cells rely on that substrate more than others
Lecture 2:
How do enzymes control rate of energy production?
Energy release rate is controlled by enzyme activity in the metabolic pathway
- more enzymes = more ATP produced
Lecture 2:
What are Enzymes?
They facilitate breakdown (catabolism) of substrates & catalyze individual reactions to produce more ATP
- they can speed up or slow down reactions based on ATP requirements
- they lower the activation energy for a chemical reaction
- end with suffix “-ase”
Lecture 2:
What is PFK Enzyme?
Facilitates production of glucose when turned on or reduces rate of production when turned off
- used in glycolysis
Lecture 2:
What is Rate-Limiting Enzyme?
Can create a bottleneck effect at an early step
- activity is influenced by negative feedback & slows overall reaction to prevent runaway reaction
Lecture 2:
How is ATP stored?
- where & how much
ATP is stored in small amounts until needed & stored in phosphate bonds in muscle
Lecture 2:
When ATP is used for energy, how is it broken down to release energy?
ATP is broken down to release energy by using ATPase enzymes
ATP + Water + ATPase —> ADP + Pi + energy
*ADP is a lower-energy compound that is less useful
Lecture 2:
How is ATP formed from by-products?
ATP is synthesized through phosphorylation & can occur in either absence or presence of Oxygen
ADP + Pi + energy —> ATP
Lecture 2:
What are the three ATP synthesis Pathways?
1.) ATP-PCr System ~ anaerobic metabolism
2.) Glycolytic System ~ anaerobic metabolism
3.) Oxidative System ~ aerobic metabolism
Lecture 2:
What is the ATP-PCr System?
- oxygen required?
- ATP yield?
- duration?
Anaerobic system (no oxygen) with substrate-level metabolism and also called the Phosphate Creatine system
- ATP Yield = 1 ATP/1 PCr
- Duration = 3-15s
- Pathway is used to reassemble ATP because ATP stores are very limited
Lecture 2:
What is PCr?
- how is it broken down in the ATP-PCr System?
PCr = phosphocreatine & used for ATP recycling
- PCr + creatine kinase —> Cr + Pi + energy
- PCr energy cannot be used for cellular work but can be used to reassemble ATP
- it replenishes ATP stores @ rest & recycles ATP during exercise until used up
Lecture 2:
What is the main enzyme used in the ATP-PCr System?
PCr breakdown is cataloged by the CK enzyme (creatine kinase)
- CK controls rate of ATP production based on negative feedback
*low ATP & high ADP causes CK activity to increase
* high ATP levels cause CK activity to decrease
Lecture 2:
What is the Glycolytic System?
- oxygen required?
- ATP yield?
- Duration?
An anaerobic system for ATP synthesis that does not require oxygen
- ATP yield = 2-3 mol ATP/ 1 mol substrate
- Duration = 15s - 2min
- breaks down glucose via glycolysis
Lecture 2:
What substrate is used in the Glycolytic System?
Uses glucose or glycogen as its substrate
- costs 1 ATP for glucose & 0 ATP for glycogen
- must convert to glucose-6-phosphate
Lecture 2:
What is the Pathway for the Glycolytic System?
- where does it occur?
- ATP yield?
Pathway starts with glucose-6-phosphate & ends with pyruvic acid
- 10-12 enzymatic reactions total
- all steps occur int eh cytoplasm
- ATP Yield: 2 ATP for glucose & 3 for glycogen
Lecture 2:
What are 3 Cons of the Glycolytic System?
1.) low ATP yield & inefficient use of substrate
2.) lack of O2 converts pyruvic acid to lactic acid
3.) lactic acid impairs glycolysis & muscle contraction as it impairs ability to produce ATP
Lecture 2:
What are 2 Pro’s of the Glycolytic System?
1.) Allows muscles to contract when O2 is limited
2.) Permits shorter-term, high-intensity exercise than oxidative metabolism can sustain
Lecture 2:
In the Glycolytic System, What enzyme is used & how?
Phosphofructokinase (PFK) is a rate-limiting enzyme that regulates ATP production.
- lower ATP = higher PFK activity… higher ATP = lower PFK activity **PFK levels also regulated by products of Krebs cycle
- Glycolysis = ~2mins max exercise… need another pathway for longer durations
Lecture 2:
What is the Oxidative System?
- Oxygen required?
- ATP yield?
- Duration?
- location?
Aerobic system that yields way more ATP than other systems & is less intense as ATP is produced slowly
- ATP Yield is dependent on substrate… 32-33ATP/1g glucose & 100+ ATP/1 FFA
- Duration = steady supply for hours
- Location = mitochondria (not cytoplasm)
- most complex system of the 3 bioenergetic systems
Lecture 2:
What are the 3 stages of the Oxidation System when Oxidizing a Carbohydrate?
1.) Glycolysis
2.) Krebs Cycle
3.) Electron Transport Chain (ETC)
Lecture 2:
Explain the Electron Transport Chain
H+ & electrons are carried to the ETC via NADH & FADH2 molecules
- H+ & electrons travel down the chain….
1.) H+ combines with O2 & forms H2O
2.) Electrons & O2 help form ATP
3.) 2.5 ATP per NADH & 1.5 ATP per FADH2
Lecture 2:
How is Fat Oxidized in the Oxidative System?
- rate of entry into muscle?
- ATP yield compared to glucose?
- slower or faster than glucose oxidation?
Triglycerides (major fat energy source) are broken down into 1 glycerol & 3 FFAs through lipolysis (carried out by lipases)
- Rate of FFAs entry into muscle is dependent on concentration gradient
- Yields 3-4 times more ATP than glucose
- slower than glucose oxidation
Lecture 2:
What is the b-Oxidation (beta-oxidation) of fat?
- how much ATP used?
The process converting FFAs (fatty acids) to acetylene-CoA before entering Krebs Cycle
- uses 2 ATP right away
Lecture 2:
How many steps in the beta-Oxidation of fat?
of steps depends on # of carbons on FFA (fatty acids)
- 16-carbon FFA yields 8 acetyl-CoA compared to 1 glucose yielding 2 acetyl-CoA
- fat oxidation required more O2 at beginning & yields far more ATP later
Lecture 2:
When discussing fat oxidation… how does the Krebs cycle & ETC work?
Acetyl-CoA enters Krebs cycle & follows same path as glucose oxidation
- different fatty acids have different #’s of carbons meaning they… yield different #’s of acetyl-CoA molecules, & Yield different ATP
Lecture 2:
What is the Oxidation process of a protein?
- how is energy yield determined?
Protein rarely used as a substrate but can be converted to glucose & Acetyl-CoA
- energy yield not easy to determine as nitrogen presence is unique & excretion requires ATP
Lecture 2:
What are the 3 key ways that muscle can use lactate?
Lactate is an important fuel during exercise & can be used by muscles in 3 ways…
1.) lactate produced in cytoplasm is taken up by mitochondria (of same muscle fibre) & oxidized
2.) lactate transported via MCP transporters to another cell & oxidized there (lactate shuttle)
3.) lactate recirculates back to liver & reconverted to pyruvate & then glucose through gluconeogenesis
Lecture 2:
How do the 3 energy systems interact with eachother?
All 3 systems interact for all activities as no single system contributes 100% but one system will often dominate
- cooperation between systems increases during transition periods
Lecture 2:
What is the Crossover Concept?
- at rest vs at intensity & their intersection
**Cross-over point is the intersection of these 2, which is affected by exercise intensity & endurance training
- at rest & exercise below 60% VO2max lipids are the primary substrate
- at high intensity & above 75% VO2max carbohydrates are the primary substrate
Lecture 2:
What are the 3 main factors that determine Oxidative Capacity of a Muscle?
Not all muscles have maximal oxidative capability’s but can be determined by…
1.) Enzyme activity
2.) Fibre type composition & endurance training
3.) O2 availability versus need
Lecture 2:
Enzyme activity & Oxidative Capacity…. What are some representative enzymes?
Not all muscles exhibit optimal activity of oxidative enzymes
- representative enzymes include; succinate dehydrogenase & citrate synthase
- levels differ in endurance-trained vs untrained individuals
Lecture 3:
What is a Neuron?
The basic structural unit of nervous system also called a nerve & is an excitable tissue that sends nerve impulses down cellular membranes
Lecture 3:
What are the 3 major regions of the Neuron?
1.) Cell body (soma)
2.) Dendrites
3.) Axon
Lecture 3:
What 2 things speed up the propagation of action potentials?
Myelin speeds up propagation & axons with a larger diameter speed propagation as well
Lecture 3:
What is myelin & How does myelin speed up action potentials?
Myelin can be a fatty sheath around the axon & called Schwann cells or not continuous layers that are called nodes of Ranvier
- saltitory conduction
Lecture 3:
Schwann Cells vs Nodes of Ranvier
Schwann cells = continuous fatty myelin sheath around the axon made of glial cells
Nodes of Ranvier = non continuous myelination
Lecture 3:
What is the Synapse & its purpose?
The junction/gap between neuron’s that serves as a site of neuron-to-neuron communication
*AP must jump across the synapse
Lecture 3:
What is the pathway of Action Potential to the synapse?
Axon —> synapse —> dendrites
Presynaptic cell —> synaptic cleft —> postsynaptic cell
**signal changes form across synapse
Electrical —> Chemical —> Electrical
Lecture 3:
How do AP’s transmit across the Synapse?
AP can only move in one direction & axon terminals contain neurotransmitters that serve as chemical messengers
- they carry electrical AP across synaptic cleft
- bind to receptor on postsynaptic surface
- stimulate GP’s in postsynaptic neuron
Lecture 3:
What are Neurotransmitters?
50+ are known
- ACh & Noepinephrine (NE) govern exercise which increases acetylcholine (ACh)
Lecture 3:
What is the role of ACh neurotransmitter?
Governs exercise & stimulates skeletal muscle contraction, & mediates parasympathetic nervous system effects
Lecture 3:
What is the role of Noepinephrine (NE) neurotransmitter?
NE mediates sympathetic nervous system effects
Lecture 3:
What is the real name of the PGC-1a neurotransmitter?
Peroxisome Profilferator-activated receptor-y coactivator 1a
Lecture 3:
What are the 4 key points of the PGC-1a neurotransmitter?
A molecule that is more available during exercise
1.) increases branching of the presynaptic terminal motor neuron
2.) increases the # of presynaptic vesicles containing acetylcholine
3.) increase the # of acetylcholine receptors on the cell membrane
4.) decreases the size of the motor end plate
Lecture 3:
What are the 2 types of Postsynaptic responses?
1.) Excitatory Postsynaptic Potential (EPSP)
2.) Inhibitory Postsynaptic Potential (IPSP)
Lecture 3:
What is the Excitatory Postsynaptic Potential (EPSP) response?
This is a depolarization, excitatory response that promotes Action Potentials
- More EPSPs = more depolarization
- if you reach threshold depolarization that AP occurs
Lecture 3:
What is the Inhibitory Postsynaptic Potential (IPSP) response?
This is a hyperpolarization, inhibitory response that prevents Action Potentials
- multiple IPSPs = more hyperpolarizing
Lecture 3:
What sections of the brain form the Cerebrum?
- Frontal lobe
- Parietal lobe
- Occipital lobe
- Temporal lobe
*basal ganglia
Lecture 3:
What is the primary motor cortex of the cerebrum?
Frontal lobe = primary motor cortex
- responsible for conscious control of muscle movement
- pathway = pyramidal cells > Corticospinal tract > spinal cord
Lecture 3:
What is the primary sensory cortex of the cerebrum?
Parietal lobe
Lecture 3:
What is the Basal ganglia in the cerebrum?
The cerebral white matter that include clusters of cell bodies deep in the cerebral cortex & initiate sustained or repetitive movements
Eg; walking, running, posture, muscle tone, etc
Lecture 3:
What are the 2 portions that form the Diencephalon?
1.) Thalamus
2.) Hypothalamus
Lecture 3:
What is the role of the Thalamus in the Diencephalon?
Serves as a major sensory relay center that determines what we are consciously aware of
Lecture 3:
What is the role of the Hypothalamus in the Diencephalon?
Maintains homeostasis & regulates internal environment using neuroendocrine control
- eg; appetite, thirst, fluid balance, sleep, blood pressure, heart rate, breathing, temperature, etc.
- controls systems typically under involuntary control
Lecture 3:
What is the role of the Cerebellum?
Controls rapid/complex movements & coordinates timing/sequence of the movements
- compares movements with intentions & initiated corrections
- accounts for body position & muscle status
- receives input from primary motor cortex (frontal lobe) to help execute/refine movements
Lecture 3:
What are the 3 sections that form the Brain Stem?
1.) Midbrain
2.) Pons
3.) Medulla Oblongata
Lecture 3:
What is the key role of the Brainstem?
To relay information between the brain & spinal cord
Lecture 3:
What is the purpose of Reticular Formation in the Brainstem?
To coordinate skeletal muscle formation/tone & control cardiovascular/respirator functions
Lecture 3:
What is the purpose of Analgesia System in the Brainstem?
Where pain is modulated by opioid substances as b-endorphins are released here with exercise
Lecture 3:
What is the Spinal Cord?
- location
Tract of nerve fibres that permit 2-way conduction of nerve impulses that is continuous with the medulla oblongata
Lecture 3:
What are the 2 tracts in the spinal cord?
1.) Ascending Afferent (sensory) fibres
2.) Descending Efferent (motor) fibres
Lecture 3:
What is the Peripheral Nervous System?
- how many cranial nerves?
- how many spinal nerves?
PNS is connected to brain & spinal cord
- 12 pairs of cranial nerves (connected to brain)
- 31 pairs of spinal nerves (connected to spinal cord)
*both types directly supply skeletal muscles
Lecture 3:
What are the 2 major divisions of the PNS?
1.) Sensory (Afferent) division
2.) Motor (efferent) division
Lecture 3:
What is the role of the Sensory Division of the PNS?
Transmits information from periphery to the brain & includes major families of sensory receptors
Lecture 3:
What are the 5 major families of sensory receptors in the PNS?
1.) Mechanoreceptors - physical forces
2.) Thermoreceptors - temperature
3.) Nociceptors - pain
4.) Photoreceptors - light
5.) Chemoreceptors - chemical stimuli (changes in o2 levels etc)
Lecture 3:
In the sensory division of the PNS, what are Joint Kinesthetics Receptors?
Receptors sensitive to joint angles & rate of angle change (degrees of flexion or extension)
- they sense joint position & movement
Lecture 3:
In the sensory division of the PNS, what are Muscle Spindle Receptors?
- specialized intramural muscle fibres innervated by g-motor neurons
Sensory fibres/nerve clusters sensitive to muscle length & rate of change - they sense muscle stretch and rate/amount of stretch
Lecture 3:
In the sensory division of the PNS, what are Golgi Tendon Organ Receptors?
They are sensitive to tension in the tendons & sense strength of contractions
Lecture 3:
What is the role of the Motor Division of the PNS?
- 2 subdivisions
Transmit information from the brain to periphery & has 2 subdivisions:
1.) Autonomic - regulates visceral activity
2.) Somatic - stimulates skeletal muscle activity
Lecture 3:
In the Motor Division of the PNS, what is the Autonomic Nervous System?
Regulates visceral activity & controls involuntary internal functions
- helps with exercise-related autonomic regulation such as heart rate, blood pressure, & lung functions
Lecture 3:
What are the 2 complimentary divisions of the Autonomic Nervous system?
- one key point on each
1.) Sympathetic Nervous System - fight or flight (prepares body for exercise)
2.) Parasympathetic Nervous System - rest & digest (state of conserving energy)
Lecture 3:
What is the Sympathetic Nervous System of the ANS?
- what happens when stimulation increases?
The fight or flight response in preparation for exercise… when stimulation increases…
- heart rate & blood pressure increase
- blood flow to muscles increase
- airway diameter increases (bronchodilation)
- metabolic rate, glucose levels, and FFA levels increase
Lecture 3:
What is the Parasympathetic Nervous System of the ANS?
- what happens when stimulation increases?
The rest & digest activity that opposes sympathetic effects as trying to conserve energy for next sympathetic event
- digestion & urination increases
- heart rate decreases
- diameter of vessels & airways decreases
Lecture 3:
What is Sensory-Motor Integration?
The communication & interaction between sensory & motor systems
Lecture 3:
What are the 5 Sequential Steps of Sensory-Motor Integration?
1.) Stimulus sensed by sensory receptor
2.) Sensory AP sent to sensory neurons in CNS
3.) CNS interprets sensory info & sends out response
4.) Motor AP sent out on alpha-motor neurons
5.) arrives at skeletal muscle & response occurs
Lecture 3:
What happens when level of control moves from spinal cord to cerebral cortex?
As level of control moves from spinal cord to cerebral cortex, movement complexity increases
Lecture 3:
What is the motor reflex activity like during sensory-motor integration?
Motor reflex is an instant, preprogrammed response to stimulus & is identical each time
- occurs before conscious awareness
- impulse is integrated at lower, simple levels
Lecture 4:
What is the role of the Endocrine System?
It’s a chemical communication system that maintains homeostasis via hormones
Lecture 4:
What is the speed of the endocrine system compared to the nervous system?
endocrine system is slower to respond than the nervous system but is longer lasting
Lecture 4:
What are the 2 key ways the endocrine system maintains homeostasis?
1.) controls substrate metabolism
2.) regulates fluid & electrolyte balance
Lecture 4:
What are the 4 key organs of the endocrine system we are going to look at?
Thyroid gland, adrenal glands, pancreas, & kidneys
Lecture 4:
What are steroid hormones?
- derived from what & soluble or not?
Derived from cholesterol & are lipid soluble as they can diffuse through membranes
- aldosterone is an important for fluid balance
Lecture 4:
What are the 4 major glands that secrete Steroid Hormones?
- & what hormone is secreted?
1.) Adrenal Cortex - cortisol & aldosterone
2.) Ovaries - estrogen & progesterone
3.) Testes - testosterone
4.) Placenta - estrogen & progesterone
Lecture 4:
What are Non-steroidal Hormones & their 2 types?
Non lipid-soluble hormones that are unable to cross membranes & include 2 types; Protein/Peptides & Amino-Acid Derived
Lecture 4:
What are the Protein/Peptide Non-Steroidal hormones?
The most common type of non-steroidal hormones that are secreted from the pancreas, hypothalamus, & pituitary glands
Lecture 4:
What are the Amino-Acid Derived Non-Steroidal hormones?
Includes the thyroidal hormones (T3 & T4) and the Adrenal Medulla Hormones including epinephrine & noepinephrine
Lecture 4:
How are Hormones secreted?
Secreted in bursts (pulsatile) as plasma concentrations fluctuate over minutes/hours & days/weeks
Lecture 4:
How is Hormone Secretion Regulated?
Regulated by negative feedback as hormone release causes a change in the body
- large downstream change reduces secretion
- small downstream change increases secretion
- eg; home thermostat
Lecture 4:
What is downregulation (when discussing hormone actions)?
The decrease in # of receptors during high plasma concentration & causes desensitization for receiving hormones
Lecture 4:
What is upregulation (when discussing hormone actions)?
The increase in # of receptors during high plasma concentration & causes sensitization for hormones
Lecture 4:
How do hormone receptors work?
Use hormone-specific receptors to limit the scope of their effects & bind to correct receptors
*if no receptors than there is no hormone effect
Lecture 4:
Why is there no hormone effect if there is no receptor on the cell surface?
1.) hormone affects only tissues with specific receptors
2.) hormone exerts effects after binding with receptors
- typical cells have 2,000-10,000 receptors
Lecture 4:
Where are steroid hormone receptors found & their actions?
Inside the cell in the cytoplasm or nucleus
-hormone-receptor complex enters nucleus & binds DNA to direct gene activation & regulate the synthesis of mRNA & proteins
Lecture 4:
Where are non-steroid hormone receptors found & their actions?
Receptors on cell membranes go to second membrane systems to carry out hormone effects
Lecture 4:
What are the 3 common second messengers of non-steroidal hormones & their roles
Second messengers carry out & intensify the effects of hormones
1.) Cyclic Adenosine Monophosphate (cAMP)
2.) Cyclic Guanine Monophosphate (cGMP)
3.) Inositol Triphosphate (IP3) & Diacylglycerol (DAG)
Lecture 4:
Where is the Pituitary Gland located?
Attached to the inferior hypothalamus of the brain
Lecture 4:
What are the 3 lobes of the Pituitary gland?
1.) Anterior (most important)
2.) Intermediate
3.) Posterior
Lecture 4:
What is the role of the Pituitary Gland?
Secretes hormones in response to hypothalamic hormone factors:
- releasing & inhibiting factors
- exercise increases secretion of all anterior pituitary hormones
Lecture 4:
What is the most common hormone released from the Anterior Pituitary Gland?
- what is it’s role
Growth Hormone (GH) is a potent anabolic hormone that’s release is proportional to exercise intensity (increased GH release when increase in intensity)
- helps build tissue & organs, promotes muscle growth (hypertrophy), & stimulates fat metabolism
Lecture 4:
What are the 2 key hormones released from the Thyroid Gland?
Triiodothyronin (T3) & Thyroxine (T4)
Lecture 4:
In the Thyroid Gland, T3 & T4 led to increases in what?
T3 & T4 increase…
- metabolic rates of all tissues
- protein synthesis
# & size of mitochondria
- glucose uptake by cells
- rate of glycolysis & gluconeogenesis
- FFA mobilization
Lecture 4:
How is the release of T3 & T4 stimulated?
1.) The Anterior Pituitary releases thyrotropin (Thyroid-stimulating hormone/TSH) that travels to the thyroid gland and stimulates release of T3 & T4
2.) Exercise speeds up release of TSH
- short exercise = T4 increases & long exercise = T4 constant & T3 decreases
Lecture 4:
What is the role of the Adrenal Medulla?
Releases catecholamines (80% Epinephrine & 20% NE) that help with the fight or flight response
- exercise increases which increases SNS & increases release of E & NE
Lecture 4:
When Catecholamines are released from the Adrenal Medulla, what 3 things are increased?
1.) heart rate, contractile force, & blood pressure increase in the heart
2.) Glycolysis & FFAs increase
3.) Blood flow to skeletal muscle increases
Lecture 4:
What hormones are released from the Adrenal Cortex?
Releases corticosteroids which include:
- glucocorticoids
- mineralocoticoids
- gonadocorticoids
Lecture 4:
What is the most common glucocorticoid released from the Adrenal Cortex?
- function?
Cortisol is the major glucocorticoid & stimulates glucogenesis while increasing FFA mobilization & protein catabolism
- acts as an anti-inflammatory & depresses anti-immune reactions
Lecture 4:
What are the 2 key hormones in the Pancreas & their main function?
1.) Insulin - used to lower blood glucose levels
2.) Glucagon - used to raise blood glucose levels
Lecture 4:
How does insulin work when released from Pancreas?
Lowers blood glucose by countering hyperglycaemia and opposing glucagon
- facilitates glucose transport into cells
- enhances synthesis of glycogen, protein, & fat
- inhibits (stops) gluconeogenesis
Lecture 4:
How does Glucagon work when released from the Pancreas?
Glucagon raises blood glucose levels by countering hypoglycemia & opposes insulin
- promotes glycogenolysis & gluconeogenesis
Lecture 4:
3 key ways of regulating carbohydrate metabolism during exercise?
1.) Glucose must be available to tissues
2.) Adequate glucose during exercise requires glucose re;ease from liver & glucose uptake by muscles
3.) some hormones help increase circulating glucose such as; glucagon, epinephrine, noepinephrine, & cortisol
Lecture 4:
What is Glycogenolysis?
The process of turning glycogen into glucose
Lecture 4:
What is Gluconeogenesis?
The process of turning FFAs & proteins into glucose
Lecture 4:
How does Growth Hormone affect glucose circulating during exercise?
GH causes an increase in FFA mobilization which causes a decrease in cellular glucose uptake
Lecture 4:
How do T3 & T4 hormones affect glucose circulating during exercise?
T3 & T4 hormones cause an increase in glucose catabolism & fat metabolism
Lecture 4:
What does the amount of glucose released from the liver depend on?
Exercise intensity & duration
Lecture 4:
When discussing the regulation of Carbohydrate Metabolism during exercise, what happens when exercise intensity increases?
- catecholamine release increases
- glycogenolysis rate increases in liver & muscles
- muscle glycogen is used before the liver glycogen
Lecture 4:
When discussing the regulation of Carbohydrate Metabolism during exercise, what happens when exercise duration increases?
- more liver glycogen is sued
- increase in muscle glucose uptake causes increase in liver glucose release
- glycogen stores decrease causes glucagon ;evils to increase
Lecture 4:
During Exercise, what happens to insulin levels?
Insulin concentrations decrease & cellular insulin sensitivity increases causing more glucose to be taken up into the cells & less insulin is used
Lecture 4:
How does the CNS interact with the Endocrine SYstem?
CNS regulates carbohydrate metabolism through hormones (insulin) & nutrients (glucose, FFAs, & amino acids)
- brain sensitive to glucose & helps control insulin release
- Leptin & GLP-1 hormones are released by adipose tissue & act through the CNS to decrease glucose production
*glucose is the only substrate for brain metabolism
Lecture 4:
How is Fat Metabolism regulated during exercise?
FFA mobilization & fat metabolism is critical to endurance exercise as glycogen is depleted & fat energy is required, causing lipolysis acceleration
- Triglycerides broken down into FFAs & glycerol
Lecture 4:
During exercise, how are triglycerides broken down to maintain metabolism using the fat substrate?
Tryglycerides broken down into FFAs & Glycerol
- fat is stored as tryglycerides in adipose tissue
- broken into FFAs & transported to muscles
- rate of this breakdown is a possible determinant of the rate of cellular fat metabolism
Lecture 4:
What is Lipolysis & how is it stimulated?
Lipolysis is the breakdown of fat & is stimulated by:
- decreased insulin levels
- epinephrine & norepinephrine
- cortisol
- Growth Hormone
*they stimulate lipolysis via lipase enzyme
Lecture 4:
During exercise, plasma volume decreases in the blood. What does this cause?
1.) increases hydrostatic pressing & tissue osmotic pressure
2.) decreases plasma water content through sweating
3.) increases heart strain, which decreases blood pressure
Lecture 4:
During exercise, hormones work to correct fluid imbalances, where are these secreted from?
- name 3 organs/glands
1.) Posterior Pituitary Gland
2.) Adrenal Cortex
3.) Kidneys
Lecture 4:
How does the Posterior Pituitary gland help regulate fluid & electrolytes during exercise?
- what is the main hormone?
Posterior pituitary secretes Antidiuretic hormone (ADH) & oxytocin which are produced in the hypothalamus & travel to posterior pituitary & secreted when brain signals from hypothalamus
- Only ADH is involved with exercise to increase water reabsorption in kidneys & less water in urine (antidiuresis)
Lecture 4:
How is the ADH hormone from the Posterior Pituitary stimulated to regulate fluid & electrolytes?
1.) decrease in plasma volume (hemoconcentration) causes increase in osmolality
2.) increases osmolality & stimulates osmoreceptors in hypothalamus
*ADH is released & increases water retention by kidneys (minimizes water loss & severe dehydration)
Lecture 4:
What hormones do the Adrenal Cortex release to maintain fluid & electrolyte regulation?
They secrete mineralocorticoids, the main one is aldosterone which acts on kidneys & causes sodium retention from urine into the blood so water is reabsorbed to maintain osmolaty
Lecture 4:
What effects does Aldosterone have on Fluid & electrolyte retention?
Aldosterone released from the Adrenal Cortex causes…
1.) increases Na+ retention by kidneys
2.) increases Na+ retention to increase water retention via osmosis
3.) increases Na+ retention to increase K+ excretion
Lecture 4:
What is the stimuli for Aldosterone release?
Decrease in plasma Na+
Decrease in blood volume & blood pressure
Increase in Plasma K+
Lecture 4:
How do the kidneys help regulate fluid & electrolytes?
Kidneys are target tissues for ADH & they secret erythropoietin (EPO) & renin
Lecture 4:
How does EPO (erythropoietin) released from the kidneys work to maintain fluid & electrolyte balance?
EPO released in response to low blood O2 in the kidneys
- simulates red blood cell production which is critical for adapting to training & altitude
Lecture 4:
What is the stimulus for renin (enzyme) release from the kidneys?
Decreased blood volume & decreased blood pressure
- sympathetic nervous system impulses
Lecture 4:
What is the Renin-Angiotensin-Aldosterone Mechanism?
Process where renin converts angiotensinogen into angiotensin I & then ACE converts Angiotensin I into Angiotensin II which stimulates the release of Aldosterone
Lecture 4:
What does Angiotensin II hormone do?
Constricts blood vessels to increase pressure causes kidneys to release aldosterone & brainstem to increase thirst to increase water intake
Lecture 4:
What is Osmolality?
The measure of concentration of dissolved particles (proteins, ions, etc) in the body’s fluid compartments
- normal value + ~300mOsm/kg
Lecture 4:
How does Osmolality & Osmosis help with fluid & electrolyte regulation?
If compartments osmolality increases than water is drawn in but is compartment osmolality decreases than water is drawn out (osmosis)
Lecture 4:
Relationship between Aldosterone & Osmosis & what does osmotic water movement minimize?
Na+ retention causes increased osmolality which leads to increased water retention because where Na+ moves, water follows
- Osmotic water movement minimizes loss of plasma volume & maintains blood pressure
Lecture 5:
What is Direct Calorimetry?
The measurement of temperature change from heat produced during energy production/expenditure
Lecture 5:
When turning substrates into energy, what is metabolism efficiency of it?
40% of substrate energy turns into ATP
60% of substrate energy turns into heat
Lecture 5:
What are the 2 laws of Thermodynamics?
1.) Energy can be created or destroyed
2.) any chemical reaction in the body will release heat
Lecture 5:
What happens to heat as energy is produced?
Heat production increases with energy production
- can be measured with calorimeter
- water flows through walls & body temp increases the water temp
Lecture 5:
What are 2 Pros of Direct Calorimetry?
1.) Accurate over time & more precise
2.) Good for resting metabolic measurements
Lecture 5:
What are the 4 Cons of Direct Calorimetry?
1.) expensive & slow (box is very pricey)
2.) heat added by exercise equipment (eg; treadmill creates friction heat)
3.) Measurement errors created by sweat
4.) Neither practical nor accurate for exercise
Lecture 5:
What is Indirect Calorimetry?
- what does it measure?
Way of measuring expiratory gases under certain conditions & estimates total body energy expenditure based on O2 used & CO2 produced
- measures respiratory gas concentration
Lecture 5:
When is Indirect Calorimetry accurate?
Is accurate for steady-state oxidative metabolism
**older methods are accurate but slow & newer methods are faster but expensive
Lecture 5:
What is VO2 & how is it calculated?
VO2 = volume of O2 consumed per minute (rate of O2 consumption) & units = L/min
*volume of inspired O2 minus volume of expired O2
Formula = (Vi x FiO2) - (Ve x FeO2)
Lecture 5:
What is VCO2 & how is it calculated?
- formula & units?
The volume of CO2 produced per minute (rate of CO2 produced) & units = L/min
*VCO2 = volume expired CO2 minus Volume inspired CO2
*Formula = (Ve x FeCO2) - (Vi x FiCO2)
Lecture 5:
When Calculating VCO2 & VO2, what does FiO2 & FeO2 represent? FeO2 & FeCO2?
FiO2 = fraction of O2 in the air we inhale
FiCO2 = fraction of CO2 in the air we inhale
FeO2 = fraction of O2 expired into the air
FeCO2 = fraction of CO2 expired into the air
Lecture 5:
What is the % of FiO2 always?
Always 20.93% or 21%
Lecture 5:
What is the % of FiCO2 always?
Always 0.03%
Lecture 5:
What is the Respiratory Exchange Ratio (RER)?
- formula?
- units?
The ratio between rates of CO2 production & O2 usage
- RER = VCO2/VO2
- no units as it is a ratio
Lecture 5:
What does O2 usage during metabolism depend on?
Depends on type of fuel being oxidized
- more carbon atoms = more O2 needed
Lecture 5:
What does RER predict?
Predicts substrate usage & how much energy is required which is measured in Kcal/O2 efficiency
RER = efficiency of energy substrate
Lecture 5:
What is the typical range for RER?
Between 1.0 & 0.7
*use chart to see these ratios
Lecture 5:
What are the limitations of Indirect Calorimetry?
1.) CO2 production may not = CO2 exhalation
2.) RER is inaccurate for protein oxidation
3.) RER near 1.0 may be inaccurate when lactate buildup increases CO2 exhalation
4.) Glucogenesis produces RER <0.70
5.) doesn’t work on someone malnourished
Lecture 5:
What are the 5 steps to solving indirect Calorimetry questions?
1.) Calculate VO2
2.) Calculate VCO2
3.) Calculate RER
4.) use RER to obtain kcal/LO2 (on chart)
5.) Use kcal/LO2 & VO2 to calculate EE
Lecture 5:
What is Metabolic Rate & what is it based on?
The rate of energy use by the body based on whole body O2 consumption & corresponding caloric equivalent
*@ rest RER = 0.80 & O2 = 0.3L/min
* @ rest metabolic rate = 2,000 kcal/day
Lecture 5:
What is Basal Metabolic Rate?
BMR = rate of energy expendature @ rest
- found when in supine position, thermoneutral environment, & after 8hrs of sleep & 12hrs fasting
Lecture 5:
What are a few things that affect BMR?
BMR find the minimum energy required for living & can be affected by body surface area, age, stress, hormones, body temp, etc
Lecture 5:
What is Resting Metabolic Rate (RMR)?
Typically what we measure as rules are not as strict & is like BMR but easier (within 5-10% range)
- stringent standardized conditions not required
- 1,200 - 2,400 kcal/day
- looks @ total daily metabolic activity
Lecture 5:
What occurs to energy expenditure during submaximal aerobic exercise?
- metabolic rate increases with exercise intensity
- slow component of O2 uptake kinetics (at higher outputs, VO2 increases as more Type II fibre recruitment occurs)
- VO2 drift = upward drift at low power outputs possibly due to ventilators hormone changes (occurs when recruiting Type II fibres)
Lecture 5:
What occurs to energy expenditure during submaximal aerobic exercise?
- metabolic rate increases with exercise intensity
- slow component of O2 uptake kinetics (at higher outputs, VO2 increases as more Type II fibre recruitment occurs)
- VO2 drift = upward drift at low power outputs possibly due to ventilators hormone changes (occurs when recruiting Type II fibres)
Lecture 6:
What are the 2 Definitions of Fatigue?
1.) decrements in muscular performance with continued effort, accompanied by sensations of tiredness
2.) inability of muscle(s) to maintain required power output to continue muscular work at given intensity
Lecture 6:
Is fatigue reversible?
Fatigue is reversible by rest & isn’t necessarily catastrophic but is a continuum @ reduced rate
Lecture 6:
What are the 4 major causes of fatigue?
1.) inadequate energy delivery/metabolism
2.) accumulation of metabolic by-products
3.) failure of muscle contractile mechanism
4.) altered neural control of muscle contraction
Lecture 6:
How does PCr depletion coincide with fatigue?
PCr (phospho-creatine) is used for short-term, high-intensity effort & gets depleted more quickly than total ATP (Pacing helps defer depletion)
*Pi accumulation may be potential cause
Lecture 6:
How is Glycogen Depletion associated with Fatigue?
Glycogen depletion is correlated with fatigue as reserves are limited & get depleted quickly
- fatigue related to total glycogen depletion but unrelated to rate of glycogen depletion
Lecture 6:
Does glycogen depletion increase or decrease with intensity?
Glycogen is depleted more quickly with high intensity & depleted more quickly during first few minutes of exercise
Lecture 6:
How is glycogen depleted in fibres recruited first?
Fibres recruited first/most often get depleted fastest
- type I fibres depleted after moderate endurance exercise
Lecture 6:
How are Muscle fibre types recruited (what order)?
- Type I fibres recruited first (for light/moderate intensity)
- Type IIa fibres recruited next (for moderate/high intensity)
- Type IIx fibres recruited last (for maximal intensity)
Lecture 6:
What is glycogen depletion like in different muscle groups?
Activity-specific muscles are depleted faster as they’re recruited the earliest & for he longest time
Lecture 6:
How is glycogen depletion & blood glucose levels related?
- role of liver?
When muscle glycogen isn’t enough for prolonged exercise, liver glycogen turns to glucose & enters blood stream
- when muscle glycogen decreases, liver glycogenolysis increases
Lecture 6:
What are the 3 Metabolic By-Products that cause fatigue?
1.) Pi - from rapid breakdown of PCr to form ATP
2.) Heat - retained by body & core temp increases
3.) Lactic Acid - product of anaerobic glycolysis
Lecture 6:
How does Heat alter metabolic rate?
- how does heat impact muscle function?
Heat increases rate of carbohydrate utilization
& speeds up glycogen depletion
- high muscle temperature may impair muscle function
Lecture 6:
How does time to fatigue change with surrounding temperatures?
- what degree is longest to fatigue? Which is shortest?
- longest time to exhaustion = 11degC
- shortest time to exhaustion = 31degC
- *muscle precooking prolongs exercise
Lecture 6:
If lactic acid isn’t cleared immediately from the muscles, what does it convert to?
Lactic acid converts to Lactate & H+ which causes decrease in muscle pH (causing acidosis)
Lecture 6:
What happens when muscle pH levels drop below 6.9? PH = 6.4?
pH <6.9 inhibits the glycolytic enzymes used for ATP synthesis
pH = 6.4 prevents further glycogen breakdown
Lecture 6:
How does fibre recruitment contribute to fatigue?
Fibre recruitment may be reduced due to…
- stress of exhaustive exercise may be too much
- someone may be unwilling to endure more pain
- discomfort of fatigue is a warning sign to stop
- elite athletes learn proper pacing to tolerate fatigue
Lecture 6:
What is Muscle Soreness & what does it result from?
Muscle soreness = accuse soreness during & immediately after exercise & felt anytime (delayed-onset 1-2 days later)
- Results from exhaustive/high-intensity exercise (especially when performed for the first time)
Lecture 6:
What is Acute Muscle Soreness?
- duration?
Felt during or immediately after strenuous/novel exercise caused by accumulation of metabolic by-products (H+) & disappears in minutes-hours
Lecture 6:
What is tissue Edema?
Tissue edema occurs due to plasma fluid in the interstitial place & causes acute muscle swelling
Lecture 6:
What does DOMS stand for?
Delayed-onset muscle soreness
Lecture 6:
What are DOMS?
- major cause of them?
Delayed-onset muscle soreness that appears 1-2 days after exercise causes predominantly by eccentric contractions
- stiffness to restrictive pain
-eg; level-run pain < downhill-run pain (not caused by increase in blood lactate oncentrations)
Lecture 6:
How is structural damage of muscle indicated in DOMS?
Structural damage caused by DOMS is indicated by muscle enzymes in blood
- enzyme concentrations in blood increase 2-10 times after heavy training
- onset of DOMS parallels the onset of increased muscle enzymes in blood
Lecture 6:
Hoe are DOMS and inflammation connected?
Inflammation & DOMS are connected as white blood cells count increases with soreness and neutrophils are released due to damaged muscle cells
Lecture 6:
What are some sequence of events in DOMS?
Increase muscle tension leads to structural damage to muscle/cells
- membrane damage disturbs Ca2+ homeostasis & inhibits cellular respiration causing activation of enzymes that degrade Z-disks
- circulating neutrophils increase as products of macrophage activity accumulate & stimulate pain
- fluid & electrolytes shift to the area & create edema
Lecture 6:
How do DOMS impact Performance?
- 3 factors causing loss of strength?
DOMS reduce muscle force generation as there is a loss of strength due to 3 factors…
1.) physical disruption of muscle
2.) failure in excitation-contraction coupling
3.) loss of contractile protein
Lecture 6:
3 Strategies for reducing DOMS?
1.) minimize eccentric work early in training
2.) start with low intensity & increase slowly
3.) start with higher-intensity (exhaustive training) - soreness starts bad but much less later on
Lecture 6:
What are EAMC Muscle Cramps?
- caused by…?
- reduced by…?
EAMC = exercise-associated muscle cramps that are localized to an overworked muscle
- due to lack of conditioning, improper training, & depletion of muscle energy stores
- treated with stretching & reduced by changing excitatory properties of neuron
Lecture 6:
What are heat cramps?
Associated with large sweat & electrolyte losses (sodium & chloride)
*coupled with dehydration
- treated with high sodium solution, ice, & massage
Lecture 7:
What are the 6 Major functions for the Cardiovascular System?
1.) Delivers O2 & nutrients
2.) removes CO2 & wastes
3.) transports hormones & other molecules
4.) Supports temperature balance & fluid regulation
5.) maintains acid-base balance
6.) regulates immune function
Lecture 7:
What are the 3 major circulatory elements of the Cardiovascular system?
1.) Heart (pump)
2.) Blood Vessels (channels/tubes)
3.) Blood (fluid medium)
Lecture 7:
What is the role of the right side of the heart?
- route of the blood flow?
Pulmonary circulation ( deoxygenated blood from body & pumped to lungs)
- superior & inferior vena cava to RA to tricuspid valve to RV to pulmonary valve to pulmonary arteries to lungs
Lecture 7:
What is the role of the left side of the heart?
- route of the blood flow?
Systemic Circulation (pumps oxygenated blood from the lungs to the body)
- lungs to pulmonary veins to LA to mitral valve to LV to aortic valve to aorta
Lecture 7:
what is Myocardium?
Myocardium is heart muscle & left ventricular has most myocardium beacause it must pump blood to entire body so its largest & has thickest walls
Lecture 7:
How are cardiac muscle fibres of the myocardium connected?
Connected by intercalated discs with desmosomes holding the cells together
- gap junctions rapidly conduct action potentials
Lecture 7:
What is the difference between Myocardium & Skeletal Muscle?
Skeletal muscle: large, long, unbranded, multinucleated cells with intermittent, voluntary contractions & Ca2+ released from SR
Myocardial Cells: small, short, branched, single nucleus cells with continuous, involuntary rhythmic contractions & calcium-induced calcium release
- high capillary density & mitochondria count
Lecture 7:
What is the route of electrical signal through the heart?
Sinoatrial (SA) Node —> Atrioventricular (AV) Node —> AV bundle (bundle of his) —> Purkinjee fibres
Lecture 7:
How do electrical signals spread through the heart?
Electrical signals spread through gap junctions
Lecture 7:
What is the role of the SA Node in the cardiac conduction system?
SA node initiates contraction signals
- made of pacemaker cells in the upper posterior RA wall
- signals spread from SA node via RA/LA to AV node
- stimulates
Lecture 7:
What is the role of the AV Node in the cardiac conduction system?
The AV node, located in the RA (right atrial) wall, delays the signal & relays it to ventricles
- the delay lets R&L atrial to contract before R&L ventricles
- then relays signals to AV bundle
Lecture 7:
What is the role of the AV Bundle in the cardiac conduction system?
AV bundle relays signal to R&L ventricles which travels along interventricular septum (which then splits into R&L bundle branches) & sends signal to the apex of the heart
Lecture 7:
What is the role of the Purkinje Fibres in the cardiac conduction system?
Purkinje fibres forming the terminal branches of R&L bundle branches send a signal into the R&L ventricles & spread it through the entire ventricle wall
- contraction of R&L ventricles
Lecture 7:
How does the Parasympathetic Nervous System help with Extrinsic control of the hearts activity?
- 3 key points
1.) PNS accesses heart through vagus nerve (cranial nerve X)
2.) PNS carries impulses to SA & AV nodes as it releases Acetylcholine to hyper-polarize cells (brings membrane potential down to decrease threshold & heart-rate)
3.) PNS decreases HR below intrinsic HR (100bpm)
Lecture 7:
What is intrinsic heart rate normally? Normal resisting heart rate? Resting heart rate in endurance athletes?
1.) intrinsic = 100bpm
2.) resting = 60-100bpm
3.) elite endurance athletes = 35-45bpm
Lecture 7:
What effect does the Sympathetic Nervous System have on heart activity?
Opposite effect of the PNS
- carries impulses to the SA & AV nodes which release NE for depolarization (increases HR & contractile force)
- increases HR above intrinsic HR (determines HR during physical & emotional stress)
Lecture 7:
What is the max HR someone can have?
250bpm
Lecture 7:
Define Cardiac Cycle
- 2 periods?
Tall mechanical & electrical events that occur during one heart beat
- 2 periods; diastole (relaxation phase, chambers fill with blood, & 2x length of systole) & systole (contraction phase to pump blood to body)
Lecture 7:
In the Cardiac Cycle, what occurs during Ventricular Systole?
- how is it shown on an electrocardiogram?
1/3 of the cardiac cycle where contraction begins as a result of…
- increased ventricular pressure
- AV valses closing (heart sound 1 “lub”)
- semilunar valve opens & blood is ejected
*End-systolic volume (ESV) is the blood remaining in the ventricle
*QRS complex to T wave on electrocardiogram
Lecture 7:
In the Cardiac Cycle, what occurs during Ventricular Diastole?
- how is it shown on an electrocardiogram?
2/3 of the cardiac cycle where relaxation begins due to the ventricular pressure dropping
- semilunar (SV) valves close (heart sound 2 “dub”)
- AV valves open & ventricle fills 70% passively & 30% by atrial contraction
*End-diastolic volume (EDV) = amount of blood in ventricles
* T wave to the next QRS complex
Lecture 7:
What is Stroke Volume (SV)?
- calculation for SV?
The volume of blood pumped out of heart in one heartbeat
- occurs during systole where most, not all, blood is ejected
- EDV - ESV = SV
Eg; 100mL - 40mL = 60mL
Lecture 7:
What is Ejection Fraction (EF)?
- formula for calculating
The % of EDV pumped
- SV / EDV = EF
Eg; 60mL/100mL = 0.6 =60%
- clinical index of heart contractile function
Lecture 7:
What is Cardiac Output (Q)?
- units & formula?
The total volume of blood that is pumped per minute measured in L/min (Q= HR x SV)
- Resting cardiac output = ~4.2 - 5.6 L/min
(Average total blood volume is ~5 L & total blood volume circulates once every minute)
Lecture 7:
What is Functional Syncytium?
The pumping of the heart as one unit
Lecture 7:
What is Torsional Contraction?
- explain how it works in systole & diastole
The increased contractility during intense exercise to enhance left ventricle filling
*Increases hearts efficiency
- Systole: heart twists gradually, storing energy like a spring
- Diastole: abrupt untwisting that allows atrial filling (dynamic relation)
Lecture 7:
What are the 5 things that form the vascular system?
1.) Arteries - carry blood away from heart
2.) Arterioles - control blood flow & feed capillaries
3.) Capillaries -site for nutrient & waste connection
4.) Venules - collect blood from capillaries
5.) Veins - carry blood from venules back to heart
Lecture 7:
What is Systolic Blood Pressure (SBP)?
Highest pressure in the artery that occurs during systole (contraction)
- top number of blood pressure (~110 to 120 mmHg)
Lecture 7:
What is Diastolic Blood Pressure (DBP)?
The lowest pressure in the artery that occurs during diastole (relaxation)
- bottom number of blood pressure (~ 70-80 mmHg)
Lecture 7:
What is Mean Arterial Pressure (MAP)?
The average pressure over entire cardiac cycle & is important for pressure differential
- MAP = 2/3 DPB + 1/3 SBP
Lecture 7:
Define General Hemodynamics
The way your blood flows through your arteries and veins and the forces that affect your blood flow
Lecture 7:
What is Pressure & why is it important to blood flow?
The force that drives blood flow & provided by heart contraction
- blood flows from area of high pressure (LV, & arteries) to are of low pressure (veins, & RA)
*pressure gradient = 100mgHg
Lecture 7:
What is Resistance & how does it impact blood flow?
The force that opposes blood flow & is provided by physical properties of vessels
- radius of vessels is most important
- controls pressure differences through the body
Lecture 7:
What is the easiest way to change blood flow in the body?
1.) Change the radius of vessels through; vasoconstriction (smaller diameter) & Vasodilation (larger diameter)
2.) Arterioles (resistance vessels) - site for most VC & VD & responsible for 70-80% of pressure drop from LV to RA
Lecture 7:
How is blood distributed throughout the body?
- distribution @ rest vs @ heavy exercise
1.) blood flow (BF)s to sites where there is most need
- regions of high metabolism have increased BF
2.) @ rest cardiac output (Q) = 5L/min
- liver & kidneys receive 50% of Q
- skeletal muscle receives ~20% of Q
3.) Heavy exercise (Q = 25 L/min)
- exercising muscles receive 80% of Q via VD
- flow to liver & kidneys decreases via VC
Lecture 7:
What are the 3 types of Intrinsic Control of Blood Flow?
1.) Metabolic
2.) Endothelial
3.) Myogenic
Lecture 7:
When discussing Intrinsic Control of Blood Flow, How do Metabolic Mechanisms help?
Metabolic mechanisms (VD) form a buildup of local metabolic by-products such as a decrease in oxygen levels and increase carbon dioxide, K+, H+, & lactic acid
Lecture 7:
When discussing Intrinsic Control of Blood Flow, How do Endothelial Mechanisms help?
Endothelial mechanisms (mostly VD) include substances secreted by vascular endothelium & includes nitric oxide (NO), prostaglandins (relax smooth muscle), & EDHF (hyperpolarizing)
Lecture 7:
When discussing Intrinsic Control of Blood Flow, How do Myogenic Mechanisms help?
Local pressure changes that causes VC & VD
- increase in pressure causes increased vasoconstriction whereas decreased pressure causes increased vasodilation
Lecture 7:
What are a few things that help with the extrinsic control of blood flow?
Autonomic process where blood flow may be redistributed to a different organ at same level
SNS (@autonomic branch) innervates smooth muscle in arteries & Arterioles and increase in sympathetic activity increases VC but decrease in activity leads to decrease in VC
Lecture 7:
How does the Local Control of muscle Blood Flow work?
Blood flow to exercising muscle increases to match its metabolic demand
This is seen through local alteration of blood flow & improved extraction at tissue level)
Lecture 7:
How does Functional Sympatholysis help with local control of muscle blood flow?
Functional Sympatholysis is the inhibition of sympathetic vasoconstriction by reducing vascular responsiveness to adrenergic receptor activation
*sympathetic nerve cannot do job bc we’ve inhibited neurotransmitters by EDHF + ND inhibitors
*review slide 38
Lecture 7:
What are Baroreceptors and how do they control blood pressure?
Assist with integrative control of blood pressure
- sensitive to changes in arterial pressure
- Afferent signals sent from baroreceptors to brain
- Efferent signals from brain sent to heart & vessels
- Adjustments of arterial pressure are back to normal
Lecture 7:
What three mechanisms assist with blood return to the heart?
1.) One-way venous valves
2.) muscle pump
3.) respiratory pump
*upright posture makes venous return to heart more difficult (eg; compared to laying down)
Lecture 7:
How does the Muscle Pump work to assist with blood return to heart?
Skeletal muscles contract and increases pressure in vein causing the superior valve to open so the blood can rush through
Eg; walking helps activate muscle pump so blood doesn’t pool in legs & decreases risk for deep vein thrombosis
Lecture 7:
What are the 3 major functions of blood?
1.) transportation (O2, Nutrients, & waste)
2.) temperature regulation
3.) acid-base (pH) balance
Lecture 7:
How much blood volume typically in a male? In a female?
Male = 5-6L Female = 4-5L
Lecture 7:
What is the composition of blood?
1.) Plasma - 55-60% of blood volume
2.) Formed Elements - 40-45% of blood volume
- includes… red blood cells, white blood cells, & platelets
Lecture 7:
How can blood plasma levels increase & decrease?
- composition of plasma?
- can decrease by 10% with dehydration in heat
- can increase by 10% with training & heat acclimation
- 90% water, 7% protein, 3% nutrients & ions
Lecture 7:
What are the 3 things that make the formed elements of blood?
- their percentages
- red blood cells (erythrocytes) - 99%
- white blood cells (leukocytes) - <1%
- platelets - <1%
Lecture 7:
Define “Hematocrit”
The total percent of blood volume composed of formed elements
Lecture 7:
What are Red Blood Cells?
- Composition?
- lifespan?
Red blood cells have no nucleus & cannot reproduce
- replaced by hematopoiesis
- lifespan of 4months
- produced & destroyed @ equal rates
Lecture 7:
What is Hemoglobin & its role in red blood cells?
An oxygen-transporting protein found in red blood cells
- 250million hemoglobin per red blood cell
- carries 20mL O2 per 100mL of blood
Lecture 8:
What is the Purpose of the respiratory system?
To carry Oxygen to & remove CO2 from all body tissues
Lecture 8:
What are the 4 Processes of the Respiratory System?
1.) Pulmonary Ventilation
2.) Pulmonary Diffusion
3.) Transport of Gases via Blood
4.) Capillary Diffusion
Lecture 8:
What is Pulmonary Ventilation?
- 2 zones?
Process of moving air into & out of the lungs
- transport zone & exchange zone
- Pathway = nose/mouth > Nasal conchae > pharynx > larynx > trachea > bronchial tree > alveoli
Lecture 8:
What occurs during Inspiration of Pulmonary Ventilation
An active process where the diaphragm flattens, ribcage/sternum move up & out, and the thoracic cavity expands thus increasing the volume of thoracic cavity & lungs
Lecture 8:
What happens to lung volume & intrapulmonary pressure during inspiration?
Lung volume increases & intrapulmonary pressure decreases
- boyles law helps explain this movement
- due to pressure difference, air passively rushes in due to pressure difference
Lecture 8:
What additional muscles are used for forced breathing?
Scalenes, sternocleidomastoid, & pectoralis
- ribs raise even further
Lecture 8:
What occurs during Expiration of pulmonary ventilation?
A passive process where inspiratory muscles relax, decreasing lung volume & increasing intrapulmonary pressure
- air is forced out of the lungs
Lecture 8:
What occurs during forced breathing when exhaling?
- what muscles are used?
Forced breathing, is an active process where internal intercostals pull ribs down
- uses latissimus dorsi, Quadratus lumborum, and abdominal muscles to force diaphragm back up
Lecture 8:
What is Pulmonary Diffusion?
The gas exchange between alveoli and capillaries (alveoli are surrounded by capillaries)
- air path = bronchiole tree to alveoli
- blood path = right ventricle > pulmonary trunk > arteries > capillaries
Lecture 8:
what are the 2 major functions of Pulmonary Diffusion?
1.) Replenishes blood oxygen supply
2.) Removes Carbon dioxide from blood
Lecture 8:
During Pulmonary Diffusion, How does the blood flow to the lungs?
- how much? How fast? Where from?
At rest, lungs receive about 4-6 L of blood/min
- RV cardiac output to lungs = LV cardiac output
*lung blood flow = systemic blood flow
- Blood moves to lungs via Low Pressure Circulation
- Lung MAP = 15mmHg vs aortic MAP = 95mmHg
- small pressure gradient (15 to 5 mmHg)
* resistance much lower as vessel walls thinner
Lecture 8:
What is Oxygen’s diffusion capacity?
- normally? at rest? At exercise?
O2 diffusion capacity is the O2 volume that is diffused /min/mmHg of gradient
*gradient calculated from capillary mean PO2 (11mmHg)
- @ rest = 21mLO2/min/mmHg of gradient OR 231mLO2/min for 11mmHg gradient
- @ max exercise = venous O2 levels decrease & PO2 has a bigger gradient (diffusion capacity increases by 3 times)
Lecture 8:
Why is Oxygen diffusion capacity limited at rest?
Limited due to incomplete lung perfusion
- only bottom 1/3 of lung perfused with blood & top 2/3 lung surface area has poor gas exchange
Lecture 8:
Why does Oxygen diffusion capacity increase with exercise?
Increases with exercise as there is more even lung perfusion as systemic blood pressure rises to open the top 2/3 of lungs for perfusion
- gas exchange now occurs over entire lung surface area
Lecture 8:
What is the carrying capacity of blood for oxygen transport?
Carrying capacity is 20mL O2/100mL blood
Approx 1L O2/ 5 L blood
Lecture 8:
How is oxygen transported in blood?
- greater than 98% of O2 is bound to hemoglobin (Hb) in red blood cells (oxyhemoglobin if carrying o2 & deoxyhemoglobin if not carrying)
- less than 2% of O2 dissolved in plasma
Lecture 8:
Review Oxyhemoglobin Dissociation Curve
Slide 25
Lecture 8:
What are 2 factors that affect Hemoglobin Saturation?
1.) Blood pH - more acidic = more O2 unloaded @ acidic exercising muscles (Bohr effect as O2Hb curve shifted to right)
2.) Blood Temp - warmer blood causes more tissue O2 unloading during exercise (causes O2Hb curve to shift right)
Lecture 8:
What happens to hemoglobin oxygen-saturation during rest? During exercise?
@ rest, Hb is 98-99% saturated with 0.75 seconds of transit time
During exercise, Hb saturation levels lower ( transit time is shorter than at rest)
Lecture 8:
What are the 3 ways Carbon Dioxide is transported in the blood?
1.) as bicarbonate ions
2.) dissolved in plasma
3.) bound to Hb (carbaminohemoglobin)
Lecture 8:
What is the role of Bicarbonate Ions for Carbon dioxide Transport?
Bicarbonate ions transport 60-70% of CO2 in blood to lungs
1.) CO2 & water forms carbonic acid (H2CO3) - in red blood cells & catalyzed by carbonic anhydrase
2.) Carbonic acid dissociates into bicarbonate - H+ binds to Hb & triggers Bohr Effect
- bicarbonate ion diffuses from red blood cells into plasma
lecture 8:
What is a Carbaminohemoglobin?
A hemoglobin molecule in the blood with CO2 bound to it for transport
Lecture 8:
How is Carbon Dioxide Transported with Carbaminohemoglobin?
20-33% of CO2 transported is bound to Hb
- CO2 binds to protein (-globin) part of Hb
- deoxyhemoglobin binds CO2 more easily as PCO2 levels affect CO2 binding
*higher PCO2 = easier to bind CO2
* lower PCO2 = easier CO2 dissociation
Lecture 8:
What is the difference between Arterial and venous Oxygen?
The difference reflects the tissue O2 extraction (higher exteraction = venous O2 lower& difference increases)
- Atrial O2 content = 20mL O2/100mL blood
- Mixed Venous O2 = 15-16mLO2/100mL blood (rest) or 4-5mLO2/100mL blood (exercise)
Lecture 8:
How is Oxygen Transported in muscle?
Myoglobin
- similar structure to hemoglobin but higher affinity for O2
Lecture 8:
3 key factors influencing Oxygen delivery & uptake
1.) O2 content of blood - represented by PO2 & Hb % saturation
2.) Blood flow - decreased blood flow = decreased opportunity to deliver O2 to tissue… increase exercise = increase blood flow to muscle
3.) Local conditions (pH/Temp) - shift in O2Hb dissociation curve & decreased pH causes increased temp to promote O2 unloading in tissue
Lecture 8:
3 ways to regulate pulmonary ventilation
1.) maintain bodies homeostatic balance between blood PO2 & PCO2 & pH
2.) coordination between cardiovascular & respiratory systems
3.) coordination via involuntary regulationn
Lecture 9:
During acute exercise, what are some cardiovascular responses?
- heart rate
- stroke volume
- cardiac output
- blood pressure
- blood flow
- blood
Lecture 9:
What are the normal Resting Heart Rate (RHR) levels?
- untrained vs trained
- how is RHR affected?
Normal ranges of untrained RHR = 60 to 80 bpm
Trained Ranges of trained RHR = 30 to 40 bpm
* RHR affected by neutral tone, temperature, & altitude
* anticipatory response increases heart rate above RHR before exercise starts
Lecture 9:
What is heart rate during exercise directly proportional to?
Heart rate when exercising is directly proportional to exercise intensity
Lecture 9:
What is Maximum Heart rate?
- how is it calculated?
HR max is the highest HR achieved in all-out effort to volitional fatigue
- it’s highly reproducible & see slight decline with age
- Estimated HRmax = 220 - age
- Better Estimated HRmax = 280 - (0.7 x age)
Lecture 9:
What is Steady-State HR?
The point of plateau & the optimal HR for meeting circulatory demands at a given submaximal intensity
- increase intensity = increased steady-state HR (2-3mins to adjust)
-It is a basis for simple exercise tests estimating aerobic fitness & HRmax
Lecture 9:
Why does heart rate fluctuate during exercise?
- causes & influencing factors?
Measure of HR rhythm fluctuates due to continuous changes in sympathetic & parasympathetic balance
- influenced by; body core temp, sympathetic nerve activity, respiratory rate, etc
- analyzed in respect to frequency (not time)
Lecture 9:
How does Stroke Volume respond during acute exercise?
- does it increase or decrease?
SV increases with intensity to 40-60% of VO2max (past this is plateau leading to exhaustion)
- max exercise SV is approx. double standing SV but only slightly higher than supine SV
* supine SV Musca higher than Standing SV due to supine EDV being way larger
Lecture 9:
What are 3 factors that increase Stroke Volume (during exercise)?
1.) increased preload (end-diastolic ventricular stretch) = frank-starling mechanism
- increase stretch = increase contraction strength
2.) increased contractility (inherent ventricle property)
- increase in epinephrine or NE which increases contractility
3.) decreased after load: aortic resistance
Lecture 9:
How is blood pressure altered during exercise?
- systolic BP up or down? Diastolic?
During endurance exercise, there is an increase in mean arterial pressure (MAP)
- systolic BP increases in proportion to intensity
- diastolic BP has a slight increase or decrease
L:ecture 9:
How is MAP calculated during exercise?
MAP = Q (cardiac output) x total peripheral resistance (TPR)
* Q increases & TPR slightly decreases
Lecture 9:
How is blood distribution altered in acute exercise?
cardiac output increases causing an increase in available blood flow
- increase in blood flow redirected to areas with greatest metabolic need (working muscle)
- blood is shunted away from less active regions by sympathetic vasoconstriction
- local vasodilation allows additional blood flow to exercising muscle (triggered by metabolic products)
Lecture 9:
How does cardiovascular drift assist in cardiovascular response during exercise?
Cardiovascular drift is associated with increased core temp & dehydration
- Stroke Volume decreases as skin blood flow increases & plasma volume/venous return & prelod decrease
- Heart Rate drift increases to compensate
Lecture 9:
How is plasma volume altered during exercise?
Upright exercise causes a decrease in plasma volume to compromise with exercise performance
- decreased plasma volume causes increased MAP & capillary hydrostatic pressure
- sweating further decreases plasma volume
Lecture 9:’
What does the decrease in blood plasma lead to?
Hemoconcentration of blood due to decrease in fluid % in blood & increase in cell %
(Hematocrit increases up to 50%)
Lecture 9:
What are the net effects of Hemoconcentration during exercise?
Red blood cell concentration increases as plasma levels decrease
- hemoglobin concentration increases, thus increasing O2 carrying capacity
Lecture 9:
What stimulates rapid changes in HR, Q, & BP during exercise?
1.) precede metabolic buildup in muscle
2.) HR increases within 1s of onset of exercise
3.) Central Command - higher brain centers & coactivation of motor & cardiovascular centers
Lecture 9:
When exercising what is the first priority of cardiovascular response?
First priority is to maintain blood pressure
- blood flow is maintained as long as BP is stable
- BP prioritized before other needs
Lecture 9:
How is Ventilation changed during exercise?
There is an immediate increase in ventilation that occurs before muscles contract due to anticipatory responses from central command
- second phase of ventilation increase is driven by chemical changes in arterial blood (increase in CO2 & H+ triggers chemoreceptors)
Lecture 9:
What is ventilation increase proportional to?
- what changes from low intensity to high intensity activities?
Ventilation increase is proportional to metabolic needs of the muscle
- at low intensity, only tidal volume increases but at high exercise ventilation rate increases also
Lecture 9:
How long is ventilation recovery & what is it regulated by?
Ventilation recovery occurs several minutes after delay of exercise
- regulated by blood pH, PCo2 & temperature
Lecture 9:
When discussing breathing irregularities, what is Exercise-Induced Asthma?
Occurs due to lower airway obstruction & more water being evaporated from airway surface
- related to disruption of airway epithelium & injury to microvasculature
- results in coughing, wheezing, or dyspnea
Lecture 9:
When discussing breathing irregularities, what is Dyspnea?
Dyspnea is shortness of breathe that is common with poor aerobic fitness & caused by the inability ro adjust to high blood PCO2 & H+
- fatigue in respiratory muscles
Lecture 9:
When discussing breathing irregularities, what is Hyperventilation?
Excess ventilation/breatjing that may be anticipatory or anxiety driven
- caused by increase in PCO2 gradient between blood & alveoli
- must decrease blood PCO2 to decreased drive to breathe (slow breathing)
Lecture 9:
When discussing breathing irregularities, what is Valsalva Maneuver?
A potentially dangerous irregularity accompanied with certain exercises that causes the glottis to stay closed (increased intra-abdominal Pressure & intrathoracic Pressure)
- the great veins collapse from high pressures causing decrease in venous return, decreased cardiac output, & decreased arterial BP
Lecture 9:
What is Ventilatory Threshold?
The point where Litres of air breathed is greater than Litres of O2 consumed
- associated with lactate threshold and increased PCO2
Lecture 9:
Is Ventilation normally a limiting factor on exercise performance?
Ventilation normally not a limiting factor as respiratory muscles are very fatigue resistant (account for 10% of VO2 & 15% of cardiac output [Q] during exercise)
