Biomechanics Exam PDF

Muscle - Tissue Composition, Properties and Roles Muscles The engines of the musculoskeletal system Enable capacity for motion and provide stability (eg spine) Three types of muscle Skeletal muscle (40-45% of Smooth muscle Cardiac muscle total body weigh...

Muscle - Tissue Composition, Properties and Roles Muscles The engines of the musculoskeletal system Enable capacity for motion and provide stability (eg spine) Three types of muscle Skeletal muscle (40-45% of Smooth muscle Cardiac muscle total body weight) - Usually attached to - Surrounding vessels in - Heart bones (via tendons) gastrointestinal system - Involuntary - Voluntary control - Involuntary Muscle morphology and hierarchical structure - Basic structure is the muscle cell (myocyte) - Muscle fiber is full of multiple myofibrils - myofibrils contain sarcomeres arranged in series - Myofibrils contain: - Sarcomere - Overlapping structure of: - Actin filaments (thin) - diameter of 5-8 nm - Myosin filaments (thick) - diameter of 12-18 nm - Multiple nuclei - Many mitochondria (energy production) - Very long spindle shaped cells (longer than they are wide) - 10-100 um in diameter - Up to 30 cm long  - Muscle fibers = muscle cell Two types of muscle fibers based on energy production (ATP) Aerobic: ATP produced with O2 Anaerobic (glycolytic): ATP without O2 - Related to endurance - Related to fast contraction - Muscles able to hold for long duration - Rapidly fatigues - not able to hold load - Most predominant in postural (deep for extended time (those muscles muscles in your abdomen, pelvis, and involved in sprinting or lifting heavy back) weights) Types of fibers - based on myosin heavy chain composition 2A ⇒ fast twitch oxidative glycolytic 2B ⇒ fast twitch glycolytic 2X ⇒ type 2X (half way between 2A and 2B) - Most muscles are a spectrum of fiber types - Fiber can shift depending on muscle use (training) Muscle contraction - cross bridge theory (sliding filament) - Unactivated state: tropomyosin covers actin binding sites 1. Motor neuron potential ⇒ signals release of Ca2+ - Ca2+ binds to troponin on actin ⇒ causes tropomyosin to move off of actin - Therefore, opening up myosin binding sites - While this is happening, myosin heads (with bound ATP) bind to actin on the myosin binding sites 2. Step 2 a. ATP cleavage ⇒ Mg2+ causes cleavage of ATP ⇒ loss of PO43- ⇒ tipping of myosin head ⇒ pulls actin filament i. The ATP on the myosin head breaks down into a phosphate group and ADP through the help of magnesium ⇒ called cleavage of ATP b. ADP discarded ⇒ final tip of myosin head i. After the myosin head has tipped and pulled the actin, it gets rid of the ADP. The myosin head then finishes its movement, completing the pull on actin filament. 3. ATP binds to the myosin head to release myosin head from actin and cause relaxation 4. Myosin head relaxes and (provided there is still Ca2+ present) binds to next actin site Fun facts - Ca2+ released from longitudinal tubules of sarcoplasmic reticulum ⇒ gets rapidly sequestered - Single release ⇒ single twitch - Sustained release of Ca2+ causes tectonic muscle contraction - Role of troponin and tropomyosin is to expose actin-binding sites and therefore control myofibril contraction - Binding of Ca2+ to troponin moves the tropomyosin, exposing binding sites, and allowing myosin cross-bridges to bind to actin Myosin - Myosin acts like a “motor” that moves along another protein called actin to cause muscles to contract - It is a long thick protein with a head and a tail ⇒ head attaches to actin filaments - Heads work by being little “hands” that grab onto actin and pull it ⇒ therefore, they pull the actin filaments together which leads to shortening of the sarcomere and causes a contraction Twitch of a muscle fiber in response to a single action potential - Notice the latent period between the action potential and the mechanical contraction Characterization of muscle behaviour - Tests of isolated muscle bundles (fibers) - ex vivo Isotonic (constant tension) Isometric (constant length) - F(t) = constant - x(t) = constant - Measure displacement/length x(t) - Measure force generated during contraction F(t) Latent period is isometric and isotonic twitches - Isotonic twitches have a larger latent period because the muscle has to overcome a large applied force (load) - As the load increases, the latent period increases and the distance shortened decreases Repeated stimulus frequencies - As the stimulation frequencies increase, the twitch becomes larger - Muscle contraction is a succession of multiple action potentials - Subsequent potentials build on previous contractions - At sufficient frequency (>30 Hz) - Fused tetanus (tetanic contraction) normal physiological muscle contraction  - This is how muscles generally work in day to day life like when you’re holding something Muscle constitutive modeling - Vertical axis: isometric tetanic tension in an isolated frog skeletal muscle (expressed as a percentage of the maximum attainable tension) - Horizontal axis: measure of sarcomere length - Start looking at the graph from the right side Tension generated during muscle contraction depends on 3 main factors ⇒ length, velocity, and time - ON EXAM 1. Load-length relationship - Length ⇒ related to overlap of myosin heads of actin ⇒ causes an increase in binding which increases forces - A(1) ⇒ sarcomere is too long so there's no binding and therefore no force (3.65 um) - B-C(2) = optimal binding so all myosin heads are bound to actin ⇒ creates the greatest force (2-2.25 um) - Optimal length for force generation = 2.18 um - C-D(4-5) = excessive overlap ⇒ actin interference with opposing myosin ⇒ reduction in tension 2. Load-velocity - Tetanized muscle contracts faster at lower external loads - Hill model:  - (P + a)(V + b) = b(P0 + a) where P = external load, V = velocity of contraction, a, b, P0 = constants for a muscle - Load-velocity relationship for isotonic tetanized muscle under different loadings 3. Time a. Latency period: time from arrival of the action potential to the development of tension (or displacement) b. Viscoelastic response of the whole muscle which includes dense connective tissue i. Elastic and viscoelastic (damping) behaviour c. Graph shows the measured time course of muscle tension T(t) during an isometric twitch of a frog  - What does this picture represent? - Shows latency period Circulatory System Vascular distribution - Consists of heart and blood vessels - Vasculature includes: - Arteries - Arterioles - Capillaries - Venules - Veins Two pain pumping systems Pulmonary Systemic - Lungs - exchange of O2/CO2 - Supplies O2 and nutrients, does - Low pressure waste removal - High pressure - Big veins have a larger diameter than large arteries - Don’t have many of the big arteries/veins ⇒ have many of the small vasculature like capillaries and venules - Capillaries and venules have big surface areas ⇒ venules have a much bigger Primary functions of circulatory system 1. Enable mass transfer between blood and surrounding tissue ○ Performed at capillary level In tissues (systemic) and lungs (pulmonary) Enables a large surface area 2. Regulate distribution of blood in response to local metabolic demands Greatest resistance to flow occurs at the capillaries Arteriole flow can be regulated by smooth muscle cells Shunt blood away from regions where blood is in less demand (eg having cold feet in winter) 3. Maintain reservoir of blood in case of loss ○ Reservoir in veins (large volume) ~ 60% of total volume Aortic root with age The aortic root refers to the section of the aorta (the large artery that carries blood from the heart) that is closest to the heart. As you get older, your aortic root gets bigger due to a loss of elastin with age ○ With a lack of elastin, your aorta cannot expand and contract with each heartbeat so it expands to compensate for this loss of elasticity Pericytes regulating blood flow Pericytes (smooth muscle cells) can relax or contract to alter the caliber of the arteriole to regulate flow resistance and blood distribution to the distal capillary beds Heart - Basically two positive displacement pumps in series Two Systems - Pulmonary: right side = low pressure - Systemic: left side = high pressure Pump outputs volume and pressure (work) - Able to adapt the output in response to demand (rest vs exercise) - Does this in two ways: - Increase in frequency of pump contractions (heart rate) - Increase in pressure of output - Frank-Starling mechanism ⇒ increased stretch of the ventricular muscles due to increased incoming blood ⇒ greater contractile force Anatomy of the heart - Paired anatomical structures - Ventricles - pumping chambers - Atria - holding chambers - Valves - passive, pressure regulated - Between atria and ventricles - Atrioventricular (AV) values - Right tricuspid - Left bicuspid (mitral) - Secured from eversion by chordae tendineae - Aortic valve (LT ventricle and aorta) - Pulmonary valve (RT ventricle and pulmonary artery) Heart beating system Two main portions of the cardiac cycle Systole Diastole The period starting with AV valve Remainder of cardiac cycle closing and ending with aortic valve closing Stages in detail Stage 1: Ventricular filling Latter stage of diastole AV valves open - atria empty into ventricles Atrial contraction Volume increases Stage 2: Isovolumetric First part of systole contraction All valves closed Ventricular muscles contract against constant blood volume Volume constant Pressure increases Stage 3: Ventricular ejection Second part of systole Aortic/pulmonary valves open Blood is pushed out of ventricles Volume decreases Pressure peaks and then decreases Stage 4: Isovolumetric First part of diastole relaxation All valves closed Ventricle muscle fibers relax with no change in volume Volume constant Pressure decreases The heart - the work diagram Plot of left ventricular volume (mL) on the x axis and left ventricular pressure (mmHg) Key Points Created for the left ventricle (high pressure) Cyclic stages of the heart: systole & diastole Two key points: ○ EDV: end diastolic volume ⇒ mitral valve closes ○ ESV: end systolic volume ⇒ aortic valve closes EDPVR (end diastolic pressure-volume relationship) ○ ↑ volume from atrium ○ Limited by passive elastic properties of left ventricle muscle ESPVR (end systolic)  ○ Function of “afterload” on heart ⇒ systemic blood pressure ○ ↑ pressure of aortic valve closing due to arterial back pressure Two possible issues Arterial pulse propagation Thin solid line = local arterial pressure Heavy line = pressure in the sphygmomanometer cuff A = systolic pressure when artery is just opening (ticking noise) B = diastolic pressure (no noise) Pressures generated by the heart propagate through arterial vessels Blood pressure determined by maximal (systolic) and minimal (diastolic) pressure Blood pressure = systolic pressure / diastolic pressure Windkessel model The heart = variable current source Distensible arteries = compliant chamber Peripheral vessels = resistor Finish later Arterial wall structure and elasticity Three layers Layer 1: Tunica intima ○ Inner layer ○ Endothelial cell - barrier between blood and artery wall ○ Basal lamina - type IV collagen, fibronectin, laminin Layer 2: Tunica media ○ Middle layer ○ Smooth muscle cells ○ Elastin, type I, III, IV collagen, proteoglycans ○ Determines mechanical properties & behaviours of the vessel ○ Proximal to the heart (aorta) = ↑ elastin, ↓ smooth muscle ○ Distal to the heart = ↑ smooth muscle, ↓ elastic Layer 3: Tunica adventitia ○ Outer layer ○ Fibroblast ○ Type I collagen, elastin, nerve fibres ○ Forms attachment between blood vessel and surrounding tissue Arterial wall mechanics For normotensive, the fully relaxed VSM is the same as the normal VSM For hypertensive, the fully relaxed VSM has a higher radius than the normal VSM Pulse propagation through arteries Arterial flow ○ Effect of elastic waves (arterial distension) due to oscillatory pressure from the heart (on the blood) ⇒ vessel expanding from high pressure creates pulse ○ Wrist (radial pulse)/carotid artery pulse is caused by distal pressure wave ○ Oscillatory flow superimposed on mean (net forward) flow Increase in vessel stiffness ⇒ decreased distensibility ○ Decreased change in radius (less vessel expansion) ○ Increased velocity of wave propagation downstream (not the same as fluid velocity) ⇒ high blood pressure Characteristics that affect blood flow 1. Viscous losses a. High fluid viscosity ⇒ higher resistance to flow ⇒ lower pulse pressure b. Lower arterial wall viscoelasticity ⇒ viscoelasticity allows arteries to absorb and dissipate energy from the pressure pulse to smooth blood flow and maintain pressure ⇒ when viscoelasticity is reduced, it leads to diminished buffering of the pressure pulse and makes it harder for blood to flow c. Effects: Dissipates energy, diminishes pressure pulse, impedes fluid motion 2. Variation of arterial properties a. Arteries increase in stiffness and decrease in diameter distally from the heart (change in content of tunica media) b. Pulse speed should increase as you move distally from the heart 3. Effects of branching and tapering a. Curvature and branching of arteries - pulse wave velocity and area in distal arteries will be different than in proximal artery - difference impedance i. Pulse wave velocity increases as your move away from the heart because distal arteries are smaller and stiffer b. Difference impedance to pressure pulse causes reflection of some of the incident pulse  i. At points of branching or changes in vessel diameter, there's a mismatch in impedance (resistance to pressure wave transmission) ⇒ causes partial reflection of the pressure wave back to the heart ii. Reflected waves add to the incident wave, increasing pressure in certain regions (especially distal arteries) ⇒ explains why systolic pressure can be higher in peripheral arteries than in central arteries c. Increased pressure in more distal vessels but loss of energy due to loss of velocity i. Some pressure energy is converted into heat due to viscous losses and friction. ii. The velocity of the blood decreases due to increased resistance and branching, dissipating energy and reducing wave amplitude. iii. This energy dissipation results in damping of the pressure pulse by the time blood reaches the capillaries, ensuring smoother and continuous blood flow at the microvascular level. d. Pressure energy is damped out in capillaries i. By the time the pressure wave reaches the capillaries, most of the pulsatile energy has been absorbed or dissipated ⇒ ensures capillaries experience a much steadier flow which is important for neutral and gas exchange e. Overall i. Impedance mismatches cause partial reflection of the pressure pulse, which contributes to increased pressure in distal arteries. ii. Energy and velocity are progressively lost as the pulse wave travels through the vascular tree, leading to damped pressure in the capillaries, facilitating efficient exchange.