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Homeostasis
The state of equilibrium in the living body with respect to various functions and to chemical composition of the fluids and tissues
Examples of homeostasis
Body temp, pH, blood pressure, heart rate, oxygen and hydration
Regulation
Maintained within very narrow limits
Control
Can vary widely from their normal steady state with no harm caused
Controls are required
to achieve regulation
Ie: change in heart rate can alter how blood pressure is controlled
The control system
A group of interconnected and interacting components relating a given input to a given output
(blood pressure: heart, vasoconstriction/dilation)
Output =
Input in many closed systems
Components of a Control System
Measure of a system by output ( the regulated component)
Controlled system produced by the output
Sends signal to integrator usually in CNS
Integrator takes note of whether or not the output is correct based on the input
Error sent to the controller usually in the CNS controls the signal to that system
If no error system continues normally
In error state they send a signal to indicate what needs to change within the controlled system
Closed Loop
Continuous loop ( most physiological properties are closed loop) Output=Input
Open Loop
Output doesn't regulate input (something requiring lots of power in a short time, like kicking a ball)
Setpoint
Set area that the input wants you to be at (preferred point of variable) can change temporarily
Servomechanism
The control system, what responds to change in output
Gain
Ratio of output to input when =1 it's a steady state and nothing is changing
Steady-States
Ratio = 1
Transient response
Between steady states, period of adaption (time that it takes is called the lag time)
HR (msec)
Some adjust quickly some slowly (lag time changes)
Blood Glucose example
Regulated based on availability
Insulin: controlled
Anaerobic
Can occur in an oxygenated state but also without oxygen
Requires glucose and energy investment step
NADH and ATP may go to ETC
In absence of oxygen only makes ATP and Lactate
Occurs in cytosol
ATP is _____ in Myokinase
AMP
PCr
In muscle with fairly limited store can come with ADP to create ATP (can only sustain power outage for about 10 seconds)
Energy stores
Horse has a massive amount of glycogen in muscle: gives greater anaerobic capacity
Production of NADH and FADH
Occurs in the mitochondria
Fatty Acid Oxidation
through beta oxidation allows for use into ATP (small energy investment step)
129-130 ATP production
"Fat burns in a flame of carbohydrate" Why?
Oxaloacetic acid is a byproduct of glycolysis and is required for complete oxidation of FFAs
"Fat burns in a flame of carbohydrate" What does this mean?
MUST have some level of glucose/glycolysis to utilize FFAs, can never completely rely on fat as an energy source CHOS always required
Energy Sources
CHOs
-Glycogen
-Blood Glucose
Fat
- Intra- and extra-
stores
Protein
Major sites of glycogen storage
liver and muscle
Glycogen can be depleted by
a lot of exercise
Blood glucose is an
immediate source of CHOs but if no other source of CHOs you will fatigue
Fatty acids
Muscle does not contain some fat, immediate energy store
Protein
Can be used but it is not desirable, it is pulled from broken-down muscle, generally a last resort
(I.e.: starvation, long or high intensity can also cause this)
Aerobic Respiration
Respiration that requires oxygen
CHO, fat and protein substrates
36-138 net ATP
CO2 end product
Slow rxn time
lasts hours
Fick Principle
Can measure extraction/utilization of a substance using venous and arterial concentrations and flow rates
Fick Principal Equation
VO2 = Q x (a-v) x O2
Q= Cardiac Output
A= Arterial
V= Venous
O2= Hormone/ metabolite
High arterial concentration indicates
Usage
High venuous concentration indicates
production
Respiratory Exchange Ratio
RER = VCO2/VO2
RER meaning
> 1.0 = anaerobic
1.0= CHO
0.7-0.8 = CHO, Fat
<0.7 = Fat
Energy Expenditure
VO2: Oxygen uptake (measure of aerobic metabolism of an individual)
VO2 max: max aerobic capacity of an individual
Relative value is the ratio of the two
Body cares about relative cost of VO2 max
VO2 max is effected by
Health
Age
Fitness status
Altitude
Effect of Speed and Slope on VO2
VO2 max will plateau at a certain point, and is adaptable based on a variety of factors
Oxygen deficit
Lag in consumption at the start of exercise
EPOC
Oxygen debt (excess post exercise oxygen consumption)
Always larger than the deficit because slow phase takes more time to achieve homeostasis
Fast phase
Primarily the drop off
Slow Phase
Replenishing enzymes, protein repair and tissue repair
Metabolism
Sum of all chemical rxns occurring in a living organism
Energy conservation
Chemical energy -> electrical or mechanical energy -> heat
Catabolism
Breakdown of complex substances
Anabolism
Build up of complex substances
When there is a catabolic and anabolic balance
No net charge
Greater catabolism there is
a loss of process
Ie. Bone loss
Greater anabolism
there is growth
Appropriate in young animals
Inappropriate can result in tissue damage or injury
Energy Metabolism
Energy usage by an organism
The rate at which organized energy is converted into heat
Direct calorimetry
Measure of heat production (kJ or Cal) Primarily through O2 consumption, good for aerobic metabolism
Indirect calorimetry
Measure chemical changes
exercise harder to perform due to equipment needed
C6H12O6+ 6O2 -> 6CO2 + 6 H2O + Energy (673 Cal , 2820 kJ)
CO2 production
is not as effective a measure of energy metabolism as O2 consumption
Can change easily through non-metabolic processes
I.e. hyperventilation
Energy yield per mL of Co2
varies greatly
What effects metabolic rate
Physical activity: individuals with greater lean mass have greater metabolic rate
Environmental Temperature: cold raises basal metabolic rate
Digestive processing
Body Size
Age: slows as you age
Sex: males have higher metabolic rate
Endocrine Activity
Circadian Rhythms: decreases as you sleep
Basal Metabolic rate
BMR
Temperature in thermal neutral zone
Fasting
Resting
Amount of energy an organism needs just to stay alive
Surface Area
Body mass
Horse: large body mass not a lot of surface area
Dog: less body mass to surface area
Gravity effects
Circulation
Movement and Locomotion
Surface area/ Volume ration effects
Respiration
Digestion
Water Balance
Thermoregulation
Bipedal vs Quadrupeds
Metabolism and body size
Smaller animals have higher metabolic rate than larger animals
Kleiber's Rule
For eutherian mammals
Oxygen consumption (VO2)=(Mass)^0.75
Small animals have relatively more per gram VO2 as an elephant
Roles of skeletal system
Locomotion
Protection of vital organs
Provides structure
Bones and joints create levers
Attachment for muscles
Functions below physiological limit
7-10x normal force to cause failure
Tendon and Ligament structure
Mostly extracellular matrix
Very few actual cells, with exception of fibroblasts
Water is a very important component that acts as a lubricant
Allows college to freely stretch
ECM
Proteoglycans
Glycosaminoglycans
Collagens
Crimp Pattern
Organized become more linear as they stretch, if damaged pattern is disturbed fibroblasts produce extracellular proteins
Bone Structure
Weight bearing bones, mostly long bones
Site of red and white blood cell development
Compressive forces are supported by inorganic mineral content to provide resistance to outside forces
Bone cells minor component
Tissue Turnover
Normal
Repair/regrowth of damaged tissue
Rate dependent on tissue
Tissue Turnover: tendons and ligaments
Very slow process
Very few fibroblasts and are relatively inactive therefore takes longer
Metabolic capacity is limited
Tissue Turnover: Bone
Repairs much faster but still limited
More metabolically active can repair quicker
An entire skeletal system can turnover in three years
Bones respond relatively rapidly when new pressure is exerted
Modeling
Change in the size or the shape of the tissue
In bone an independent action of osteoclasts and osteoblasts which results in change in shape or size of bone
Tissue needs change such as muscle mass growth due to power lifting
Remodling
Coordination reaction of absorption and growth
Osteoclast resorb and osteoblast replace tissue
Size and shape do not change
Tissues needed to adapt to activity or changes in activity such as damage occurring
Inactivity
Joint immobilization, bed rest, horse on stall rest
Changes in composition
Less collagen fibril density, fewer small fibers and greater amount of larger fibers impacts flexibility of that tendon or ligament, decreased water and proteoglycan content (decrease lubrication properties) can disrupt parallel nature of collagen fibers
Cannot stretch as well
Activity
Maintain tendons and ligaments to 80-90% of their maximal capacity, only 10-20% increase during
Increase in proteoglycan content, increased collagen. Actual change is fairly limited
Functional Adaptation
Long term exercise will increase bone mineral density which increases the strength of the bone, increases in cross sectional area of the bone, allows the pressure on the bone to be distributed over larger surface area so there is a decrease in stress
Structural Changes
Changes in bone size and thickness: increase amount of bone
Material Changes
Important to consider, new bone first starts as collagen and first has different mechanical properties, can have areas that are stronger than other areas. Progression and will have different properties until calcification
Negative Effects of adaptation
Extremely intense or frequent exercise can cause micro damage in the bone and without rest can become micro fractures which lead to fractures. Rest is crucial for positive effects to bone
Bone Mass
influenced by age
Peak in late teens and early 20s
Rate of loss more rapid when exercise is stopped
Cardiovascular: swimming, biking not much load bearing on bones
Running: increase bone mass
Mechanotransduction
How a cell interprets mechanical cell/movement
Mechanocoupling usually through a sensor: such as stretch
Different cell types have different mechanosensors
Biomechanical coupling
on a cell membrane or in a cell: the receptor changing the signal it is receiving, stimulation of cell signaling pathways, release of paracrine or autocrine factors
Changes in gene and protein expression which changes function
Cell to Cell signaling
Not usually one cells that receiving the signaling, many cells working together to carry out the response
Hierarchal Tissue
Muscle fibers grouped together: surrounded by connective tissue
Vasculature
Blood supply
Myofibrils
Arranged in a way that they can contract
Multi nucleated
Support metabolism of that cell, many mitochondria
Muscles are arranged in
sarcomeres, stacked end on end, smallest unit of contraction, the shorter to allow contraction. Fibers slide along each other
Terminal of cisternae
T Tubule responsible for ca 2+ storage and release critical for contraction
sarcoplasmic reticulum
Criss-crosses inbetween myofibrils
Myosin
Thick filament
Actin
Thin filament
In resting state actin and myosin
overlap
In contracting state actin and myosin
they slide along each other, the length of actin and myosin filaments is constant
Head walks along myosin
Z line
Where sarcomeres attach end to end: it wouldn't shorten muscle if there were mitochondria in the sarcomere
Neuromuscular Junction Outline
Nerve impulse reaches end of motor nerve
Acetylcholine released, binds with receptors on motor end plate
Depolarization of sarcolemma
Initial Muscle Contraction steps
Neural signal is stimulated to contract by motor neurons, into motor end plate
As action potential reaches end of motor neuron acetylcholine is released and disperses across the synaptic cleft between neuron and muscle membrane and binds with receptors at the end plate
Depolarizes the sarcolemma which makes it permeable to sodium which reverses the polarization called the end plate potential
Depolarization also travels along the membrane and throughout the cell is the start of contraction
Excitation Contraction Coupling
Depolarization is the action potential
Travels across the muscle membrane and comes in the t tubules around the muscle fibrils : Ca2+ release from the sarcoplasmic reticulum calcium binds to troponin and sits on tropomyosin and is bound to the actin molecules
When calcium binds to troponin it causes it to changes shape which pulls troponin and actin and uncovers a myosin binding sit on actin
Myosin binds to actin and causes ATP to be hydrolyzed to ADP and it causes the binding arm to twist and shortens the whole thing
This process will continue as long as calcium is bound to troponin and ATP is present calcium is sequestered into the SR and causes tropomyosin to go back to the original shape and actin has no where to bind (active requires ATP)
Cross Bridge Cycle
ATP requirement to activate myosin and myosin detach, calcium pumps is an active process, runs out of ATP it stays contracted (rigor mortis)
Contractions are
repeated movements