KINE 1020 Winter Term Exam Notes.docx

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Chapter 17-Muscular Structure and Function 3 Main types of muscles Cardiac muscle • The muscle within the heart • Striated-aligned structures • Electrically coupled cells –if one is activated, the next one is also activated • Involuntary-controlled by theAutonomic Nervous System Smooth muscle • No striated muscle • Responsible for blood vessel tone (vasoconstriction or vasodilation) • Involuntary • Muscle surrounds the blood vessels and controls blood vessel size • Lines intestines, stomach Skeletal muscle • Striated – aligned structures • Not electrically coupled and voluntary • Helps in locomotion, with posture, and heat production in cold stress • 600 skeletal muscles Skeletal Muscle Structure − Muscle – composed of a number of fasciculi − Fascicle – bundle of muscle cells − Muscle cell – elongated structure unlike other cells − Myofibril – contractile unit, also the cause of striation in muscles, responsible for force and speed is generated by muscle Sarcomere • Located within myofibrils • Responsible for the action produced by a muscle • The different regions are categorized by the amount of protein found in the various regions of the sarcomere • Aband: more protein thus appears darker in the muscles, composed of actin • I band: fewer proteins thus appears lighter • H band: composed of myosin Muscle Proteins Actin • Composed of globular proteins that binds together to form microfilaments • Two F-actin(filamentous) wind together into a double helix, together with troponin and tropomyosin to form the thin filament • Actin is a structural protein that acts like scaffolding Tropomyosin • Long, double-stranded protein that weaves around the F-actin in a double helical arrangement • During rest: the tropomyosin blocks the active sites on actin so myosin cannot bind Troponin • Aglobular protein made up of 3 sub-units(Troponin C, I & T) • Troponin-T binds the troponin to the tropomyosin • During contraction: the calcium will bind to troponin-C and cause it to change shape and removes the tropomyosin exposing the active binding sites on actin • Troponin-I inhibits this process during resting state Myosin • Has 2 globular head regions and a rod-like tail region • Myosin form the thick filament with the tail regions coming together in a thick rod like structure with the heads extending outwards • Each head has two reactive sites: one for binding to actin and the other to bind toATP Intermediate proteins Titan − One of the largest proteins located from Z-line to M-line − 1 titan protein extends half the length of a sarcomere thus providing a scaffolding structure for the sarcomere − This allows for the force transmission at the Z-line and contributes to the passive stiffness of muscle Desmin − Acts as a scaffolding anchoring the Z-line to the Z-line of the next later sarcomere. − Titan provides support lengthwise and desmin is more like the cord that binds all the sarcomere chains (myofibrils) together via Z-lines C-protein − Located in the middle of theA-band − Binds myosin tail region − Maintains thick filaments of myosin Sarcoplasmic Reticulum • Site of storage for calcium • T-tubule interacts with the exterior of the cell, to regulate calcium levels in the cell • Nerve impulse (action potential) sends signal entering through T-tubule thus releasing calcium • After the movement (during rest) calcium is taken up again into the reticulum Muscle Contractions http://www.youtube.com/watch?v=BMT4PtXRCVA Muscle Fibre ContractileActivity 1. Nerve stimulation is followed by action potential called the latent period (takes 1-2 msec). During this time there is no muscle contraction or force production 2. The contraction begins. There is a gradual increase in the force/tension until the force reaches the climax. Referred to as contraction time (lasts 40-120 msec) 3. After the climax the muscle force/tension returns to rest called relaxation time(lasts 50-200 msec) Motor Unit Recruitment • Composed of a motor nerve that innervates a particular # of muscle cells or muscle fibres • When activated, all muscle fibres in a motor unit are activated • The more motor units activated, the stronger the contraction Motor Unit Type: Fast Fatiguing vs. Fatigue Resistant Type I Slow Twitch − Slow contracting − Fatigue resistant − Maintains posture − Produce less force but can sustain the force production for a very long time Type IIa Fast Twitch: Fatigue Resistant − Fast contracting − Moderate resistance to fatigue − Produce more force than slow twitch but cannot sustain the force production for as long before fatiguing − Used for non-exertive movement (walking) Type IIx Fast Twitch: Fast Fatiguing − Fastest contracting − Produce much more force than Type IIa but are more easily fatigued than Type IIa − Used for powerful movements with quick bursts of energy (sprinting, jumping) Frequency Summation • Staircase effect: summation of first stimulus and second stimulus (2 action potential) Fibre length − Ensures sarcomere length is within optimal length, for optimal actin and myosin interactions Force transmission – Series Elastic Components • Contractile Component:A-M cross bridges • Parallel Elastic Component: Intermediate filament inside myofibrils • Series Elastic Component: ligaments and tendons which may increase or decrease tension in muscle Characterizing Muscle Contractions Work − Force multiplied by the distance. No movement means no work done − Work (kg x m) = force (kg) x distance (m) Power − How quickly the work is done, work done in less time is said to be more powerful, alternatively, more work over the same period of time is also said to be more powerful − Power can be expressed as kg x m/s or watts which is equal to 1 joule/sec − Power (kg x m/s) Work (kg x m) + time (sec) Types of Muscle Contractions Static or Isometric • Contractions wherein force is generated but there is no movement or shortening of the muscle Dynamic • Contractions that result in movements that are subdivided into two categories: concentric(shortening) & eccentric (lengthening) Chapter 18 – Energy Metabolism and Bioenergetics  This is the flow of energy in a biological system resulting in the ability to do work, produce heat etc.  Body chemical energy is converted to thermal (heat) and mechanical energy (work) through chemical reactions 2 Main Types of chemical reactions Exergonic reactions − Energy releasing reactions ( free energy – negative delta G) G refers to the net energy in the system, so releasing energy will result in an overall reduction in the net energy left in the system − i.e., breaking downATP or Glycolysis Endergonic reactions − energy consuming reaction ( free energy – positive delta G) − i.e., producingATP Enzyme Catalyzed Reactions Catabolic − breakdown of larger molecules into smaller molecules − i.e., breakingATP intoADP+Pi Anabolic − Synthesis of larger molecules from smaller molecules − i.e., producingATP fromADP and Pi Chapter 19 – Energy Systems  Biological energy systems 3 main types: phosphagen system, glycolysis, and oxidative phosphorylation  All produceATP but at different capacities i.e., how much and how fast ATP was created Adenosine TriPhosphate (ATP) • Tissues need energy to be converted toATP in order for it to be used by biological tissues to produce work • Metabolic pathways convert food intoATP • Each molecule ofATP releases 7.3 kcal/mol of energy each. Considered an intermediate level energy substrate • During muscle contractions, myosin ATPase hydrolyzes ATP so that energy is released as mechanical movement (~25%) and heat (~75%) • ATP levels in biological tissues such as muscle star relatively constant, and even during fatiguing intense exercise ATP levels remain within 10-15% of baseline levels • You cannot get more ATP with enhancements and the ATP you have during muscle contraction must be restored at the same rate otherwise work rate will decrease • Aerobic processes require oxygen & anaerobic processes do not require oxygen • Metabolic pathways convert food intoATP ATP-Phosphocreatine (PCr) − The muscle uses ATP immediately present in the muscle but only lasts 2-3 seconds − The ATP-PCr can reform ATP from PCr and ADP very rapidly. Does not require oxygen and doesn’t produce lactic acid but supplies 6-8 seconds of energy − Used for activities less than 10 seconds with lots of energy − Occurs in the sarcoplasm allowing the recharge of ATP − ATP+Cr ----- creatine kinase ----- ADP+PCr+H+ ( bi-directional equation meaning it can do right or left depending on the concentrations of substrates available) − During muscle contraction, there is an increase in the concentration of DP and hydrogen ions and a decrease in the ATP thus if PCr is available, the equation above will be driven from right to left to restore ATP levels to equilibrium − Alternatively, when PCr levels are low, two ADP molecules can form ATP and AMP. However this reaction does not use up the excess hydrogen ions created from the breakdown ofATP which is still problematic for fatigue − 2 ADP -----adenylate kinase or myokinase -----ATP+AMP Glycolysis • Anaerobic energy source that can provide energy for a longer period of time thanATP-PCr but at a slower rate • Together the ATP-PCr & glycolysis provide the most (~60%) of energy for activities less than 2 minutes of all-out activity • Glycolysis converts glucose-6-phosphate into 2 molecules of pyruvate and a net of 2ATP • Occurs in the sarcoplasm and the rate of glycolysis is limited by the activity of phosphofructokinase (PFK) converting Fructose-6-phosphate to Fructose-1, 6-biphosphate. • Higher PFK activity allows for increase rate of glycolysis & lower PFK slows the rate of glycolysis • AMP and ADP are important controllers of PFK activity, thus high AMP or ADP increases PFK activity to increaseATP production Anaerobic Glycolysis − The conversion of muscle glycogen to G6P is catalyzed by glycogen phosphorylase − The conversion of pyruvate to muscle lactate is catalyzed by lactate dehydrogenase − The capacity for anaerobic glycolysis to produce energy is related to the amount of muscle glycogen available − Glycogen loading can help to increase the capacity for anaerobic glycolysis − The amount of lactate that is produced and accumulates in the muscle is a major factor − Anaerobic glycolysis can only continue if there is sufficient NAD to form NADH (the final factor is the NAD/NADH ratio) Aerobic Glycolysis • Blood glucose is used to produce G6P catalyzed by hexokinase • Blood glucose is a source substrate and not limited like muscle glycogen • Blood glucose is replenished more easily and faster than muscle glucose from the liver or with dietary intake • Calcium and insulin are factors that help blood glucose to enter aerobic glycolysis • The pyruvate enters the mitochondria and is converted to acetyl-CoA entering the Krebs Cycle and the oxidative system • If acetyl-CoA accumulates there will be a negative feedback of glycolysis which limits the potential for aerobic glycolysis • Oxygen amount in mitochondria is important for acetyl-CoAto continue down the metabolic pathway • In aerobic glycolysis, NADH is converted to NAD and so insufficient NADH can also limit entry of pyruvate into mitochondria LacticAcid System − When your body needs more energy, glycolysis can create pyruvate faster than aerobic metabolism can use it − The accumulation of pyruvate will inhibit glycolysis and slow the rate of ATP production − The lactic acid system can temporarily reduce the pyruvate accumulation by converting some of the pyruvate to lactate which then can become lactic acid catalyzed by lactate dehydrogenase (LDH) − The accumulation of lactate will inhibit the LDH and the accumulation of lactic acid decreases the pH, eventually the accumulation will denature enzymes and inhibit or slow metabolism − Lactate can be transported to the liver and converted to glucose Oxidative (Aerobic) Phosphorylation System • Provides nearly all the energy required in long term exercise (greater than 120 min) • Provides energy at only 25% of the rate of theATP-PCr system • Uses oxygen to fully break down the glucose molecule into CO2, H2O & energy • 38 ATP for 1 glucose formed in oxidative metabolism • Oxidative metabolism is very important for energy production and normal functioning • After glycolysis, the pyruvate enter the mitochondria and is converted into acetyl-CoA which then enters the Krebs Cycle (also known as citric acid or tricarboxylic acid cycle) • Acetyl-CoAcan also be made not only from carbohydrates but also from fat and protein • In the Krebs Cycle: acetyl-CoA is broken down into ATP, CO2 (removed as waste), and NADH (enter oxidative metabolism) • The electron transport chain (ETC) is a complex series of chemical reactions where hydrogen ions from NADH & FADH2 combine with oxygen to form H2O • The rate limiting step for ETC is cytochrome C which occurs in the wall of the mitochondria and this process generates 38ATP per 1 molecule of glucose • The rate of aerobic metabolism at the mitochondrial level is dictated by the concentration of acetyl-CoA and oxygen • At the muscle level, aerobic metabolism is relates to the muscle fibre type (percent slow twitch), the volume of mitochondria and blood flow to the muscle Contribution of the Energy Systems Energy Systems Mole ofATP/min Time to fatigue Immediate: ATP-PCr (ATP & 4 5 to 10 sec phosphocreatine) Short Term: Glycolytic (Glycogen – 2.5 1 to 2 min LacticAcid) Long Term: Oxidative 1 Unlimited time Chapter 20 – Musculoskeletal Health and Fitness Low Back Pain • The leading cause of work absenteeism 6.3-15.4% of individuals experience low back pain at some time in their life, with the risk of increasing with age • 1/3 of low back pain people will have recurrent back pain • Range of severity from muscle ache to disability • Causes include fracture due to compressive loads or osteoporosis, bulging disc or herniation, pinched nerves, muscle sprains, arthritis, inflammation or spondylolishthesis (forward movement of a vertebrae relative to the one below) • Difficult to determine because it is not visible in medical images • Related to muscle flexibility and strength, abdominal obesity or low back strain or injury • Decrease the chance by proper lifting techniques and limit the twisting or torsion Occupation Related MSK Disorders − Injuries lead to impaired work performance and disability − Involves the upper extremity – impact can involve the hand and/or foot − Common types of occupation-related MSK include carpal tunnel syndrome, back pain, hernia, tendonitis or any joint pain Osteoarthritis • 2 main forms of arthritis: rheumatoid & osteoarthritis (most common) • Osteoarthritis results from the wearing down of the protective cartilage on the ends of the bones (knee and hip are most prevalent • Symptoms: stiffness & pain in the joints that is worse after exercise, swelling, or cracking or grating sounds when moving the joint (crepitation) • Medications: corticosteroids injected into the joint to reduce pain and swelling, pain medication, anti- inflammatory drugs and glucosamine and chondroitin sulfate for stimulating cartilage growth Osteoporosis − Condition characterized by lower bone mineral density − Within the bone there is a porous matrix that gives strength to the bone, with age there is a thinning of the matrix, making the bones more porous and weak − Osteopaenia: borderline osteoporosis − Condition related to obesity, dietary and physical factors, as high as 70% in adults over 80yrs old − Common symptoms: pain in the bones and/or lower back, height loss, night cramps in legs and feet, dowager’s hump and fractures − Associated with diets lacking in calcium or vitamin D, hormone imbalance, physical inactivity, or other endocrine or nutritional disorders − Osteoclasts are specialized cells that eat away at the bone and osteoblasts re-fill; the cavities with new bone; however if the breakdown in bone exceeds the re-formation there is a net loss overtime − The balance of osteoclast and osteoblast can be influenced by hormones: estrogen and parathyroid (is the target for some osteoporosis medications) − Bones also have sensors that detect stress on the bone that results from muscle contraction or impact, this triggers increased activity of the osteoblasts to build the bones stronger Musculoskeletal (MSK) Disorders • MSK Disorders are grouped into 3 main categories: 1. Fatigue – these are transient and reversible functional and structural changes meaning that the changes are temporary and that the individual can recover function to ‘normal’quickly within minutes to hours 2. Functional limitations – injury or damage that impairs movement or activity which generally take days to years to recover from 3. Chronic disability – these injuries will be ongoing, and may contribute to further MSK disorders Skeletal Muscle Fatigue – MSK Disorder − The muscle fatigue is reversible, meaning that the muscle performance recovers with rest, but may require several days to return to normal − The return to ‘normal’ maximal fore production is quicker with electrical stimulation that with self-controlled contraction − This suggests that fatigue and the recovery to normal may be related to several different types of factors that are both central (CNS) & peripheral (peripheral nervous system or skeletal muscle) limitations Sites of Central Fatigue • The components that may be related with fatigue include: the planning of involuntary movement (includes motivation), motor cortex and supraspinal outputs (includes coordinated afferent and efferent signals), upper motor neurons and lower motor neurons Sites of Peripheral Fatigue − The components that may be related with fatigue are the peripheral nervous system and skeletal muscle fibre Neuromuscular Junction − There is very little evidence that electrical transmission at the neuromuscular junction may be responsible for fatigue nor that the acetyl-CoArelease or uptake (neuromuscular blockage) is a problem Calcium Overload Hypothesis • This theory suggest that there are disturbances in calcium transport, impaired excitation of the contraction coupling, reduced calcium sensitivity of the myofibril processes and activation of calcium degradative processes • It is demonstrated that the components involved in calcium transmission (sarcolemma, t-tubule and sarcoplasmic reticulum) are impacted with fatigue • Fatigue is also associated with a drop in strength or size of the action potential that may result in insufficient signal to activate the calcium ion channels; this is typically the last calcium regulation change that is seen with fatigue • Further, when calcium is released, there tends to be an incomplete release meaning that there will be increased calcium remaining in the sarcoplasmic reticulum resulting in decreased force generation (associated with high frequency fatigue – highly repetitive activities) Metabolic System Limitations − Fatigue can also be associated with low substrate availability or metabolite accumulation, resulting in altered ATP homeostasis meaning there is a shift in fuels used and the products that result from metabolism that ultimately contribute to fatigue − Similarly, anaerobic glycolysis can be limited when there are reduced glycogen concentrations, this is why increasing glycogen levels with training or carbohydrate loading can delay fatigue − Increased hydrogen ions from the anaerobic systems (breaking down of ATP with muscle contraction and lactic acid production) can lower pH and contribute to fatigue through the inhibition of ATP breakdown from anaerobic glycolysis − Accumulation of lactate will inhibit glycolysis and is why the ability to clear lactate from the muscle is important for recovery, and performance in interval type activities (i.e., hockey shifts, or fartlek training) − There are also by products from aerobic metabolism that contribute to fatigue, specifically the accumulation of reactive oxygen species (ROS – are highly reactive molecules due its unpaired electron, and can damage membrane structures, proteins or enzymes and will decrease the stability of the mitochondria to produce energy) from the electron transport chain can impair ATP production − In the electron transport chain, oxygen is generally used to form water, however, some of the oxygen does not follow the proper metabolic pathway and can become superoxide instead − This will contribute to additional ROS production and further damage Actin-myosin interaction • During exercise, there is a reduction inATP and a build-up of inorganic phosphate (Pi), this delays the detachment phase of the actin-myosin cross-bridges and can contribute to fatigue • Further, the increased hydrogen ions resulting from the breakdown of ATP during muscle contraction will decrease pH (more acidic) • In the muscle, the majority of lactate-lactic acid is in the form of lactate, increased acidity will decrease myosin ATPase activity • As myosin ATPase hydrolyzed (breakdown) ATP and allows for the breaking of the actin-myosin cross-bridges, the lower pH can also contribute to fatigue • Lower pH can also result in decreased sensitivity of troponin to calcium as the hydrogen ions hide the binding sites, thus making it more difficult for troponin to move tropomyosin revealing the binding site on actin for myosin to attach • FinallyADP accumulation also decreases the myosinATPase activity and may also contribute to muscle fatigue Skeletal Muscle Protein Breakdown − With physical activity, there is also structural damage that is reflected by increased skeletal muscle protein breakdown and its release in the blood − The amount and the time course of protein breakdown and release is dependent on the task that is done meaning that the peak protein breakdown, when the peak breakdown occurs and the time to recover will be influenced by the type of exercise done Functioning Limitation – MSK Disorders • Functional limitations are described as the sensation of discomfort or pain in skeletal muscle that occurs following unaccustomed movement, activity or exercise • Functional limitation can also be accompanied by myalgia (pain), muscle weakness or swelling, experience of ‘doughy’or soft feeling in muscles, edema (swelling), discoloration, nausea and/or fever Non-traumatic Causes − Include increased muscle exertion or use, heat cramps, convulsions, inflammation, drugs, toxins, and genetic conditions Traumatic Causes − Include crash injuries, electric shock, pressure necrosis(cell damage=death), arterial occlusion and surgery Stages of Functional Limitations 1. Initial Stage: the initial incident leading to the functional limitation (i.e., activity or injury). The muscle tissue (tendon or ligament) disruption and loss in function is not reversible in 24-48hrs. This stage is characterized by many of the factors seen with muscle fatigue such as lower ATP concentrations, increased calcium concentration and increased ROS 2. Autogenesis Stage: this stage occurs 36-60hrs after the initial incident. There is increased protein breakdown and degradation that does not return to normal. Neutrophils accumulate in the muscle to the site of damage, this is turn leads to monocyte and macrophage accumulation that break down tissues. This stage is characterized by swelling, decreased blood flow and pain 3. Phagocytosis Stage: this stage lasts 36-72hrs post trauma. This stage still has pain/pressure, and there is still some muscle degradation that can occur with continued macrophage activity. Increased cytokine activity direct the early clean-up of the damaged or altered proteins in muscle 4. Regeneration Stage: this stage lasts 4-10 days post trauma. With the decline in muscle breakdown, there is an increase in growth factors and increased protein synthesis and satellite cell proliferation. There is a differential expression of skeletal muscle proteins that is dependent upon the stimulus or demand that may result in muscle hypertrophy or increased skeletal muscle aerobic capacity Example of Functional Limitation Disorders - Fibromyalgia • Condition in which a person has long-term, body-wide pain and tenderness in the joints, muscles, tendons and other soft tissues • Linked to skeletal muscle fatigue but is not a WHO class of MSK disorder, also associated with sleep problems, headaches, depression and anxiety • More common in women, and the causes are unknown, but are speculated to be related to physical or emotional trauma, increased pain sensitivity, sleep disturbances, or infection • Treatments include: exercise, physical therapy, stress/relaxation techniques, symptom relieving meds and cognitive behavioral therapy Chronic Restrictive MSK Disorders − Chronic restrictive MSK conditions are injuries leading to chronic disability, degeneration and ongoing loss of muscle or muscle diseases Causes of Chronic Restrictive MSK Disorders − Vary in types, symptoms and causes & are categorized into 2 main types dependent upon the origin of disease: Primary Muscle Diseases • Have a pathology that originates within the muscle (internal membrane/metabolic/contractile disorders) Secondary Muscle Diseases • Have a pathology that originates outside the muscle (nerve – neuromuscular: Parkinson’s or muscular dystrophy; bone/joint – musculoskeletal, inflammatory, dermatomyositis, immune – autoimmune muscle disorders: multiple sclerosis, myositis, muscle rheumatism) Symptoms of Chronic Restrictive MSK Disorders Muscle atrophy and accompany muscle weakness − Aloss of muscle size and is accompanied by a loss of muscle strength − The muscle weakness can be attributed to central(brain or nerve) or peripheral (muscle) causes − The central and peripheral factors are very similar to those associated with muscle fatigue, for example, a central upper motor neuron disease would include a reduction or lack of electrical signal due to tumors, reduced blood flow, spinal cord injury or trauma Pain • Can be rooted in cardiovascular or inflammatory system • In some conditions such as amplified musculoskeletal pain syndrome, there can be an abnormal pain reflex where the nerves cause blood vessels to constrict • The lack of blood to the area deprives the muscle of oxygen and can cause the build-up of waste products resulting in pain • Peripheral vascular disease will result in restricted blood flow, particularly to the legs and can result in pain or numbness, particularly upon exertion • Inflammation is the most common reason for muscle pain and aches in lupus or other autoimmune diseases, wherein the body’s own immune system is damaging its own tissues such as muscle, resulting in muscle weakness, swelling and pain Tetany − Involuntary contractions or spasms that are caused by changing calcium levels − Generally occurs in the larger muscles of the arms and legs, but can result in laryngospasm (affects breathing or speech), seizures or even myocardial dysfunction Twitching • Due to muscle contractions from the uncontrolled firing of single motor units • Can become more severe as motor neurons die off and each neuron serves a greater # of muscle fibres Muscular Hypertrophy in dystrophy − Is accompanying muscle stiffness − In humans the increased muscle size is due to increased fat and connective tissues as opposed to true increased muscle size − There is a reduction in the absolute muscle mass, despite an increased overall muscle volume (i.e., myotonia congenital) Biochemical Parameters • Specific to the disease and the diagnostic impact is dependent of the type of chronic restriction MSK disorder (i.e., McArdle: reduced muscle glycogen, mitochondrial oxidative potential etc.) Central Factors Related to Muscle Weakness in Muscle Diseases − Strokes are an upper neuron disease that produces weakness on one side of the body but with increased muscle tone (arm is typically flexed and leg is extended) unlike lower motor neuron diseases where the muscle bulk is generally well preserved early in upper neuron diseases − Spinal cord injury or spinal cord diseases such as Lou Gehrig or amyotrophic lateral sclerosis diseases (ALS) are upper/lower motor neuron diseases that will lead to muscle wasting and denervation of muscle (denervation of muscle will lead to muscle paralysis and rapid muscle death − Peripheral Nerve Diseases are lower motor neuron diseases that have sensory disturbances that generally being in the hand and feet and progress inwards − Peripheral neuropathies are degeneration of the axons (core of nerve fibres). This can be due to damage to blood vessels either from physical or chemical causes that cause axonal neuropathy (axons can regenerate but only at a rate of 1-2 millimeters per day) − Peripheral neuropathy can also be due to degeneration of the myelin sheaths (covering around axon) − This can be due to diabetes mellitus, nerve trauma, inherited factors, infections and chronic renal failure. The symptoms are similar to axonal neuropathies but since the axons remain intact, the muscles rarely atrophy Neuromuscular Junction Diseases • Involve reduced end-plate electrical potential with lower electrical input meaning that there is a lowered action potential delivered to muscle fibre/cell • These diseases can be acquired or inherited and may the result of autoimmune disorders such as myasthenia gravis congenital disorders (failure of nerve impulses to be properly transmitted to the muscles) or toxins such as those present in botulism • People with this condition have persistent muscular weakness in the face, limbs and neck and are easily fatigued, may also have double vision and difficulty swallowing and breathing • Myasthenia is treated with high doses of corticosteroids to depress the immune response and anticholinesterase medications which improve the transmission of nerve impulses (unfortunately symptoms are not completely irreversible Peripheral Factors related to Muscle Weakness in Muscle Diseases − As with the central factors, the peripheral factors such as sarcolemma, t-tubule and sarcoplasmic reticulum modify the internal membrane functions of the muscle, whereas the metabolic systems and actin-myosin interactions are extremely varied in how they relate to muscle weakness Internal Membrane Systems • Are affected by peripheral muscle diseases resulting in reduced electrical input (smaller action potential=less signal) stimulating the calcium release from the sarcoplasmic reticulum meaning that there is reduced calcium release from the sarcoplasmic reticulum and more remaining in the sarcoplasm Metabolic Systems − Can also be affected by peripheral muscle diseases such as McArdle’s Disease which is a rare inherited condition that is characterized by the lack of the enzyme phosphorylase or myophosphorylase which is needed for the breakdown of glycogen Muscular Dystrophies • Are a type of peripheral muscle disease characterized by progressive muscular atrophy and weakness, particularly in the limbs, pelvic and shoulder muscles due to the progressive loss of muscle proteins and ultimately, muscle fibre death • The most common type of muscular dystrophy in adults is Steinert’s Disease or Myotonic Dystrophy • Duchenne Muscular Dystrophy is the most common type in children and only affects male, this condition results in the progressive loss of muscle in the pectoral, upper arm and leg areas causing them to be in a wheelchair at start of their teenage years and die by age of 20 • Becker Muscular Disease is similar to Duchenne in the muscles it affects but is milder in nature and only affects males. Individuals are able to walk but have some cardio-respiratory and/or heart problems • Emery-Dreifuss is a type of muscular dystrophy which is only preset in males and is diagnosed between childhood and teenage years. Along with the affected limb muscles (pectoral, upper arms and lower legs), patients usually have serious heart problems that are usually fatal • Limb-Girdle affects both males & females between teenage and adulthood. The muscle dystrophy begins in the hip and spreads to the shoulders and then the upper limbs. Most patients are unable to walk but can survive past mid-adulthood. This type is caused by a defect in dystrophin and increased calpain that breaks down muscle protein • Fascioscapulohumeral Muscular dystrophy affects both males & females.Almost all patients live a normal life span and half retain their ability to walk • Oculophyrangeal Muscular dystrophy affects both males & females at the age of 40yrs and older and primarily influences the muscles of the eyes and throat which can cause problems swallowing, predisposing patients to pneumonia and chocking. Aging and MSK Disorders − Causes of age-related muscle loss are unclear, but could be related to hormonal or motor unit changes or programmed cell death − With aging there is decreased testosterone and growth hormone that may be responsible for loss in muscle mass − Aging is associated with the selective loss of type II motor units resulting in a larger proportion of type I fibres and less muscle mass and strength overall − The most popular theory for sarcopenia is thought to be a result of programmed cell death due to the activation of caspases (enzymes that breakdown and degrade proteins and DNA) and apoptosis-inducing factor (AIF) − The destruction of fragmentation of DNAwill eliminate the muscle’s ability to regenerate itself − The caspases can be activated by some of the same factors that are seen with muscle fatigue.AIF can also be activated by ROS and has been shown to destabilize the nucleus which also causes the cell to die Sarcopenia • The age-related loss in muscle mass and strength which impacts 10-25% of adults under 70yrs & ~40% of adults over 80yrs.1-2% of muscle is lost per year after the age of 50yrs • The loss of strength can vary, but the loss of strength and mass is more apparent in the lower body. This is problematic as lower body functionality is more important for maintaining one’s ability to perform activities of daily living Chapter 21 – Muscle Adaptations to Strength or Resistance Training Timing of Muscle and Neural Strength Changes − In the strength/resistance study there was a dramatic increase in muscle strength but with minimal muscle gains (hypertrophy). This dramatic increase is because the majority of early strength gains are associated with changes in neural components of strength as opposed to increased muscle mass − The increases in strength associated with the neural component are related to the skill acquisition and improved synchronicity of motor unit firing meaning that the individual is better able to do the movement and their muscles are better able to work together − The gains in hypertrophy are not immediate and begin with little if any hypertrophy but are more linear and longer term slower increases in strength are more strongly related to the gains in hypertrophy Myogenesis • The formation of a new muscle fibre is called myogenesis, beginning from a satellite cell myoblastsmyotubemuscle • This process is regulated by activators (myoD and myogenin) and inhibitors(myostatin) • With resistance training, there are early increases in myoD and myogenin even with a single bout of resistance exercise that peak 36hrs post (one of the reasons why you need to rest 48hrs post resistance to allow time for the myogenesis activating factors to have their effect Muscle Fibre Type − In most people, there is approximately 50% type I and 50% type II fibres but there can be as much as 85% type II for sprinters or 90% type I for elite endurance athletes − Within type II fibres there can be an interconversion of its sub-types: type IIx fibres (glycolytic), type IIAx (intermediate) or type IIA(oxidative) fibres − There is little to no conversion of type I to type II or vice versus in humans Muscle Hypertrophy • Is the increase in muscle size with resistance training due to an increased number of myofibrils per muscle fibre as opposed to an increased number of muscle fibres (hyperplasia) • The increase in muscle fibre size is due to increased protein synthesis relative to protein degeneration • The degree to which hypertrophy occurs is related to the intensity of the training and the overload on the muscle (causing degradation) • In addition to an increased number of myofibrils is an increased density of sodium-potassium pumps, sarcoplasmic reticulums and t-tubules that can result in an improved calcium handling Factors Promoting Protein Synthesis Intensity and volume of workload − Greater intensity and volume of workload will increase the organelle disassembly and protein breakdown (i.e., increased protease activity, sarcomere disruption, etc.) − The contraction type will also influence protein breakdown and synthesis − Greater muscle tension will also result in greater membrane disruption and muscle damage − Metabolic stress will also contribute to greater protein synthesis, the greater the anaerobic contribution to ATP production during the training stimulus, the greater the growth hormone and protein synthesis response that will result Nutrient intake • Water and cellular hydration is associated with decreased protein degradation and increased protein synthesis • Creatine loading is associated with increased cellular hydration and is thought to be the major pathway by which creatine results in muscle hypertrophy as opposed to the increasedATP supply • The second major nutrient factor related with protein synthesis is increased carbohydrate intake due to the increased insulin and insulin growth factor response • The final nutrient factor is protein or amino acids intake Hormonal environment − There are several hormones and endocrine factors that influence protein synthesis; two of the major classes of hormones that promote protein synthesis are: − Androgenic: the sex hormone testosterone is related with protein synthesis and is why males increase in muscle mass with puberty − Anabolic: these are natural or synthetic compounds that stimulate muscle growth and strength gains (i.e., steroids; testosterone esters; growth hormone; testosterone enhancers). The synthetic anabolic compounds are banned and its use is considered unethical for athletes Chapter 22 – Principles of Strength/Resistance Training  When designing a strength or resistance training program, there are many different variables that need to be considered: the type of exercise, # of reps, # of sets, volume, intensity, rest and the type of muscle contraction, will all influence the gain in muscle strength, power and endurance • Repetitions: the # of complete movement cycles per set • Sets: the # of reps done in a group without rest • Volume: the amount of total work performed in an exercise • Intensity: the weight lifted relative to the maximal weight lifted in a single effort • Frequency: the # of training sessions per day of week • Exercise selection: the type of exercise performed in an exercise session or training program • Exercise order: the sequence in which the exercise are performed • Rest period: the amount of rest taken between sets/or exercises • Repetition velocity: the velocity at which the reps are performed • Muscle contraction: categorized by the changes in muscle length: eccentric (lengthening), concentric (shortening) and isometric (no change), by the speed: isokinetic (constant speed), isometric (no movement) or resistance: isokinetic (variable resistance), isometric/eccentric/concentric (constant resistance)  These factors are modified to create different strength/resistance programs; there are 5 basic principles that are generic to all programs: progressive overload, specificity, variation, individualization and reversibility − Progressive overload: the gradual increase in physical stress or demand on the whole body and/or segments, without progressive overload or ‘training stimulus’, the body or muscles will become adapted to the stressor and there will be little to no benefits − Specific: the training stimulus is specific to the muscular adaptations that are designed. The muscle actions, velocity of movement, rate of force development, range of motion, muscle groups used and movement pattern off the training program, all need to be as close to the desired characteristics − Variation: it is also important to have variation in the strength/resistance training program variables over time to optimize the training stimulus − Principle of individualization: the concept that individuals will respond differently to the same training stimuli due to inter-individual differences in genetics, training status or nutritional status − Principle of reversibility: detraining with cessation or reductions in training stimulus; the loss of function and performance will appear earlier and more quickly in individuals with higher training status than untrained individuals Chapter 23 – Balance  Balance is dependent upon signals received from the semi-circular canals in the inner ear, kinesthetic sensors in the muscles, tendons and joints, visual perception and the co-ordination of these signals (spastic lock co- ordination) Sensory signals Semicircular canals • Located in the inner ear above the vestibule (detects straight acceleration due to gravity) and cochlea (magnifies sound). They are filled with fluid with little particles and with angular acceleration (changes in movement or direction) the particles within the semicircular canals will disturb the hairs that line the semicircular canals and provide information regarding the body’s movement Kinesthetic sensors − Within the muscles, tendons and joints include the muscle spindles, Golgi tendons organs and joint kinesthetic receptors. Muscle spindles − Proprioceptors located in the skeletal muscles between the contractile (extrafusal) muscle fibres; the muscle spindles provide info to the CNS regarding muscle length, tension and load Golgi tendons − Interwoven in the tendon close to the skeletal muscle; these proprioceptors detect tension in the tendon of a contracting muscle and inhibit contraction in the muscle Joint kinesthetic receptors − Located within the connective tissue of a joint capsule; these proprioceptors respond to mechanical deformation of the joint capsule and ligaments and signal the extremes of joint range. Responds only to dynamic movement. Vision − Is simply eyesight, individuals use what It sees in the surrounding environment to assess the body’s position in space Spastic lock co-ordination − The ability of the body to take the info from the proprioceptive receptors & vision and to contract the appropriate muscles with the appropriate factor Factors Influencing Balance • An individual’s body weight in combination with their center of balance and strength and power will influence the individual’s ability to correct any deviations in balance and the likelihood that imbalance will occur. A higher body weight requires more strength and power to correct deviations in balance • A high center of balance or a small base of support meant that it is more likely that the center of balance will fall outside of the base of support resulting in imbalance • Co-ordination also influences how well an individual will be able to contract the appropriate muscles with the appropriate force to bring the centre of balance back within the base of support Balance andAging − Balance deteriorates with aging and falls are a strong risk factor for hip fractures. The major difference between those who fall and those who do not fall is not reaction time but is the rate of strength development or power − This means that strength and power training can improve balance and reduce fall risk Chapter 24 – Flexibility  Flexibility is the range of movement about one or more joints and is important for reducing risk of injury and proper joint movement and body alignment  The flexibility test that is most commonly cited to be relat