Exercise Psy Quiz 3

VO2max

the maximum amount of oxygen the body can take in and use during exercise.

Muscle Anatomy Epimysium Perimysium Endomysium Sarcolemma Myofibril fig 1

-Muscle is connected to the bone by a tendon Called the myotendinous junction. -The bone tendon interface is called the osteotendinous junction * Fascia sheet or band of fibrous connective tissue that lies deep to the skin or forms a kind of envelope for muscle and various other organs. Pericardium is example * epimysium- fascia continuous with a tendon. presents as fascia sheets creating an external ultrastructure of the muscle belly providing structural integrity. *perimysium-fascia sheets continuous with epimysium creating longitudinal compartments within the muscle belly. The compartment is called a fasciculi are fasciculus. *Endomysium within fascicle find individual muscle fiber cells that are separated by a substance called endomysium it acts as an insulator between the muscle cells not allowing the behavior of one muscle cells membrane to affect adjacent cell. * sarcolemma - the muscle cell membrane Sarco referring to muscle limit to membrane. It's similar to all cell membranes a phospholipid bi layer with electrophysiological properties in other words it's an excitable membrane. *Muscle cell referred to as the muscle fiber. It's delineated by its membrane and the sarcolemma. Also cells have a number of unique feature when compared to other cells Length it is long related to other cells the longest individual cells are in the sartorius muscle which connects the anterior pelvic bone to the posterior medial tibia. * myofibrils. These are highly organized protein-based structures within the muscle cells extending the full length of the muscle cell. Each Myofibril is approximately 3,000 Actin filaments and 1500 myosin filaments in a hexagon arrangement in cross section with the filaments running in parallel with the length of the cell. This is a three-dimensional arrangement. *Sarcomere the sarcomere is the smallest functional contractile unit of the myofibril and muscle. If we look at one small section of the myofbril we can see the arrangement of specific protein structures responsible for the contraction and regulation of the contractile state. CONTRACTILE PROTEIN- Responsible for the change of the length to in the cells are actin and myosin *Actin-The thin filament one end of each filament is embedded into the Z lines which create two end boundaries of each sarcomere.Z lines are structural proteins. A number of acting filaments are in bedded into each Z line on either end of the sarcomere projecting back towards the midline of the sarcomere but not touching each other. A unique feature of the actin filament is that they have a very high affinity for the cross bridge portion of the adjacent myosin filaments. * myosin the thick filament are a series of bluff golf club shaped structures with the clubhead which is referred to as the cross bridge staggered along the surface and over the length of the filament. These crossbrige heads have a high affinity for the actin filament and for ATP. They contain myosin - ATPase an enzyme that hyrolyzes the ATP into ADP plus P yielding energy from the terminal phosphate bonds. This is splitting of ATP. The myosin filaments live between an overlap with the actin filament's straddling the sarcomere. The cross bridge heads project up about a 45° angle towards the actin pointing away from the midline towards Z line on the other end. This angle is important. The hexagon all arrangement of the Actin myosin in the cross section. REGULATORY PROTEINS-Responsible for regulating the contractile state of the sarcomere. They are tropomyosin and troponin. * tropomyosin long thin chain like proteins run on the surface of the actin filament. * troponin- smaller globular proteins embedded in the tropomyosin along length. high affinity for calciumCA2. They are linked together in long chains is covering the surface of the actin filaments. They cover sites on Actin molecule and have a high affinity for myosin - active sites. Passive or relaxation state - troponin and tropomyosin cover the active sites preventing myosin from interacting with Actin. When CA2 binds troponin causing shape change(Conformational change in protein structure) and pulls the tropomyosin chain to the side exposing active sites on the actin filament. Myosin cross bridge heads can then attach to the active sites on Actin pulling the actin filament toward the middle, release the Actin, reset to original, attach, swivel, release, reset, splitting an ATP per swivel cycle. When the myosin cross bridge attaches to the actin filament it swivels back to the midline of the sarcomere pulling the Actin and Z line. A large number of these sarcomeres in series representing a muscle cell each pulling its own Z line in the net effect would be shortening at the ends leading to muscle shortening-active-contracted uses ATP (ATP=ADP +P+energy) and cross bridge occurs. Fig 7

Varying DURATION while holding frequency and intensity constant looks like this:

*15 minutes per bout-35% genetic potential *30 minutes for about 65% genetic potential *45 minutes for about 90% genetic potential There is little specific data on longer durations or an injury which direction but as you might imagine longer durations are likely to increase injury rate somewhere to that seen with frequency

Myofibril Contractile protein Actin Myosin

* myofibrils. These are highly organized protein-based structures within the muscle cells extending the full length of the muscle cell. Each Myofibril is approximately 3,000 Actin filaments and 1500 myosin filaments in a hexagon arrangement in cross section with the filaments running in parallel with the length of the cell. This is a three-dimensional arrangement. *Sarcomere the sarcomere is the smallest functional contractile unit of the myofibril and muscle. If we look at one small section of the myofbril we can see the arrangement of specific protein structures responsible for the contraction and regulation of the contractile state. CONTRACTILE PROTEIN- Responsible for the change of the length to in the cells are actin and myosin *Actin-The thin filament one end of each filament is embedded into the Z lines which create two end boundaries of each sarcomere.Z lines are structural proteins. A number of acting filaments are in bedded into each Z line on either end of the sarcomere projecting back towards the midline of the sarcomere but not touching each other. A unique feature of the actin filament is that they have a very high affinity for the cross bridge portion of the adjacent myosin filaments. * myosin the thick filament are a series of bluff golf club shaped structures with the clubhead which is referred to as the cross bridge staggered along the surface and over the length of the filament. These crossbrige heads have a high affinity for the actin filament and for ATP. They contain myosin - ATPase an enzyme that hyrolyzes the ATP into ADP plus P yielding energy from the terminal phosphate bonds. This is splitting of ATP. The myosin filaments live between an overlap with the actin filament's straddling the sarcomere. The cross bridge heads project up about a 45° angle towards the actin pointing away from the midline towards Z line on the other end. This angle is important. The hexagon all arrangement of the Actin myosin in the cross section.

Overtraining syndrome

A condition whereby too much training results in the maladaptations of body responses

Specificity of exercise principal

A specific training real specific add active responses to improve response performance at that specific task. What you specifically trained for is the task in which you will Improve. There is a specificity in both training and testing. Testing meaning the measurement of improvements in capacity caused by a specific type of training. SAID Principal specific adaptations to imposed demands.

Sliding filament theory Fig NM.7

Actin and myosin filaments slide over each other in both active and passive state with no change in the length of the filaments only relative to each other and the length of the sarcomere is what changes. The structure of the myofilaments can explain the change in the length the muscle in both the active and passive state. An active contraction or shortening requiring ATP is responsible for movement but the antagonist is being passively lengthened. Then muscle protein filaments are pulled passed each other as the sarcomeres are stretched due to the pulling force created at their tendon by the agonist, but no actin myosin interaction occurs and it's passive with no ATP used. The structure and orientation of the myofibrils explains both active and passive state of muscle shortening and lengthening

Motor unit recruitment - the order in which motor units are recruited by a motor unit type.

As we exercise at low to moderate intensity for extended duration greater than five minutes we require metabolism that will support longer duration exercise like aerobic metabolism. As exercise intensity increases like a sprint we require much more force from the muscle and recruit many more motor units. What happens is regardless of the motor unit type included the time course of metabolism holds true. Immediate energy sources IES followed by anaerobic glycolysis followed by aerobic Glycolysis and then beta oxidation depending on the capacity of the particular motor unit and the duration of the activity. FG does not have as much aerobic capacity as SO. ***So the same time course of metabolism occurs. Within each cell within a given motor unit as that motor unit is recruited by the motor cortex to produce force to support movement. How LONG that motor unit is active will determine which metabolic pathway will contribute and the ATP produced and the muscle cells of that motor unit. Especially true in SO FOG motor units as they have both sufficient capacity of all forms of metabolism.

A few studies have been performed to show selective recruitment of motor units in clonus in a cat model.

Clonus is a series of involuntary rhythmic muscle contractions and relaxation at the highest possible alternating frequency. This occurs when you place a piece of tape on the cats forelimb paw. The Cat flicks the paw back-and-forth trying to shake the tape off and reaches clonus. It appears it is a non-weighted situation. FG motor units can be selectively recruited allowing the movement to reach clonus.

Cerebral hemispheres figure NM.12 A-C

Cortex - thin outer layer which is gray matter. Gray matter - is composed of somas (nerve cell bodies.) White matter- which is deep to the cortex is comprised of axons extending from the neuron somas in the gray matter.

Spinal cord cross section ventral to dorsal NM.13

Dorsal fin is the back of the fish. Dorsal side is towards back. Ventral side is towards front.

Lower motor neuron's LMN specific class Alpha motor neuron (a-min)-A motor neuron that innervates and controls skeletal muscle. Gamma motor neuron Y - mn innervates and controls a sensory organ inbedded in skeletal muscle called the muscle spindle. Dorsal horn receives sensory input from the peripheral nervous system PNS.

Example Contraction of the elbow flexors. The brachialis and biceps in the motor cortex an UMN collects input from other areas of the CNS (the decision to move) and the PNS century feedback reaching threshold sending an action potential down it's axon. The axon will travel through the middle of the brain in nerve bundles (white matter) and travel down the spinal cord in the ventral white matter at approximately C5 of the spinal cord, UMN axon will enter the ventral horn Gray Matter and synapse with the soma of an a-mn. That a-mn soma will reach threshold send an action potential down an axon to its terminal where it will excite the muscle cells that innervates and bring them to threshold. These muscle cells will contract producing force. The specific muscle cells excited are in the targeted muscles. This is a semi hard wired system. Make sure you know the Excitation Contraction E-C coupling. and understand the connection of excitation by the nervous system with the contraction of muscle.

Metabolic adaptation to applied stress

Exercise training subjective is neurologic metabolic and physiological adaptations in order to improve performance in a specific task. General adaptation syndrome - GAS Overload principle -muscle is regular stressed in a specific way it will adapt better respond to that stress in the future. Individual differences

Integration of motor information in the motor cortex causing stimulation excitation of the UMN

Fig 13

A-Motorneuron is stimulated to threshold. Signal travels down the axon to each of the motor terminals. the Signal causes Synaptic vesicles with in the terminal to split and release acetylcholine

Fig 17

ACSM criteria for aerobic exercise

Frequency-3 to 5 x of activity per week Intensity - 50 to 80% VO2 max or 60 to 90% of max heart rate HR Duration 20 to 60 minutes Mode- activity using large muscle groups in a continuous and rhythmic fashion examples are running jogging hiking walking swimming skating cycle cross country or Nordic style skiing.

Neurons (nerve cells)

Highly specialized to transmit messages from one part of the body to another. They receive input from other nerve cells with their terminals synapsing on either soma or dendrites of the receiving neuron. That information sums together (temporal and spatial) moving through the neurons somas cytoplasm to the axon Hillock. If the signal is strong enough to reach the threshold an action potential is created and will be propagated down the axon to the terminal where it will communicate it's signal to the next cell. If the stimulus is not strong enough this cell will not reach threshold Fig NM.10 anterior motor neuron an example of a lower motor neuron and it's synapse with a skeletal muscle cell creating a motor unit..

There is a lot of focus on and aerobic aerobic exercise as a form of exercise as it can provide significant health benefits related to other forms of exercise primarily cardiovascular health benefits but may extend to the Immune system support and cancer risk reduction.

However defining aerobic exercise is critical to maximize the potential benefits of the activity. The American College of sports medicine a CSM an international exercise physiology and sports medicine organization supports research and this feels develops and publishers position papers and overseas certification programs for professionals. They have developed the standard criteria by which aerobic exercise is typically defined.

Unilateral resistive training there does appear to be some minor strength increases that transferred to the opposite Limb.

In metabolic adaptation we see that there is no crossover affect with aerobic training meaning that if we train only one body part it has not impact model metabolically on the opposite body part. However in resistive training there appears to be small minor strength increases with transfer to the opposite limb. The evidence suggest that there may not be a physiological explanation to opposite Limb hypertrophy but potentially some neural adaptations. The strength gains be appear to be moderate in the 7 to 10% range.

Muscular strength power VO2max

Increasing muscular RT strength power BW CT strength power BW Endurance VO2 max only

Muscular endurance - number of repetitions it can be performed in a given movement at a percentage of one RM typically 70% of one RM.

Low endurance completing fewer than 10 repetitions before fatigue high endurance would be completing 10 or more repetitions before fatigue. Do not confuse with aerobic endurance. Aerobic metabolism does not even enter the equation. For it to be aerobic it would have to be continuous in a rhythmic fashion for at least 3 to 5 minutes and would require a weight significantly less than 70% one RM. 1RM represents one lift up to fatigue 15RM weight can be lifted 15 times to fatigue. 10RM 10 x to fatigue 78% 5RM 5x to fatigue 90%

Muscle structural Organization

Muscle tendon myotendinous junction bone tendon osteotendinous junction

Specificity bicycle ergonomic

Only train one leg the right leg for four weeks using a foot strap and train to improve aerobic capacity. Then test for improvements in VO2Max with each leg separately. Results VO2Max improvement with both right and left legs NO only the right leg test because we stressed motor units in the right leg. Motor units only adapt and stress and the left leg test did not measure adaptations on the right and the left leg is not magically at that because the right leg was trained. Specificity. Some research supports contralateral adaptation in the untrained leg however it's only minor adaptations what is clear is that changes are not due to training the contralateral leg but due to the unintended use of the untrained leg.

Overtraining

Over training is a significant issue with exercise training for both an amateur an elite athlete. Techniques like Periodization are intended to reduce the likelihood of over training but the risk still exist. You need to understand the risk and understand how to minimize their appearance and treat them if they appear. Figure 16 page 177 and 427

Swim training test figure 1 Pre-training - test VO2Max and maximum exercise time MET on both a treadmill and while swimming tether. Baseline

Swim training using swim testing and treadmill testing Swim train the subjects for 10 weeks then retest both in the pool and on the treadmill to get post training data VO2Max and MET. Treadmill test - improvements in VO2Max and MET small Swim test- Much more significant because the swim test mimics the training modality swimming in there for a higher sensitivity to Adaptation. Treadmill test is not the same motor units that were stressed in the exercise of swimming. Swimming is mostly upper body and the treadmill is not sensitive to adaptations in the upper body. Only the swim test captures adaptation elicited by training. The same would be true if we reversed and trained running rather than swimming.

Histochemical techniques

The differentiation of other muscle cell divisions is not specifically quantitative in nature only qualitative. It has to do with how the differences in the cell types are assessed measured using histochemical versus bio chemical techniques. Histochemical techniques assessing the staining properties of different proteins enzymes would just show the protein existence qualitative not how much there actually is, quantitative. Well there is graded standing response to a riding concentration of enzymes is not qualitative in nature. A bio chemical assay determines the actual type and amount of each protein quantitative but determining where the protein is from us more difficult. Essays of single muscle cells are very difficult if not impossible. Table one gives us a bio chemical Sar resistant strain muscle showing the metabolic adaptation is associated with resistance training. Note that if an enzyme is not shown secured no significant change was detected.

nervous system organization Generic nerve Neuron structure Fig NM.9

The generic nerve cell neuron structure consists of a cell body (soma) with dendrites(antenna ) extending from the soma receiving information from other neurons, an axon (a long cable extending in the direction that the neuron wants to communicate information.) a terminal. The terminal representing the termination of the axon, which connects innervates and synapses with the cell (nerve muscle etc. ) that the Neuron sends information to. Axon hillock -The interface between the soma in the axon. This area has the lowest input resistance and is the easiest to bring to threshold. This is where the action potential is created.

What about the intensity of exercise. There's very little specific data that tells us the Intensity that we will see the greatest results. However intensity is the primary driver for improvement.

The higher the exercise intensity the faster the adaptation. However you can see similar results at lower intensity over longer training periods (weeks). Training at intensities above 85% VO2 max do not yield any greater adaptation. While some individuals may be able to maintain intensity of excess of 85% be able to max the quality of training suffers and the risk of over training and injury increases. There does not appear to be any adaptive advantage to exercising and intensity is above 85% be able to max only risks! Remember we are discussing longer durations 30 minutes Chronic activities. * once you reach a level of aerobic capacity and want to maintain appropriate activity is every third day is enough to maintain. However you can lose it, use it or lose it. In about two weeks of inactivity you will lose 12 to 15% of your aerobic capacity. Within 2 months almost all improvement is lost. With complete bed rest you will lose about 1% of aerobic capacity per day eventually down to your genetic minimum.

Innervation ratio

The number of muscle fibers Per a-mn

Table 1 highlights many of the changes we might expect to see in this type of aerobic training.

The training data in this table reflects two different populations 1. sedentary population untrained - in the sedentary population with continued training their adaptive values will approach their genetic potential however they will never approach the values seen in the elite aerobic athletes. 2. elite population trained-Genetically different than the sedentary population.

Motor cortex

This is the area of the brain where nerve cells somas that controls skeletal muscle are located. The projections from the spinal cord to the brain this is the CNS are the central nervous system.

Somatic nervous system - two classes of motor neurons Mn Motor neuron

Upper motor neuron and lower motor neuron —- mn Upper motor neuron UMN give rise from the grey matter of the higher centers in the central nervous system cerebral hemisphere of the brain. Lower Motor LMN and give rise from the gray matter of the spinal cord. This is a motor neurons not sensory. Motor means movement.

Adaptation - three training scenarios each designed to maximize the adaptation a specific metabolic pathway and resulting increase capacity associated with that adaptation metabolic adaptations that we describe a primary neuromuscular level specific to the motor units train.

We will describe adaptation that occur in other systems from the integral perspective. organize the adaptation in terms of metabolic pathways affected specific to the motor units recruited for the activity as well as the cardiovascular, Physiologic and respiratory adaptations. Physiological adaptations are changes in the ultrastructure of the muscle cells trained, increase cross-sectional area or changes in muscle fiber type resulting from metabolic adaptations. Adaptations to chronic training is not an acute bout of exercise. Chronic exercise in this situation will be training performed at least three times a week over a series of 4 to 6 weeks. With each successive training scenario absolute exercise intensity decreases and duration increases.

excitation contraction coupling from the arrival of the action potential in the presynaptic nerve terminal to the contraction of a muscle.Fig NM 17

1. Axon-saclike vesicles within the terminal axon release ACH Acetylcholine which diffuses across the synaptic cleft and attaches to specialized ACH receptors on the sarcolemma. 2. Muscle action potential Depolarizes transfers tubulars (T tubules) at sarcomeres A- L junction. 3. T tubule systems depolarization causes Ca2+ released from the sarcoplasmic Reticulum lateral sacs. 4. Ca2+ binds to troponin And tropomyosin in Actin filaments, which releases inhibition of Actin combining with myosin. 5. Actin joins myosin ATPase to split ATP with energy released during muscle action. Tension from energy released produces myosin crossbridge movement. 6. A muscle shortening occurs after ATP binds to the myosin cross bridge, which breaks the Actin myosin bond and allows cross bridge dissociation from the Actin and sliding of the thick and thin filaments. 7. Crossbridge activation continues when Ca2+ concentration remains high (from the membrane depolarization) to inhibit troponin and tropomyosin action. 8. When muscle stimulation ceases Ca2+ moves back into the sarcoplasmic reticulum lateral sacs through active transport via ATP hydrolysis. 9. Ca2+ removal restores troponin and tropomyosin inhibitory action. With ATP present, actin and myosin remain in the dissociated relaxed state.

Motor units SO FG FOG

1. Individual cell diameter of cross-sectional area's CSA varies with motor type. SO smallest FOG FG When it said they have 50% a motor units are SO they mean the number of motor units not the cross-sectional area or the CSA. FG motor units have more than 50% CSA and they have the potential to produce more force than FO. 2. Motor units are recruited serially but function in parallel. which means the size principal determines what we recruit motor units serially recruiting more and more as we require more force. However once we were through the motor unit we don't stop recording it as we add more motor units it is a collective force. The FG force is added on top of the SO's replacing it. The central nervous system CNS only cares about the force requirements for a movement. That is what it's program for selecting the appropriate amount of force for a given movement or series of movements jumping running etc. It is up to the organization at the spinal cord level and the motor unit system to select appropriate motor units to support that activity. They will do it as long as they have specific metabolic pathways. We cannot selectively recruit motor units in any useful in sustained way. The size principal dominates recruitment order.

Motor units SO FG FOG

1. Individual cell diameter of cross-sectional area's CSA varies with motor type. SO smallest FOG FG When it said they have 50% a motor units are SO they mean the number of motor units not the cross-sectional area or the CSA. FG motor units have more than 50% CSA and they have the potential to produce more force than FO. 2. Motor units are recruited serially but function in parallel. which means the size principal determines what we recruit recruit motor units serially recruiting more and more as we require more force. However once we were through the motor unit we don't stop recording it as we add more motor units it is a collective force. The FG force is added on top of the SO's replacing it. The central nervous system CNS only cares about the force requirements for a movement. That is what it's program for selecting the appropriate amount of force for a given movement or series of movements jumping running etc. It is up to the organization at the spinal cord level and the motor unit system to select appropriate motor units to support that activity. They will do it as long as they have specific metabolic pathways. We cannot selectively recruit motor units in any useful in sustained way. The size principal dominates recruitment order.

Spinal cord

4 subdivisions cervical 8 segments Thoracic 12 lumbar five sacrum five the lumbar and sacral region's are often combined into a single 10 segment lumbosacral region. Which skeletal muscles are controlled by what segment of the spinal cord. Example-C4 cervical segments we find the somas for the LMNs that control the shoulder muscles trapezius rotator cuff and deltoids.

Injury rate

6-7xweek-Little additional improvement only the elite athletes look for the last 5% improvement in VO2 max and then the injury rate becomes an issue. Therefore a significant consideration in injury rates versus frequency. These rates are with weight-bearing exercise however swimming and cycling have similar injury rates due to repetitive use injuries. *3xweek-10% injury rate *five x week 40% Injury rate What this means is 10% of those participating in exercise or injured at any given time if they exercise three times a week it rises significantly at five days a week to 40%. Injuries anything that limits the quality of exercise. That includes tendinitis sprain strain sore knees hips shoulders elbows and wrists.

ATP contraction of muscle.

ATP supplies energy necessary for myosin head movement and tension production in the muscle. With Contraction of the muscle Ca2+ is released into the myofibril space around the sarcomeres binding to the troponin and tropomyosin causing it to move aside expose the active sites on Actin. The activated myosin head cross bridge will attach to the active site on the Actin. While attached to the Actin the myosin head swivels producing tension in the muscles pulling the actin molecule toward the midline of the sarcomere attempting to shorten it. ADP is released from the myosin head and is replaced by another ATP. This causes the myosin head to release from the active site on the Actin. mATPase will again split ATP energizing the myosin head. CA2+ and ATP are present The cross bridge inter-action process will continue. Once Ca2 plus is removed from the myofibril the sarcomere and muscle relax. You do not need to know this do not study this

Scenario one Sprint and power-Running at near 100% effort for 10 to 20 seconds or less hundred meter run sprints a 25 m swim sprint effort is repeated 6 to 10 times per bout of exercise each bout repeated three times a week for 4 to 6 weeks.

Adaptations METABOLIC *marked increase in size of a immediate energy source pool ATP/CP * increase and glycogen storage within affected motor unit muscle cells. CARDIOVASCULAR * mild hypertrophy of the left ventricle wall. This does not necessarily lead to an increase in stroke volume. SV PHYSIOLOGIC * minor to moderate hypertrophy increase cross-sectional area a predominately fast twitch motor units recruited and trained FG/FOG. There is some hypertrophy in the SO motor units but small by comparison, the SO motor units are not as adaptable in terms of cross-sectional area where as the FGNFOG populations are. No change in motor unit types RESPIRATORY * some minor adaptations are possible due to the pulse bout hyperventilation. Note that the adaptation in terms of increased immediate energy source pool size, glycogen storage and increase cross-sectional area of the muscle cells are specific to the motor units recruited for the activity.

Scenario number 2 Intermediate distance sprint 60 to 90 second activity 90-100% effort for that distance Ie 400 meter run or 100 m swim at near maximum effort repeated 4 to 6 times per bout three times a week over 4 to 6 weeks.

Adaptations METABOLIC * marked increase in size of immediate energy source pool ATP/PCr * increase and glycogen storage within affected motor unit muscle cells * increase in anaerobic enzymes anaerobic glycolic enzymes within the affected motor unit muscle cells. Nominal increase in aerobic enzymes. *CARDIOVASCULAR * mild to moderate improvement in stroke volume SV PHYSIOLOGIC * minor hypertrophy of the fast motor units recruited. No significant S0 motor unit hypertrophy. * no change in motor unit types RESPIRATORY * respiratory musculature add apps similar to those seen in train skeletal muscles

Scenario three Moderate to high intensity activity of extended duration: any type of activity that can be sustained in excess of 20 to 30 minutes using continuous rhythmic activity without metabolic fatigue. The intensity of this activity is often measured as a percentage of maximum heart rate usually in the 60 to 85% range. three times a week for over a period of 4 to 6 weeks And the three training scenarios different types of training cause different types of physiological and neurological stress and results in a variation in the type and magnitude of adaptation to that stress.

Adaptations METABOLIC * marked increase in the size and number of mitochondria and associated aerobic metabolic enzymes * increase beta oxidation capacity *the two above leading to an increase VO2max *increase in glycogen storage CARDIOVASCULAR * increase in stroke volume both at rest and during exercise resulting in increased and maximum cardiac output *decreases in resting heart rate resulting from an increase in resting stroke volume decrease in resting blood pressure typically and better management of exercise blood pressure *mild left ventricular hypertrophy *potentially increase capillarization surrounding trained motor units typically occurs after many months of training rather than the weeks noted here. PHYSIOLOGIC * mild pepper jerky a predominantly the SO motor units which are the primary motor units recruited for this activity performed in tensely in over a longer training. More than six weeks we might see some shifts from FG to apogee but more on this later when we discuss interval training which is more likely to cause the shifts. RESPIRATORY * similar changes in the respiratory musculature as seen in the trained skeletal muscle *no significant changes in lung or capacities increase in 0BLA a percentage of the VO2 max say from 50% to 70% plus VO2Max The change in OBLA as a percent of VO2 max is due to metabolic adaptation. We see is a less accumulation of lactic 8+ delayed onset of blood lactate accumulation. The mechanisms is first and lowest impact mechanism is the quarry cycle in the liver which converts lactate back into glucose it is not fast enough during intense exercise to be much of use as either a lactate utilizer Or glucose producer. The second mechanism is called lactate shuttle. And then divide by George brooks at UC Berkeley this mechanism shuttle is lactate into the mitochondria in skeletal muscles for use as a precursor in the Krebs cycle.

Nervous System Functional organization of the nervous system somatic automatic autonomic divisions. Anatomical divisions are central and peripheral nervous system With the brain and spinal cord.

All of the nervous tissue within the bony structures of the vertebral column and cranium are part of the CNS central nervous system. Any part of the nervous system outside of these bony structures is referred to as the peripheral nervous system the PNS. Somatic nervous system which controls skeletal muscle function spans both the CNS and the PNS, Or the central nervous system and the peripheral nervous system.

Overview of the general value of chronic aerobic activity two overall health

Alleviate symptoms of depression stimulates new brain cells reduce his chances of stroke lowers blood pressure reduces heart disease risk curbs risk of certain cancers reduces pain and disability from arthritis boosts insulin sensitivity limits gain visceral fat Builds muscle increase bone mass and bone density.

Stopping a muscle contraction Ca2

At the motor cortex we stop sending the signal to contract by stopping excitation of the UMN (don't move) which will stop excitation of the a-motor neuron, which will no longer excite the muscle cell. So that stops the continued excitation but what stops The muscle cell from continuing to contracts? If CA 2+ his present in the myofibrillar space and ATP is available myosin will bind with Actin and the muscle contracts- so how do we stop this?) We must remove the CA 2+ From the Myofibrillar space back into the SR? There is an active Ca2+ pump in the SR's membrane, active meaning that it uses ATP and pumps against its concentration gradient. It's busy pumping Ca2+ back into the SR entire duration of the contraction so that only a small amount of Ca2+ is left in the myofibrillar at any given time. Once Excitation stops and only a small amount of Ca2+ will have to be pumped into the SR to stop the contraction. This is very efficient and critical mechanism and is central to motor control.

Delayed onset muscle soreness DOMS

DOMS-begins in about 12 to 24 hours after post exercise speaking at about 48 hours post exercise and begins to diminish within about 72 hours. This is not acute pain that occurs either during or immediately post exercise. Acute muscle pain may be due to muscle fatigue or muscle injury. DOMS is not due to lactic acid accumulation within the muscle cell. Lactate and lactic acid concentration normalize within minutes post exercise. This type of muscle pain is thought to be due to the sub cellular damage to the muscle at the level of the myofibrils. We are not talking about significant trauma to the muscle cell, but sub cellular damage. Can you started this damage stimulates the muscle repair mechanism which requires breaking down of the damage proteins and replacing them. During this process there is a mild to moderate inflammatory response in the connective tissue causing some minor localized information. This inflammation starts about 12 to 24 hours post injury. The localized inflammation causes pressure or pain receptors deep within the connective tissue causing pain. The type of movement that creates the greatest risk for developing DOMS is eccentric or lengthening contractions active lengthening. This speed is slower than gravity alone would move the weight. This was an active lengthening and a passive shortening of the antagonist muscle. Pain scale is 0 to 5 with five being severe pain. For each of the contraction modalities concentric or shortening,isometric, or eccentric or lengthening you can see the greatest DOMS with eccentric contraction. It has also been shown that eccentric contraction puts greater stress on the muscle and make faster strength gains than with concentric contraction of the loan. Why do eccentric contractions cause more stress. Consider that the concentric contraction you must recruit enough motor units to overcome the force of the weight to move the weight. From the contracted position to cause an eccentric contraction you reduce the number of motor units recruited to just enough to allow the muscle to lengthen them or the elbow to extend in a controlled movement slower than gravity would move it. With fewer motor units to control the same weight puts more stress on the muscle the motor units that are contracting. Each motor unit is working to contract or shorten but the external forces slightly greater than the internal force produced by the motor units recruited. The net effect is to pull or lengthen the active muscle cells which are trying to shorten. The fact is to possibly damage some of the myosin cross bridges or Actin molecules leading to DOMS.

strength acquisition-Rate Neural phase Hypertrophy phase

Depends on a few factors: intensity or volume of work which is scientifically referred to as the CNS activation. Regardless of the overload we see two distinct phases of strength acquisition... Neural phase-accounts for the strength great gains in the first 4+ weeks of initial resistance training program. The primary changes are in the way in which the motor units are recruited. In a non-resistive trained individual or even in resistive trained individuals during normal movements while not weight training motor units are recruited a synchronicity which means if they are not recruited simultaneously but are spread out over time (temporarily) to better control the application of force into the smooth movement. However with resistive training we train the nervous system to recruit the motor units more synchronousy, nearly all at once, to ensure the application of force all at once rather than spread out temporarily. and the hypertrophy phase.The net result of this is that peak force production increases without hypertrophy. We are training the muscular neuromuscular system to be more efficient and its application of force production. Additionally there is a reduction in something called autogenic inhibition, which is a mechanism built into the Nervous system designed to protect the integrity of the muscle and it's attachments from the application of too much force to quickly. This occurs of the spinal cord. With training this autogenic inhibition decreases as the muscle tendon and bone become stronger and there is less need. Hypertrophy phase- After four or more weeks we begin to see hypertrophy in the muscle cells which is exhibited by further increases in force production by the muscle. This increase in force production can continue for a number of months or even years depending on the quality of training. After strength gains have plateaued additional gains are smaller. Typically the range of strength gains across the population range between 25% and 100%. What is unclear is that the mechanism are that allowed years of incremental gains in muscle strength. Is it solely hypertrophy or is there some hyperplasia or some interaction of neural and physiological adaptation? Only further research will tell.

Training modality specificity (To test VO2max we can run on the treadmill bicycle swimming tethered in our current tank or an arm ergometer. Testing modality sensitivity

Exercise training is specific to the motor unit-If the motor unit is recorded during a series of training sessions then it is likely to adapt. If it is not recruited then it will not adapt. Cycling and running have some overlap of motor unit recruitment but not complete or identical. Some motor units trained with run training will not be recruited during bicycling test and some of the motor units recruited doing the bicycle test will not have been trained during the run training. The result will be a lower VO2Max measured using a bicycle ergometer test as compared to a run test while testing for adaptations to run training. This is important to learn it. Motor units adapt only if chronically recruited. If an activity doesn't recruit a specific motor unit or group of motor units the motor unit does not adapt. And that determines which motor units are recruited. The mode and intensity of the activity with the size principle of motor unit recruitment underlying it.

Motor units alpha - motorneuron a-mn an all of the muscle fiber (cells) that motor neuron innervates.

Four key properties *a-am can innervate from a few to 1000 muscle fibers depending on the muscle. * A muscle fiber will only be innervated by one a-mn. *a-mn soma reaches threshold and sends an action potential down is axon, all the muscle fibers that it innervates will contract. All or none principle. *All of the muscle fibers in a motor unit will have similar or homogeneous properties especially the terms of metabolism. Alpha-motoneurons axons can branch many times to innervate as many muscle fibers that it needs to. The number of muscle cells it will innervate is genetically and developmentally determined. A motor unit creates a discrete unit of force. If you excite a given a-mn to threshold at the minimum activation rate from higher centers a discrete number of muscle fibers will be excited to threshold and will contract (excitation contraction coupling) giving us a discrete amount of force. That force is dictated by the collective cross-sectional area of the muscle fibers contracted. If 10 muscle fibers are excited to contract by given a-mn (representing one motor unit)the amount of force produced will be the sum of those 10 muscle fibers. Within the motor unit increasing the fire frequency from the UMN (higher centers) can increase the force produced by the motor unit proportionally up to what is referred to as tetanus when all the muscles fibers of the motor unit contract continuously. This is important in activities requiring higher force production or isometric stability contractions but will not have much impact on how we view EC coupling.

Muscular power measured as force per unit time Ft-lbs/sec kg-m/sec

Given force moved at a given speed. The higher the rate at which the given weight can be moved the greater the power is developed by the muscle. The primary capability or performance detriment in mini power types of activities is the billeted to produce high power. Measurement requires a Cybex isokinetic testing rehabilitation. If you can produce high force at high angular velocity of a joint then you'll develop more force that can overcome inertia to move either your body or something you're trying to move. High power sports are high jump javelin throw shotput baseball golf or tennis anything that requires power. Motor unit types play a role here. FG motor units can produce more power than SO motor units due to their faster Contractions speed. Just like aerobic exercise training intensity of resistance maximizes adaptation. Research shows that training intensity is of greater than 60% of one RM will yield the best results in terms of strength. Most resistant training programs focus on slightly higher percentage of 1RM but this appears to be a threshold level. FT motor units have a greater capacity to Produce force at high speeds then ST motor units. Fig 4 comparing angular velocity of flexion of the knee against force production we can see individuals have a higher percentage of FT motor units power can produce more force at high shortening speeds as compared to the individuals with predominately ST motor units endurance or slow twitch meaning that they can produce more power which will translate into better performance at power or ballistic types of events. Power equals work time-1

Spinal cord Central area of gray matter Peripheral area of white matter

Gray matter always represents neural cells somas of LMN. LMN Give rise from the gray matter of the spinal cord. Gray matter is composed of somas nerve cell bodies. White matter represents axons of the UMN. UMN rise from gray matter of the higher centers of the central nervous system the cerebral hemispheres of the brain. White matter which is deep to the cortex is comprised of axons extending from the neuron somas in the gray matter. The spinal cord can be split into a left and right halves And the left and right sides have a ventral and dorsal horn of the gray matter. Ventral horn we find most of the lower motor neurons LMNs. The axons of the lower motor neurons will project out of the spinal nerves into the peripheral nervous system and will eventually synapse or connect to muscle.

Excitation - Contraction Coupling figure 17 This figure is a a-mn nerve terminal on the circle Lemme muscle cell membrane and then deep within a muscle cell in cross-section

High level steps of EC-Coupling Initiating a muscle contraction * integration of motor information in the motor cortex causing stimulation\excitation of UMN Fig 13 *UMN is excited to threshold sending a signal down it's Axon traveling in the ventral white matter of the spinal cord. Example upper elbow flexor muscles *UMN synapses with a a- motor neuron representing a motor unit of the elbow flexors. The synapse occurs in the gray matter of spinal cord at C5. C5 because that's where the somas a-mn of the elbow flexors are located. *The a - motor neuron is stimulated to threshold and the signal travels down the axon to each of the motor terminals. The signals causes synaptic vesicles within the terminal to split and release neurotransmitter acetylcholine. (Ach) Fig 17 * The Ach leaves the terminal, enters the synaptic cleft and binds to Ach receptors embedded in the postsynaptic synaptic membrane (sarcolemma). *Ach binding to the membrane - bound receptors causes channels to open in the postsynaptic membrane, causing the sarcolemma to reach threshold sending excitation or (an action potential) over the whole surface of the sarcolemma. *Excitation of the sarcolemma causes excitation of the T-tubules which are tubes continuous with the sarcolemma diving deep within the cell. The tubes carry this excitation to the sarcoplasmic reticulum SR causing the release of Ca2+ into the myofibrils space. The SR is essentially an intracellular storage sac for Ca2+. * ca2 plus binds to troponin\tropomyosin complex in the myofibrils causing the complex to move exposing the active sites on the actin molecule. * The myosin cross bridge heads then attach to the active sites on the actin, swivel, release, reset, attach, swivel, release, reset, splitting the ATP per cycle. * The brachialis and biceps brachii develop into a tension and shorten, the elbow flexes.

Use it or loss it

However you can lose it, use it or lose it. In about two weeks of inactivity you will lose 12 to 15% of your aerobic capacity. Within 2 months almost all improvement is lost. With complete bed rest you will lose about 1% of aerobic capacity per day eventually down to your genetic minimum.

Lo 2.2um

Humans 2.2um Functional range to produce force at about 1.6 to 2.6um Lo represents the ideal interaction between Actin myosin for all the myosin heads can interact with an action filament to produce a force .

Strength training resistive training benefits on the cardiovascular system or aerobic metabolic adaptation.

If we expect to see any cardiovascular adaptation it will be minor and the aerobic adaptation will be even less. You can however focus structure resistive forms of training like circuit training that can be focused on one system or the other. What does happen is the tendency to describe benefits to a form of exercise because you have a biased for that exercise it's called confirmation bias. In reality the evidence shows us that a mixture of resistance and aerobic exercise training appears to be the most beneficial for overall health. In addition resistance training alone does not utilize calories expended energy the way that aerobic exercise does. Most resistant training is comparable to walking on level ground in terms of caloric expenditure. There are benefits to resistive training but caloric expenditure is not one of them.

If we Vary frequency intensity and duration what impact will varying each of these parameters have on the magnitude of adaptation?

If we very FREQUENCY while holding intensity and duration constant moderate levels what improvement in VO2Max *3x week-70% of genetic potential *4-5xweek- 95% I'm genetic potential 6-7xweek-Little additional improvement only the elite athletes look for the last 5% improvement in the O2 max and then the injury rate becomes an issue. Therefore a significant consideration in injury rates versus frequency. These rates are with weight-bearing exercise however swimming and cycling have similar injury rates due to repetitive use injuries. *3xweek-10% injury rate *five x week 40% injury rate

What determines motor unit properties the nerve cell or the muscle cell?

In a cross re-Innervation study in humans most muscles are heterogeneous in terms of fiber type meaning that they have similar percentages of each type across all muscles with just a few exceptions... Soleus being primarily 80% SO. (This muscle become super sore when exercised remind me to tell you a story when I was a young PT) And animals there are some muscles that are hundred percent one motor type versus the other. In the rat the Solias muscle is 100% SO and the plantaris muscle is 100% FG. Both are plantar flexors(extensors) In this study when the soleus was re-innervated with an FG from the plantaris the SO muscle cells begin to become more FG like. In the plantaris the FG muscle cells when Re-innervated by the SO from the soleus begin to become more SO like. This suggests that the nerve determines the motor unit type which success that is why all the muscle cells in a given motor unit have a homeogenius properties. There appears to be a substance referred to as neurotrophic factor released in the nerve cell a-mn into the sarcolemma that affects the behavior of the muscle cells including changing the gene expression causing it to adapt to be a certain type of cell. This has a little applicable value from a training perspective but it helps to understand the control mechanisms.

MET Metabolic equivalent or task is measurement

Is a measurement that is intended to standardize common work rates across a range of work rates. One MET is defined as we owe two of 3.5 mL per kilogram per minute which is average resting VO2. Work rates are expressed in Mets as multiples of the resting work rate. For example at work rate 2 METS slow walking is two times that of a resting rate. Vigorous aerobic activity would be in the 8 to 10 METS range.

Results of training in triathletes training in three sports three separate modalities

Look at their differences in maximum responses to each different modality. Showing specificity of training but also specific adaptation to the specific training. Note that the testing modality is specific to each activity. The measured VO2Max for each modality declines with the Total muscle mass in gauge for each activity running first then cycling and finally swimming. Similar differences in heart rate max. You would expect VEMax to follow suit however you can see that swimming be Vemax is significantly lower because it is a mechanical issue not a physiological issue. The external compression of water along with the limited opportunities to breath with which each stroke reduces be Vemax. It impacts our ability to develop a higher VO2Max and the fact that we are using smaller total muscle mass for swimming.

Muscle Strength 1RM Muscular strength - pounds or kilograms

Maximum amount of force that a muscle can produce in a single movement. One maximum repetition or 1RM. The maximum amount of weight that you can lift one time only. If you can lift that weight a second time it's not a one RM.

Assessing exercise intensity

Measured in percentage of maximum heart rate because of its use of measurement. Max Heart rate equals 220 - age. At what percentage of your maximum aerobic capacity are you exercising, what percentage of VO2 max? There is a positive correlation between percentage of heart rate max and percentage of VO2 max but it's not directly proportional. Why? Percent heart rate max is measured from a heart rate of zero you take your max heart rate and take a percentage. Mathematically it's measuring your heart rate from zero to maximum and taking a percentage. Is your heart rate every ever zero no. To see the relationship between %heart rate max and %VO2max table 3 using a percent of max heart rate to assess aerobic exercise is not perfect but good enough. It tends to slightly underestimate aerobic exercise intensity.

Hypertrophy and hyperplasia

Mechanism by which the increase in muscle strength occurs. To potential mechanisms Hypertrophy - is defined as an increase in the diameter of cross-sectional area of the individual muscle cells. For strength training gains to occur the underlying cell diameter increases must be due to increased myofibril density. Myofibrils density is a increase in the number of myofibrils In the adapted state. Remember the myofibrils are primarily made up of the contractile proteins(Actin myosin) and their supportive regulatory structures. The increase in the number of contractile proteins in turn allows each muscle cell to produce more force more myofibrils in parallel. This allows each affective motor unit to be able to produce more force. Note that when a motor unit is stressed in this way all the muscle cells and fibers in that motor unit increases in cross-sectional area with the whole motor unit gaining in strength. Hyperplasia-this is an increase in the actual number of the muscle cells. The Text Support's hyperplasia in human models but the reality is evidence this weak. FOr hyperplasia to have any real effect on muscular strength requires functional hyperplasia a complete new muscle cell attached tendon with standard nervous intervation. It has much more efficient ways to gain muscular strength. What is difficult to assess is outside range of development is push with extreme bodybuilders. Studies in this area's are difficult to conduct and get Roci or a lot reliable results. In humans hyperplasia while possible if not probable under certain training conditions is not likely because of most strength acquisition. Hypertrophy is the source of bulk if not all of the strength gains. This is what the bulk of research shows us at birth things are relatively fixed in terms of motor unit profile in terms of contraction speed. The exception is metabolic profile. The differentiation of other muscle cell divisions is not specifically quantitative in nature only qualitative. It has to do with how the differences in the cell types are assessed measured using histochemical versus bio chemical techniques.

Reversibility of gains in aerobic capacity is driven by turnover rate of proteins. Reversing gains in aerobic capacity is primarily driven by what is referred to as the turnover rate of proteins. Enzymes are proteins. Proteins have a lifespan that varies significantly by type of protein and function.

Metabolic enzymes have a very short lifespan and are turned over or broken down naturally within days. Other proteins such as structural and contractile proteins have a much longer lifespan. As the metabolic proteins are degraded or catabolized they must be replaced to sustain the gains in aerobic capacity. If they are degraded and there is no stimulus to resynthesize the proteins (remember DNA/RNA then we will see a net loss of metabolic enzymes. If Chronic training continues there is a stimulus to continue to synthesize protein within the affected cells and maintain metabolic capacity. There can be anywhere from zero gain (maintenance) to net gain (increased VO2Max with aerobic exercise) in metabolic enzymes depending on the quality and quantity of the stress. This is why if you don't provide a regular stress to the system at least once every three days we begin to see a decrement in capacity and performance. It probably will take a week or more of an activity before you get it begin to notice significant decrements in performance.

Excitation - contraction coupling EC

Motor neuron arising in the brain or spinal cord conducts action potentials travel to hundreds of skeleton muscle fibers within a muscle the sequence of events that converts action potentials in a muscle fiber to a contraction is known as excitation contraction coupling. If we look at a single muscle fiber we see that an action potential travels across the entire sarcolemma and is rapidly conducted into the interior of the muscle fiber by structures called transverse tubules transverse or T tubules are regularly space in foldings of the sarcolemma that branch extensively throughout the muscle fiber. At numerous junctions the T tubules make contact with the calcium storing membranous network known as the sarcoplasmic reticulum or SR. Where it buts the T tubules the SR form sack like bulges called terminal cisternae. One portion of a T tubules +2 adjacent terminal cisternae is known as a triad. the membranes of the T tubule and terminal cisternae are linked by a series of proteins that control calcium release. as an action potential travels down the T tubules it causes of voltage sensitive protein to change shape. this shape change open the calcium release channel in the SR allowing calcium ions to flood the sarcoplasm. this rapid influx of calcium triggers a contraction of the skeletal muscle fiber. calcium ions are responsible for the coupling of excitation to the contraction of skeletal muscle fiber.

motor unit motor fiber types systems

Motor unit classification system table 1 and figure 20 Basic properties of different classification system is similar FaceTime different measurements assessment techniques biochemistry histochemistry physiological properties etc. Biggest problem is harvesting use for muscle tissue samples. The challenge with the biopsy is that it may not be representative sample and difficult to make statistical comparisons. Histology is based on cutting thin samples of tissue and placing it on a glass slide and staining the tissues with chemicals. Succinate dehydrogenase SDH for aerobic metabolic properties. Phosphofructokinase PFK for anaerobic properties differentiating of myosin ATPase. These are quantitative comparisons only with staining thresholds that suggest a minimum quantity of the given enzyme but not the absolute amount. Biochemical assays require emulsifying the tissues and performing primarily polymerase chain reaction PCR techniques. These give us a quantitative measures but in a heterogeneous tissue, we cannot differentiate as to what enzyme goes with what parts of the tissue, only gross assessment of the total tissue assessed.

Muscle cell

Muscle cell referred to as the muscle fiber. It's delineated by its membrane and the sarcolemma. Muscle cells have a number of unique feature when compared to other cells *Length it is long related to other cells the longest individual cells are in the sartorius muscle which connects the anterior pelvic bone to the posterior medial tibia. Average about 100 UM in diameter. Hair is about 50 UMN diameter. *Multi nucleation. Muscle cells are rare in that they are multi nucleated. The nucleus contains DNA which is responsible for coding proteins for synthesis which proteins and then what quantity are synthesized in that cell. Multinuclear help solve the problem of sufficient protein synthesis demanded by the large protein requirement of muscle cells and a large volume of the cells. * specialization muscle cells are highly specialized. Cells that can deform themselves changing in their length is rare. The complex protein organization within the cells, specialized attachments and the lever systems tendon and bones allow us to use the specialized cells to move about our environment. However without the lever or skeletal system or a little more than boneless chicken.

Muscle memory-common confusion

Once trained the muscle can remember what it was anything more quickly and easily return to that state of fitness. FALSE The reality is that muscle remembers nothing. It only response to the stress you apply to it. What remembers is your brain the central nervous system. Once you've trained the discomfort of training is less objectionable and for Some they enjoy it. There's a natural tendency to attempt to return to levels of intensity that you were when you stop training regardless of the reason. You tend to work at higher than ideal exercise intensity's for an untrained individual. As a result you adapt faster. Remember that we said the Intensity is the primary driver for adaptation. This is an example of it, but it does not come without risk of injury. Understand the risk and act accordingly.

Hypertrophy

Rat soleus is 100% slow twitch, yet we can see significant hypertrophy. Two populations of rats genetically identical. Group one is the control group which receives no training. Group 2 is the hypertrophy group which is resistant strain. A rat in a cage with the wire mesh bottom that is raised off the floor at the top of the cage is a light adjacent to the bar and the bar is pressed it releases a pallet of food. The red has to has a harness on his midsection above his hips with the chain attached the chain hangs below the wire mesh cage. If we put a weight on the chain Where is the light which the red is trying to reach up for releasing the food. The rat squats back down to eat the food. The Rat has performed one squat. Rat quickly learn to continue squats without the food incentive. Just flashing the light will stimulate them to perform. They will do Hugh quantities work more than humanly possible and we see significant hypertrophy. The muscles then remove from the wrap frozen cut into thin sections the glass slides. The control group has more space in between the cells than the hypertrophy group, the cells are larger with much less space in between the cells. In humans are appears to be a difference between males and females in terms of absolute muscle strength. Relative strength appears to be very similar. Force per MCSA (muscle cross-sectional area ) measured in newtons MCSA is approximately 6N/cm2. From an adaptive perspective as we train we see an increase in force production from the muscle. We also see selective increase in CSA in predominately the fast motor units as compared to the Slow motor units. SO motor units do hypertropy but just not as much as the FG when the FG's are recruited and trained repetitively.

Size principle of motor unit recruitment determines the order of motor unit recruitment. What determines the sequence of motor unit recruitment?

Recruitment order is primarily determined by the size of the a-mn soma. SO smallest FOG next FG closely intermingled Smaller somas have a lower voltage threshold for threshold for excitation and a smaller internal cellular space allowing inputs to more easily sum or add together temporarily and spatially. This mean that less input stimulation from the motor cortex is required to bring them to threshold. If you have a motor neuron pool for elbow flexors in the ventral horn of the spinal cord C5 segments you have an input into the pool from the motor cortex via the UMNs. UMNs will synapse with a variety of a-mn somas SO FOG FG that represent the elbow flexors. What will determine which motor units are actually recruited is the intensity of the stimulation from the motor cortex balanced against theProperties of the a-mn soma above. With a low level stimulation possibly a few SOs will be recruited as the intensity the simulation increases more force is being requested by the motor cortex and more motor units will be recruited. Initially almost all SOs then FOGs then FG's when a lot more force is required. The only thing the motor cortex is concerned with is force production. It is the organization at the spinal cord level that determines which motor units will be recruited and how long the force can be recruited and maintain without fatigue. Greater percentage of SOS and FOGs an individual has the more force that can produced for longer periods of time without fatigue. If the individual has a greater percentage of FG motor units their capacity for extended duration activation of motor units is limited by their limited aerobic capacity. It's not to say that they have no aerobic capacity it's only that they have more limited capacity compared to the SO motor units. Average individual has about 50% SO 50% FG FOG nominal percentage Individuals with the propensity to excel aerobic activities may be more in the 60 to 70% SO with a balance of FOG/FG. Individuals that excel in sprint power types of activities tend to be more 60 to 75% FG with a balance S0. This is fixed at birth and genetic and we will not see any changes in terms of slow versus fast percentage. But we can change is the metabolic profile and that changes with specific types of training regardless of your initial motor unit profile that's genetic. Fast versus slow is genetically determined., We can't change that with training. We may see some shifts from FG to FOG and vice a versa. If you stress and FG motor unit long enough and hard enough as with aerobic exercise not resist at the motor unit may start to develop more mitochondria in response to the stress and eventually become more FOG like.

Regulatory proteins Fig NM.5

Responsible for regulating the contractile state of the Sarcomere. * tropomyosin long thin chain like proteins run on the surface of the actin filament. * troponin- smaller globular proteins embedded in the tropomyosin along length. high affinity for calciumCA2. They are linked together in long chains is covering the surface of the actin filaments. They cover sites on Actin molecule and have a high affinity for myosin - active sites. Passive or relaxation state - troponin and tropomyosin cover the active sites preventing myosin from interacting with Actin. CA2 binds troponin causing shape change(Confirmational change in protein structure) and pulls the tropomyosin chain to the side exposing active sites on the actin filament. Myosin cross bridge heads attached to the active sites on Actin pulling the actin filament toward the middle, release the Actin, reset to original, attached, swivel, release, reset, splitting an ATP per swivel cycle. When the myosin cross bridge attaches to the actin filament it swivels back to the midline of the sarcomere pulling the Actin and Z line. A large number of these sarcomeres in series representing a muscle cell each pulling its own Z line in the net effect would be shortening at the ends leading to muscle shortening-active-contracted uses ATP (ATP=ADP +P+energy) and cross bridge occurs.

Somatotopic organization of the cerebrum Fig 16

Superior view of the left and right hemispheres. Purple shaded ridge represents motor cortex. Blue ridge -sensory cortex. Motor cortex gives rise to the upper motor neuron's UMN that will eventually excite and lead to the contraction of skeletal muscle cells. The nervous system including the cerebrum has bilateral symmetry meaning if you divided in half there's a left and right side. One side is responsible for the right side of the body and the other side the left. URE after cerebrum the surface of both sensory and motor cortex is represented in cross section. There is somatotropic organization of both the motor and sensory cortexs. In the motor cortex this means there's a mapping over the surface of the cortex cortex representing the muscle cells that each area controls. Large area for hands face tongue pharynx/larynx which is the need for fine control of the hand and ability for expressions of the face and speech. Excite a elbow flexor when the area stimulated the signal is Carryed down the axon of the UPN into those cells in the muscle and causes contraction of flexion of the elbow.

Motor units with small innervation ratios (a small number of muscle fibers per a-mn in the eyes hands and face anywhere where we find fine motor control is required. If you need to increase force production in small increments find movements of the hand you would want to have a large number of small motor units allowing you to increase the force in much smaller increments as you recruit them serially allowing for much finer control of the movement. Largest Innervation ratios are in the legs especially the quadriceps. Much larger force requirements regardless of fine control, all movements are quite gross compared to the hands and face.

The a-mn somas are located in the ventral horn of the spinal cord gray matter (figure 13b) there generally grouped by function. Elbow flexors-C5 segment. They receive input from the UMNs representing the flexor area in the motor cortex. This is hardwired fixed at birth with only very minor alterations possibly in terms of connectivity usually post natal. Research shows plasticity possible within the central nervous system and somewhat in the peripheral nervous system but it usually requires significant intervention to elicit adaptation.

Athletic predisposition a.k.a. individual differences and motor unit profile

The motor unit profile appears to be genetically fixed at birth. The challenge is to understand that genetic limitation and work to maximize what you have. Most of us were born with approximately 50/50 split between SO and FG motor units which predisposes us to athletic mediocrity separate from the issue of skill. Skill is learned and some individuals have faster neural networks and reaction times that are inherent, so genetics plays a role here as well although maybe not as much is the metabolic profile. The central nervous system is more plastic moldable then are metabolic capacities (minimum and maximum) and can be trained to maximize skill acquisition ...tennis stroke golf swing baseball bat shotput etc. Once we understand our genetic limitations we can work up or genetic potential. Elite athletes are predisposed genetically to perform well at their chosen activity. Often the activity chooses us more than we choose it. Most of us prefer to excel if possible at least be competent. Collegiate level to world-class sprinter (swim run cycle). typically has a larger percentage of FG motor unit 60 to 80%. Elite distance or aerobic athlete typically have a larger percentage of SO motor unit 60 to 80%. Understanding our limitations and learning to explode our maximum potential is the ultimate goal for training for maximum performance. Not everyone's goal is training for maximum support performance.

Strength Determinates of strength

The primary determinant of the ability to develop muscle strength much like anything else in the biological system is genetics. Second to that would be developmental status primary nutrition. The key determinant of strength development is applied stress specifically resistive exercises using the overload principle which is a variation of the GAS or General Adaptation Syndrome. The overload principle essentially states if a muscle is regularly stress to fatigue, short duration, high intensity resistive movements the muscle will adapt by becoming stronger to resist that stress in the future.

Aerobic exercise with 6 to 10 weeks of training you can expect a 5 to 45% increase VO2 max

The range of adaptation is determined by the quality of the exercise training, initial aerobic fitness level and genetic limitations. Genetic limitations you can do very little about but it is the most significant limitation. Everyone has a genetic floor or minimum and a genetic potential or ceiling maximum in terms of their VO2Max. There are some individuals small percentage that are considered nonresponders no matter how much they train aerobically they experience very little aerobic adaptation. With the broader population as we vary frequency intensity and duration we see adaptation.

There is a way to equilibrate comparing %heart rate max and %VO2 max developed by MJ Karvonen MD Finnish in the 1950s. This will not be tested

The result you get is the percentage of maximum heart rate reserve(%MHRR) which will equal the same percentage of VO2 max. The key difference rating term here is "reserve". Essentially what it does is measure your percent of maximum heart rate from your resting heart rate to your maximum heart rate which makes it directly proportional to the same percentage of VO2 max. And assessing your functional heart range, from rest to maximum, not 0 to maximum as in %heart rate max does. Karvonen formula you use the same percentage ranges as the ACSM uses % VO2Max 50 to 85%. The practical value of the car Varian mark formula is open to question and the ranges of choice must be recalculated as resting heart rate changes with adaptation, but I want you to be aware of us existence, more portly to understand that a given percentage of heart rate max does not equal the same percentage as VO2Max this will not be tested.

Length tension relationship of skeletal muscle - basis of the Frank starling mechanism it is based on the length of the sarcomere during the contraction (systolic in the myocardium.)

There is a small range of sarcomere lengths which skeletal muscle produces the maximum amount of force and is referred to as Lo. Humans Lo 2.2 um with a functional range to produce a force of about 1.6-2.6um Lo Is the ideal interaction between actin and myosin were all the myosin heads can interact with an actin filament to produce a force. When Z lines are stretched ,(sarcomere length of greater than 2.6 um) the number of myosin heads that can grab in Actin is reduced and thus less force can be produced. Shorter than 1.6 UMS the myosin molecules are being pushed up against the Z line the same is true. This variation in force production of the functional length of the sarcomere whole skeletal muscle is less than 20%. In vivo range 1.6-2.6um *** when skeletal muscle is loaded with a lever system the actual force at the end of the lever for example the hand at the end of the arm is a function of the torque produced at the rotational movement at the osteotendinous Junction and the length of the lever arm. The combination of varying sarcomere lengths during a contraction among the changing moment arm in the anatomical system tend to cancel each other out and not a real consideration in assessing movement and measuring force production.

Borg scale of perceived exertion or RPE rate of perceived exertion developed by gunner board PhD Swedish physiologist in 1970. This scale commonly used to assess exertion during clinical stress testing but you can also be used in recreational settings. In the right 2 column u see a comparison a percentage of heart rate max and the percentage of VO2 max. They are different percentages which is why the ACSM exercise intensity scale uses different ranges depending on if you are measuring %heart rate max or %VO2max.

This scale commonly used to assess exertion during clinical stress testing but you can also be used in recreational settings. In the right 2 column u see a comparison a percentage of heart rate max and the percentage VO2 max. They are different percentages which is why the ACSM exercise intensity scale uses different ranges depending on if you are measuring %heart rate max or %VO2max.

SO FOG FG Motor unit classification system Table 1 2

Three key parameters of each type: 1. The speed of the motor unit as measured by muscle contraction speed.-determined by myosin - ATPase type, ATPase is an enzyme in the myosin cross bridge that the Facilitate the splitting of ATP for muscle contraction. There are two speeds of ATPase, a fast one and a slow one the fast one being 2.5 times faster. This means that ATPase type will determine how fast the myosin cross bridge heads can channel, which will determine how fast the muscle cell can contract. This is genetic. In each muscle cell, gene expression will determine whether the fast type or the slow type of mATPase type is produced but not both because it's an enzyme a protein and synthesize within a given muscle cell as determined by the DNA. Metabolic profile so much more adaptable 1. Aerobic metabolic profile.-Oxidative profile-SO(slow oxidative-Slow contracting -slow mATPase- high oxidative high aerobic capacity and low not absent anaerobic). 2. Anaerobic metabolic profile.-Glycolytic profile-FG(fast glycolytic-Fast contracting -fast mATPase- high glycolytic high anaerobic capacity) 3. FOG Fast contracting fast mATPase high oxidative and high glycolytic capacities. The slow is relative to fast, the height aerobic capacity relative to low aerobic capacity, a high glycolytic capacity relative to a low anaerobic capacity. The aerobic profiles are adaptable to a certain extent. They can be changed through some type of chronic stress like exercise. The type quantity quality of exercise will determine the type and magnitude of the adaptation. A-mn of a given motor unit share similar properties to that of the muscle cell that it innervates. SO motor unit the soma is small, the axon is small in diameter, (slower conducting) the nerve terminal has a larger quantity of mitochondrial compared to the FG and a muscle cells it innervates all have SO properties. The increase mitochondrial density in the nerve terminal supports a greater need for neurotransmitter synthesis to support chronic stimulation with regular or long duration activity. The FG motor unit somas are large, axons are large diameter, faster conducting, less mitochondria in the terminal and all the muscle cells intermediate have FG properties. FOG Is very similar to FG excepted has a greater aerobic capacity both in the nerve terminal and in the muscle cell remember the soma size is greater.

Periodization Injuries and over training periodic cycle every three levels 1. macrocycle one complete training cycle 4 months 2. mesocycle 1/4 of a macrocycle 4 meso cycles per macrocycle - each mesocycle 1mo.3.Microcycle daily weekly cycle typically 2 to 3 bouts for muscle group per week 1st mesocycle Preparatory phase Strength development for one month High volume 3 to 5 sets 8 to 10 repetitions low intensity 50 to 70% 1RM 2nd Mesocycle first transition phase Strength development one month moderate volume 3 to 5 sets 5-6 repetitions moderate intensity 70-90% of 1RM 3rd mesocycle Competition strength optimization one month low volume 3 to 5 sets to the four repetitions high intensity 90 to 95% one RM 4th Mesocycle second transition phase recovery one month emphasize recreational activities along to moderate intensity activities using various exercises modes

To prevent over training with resistive exercise or any form of exercise training a periodization schedule is recommended. The goal is to minimize risk of injury and the focus on training technique. The value of resistive training to aerobic athlete has been somewhat controversy. ACSM has released a position paper supporting the value of resistive exercise as an adjunct aerobic exercise for Optum Health. Muscle atrophy with disuse in particular as we become less active with age. Studies done was 70 and €80 populations have shown dramatic improvements in muscle strength with resistive training and an overriding benefit was a better ability to perform activities of daily living. to the aerobic athlete resistive training stress is the muscles in ways that aerobic exercise does not. In particular stressing the myotendonness and osteotendoness junctions as well as the ligaments tendons and bones that strengthen them to reduce injury.

The change in OBLA as a percent of VO2 max is primarily due to metabolic adaptation

We see is a less accumulation of lactate thus delayed onset of blood lactate accumulation. The mechanisms is first and lowest impact mechanism is the Cori cycle in the liver which converts lactate back into glucose. It is not fast enough during intense exercise to be much of use as either a lactate utilizer Or glucose producer. The second mechanism is called Lactate Shuttle. And then divide by George Brooks at UC Berkeley this mechanism shuttles lactate into the mitochondria in skeletal muscles for use as a precursor in the Krebs cycle. As more mitochondria are developed as a result of the chronic intense aerobic exercise training, during about of exercise, more lactate is shut old into the mitochondria in which it was produced and less into the plasma, which decreases the accumulation of blood lactate. Lastly, lactate is preferred metabolic substance of the myocardium during exercise and further in scree says it's reliance on lactate with aerobic training. There is an isozyme of lactate hydrogenous LDH that converts Lactate into Pirate Bay, it's produced primarily in the myocardial cells instead of the type of LDHM that converts pyruvate into lactate that we see in the skeletal muscle cells. That is why the myocardium is essentially 100% aerobic, very little anaerobic capacity (which converts pyruvate into lactate)so with this we see less accumulation of lactate in the plasma for a given intensity of activity.