Physiology - Soft Tissue Flashcards
What does the PNS consists of
All axons and ganglia outside CNS
Autonomic and somatic system
Cranial nerves (except II)
Divisions of autonomic nervsous system
Parasympathetic
Sympathetic
Motor nerves in somatic nervous system
Efferent
Afferent
Effernet motor nerves
Run from CNS to periphery
Afferent. motor nerves
Run from periphery to CNS
Motor unit
Motor nerve axon
All the muscle fibres it innervates
What determines the size of motor unit recruited
Type of task and force
Te reusing potential of the cell membrane
BIG differences between the electrical potential inside the cell compared to the outside (-70 to -90 mv)
Big differences between intracellular and extracellular ionic conc. Na is low inside and high outside and K is high inside and low conc
Sodium ATPase pump
Na-K ATPase pump moves 2K+ molecules into the cell in exchange for 3Na+ molecules moved out
Maintains conc gradient of Na and K
Small direct effect on membrane potential
Initiation of AP
Sensory receptors transducer energy to change potential of axon
Threshold is reached and VgNa channels open, starting the ap
Steps of the action potential
Depolarisation
Repolarisation
Hyperpolarisation
Depolarisation
The inside of the cell becomes less negative with respect to the outside. VgNa channels are open (Na+ moves in) and VgK channels are closed.
Repolarisation
The cell is trying to restore balance and bring the potential difference of the cell more -ve than the outside. VgNa channels are closed and VgK channels open (K+ moves down the electrochemical gradient)
Hyperpolarisation
The eflux of K+ causes the inside of the axon to become TOO negative so the resting potential is restored using the Na-K ATPase pump
Refractory period
The duration before another AP can be generated, regardless of stimuli
Propagation of AP
Slight excess of +ve charge inside the axon hillock and excess of -ve charge outside so a potential difference builds up between the diff regions of the axon. This causes local circuit currents, opening VgNa channels so the action potential can advance
Increasing nerve conduction velocity
Larger diameter
Insulation
What is muscle
Bundle of fibres that can contract to produce movement; this can be voluntary or involuntary
Types of muscle
Striated (skeletal) muscle – locomotion and posture
Smooth muscle – peristalsis
Cardiac muscle – heart contraction
Contraction
Shortening
Elasticity
Returning to resting state
Hypertrophy
Increase in size
Hyperplasia
Increase in number (usually muscle cells)
Structure of skeletal muscle
Tendon attaches to bone
Epimysium – muscle
Perimysium – fascicle
Endomysium – fibre
What are muscle fibres filled with
Myofibrils
Sarcolemma
Plasma membrane of muscle fibre
Sarcoplasm
Cytoplasm inside muscle fibre
Sarcolasmic reticulum
Smooth endoplasmic reticulum acts as a storage organelle for Ca2+
Transverse tubular system (TT)
Invaginations of sarcolemma
Triad
Terminal cisternae of 2 SR and TT in close proximity
Sarcomere
Unit of contraction of the myofibril
Z line
Either ends of the sarcomere; thin filaments insertion
M line
Origin of thick filaments, middle of sarcomere
A band
Overlap of thick and thin filaments
I band
Only thin filaments
What does the myosin head bind to and what features allow this
Actin
2 alkali light chains help stabilise myosin head
Hinge region allows movement of myosin head
What is the myosin tail formed of
2 intertwined heavy chains
What allows ATPase activity on myosin
2 regulatory light chains
Actin
Binding site for myosin
Thin filaments
What does tropmyosin do
Block myosin receptors
What does troponin do
Control tropomyosin position
What happens to the sarcomere during contraction
All bands and H-zone gets smaller
Excitation-contraction coupling
AP motor nerve end plate propagates along membrane and down TT
Opens Vg L-type Ca2+ channels on TT
Coupling between DHP receptor and Ca2+ release channels, releases the Ca2+ from the SR
Ca2+ released into myofibril activating troponin C and cross-bridge cycling
Initiation of cross-bridge cycling
Tropomyosin blocks myosin binding site
When Ca2+ binds to the high affinity sites on troponin C a conformational change takes place in the troponin complex
Troponin I moves away from the actin filament
Troponin T pushes tropomyosin away from myosin binding site on actin
Myosin head binds to actin
How does calcium modulate contraction
Through regulatory proteins rather than direct interaction w/ actin and myosin
Types of troponin
C: binds Ca2+
I: anchors complex to actin
T: binds to tropomyosin
Cross-bridge cycle in skeletal muscle
Initially myosin head attached to actin filament after ‘power stroke’ from previous cycle – can remain in this state for indefinitely longer period, as occurs in rigor mortis Step 1 – ATP binding Step 2 – ATP hydrolysis Step 3 – cross-bridge formation Step 4 – release of Pi from myosin Step 5 - ADP release
Terminating muscle contraction
Ca must be removed from cytoplasm
Na-Ca exchanger
Ca pump at plasma membrane
Ca reuptake into SR and binds to calsequestrin
How can muscle force be determined
By no. individual muscle fibres stimulated at a given time
What does amount of muscle force generated depend on
No. active muscle fibres Cross-sectional area of muscle Initial resting length of muscle Rate at which muscle shortens Frequency of stimulation
Isometric contraction
Muscle length fixed, stimulation of muscle will cause increase in tension but no shortening
Analogy for isometric contraction
Similar to holding a weight in your hand w/ your arm outstretched, you will feel that the muscle is working w/out changing length
Isotonic contraction
Muscle length not fixed
Stimulation of muscle will cause muscle shortening provided tension generated is stronger than opposing load
Analogy for isotonic contraction
Similar to holding a weight in your hand and lifting and lowering your hand, bending at the elbow
Passive tension
Tension measured before muscle contraction
Length tension rship
At any fixed length if muscle is contracted an addn. active tension develops due to cross-bridge formation
Length-tension relationship is direct result of the anatomy of the thick and thin filaments overlapping within individual sarcomeres
Force-length rship
As velocity increases, force decreases
At maximum power is generated at approx. 1/3 shortening velocity
Summation in single muscle fibres
One AP will lead to single skeletal muscle twitch
As muscle twitch far exceeds duration of AP it is possible to generate a 2nd AP before 1st contraction has subsided
Tetanus state
Twitches – AP generated faster than muscles can react
Types of muscle fibres
Red
White
Intermediate
Red muscle fibres
Slow twitch and fast twitch, requires oxygen and glycogen
White muscle fibres
Fast twitch, glycogen is main energy store, gets fatigued quickly
Fast twitch (2b) muscle fibres
Fatiguable
White
Glycolytic metabolism
High levels of glycogen
Slow twitch muscle fibres
Resistant to fatigue
Red (myoglobin)
Oxidative metabolism
Low levels of glycogen
What determines strength of skeletal muscle
Size
What is the cross sectional area of muscle fibres proportional to
The strength that can be generated
What are long muscle fibres good for
Rapid movement
What are shirt muscle fibres good for
Large forces
Fast twitch (2a) muscle fibres
Red
Either endurance or rapid force
Quickly fatigue
Concentric isotonic contraction
Length of muscle changes in direction of contraction
Eccentric isotonic contraction
Length of muscle changes opposite to direction of contraction
Effects of endurance exercise training
Increased mitochondrial function –> increased O2
Hypoxia inducible factors (HIFs) involved in gene control of red muscle cell production and regulation of glycolytic enzymes
Increased [Hb]
Individual variation in proportion of diff fibre types
Training does not significantly change proportions of fibre types
Athletes find the sport that fits their abilities
Respiratory substrates in intense short-term exercise - 10-15s
Creatine phosphate
Respiratory substrates in intense short-term exercise -up to 2 mins
Glycogen to glucose-6-phiosphate
Respiration inintense short-term exercise - several min
Lactic acid build up
Oxygen debt
About 2L of oxygen required to replenish ATP and creatine phosphate
Respiration in longer, less intense exercise
Glycogen from circulation
Glucose from plasma
Hepatic glucose production increases
What happens when hepatic glucose increases
Short term glycogenesis
Longer term gluconeogenesis – muscle proteolysis, glucagon and insulin, fatty acid release
VO2 max
Oxygen usage under maximal aerobic activity
EPOC
Excess post exercise oxygen consumption
Fast component of recovery phase
Resting levels of ATP and CP restored
Slow component of recovery phase
Lactic acid converted to glucose in liver
Lactic acid converted to pyruvic acid
How is the increased oxygen demand met during exercise
Increase in ventilation rate
Increase in tidal volume
Tidal volume
Volume of air displaced during respiration
Changes in blood gases during exercise
Arterial O2 and venous CO2 do not change significantly during exercise
Respiratory system can provide adequate aeration
Oxygen consumption during exercise
Oxygen consumption increases
Similar rate for first few seconds reaches steady state where lactate acid accumulation is minimal
Other factors like fuel availability limit exercise
VO2max when steady state oxygen consumption doesn’t increase w/ work intensity
Changes in alveolar diffusion during exercise
Oxygen and carbon dioxide diffusion capacity increases w/ exercise
Related to increase in perfusion more than ventilation
Redistibutrion of blood flow during exercise
As exercise continues, blood flow to the muscles increase substantially
Cardiac changes in exercise
Increased cardiac output by increased stroke volume and increased heart rate
Stroke volume
How much blood pumped out with each cycle
Control of cardiac output
Increase in activity of sympathetic nerves –> increases stroke volume, ventricular myocardium
decrease ion parasympathetic nerves –> increases hr, SA node
These both increase cardiac output
Control of stroke volume
Decreased venous return –> increases end-diastolic volume
Increased sympathetic activity/ epinephrine –> increases contractibility of ventricle
Arterial pressure also decrease
These increase stake volume
What does change in central venous pressure change
Diastolic filling pressure, more blood available to fill heart
What does total peripheral resistance change
Ability to expel blood into arterial system
Starlings Law
The fuller the heart is, the harder it will contract increasing the stroke volume (ventricular performance)
Benefits of exercise and reducing cardiovascular disease risk
Reduced blood pressure
Increased circulating HDL and reduced Triglycerides
Changes in arterial wall homeostasis reducing atherosclerotic disease
Improved aortic valve function and reduction in calcification
Increased ventricular chamber wall thickness
Increased red cells (to a point)
Changes in cardiac vasculature to increase oxygen availability
Exercise and depression
Moderate clinical effect in a decline in depression
Long term follow up on mood found in favor of exercise
No more effective than psychological or pharmacological treatments
Important for those who do not want pharmacological treatment
