KIN 399 Final study guide
KIN 399 Final study guide KIN 399
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This 41 page Study Guide was uploaded by Annmarie Jaghab on Sunday May 1, 2016. The Study Guide belongs to KIN 399 at University of Miami taught by Dr.Sig in Spring 2016. Since its upload, it has received 29 views. For similar materials see Neuromuscular basis of training in PHIL-Philosophy at University of Miami.
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Date Created: 05/01/16
KIN 399 final study guide Overload and bioenergetics -training specificity: The change made by a biological organism is a direct reflection of the nature of the stress to which it is exposed. -factors associated with specificity include: 1) Enzyme structure, concentration and distribution 2) Organelle structure, concentration and distribution 3) Changes in fiber type and related structures 4) Hormones -phosphagen system: (anaerobic) ADP+PCr+H+ATP +Cr. Catalyzed by creatine kinase. Has buffering capacity from the H+ -The myokinase/AMP Kinase reaction is especially prevalent during high-speed work or heavy resistance training, and is more common in Type II (fast twitch) muscle. ADPAMP +Pi + Energy. This energy is combined with ADP +Pi ATP -oxidation: loss of electrons/hydrogen -reduction: gain of electrons/hydrogen -conversion of glycogen to glucose 1 phosphate is triggered by? ADP, AMP, IMP, adrenaline, Ca, Mg -conversion of glycogen to glucose 1 phosphate is inhibited by? ATP, H+, G6P -G1P changes to G6P via phosphoglucomutase -F6P changes to F1-6DP via PFK -conversion of F6P to F1-6DP is triggered by? F6P, F1-6DP, F2-6DP, G1- 6DP, P, ADP, AMP, NH3, cAMP -conversion of F6P to F1-6DP is inhibited by? ATP, H+, K+, Mg, PCr, Citrate, 2-3PG, PEP -conversion of pyruvate to acetyl coA is triggered by? Ca, Mg, ADP, H+ -conversion of pyruvate to acetyl coA is inhibited by? ATP, citrate, P -aerobic glycolysis would involve entering the kreb’s cycle -aerobic glycolysis is Beta oxidation. Makes FADH, NADH, and coA -enzyme lowers activation energy -Covalent modification of a specific amino acid subgroup affects the activity of the enzyme drastically by acting as an on/off switch. The most common example is the activation of protein kinases (intermediate enzymes) by phosphate groups. It is very important in metabolism as major effectors of energy needs within the cell -Allosteric enzymes regulate enzyme activity: Binding of molecules other than substrate at sites other than the active site. Can be affected by positive or negative effectors. Exhibit a sigmoidal curve due to cooperatively among subunits. Very important in metabolism as major effectors of energy needs within the cell -positive modulators of enzyme activity: 1) Cofactors = metal ions such as Zn , Mg , or Mn . +2 2) Coenzymes = organic molecules which activate the enzyme. -apoenzyme (inactive) + cofactor = holoenzyme (active) -isozymes/ isoenzymes: Different molecular forms of the same enzyme that catalyze same reaction through same mechanism. They provide different kinetics. Usually oligomeric enzymes with complex structure (multiple subunits). Ex. LDH1 and LDH2 are in heart and slow twitch skeletal muscle. LDH3 are in all. LDH4 and LDH5 are in fast twitch skeletal muscle. -High Intensity Exercise = Anaerobic and Glycolysis = Lactate production. LDH4 and 5, pyruvate to lactate -Low Intensity Exercise = Aerobic and Glycolysis = Lactate removal. LDH 1 and 2, lactate to pyruvate -Myosin light and heavy chains differ in different skeletal muscle fiber types -Every time the body is trained in a specific way it restructures its metabolic machinery (enzymes) to meet the specific need, often at the cost of other enzyme systems. -organelles are like cellular organs -For a muscle to be able to meet the specific needs demanded by an overload, what changes should it make in its organelles? Example: Distance running versus sprinting, distance runner has a much higher mitochondrial count than in a sprinter. Capillary density is more in a distance runner. For both the absolute number of capillaries may go up. -rates of ATP regeneration: •Max rate of ATP breakdown rate = 11.2mmolATP/kg d.m.w./s •CP = 8.6mmolATP/kg d.m.w./s app. or 76.8% of ATP breakdown rate •Anaerobic glycolysis = 5.2mmolATP/kg d.m.w./s app. or 46.4% of ATP breakdown rate •Aerobic glycolysis = 2.7mmolATP/kg d.m.w./s app. or 24.1% of ATP breakdown rate •Aerobic breakdown of fat = 1.4mmolATP/kg d.m.w./s app. or 12.5% of ATP breakdown rate -as you increase the exercise duration, the more energy comes from aerobic sources -fatigue can be attributed to: 1) a lack of available ATP for actin-myosin coupling, Na/K pumping, and Ca uptake by the SR 2) an inhibition of any of the above by various metabolic products 3) alterations of excitation contraction coupling from the action potential to Ca release from the SR -pedaling with creatine vs. placebo: faster with creatine -pedaling with bicarbonate vs. placebo: faster with bicarbonate Sprint Training and bioenergetics -Metabolic adaptations to sprint training, and to a certain extent the subsequent detraining adaptations, are largely dependent on the type of sprint training undertaken. Indeed, the bioenergetics of sprint exercise bouts differs markedly depending on the sprint duration and recovery intervals -Energy for muscle contraction during brief maximal exercise of 10 seconds or less is primarily derived from the breakdown of stored muscle phosphagens, such as ATP and PCr, and glycolysis. However, when short sprints are repeated or when sprint exercise lasts for up to 30 seconds, the contribution of anaerobic energy production to the energy yield decreases and a significant amount of energy is derived from aerobic metabolism -Recent evidence suggests that 13% of energy during a 10s sprint and 27% of energy during a 20s sprint is generated aerobically. In fact, no form of exercise can be purely anaerobic or purely aerobic. Given the differences in metabolic demands, it follows that intramuscular adaptations depend on the nature of the sprint-training program and that adaptations in both anaerobic and aerobic energy systems will occur in response to training. -overload causes changes in enzyme activity: Elite sprint athletes have showed the capacity to deplete PCr levels by over 60% during a 60m sprint. Myokinase activity has been shown to increase (~20%) after short (5-second work intervals with 25- to 55-second recovery). Work:recovery duty cycles -looked at enzyme profiles of healthy males doing sprint training: Mg ATPase, MK, and CPK increased -Mg2+ ATPase went up meaning you increase the rate at which you utilize energy, which increases the rate of the cross bridge cycle, which increases the rate at which the muscle contracts meaning you can increase power output and fiber type activity is changing -long sprints and short recovery leads towards aerobic systems because you don’t have time to recover so you are out of breath -the longer the work period the more utilization of aerobic metabolism -a longer recovery gives greater utilization of anaerobic sources because there is a longer amount of time to replace high energy phosphates. -Longer sprints / long recoveries lean toward aerobic systems but PFK elevation indicates improved carbohydrate utilization -PFK and hexokinase are markers of both aerobic and anaerobic glycolysis so you can’t use that to distinguish -a relatively large activity of CPK is evident in the muscle of sedentary individuals and the stress induced by a period of sprint training may not be sufficient enough to stimulate an increase in CPK activity. Therefore, although higher level sprinters are able to use PCr more rapidly than others, sprint training consisting of prolonged sprint repetitions does not appear to be able to elicit any change in CPK activity (CPK is very high in sedentary individuals. Constantly at a high enough level so it’s hard to see changes in it) -adenylate cyclase going up shows an increase in the phosphagen system -the LDH-M marker shows the greater increases (even if aerobic enzymes are increasing) to show anaerobic preference Resistance Training and Enzymes -event cascade in resistance training that signals long-term adaptation: Resistance exercise stimuluslactic acid accumulationaltered muscular environmentenhanced stimulus (motor unit recruitment, hormones, muscle damage)cumulative training responseincrease force generating capacitystrength and power adaptation -Muscle fiber types of women after resistance training, quantitative ultrastructure and enzyme activity study was done with 12 college aged women and they did heavy resistance training twice weekly. Results showed that all fiber types increased. The results suggest that this type of high-repetition resistance training causes the intracellular components of all fiber types to increase proportionally with an increase in fiber size. In addition, the enzyme analysis indicates the muscle as a whole may increase its oxidative phosphorylation capacity in conjunction with the decreased percentage of type IIB fibers. -Adaptations in rat skeletal muscle following long-term resistance exercise training. Ten male Wistar rats (3 weeks old) climbed a 40-cm vertical ladder (4 days/week) carrying progressively heavier loads secured to their tails. After 26 weeks of training the rats were capable of lifting up to 800 g or 140% of their individual body mass for four sets of 12-15 repetitions per session. -tested each muscle and found that resistance training had the greatest impact on the fibers of each muscle with the lowest SDH activity -Despite an increased ability of the rats to lift progressively heavier loads, this heavy resistance training model did not induce gross muscle hypertrophy nor did it increase the force-producing capacity of the EDL or soleus muscles. -Increased muscle oxidative potential following resistance training induced fibre hypertrophy in young men. -We conclude that resistance training provides a stimulus for improving muscle oxidative potential as reflected by the increased activities of CS and β-HAD following resistance training induced hypertrophy. -Maintenance of myoglobin concentration in human skeletal muscle after heavy resistance training. -These subjects were divided into two groups: those undergoing the bodybuilder protocol (interval RT group, IRT, n=6) and those performing the power-lifter protocol (repetition RT group RRT, n=6). Results suggested that myoglobin and mitochondria enzymes were regulated by different mechanisms in response to either type of RT. Moreover, the maintained [Mb] in hypertrophied muscle should preserve oxygen transport from capillaries to mitochondria even when diffusion distance is increased. -looked at body builders, Olympic, and power lifters vs control. Control had higher CS and HAD activity. Fast twitch fibers of lifters had a significantly lower level of oxidative capacity than the control group. LDH and MK were higher in the lifters than the control. If we look at the activity of LDH we know it is higher in the resistance training group vs control regardless of what isozyme it is. -LDH and MK were higher in fast twitch muscle fibers. -acyl coA dehydrogenase was faster in slow twitch -results suggest that long-term heavy resistance training results in specific metabolic adaptations of Type 2 and Type 1 muscle fiber types. These changes appear to be influenced by whether the individuals are engaged in hypertrophy or Olympic/Power Lifting type training. Endurance Training and bioenergetics -The cellular processes behind muscle plasticity involve qualitative and quantitative alterations in muscle fiber cells and associated structures. Alterations to endurance training over a period of weeks to months involve differentiation of the muscle fibers towards a phenotype with a high mitochondrial volume density. PGC-1 a peroxisome proliferator- activated receptor activates a transcription factor and increases organelle biogenesis. -mitochondrial content within skeletal muscle can be reduced in mitochondrial myopathies, aging or low physical activity. This leads to decreases in endurance performance. Time and intensity dependent increases in daily physical activity influence mitochondrial volume and function such that deficiencies in energy production can be ameliorated and increases in endurance performance can be re- established. At the molecular level, the signals are triaggered with each bout of exercise likely arise from a combination of rapid ATP turnover and altered calcium levels that when sustained for sufficient durations and amplitude result in mitochondrial proliferation. These signals activate signal transduction cascades resulting in changes in TF activity and the up-regulation of diverse genes, including those involves in organelle synthesis and oxidative phsophorylation. The recent identification of PGC1 has enhanced our understanding of the mechanisms underlying the formation of the organelle. The precise role of PGC1 in coordinating contractile activity induced mitochondrial bioenergenesis is currently under investigation. This enhanced organelle biogenesis provides a negative feedback mechanism to reverse the initial deficit in mitochondrial function and content. -Time-course training/detraining adaptations in mitochondrial content of skeletal muscle show that 50% of the increase of mitochondrial content was lost after 1 week of detraining and that all of the adaptation was lost after five units of detraining. Also, it took 4 weeks, of training to regain the adaptation lost in the first week of detraining. So it takes less time to retrain than to train from scratch -MCT is monocarboxylate transporters, they transport lactate -endurance training effects on the isoforms of LDH: data suggest that MCT1 expression in muscle fibers may reflect the extent to which transport of lactic acid into the cell is required for its oxidation as a respiratory fuel. The presence of high levels of MCT1 in heart muscle is consistent with this view. MCT4 is present in all muscles, but at a lower concentration in predominantly oxidative muscle such as soleus which suggests that this isoform is most important for lactic acid efflux from muscles that rely more on glycolytic metabolism. Endurance training increases expression of MCT1 in muscle because of insertion of MCT1 into both sarcolemmal and mitochondrial membranes, training has variable effects on sarcolemmal MCT4, and both MCT1 and MCT4 participate in the cell-cell lactate shuttle, whereas MCT1 facilitates operation of the intracellular lactate shuttle. Biomechanical Training Specificity -biomechanical specificity relies on: •Specific muscle groups •Specific joints •Specific joint angles •Specific contractile states •Specific movement speeds •Specific loads •Specific motor patterns •Structural changes -testing tool: multi-camera 3D movement analysis with synchronized force plate and EMG. Combination gyroscopic accelerometer units. High speed camera. - what causes the differences in strength curves we see between studies and movements? •Population: Age, Gender, Body type •Psychological Factors: Motivation, Fear of Injury •Physiological Factors: Muscle Fiber Type, PCSA, Recruitment Pattern, Fatigue levels •Geometric Factors: Location of axis of rotation, Muscle attachment points, Muscle line of action, Joint range of motion, Joint degrees of freedom. •Exercise Conditions: Type of contraction, Contractile speed, Number of joints in the kinetic chain, Involved joint configurations, Uninvolved joint configurations, Line of COG -It was found that cyclists tended to be stronger at short compared with long rectus femoris lengths, whereas the opposite was true for runners. This finding may be associated with an adaptation of the rectus femoris muscle to the requirements of cycling and running. -the knee extensor profiles of young female athletes show an age- related angle specificity that should be accounted for when treating athletes within the age range examined. -Contractile states: 1) isometric: constant joint angle 2) isoinetrial: the outside load is the same all the way through 3) isokinetic: constant speed ex. Biodex machine -Improvements due to training are optimized in the contractile state in which training occurs -concentric training is preferable for development of concentric strength and eccentric training is preferable for development of eccentric strength -for force velocity curve, force increases as velocity decreases -shift in force velocity curve with explosive weight training increases the force component -exercise prescription should target the specific muscles which are to be used in the sequence which is required for successful movement. -Older individuals develop a lifting strategy targeting the upper extremity muscles rather than resorting to lower extremity power. This indicates lower extremity muscles should be strengthened -It is our hypothesis that training older subjects using cables will increase core utilization, shifting them to a more efficient movement strategy for this and other transfer tasks. Speed Specificity -mechanisms for speed specificity: •Changes in Force/Inertia relationship •Changes in enzyme profiles or myosin ATPase activity •Contractile property changes within fiber types •Selective activation of motor units •Length adaptations by agonist and antagonist muscles •Increases in stored energy transfer during stretch-shortening cycle •Sequential firing of multiple joints •Synchronization of synergistic muscles •Reduction in tri-phasic “braking” •Motor unit firing frequency -study looked at speed specific changes in power with 22 College-aged males, Two-leg isokinetic leg extension, three times / week -found load specific changes in the force velocity and power curves -looked at skeletal muscle plasticity with marathon training in novice runners. The purpose of this study was to investigate leg muscle adaptation in runners preparing for their first marathon. 13 weeks progressive training 4 times per week starting with 10 miles/wk and concluding with 36 miles/wk. This was followed by a 3 week taper -in the face of increases in oxidative capacity of the less oxidative muscle fibers and selective increases in cross-sectional area of the quad MHC I dominant fibers. There was also a decline in shortening velocity, absolute power and power per unit body weight for the quads…an indication of speed, and perhaps contractile, specificity -According to the Henneman size principle, during any muscle contraction, the smaller, slow-contracting and fatigue-resistant motor units are recruited before the larger, fast-contracting fatigable units -training could change the size principle. In complex muscles, motor units form subgroups, and the composition of the subgroup depends on the task. Within each subgroup or “task group,” recruitment occurs according to the size principle. Muscle Fiber Types -methods for fiber typing: 1) histochemical staining: in acid, type I fibers stain dark and type II stain light. In base, type I fibers stain light and type II stain dark (opposite seen) 2) immunocytochemical staining: antibodies are created to mark different forms of the myosin heavy chains 3) electrophoresis: separates based on charge and density 4) Immunofluorescent staining: different fiber types glow different colors -fiber type specific programs of gene expression are not restricted to the MHC isoforms, but exist for many other muscle proteins. Fiber type specific isoforms exist for: the essential and regulatory myosin light chains (MLC), the three troponin subunits, tropomyosin, a-actinin, Ca regulatory proteins (such as SR Ca ATPase, Calsequestrin, and the a subunit of the DHPR). -energy supply and ATP production lead to membrane excitability and action potentials EC coupling, control of cytosolic Camolecular motors, energy conversion. Muscle contraction function requires the coordinated activity of four major cellular functional compartments (membrane excitation, excitation-contraction coupling, contraction, and energy supply) whose molecular composition and functional properties diverge among muscle fiber types -FATZ: tether calcineurin to alpha-actinin at the z-line -ZASP: mechano-sensing protein -Myotilin: formation and stabilization of sarcomeres -Myopalladin tethers nebulin -FHL1 loss associated with muscular dystrophy -Myomesin interacts with myosin and titin, possibly connecting thick filaments with the third filament system -the levels of some proteins vary in a fiber type-specific manner. These quantitative differences may be graded (e.g., the fast Ca+-ATPase isoform SERCA1, which is expressed at higher levels in type IIB fibers compared to type IIA fibers), or all or none (e.g., phospholamban in type I but not in type II fibers or parvalbumin in type II but not in type I fibers). -5 women and 5 men, 6 week training study on bicycle ergometers. After 6 weeks of training there were significant changes such as an increase in VO 2MAX an increase in the percentage of type I fibers, and a decrease in the percentage of type IIB fibers. Changes in the volume densities of mitochondria increased 35% in type I, 55% in type IIA and 35% in type IIB fibers. The relative increase in subsarcolemmal mitochondria was larger than in interfibrillar mitochondria in all fiber types. There was also a significant increase in the volume density of intracellular lipid in type II fibers. It is concluded that high intensity endurance training leads to an enhancement of the oxidative capacity in all muscle fiber types. -looked at patients with stable chronic heart failure and put them in a bicycle test. Mitochondrial ultrastructure of skeletal muscle was analyzed by ultrastructural morphometry; Cytochrome c oxidase activity was visualized by histochemistry and quantified by morphometry. The fiber type distribution was determined by adenosine triphosphatase staining. Concluded that patients with CHF who engage in regular physical exercise show enhanced oxidative enzyme activity in the working skeletal muscle and a concomitant reshift to type I fibers. Fiber types Study took untrained older men and looked at muscle fiber characteristics and nucleo-cytoplasmic relationships -when a muscle gets bigger we create more myonuclei via satellite cells (outside the nucleus, but we activate them and incorporate them as myonuclei) -took a cross section of the vastus lateralis of an untrained elderly man, dystrophin antibody -time by group interaction (difference between the two groups) -showed cross sectional length and area can both be changed with training -in the trained group, there was an increase in cross sectional area which was greater than the slight decrease in the control -even though the muscle grew in cross sectional area and length, it still structurally reorganized itself to maintain the right number of nuclei to maintain protein synthesis. -so we maintain a proportion between length, cross sectional area, and number of muscle nuclei in a cell -when looking at the percent fiber type changes, we see that type IIB (fast twitch glycolytic) fibers decrease post training and type IIA (fast twitch oxidative) fibers increase. This is expected from resistance training because we want muscle fibers to become more oxidative Study looked at single muscle fiber diameter, peak force, and specific tension of vastus lateralis muscle fibers in older women before and after resistance training -there was an increase in the type I fibers but not in the type IIA fibers meaning there might be a slight gender inclination to greater increases in cross sectional area in type I fibers. -from pre to post, there were increases for peak force in both MHCI and MHCIIA (we see a significant increase in the amount of force produced in MHCIIA even though the cross sectional area didn’t change much. So it is not necessarily true that an increase in cross sectional area is parallel to an increase in force production since there are many other factors (no absolute relationship) -found no significant difference and no time effect -type IIA was always faster than type I (no time by condition interaction) -we can increase power in these women specifically in the load portion since there is no change on the velocity side -absolute power is how much force produced contracted at a certain speed -normalized power is how much force was produced per cross sectional area -once you take out the impact of cross sectional area, the difference in power is not that great meaning that most of the improvement had to do with the fact that the muscle got bigger. -the impact of cross sectional area on force production in the study was greater in type I than type IIA Study now compares the men and the women MHCI fibers -diameter and force went up in both men and women -in the men, force per cross sectional area went up but in the women, it went down. This is because force production is more dependent on cross sectional area in the women than the men -velocity only increased in the men -absolute power went up significantly in the men but not in the women -normalized power went up in the men but in the women it went down. Shows the interdependence between cross sectional area and force with a dependence on velocity since no change in velocity for women. Study now compares the men and the women MHCII fibers -the data shows that PRT in elderly women increases muscle cell size, strength, and peak power in both slow and fast muscle fibers which was similar to older men. In contrast to the older men, the older women showed no change in velocity or normalized power. This suggests that older men and women respond differently at the muscle cell level to the same resistance training stimulus. Study looks at muscular adaptations in response to three different resistance training regimens and specificity of repetition max training zones -3 REP ranges tested -there is a training continuum. At the highest rep figures, there are the lowest loads. At the lowest rep figures, there are the highest loads. -expect strength increases with 3-5RM -9-11RM good for hypertrophy -found a significant drop in Ve (amount of air moved per minute) which was just a finding that came up -both max power and time to exhaustion went up only in the high rep group. Train fast you get faster. -to improve muscular endurance, do high repetition work -to increase strength, do low repetition work -showed increases in MHCIIA and decreases in MHCIIB in all rep groups meaning that fibers are in transition from IIB to IIA (first switched to IIAB then more towards IIA) -cross sectional area went up for all fiber types (cross sectional area in all fiber types can go up if given sufficient stimulation) -intermediate group increased capillaries. need capillaries to send the lactate to another muscle so could be due to a greater dependence on oxidative metabolism and the need for a system to get rid of waste products -both physical performance and the associated physiological adaptations are linked to the intensity and number of repetitions performed, and thus lend support to the strength endurance continuum Study looks at skeletal muscle and hormonal adaptations to circuit weight training in untrained men -minimal rest, so hard to renew phosphagen systems -a more aerobically leaning type of training (a lot of work and minimal recovery in a short amount of time) -the only significant increase in cross sectional area was seen in type IIA -significant changes in MHC IIA increase and IIB decrease -overall, the circuit training did not alter percent fiber types. Increase in cross sectional area for type IIA fibers. Increase in the relative percent of MHC expression for IIA and decrease for IIB Study looks at resistance training in the very old for muscle strength, fiber types, fiber size, and MHC isoforms -at every speed there was an increase in strength but testing individuals isokinetically that have been trained isoinertially would be better trained isoenertially -when looking at the pure MHCs, MHC1 went down in favor of increase in IIA (trying to shift back up to faster contracting fibers since in older people there is a shift to type I slow fibers). The increase in IIA came from a decrease in I because there was a huge amount of type I fibers to begin with in elderly. -overall shows an increase in fiber size of the fast muscle fibers and an overall increase in the relative fast MHC IIA lead to both a stronger and more powerful skeletal muscle. There are more than three fiber types and they can be changed with training within the genetic capacities of that person Neuromuscular training -neuromuscular training shows the demands that the nervous system puts on the muscle. It dictates the muscle fiber type. -open environment: the environment is moving and a ball is moving and this dictates where you will go ex. Tennis -closed environment: nothing is moving ex. Golf -what dictates playing is an open environment is the area of movement. In an open environment, you have to restrict the area of movement. Ex. Tennis court has boundaries. In a closed environment, you make the skill more difficult. Areas of change -each cortical region has a number. Named brodman areas 1) motor cortex: area of the brain that sends out patterns of movement (when you send a movement to your muscles to do something, it is a train of movement that is constantly being modified) 2) sensory cortex: get information sent back 3) cerebellum: comparator 4) basal ganglia: comparator that says how well am I doing this 5) motor nerve: sends message to the muscle 6) neuromuscular junction: nerve talks to muscle The motor Homoculus -what dictates the amount of space taken up across the motor cortex is fine motor movement. -the motor homoculus is susceptible to change The sensory Homoculus -the sensory homoculus looks like the motor homoculus and they mirror each other Changes to Homoculus occur with training -increased branching of dendritic tree, decreased neuron/cell body density -there is a reporportioning of the surface maps of the sensory and motor homoculi Study looks at interhemispheric structural asymmetry induced by a lateralized reaching task in the rat motor cortex -trained rats always had greater cortical thickness because increased dendritic branching -look at cell counts in anterior and posterior cortical areas and see no significant differences between hemispheres of control and trained anterior (non-forlimb), but there are significantly lower cell counts in the trained vs untrained posterior hemispheres for trained rats. This is because neurons were pushed further apart meaning that there was an increase in the density of the dendritic tree -after training, cortical thickness increased, cell bodies decreased because the larger bodies pushed the cells more apart. The more messages you can send, the finer the movement can be -higher cell count=less branching=less thickness=fewer signals -lower cell count=more branching=more thickness=more signals -results show that the area representing the dominant working forelimb was increased in size by the lateral reaching task. The lower cell count seen in the trained hemisphere (contralateral to the limb) of the trained animals is indicative of greater dendritic arborization/branching due to training) -the brain will increase the number of connections in the specific area that represents the limb being used. The change then favors use of that limb or body part. So you should target the body parts most important to the skills you wish to improve study looks at functional MRI evidence for adult motor cortex plasticity. Looked at MRI for local blood oxygenation in primary cortex -it is a quantification method of measurement. Increase in blood flow means more dendrites related to that movement -finger tapping task was done using two different sequences -there was an increase in the thickness and in dendritic branching for the limb that was used. -it is a repeated measure study because one person is doing two different tasks -the same fingers are being used, so the question is not how you change the brain using different body parts. It says if you change the movement patterns of the same body parts can you change the brain in such a way that it will get better at performing a certain sequence -there was a significant increase in performance plateauing by week 3 (they got as good as they were going to get at that sequence) -during the initial training sessions, the sequence performed first yielded the highest blood flow followed by reduced flow (habituation) (this is an initiation period so more blood flow to the area, there have been no dendritic connections set up yet) -by the 4 session (day 4), the pattern had changed and the greatest blood flow was consistently seen during the practiced sequence (enhancement) (now, the practice skill requires more blood flow since there are greater dendritic connections facilitated with the practiced skill compared to the unpracticed skill. -when looking at the MRI we see that there is more blood flow during the trained movement than the untrained movement study looks at functional reorganization of the rat motor cortex following motor skill learning -for the skilled rats, since they had to reach for the food, a greater proportion of the brain is devoted to the wrist and digits -for the unskilled rat, since they had to push down lever for food, a greater portion of the brain is directed to the elbow/shoulder -the increases in specific areas for one muscle group were accomplished through the reduction in area for the less involved muscle group for that specific movement pattern (we train the neurons to get at performing a specific activity) Cerebellum and basal ganglia feedback loops -motor memory does not just reside in the motor cortex, we can modify every structure of the nervous system. -as you practice a skill, a pattern gets built up in the basal ganglia and it acts as a comparator to the message you are sending down -basal ganglia does not get information from the periphery -basal ganglia is knowledge of action -cerebellum is knowledge of results The cerebellum (lower loop) -the cerebellum acts as a comparator. It compares the actual movement being made to the motor plan being sent so that minute changes can be made to perfect the movement as it is happening. This is a peripheral feedback loop using knowledge of results to adjust the movement as it is occurring. -smoother: the cerebellum also has inhibitory cells that act like neural shock absorbers to reduce the chatter in the system -cerebellum is a number of individual cells that have positive and negative outputs that all work together and allow the movement to be smooth -the cerebellum gets input from vision, balance, propioceptor, GTO’s, joint receptors, pressure, and pain receptors Learning dependent synaptic modifications in the cerebellar cortex of the adult rat persists for at least four weeks -an examination of the number of synaptic connections per purkinje cell due to the performance of an endurance task vs an acrobatic movement task Circuitry within the cerebellar cortex -blue thing is a purkinje cell (p). the + is telling the purkinje cell to give it output from the cortex. The – sign tells it to slow down -CF are climbing fibers and give out a compound signal -MF are mossy fibers and give out one pulse after another after another like an action potential. They send out single spikes and attach to granular cell which then send the message up to the parallel fibers and the granular cell excites the purkinje cell -gave rats an obstacle course(AC) and another just runs in a straight line(MC). -significant increase in synapses for the obstacle course group -results show that complex motor tasks have a much greater ability to stimulate synaptic connections than simple motor tasks do -results also show that once a motor task has caused increase synaptic connections, these connections tend to persist for at least 3 weeks during detraining Basal Ganglia -the upper loop -sends a message from the motor cortex that says to do something, allows you to do a pattern over and over again because the basal ganglia has to capacity to hone in movements -as you send the message out, a copy of the message is being sent to the basal ganglia and it examines that copy and sends a message back up to the motor cortex and as you continue to send the sequence of signals that dictate that movement, you memorize that sequence so it is not unique and you just need to make sure everything is in the right place to do that movement A neostratiatal habit learning system in humans. A comparison of non-demented parkinson’s patients (basal ganglia damaged) and amnesiac patients (limbic diencehalic damage) on a learned motor task -if you messed up basal ganglia you would be able to say what the weather is but not point to it -if you had an amnesia problem you wouldn’t be able to vocalize if it was going to rain or not but you would be able to point to the sun or the clouds to tell -memory, in part, resides in the basal ganglia The motor nerve -we can make it get faster and give it more myelenation Ablation -the soleus is 70% slower contracting muscle and 30% faster contracting -the plantaris is 80% fast contracting fibers -if you put together the fiber type compositions of the soleus and gastracenmius you would have more slow twitch fibers than the plantaris -the gastrocenemius is 50% fast and 50% slow -there is more slow twitch activity (2.5 times more) in the overload plataris because it needs to compensate for the loss of the other muscles so it modifies its fiber types because the pattern it has to hold is at a more slow level Study looks at motor unit activation in the young and the old -takes a while for tissues to adapt (that is why you have to wait for strength increases so that the tissues can catch up to the neural increases) Synchronization of synergistic muscles -tried to see if through training they can get the synergistic nature of the two heads of the biceps to be in sync and fire at similar times -the nature of the conduction along a motor nerve and/or the prevailing connection can be changed with training to such an extent that even the predominate nature of the motor unit dominating that muscle can change. -the first changes that occur with training are neuromuscular rather than muscular so be careful not to proceed too quickly -people get stronger than their tissues can handle, so caution must be taken motor end plate -message is sent from the motor cortexbasal gangliacerebellum motor nerveneuromuscular junction where the motor nerve will speak to the skeletal muscle fiber and tell it how to contract through acetylcholine attaching to acetylcholine receptors -a new action potential starts with acetylcholine since it is a sodium/potassium gated channel. Sodium goes through first because of the concentration gradient as well as the electrical gradient. Then potassium goes out after due to the new concentration and electrical gradients -motor end plate has arborization (branches) The effects of exercise training of different intensities on neuromuscular junction morphology -HIT went up in arborization but LIT went down -the patterns already honed in on the animal were modified to a more simplistic level so that is why the arborization went down -with the HIT, the total overall branch length went up -more terminal branches need more docking spaces to unload acetylcholine to receptors, so the number of action potentials being sent across the sarcolemma of the muscle will increase per unit time -to distinguish between faster or stronger, use frequency coding. The number of trains sent per unit time tells you how fast you will move -the amount of action potentials per train tells you how forceful it will be -if you increase both force and time you increase power -complexity index: multiplies the number of branches by the length of each branch -high intensity training increased the complexity index while the low intensity index decreased the complexity index -overall, the more intense the training, the greater the complexity of the neuromuscular junction Muscle acetylcholinesterase adapts to compensatory overload by a general increase in its molecular forms -the faster you can open the receptor sites for acetylcholine to attach, the faster the signal -the rats underwent ablation of MG synergists, LG, soleus, and plantaris -nature of ach molecular forms: A12 all muscle types A8 and G2 slow G1 hypertophied G4 fast -we want a faster acetylcholinesterase so that acetylcholine can be broken down fast so the receptors can be opened fast and are ready for new acetylcholine to bind and increase rate coding (best would be to have highly branched neuromuscular junction and acetylcholinesterase). -looked at type A12 which is in every muscle and in both running and walking it increased -A8 (slow) only the walking increased significantly -G4 (fast) only the running increased significantly -G2 (slow) only the walking increased significantly -G1 is a hypertophy isoform and went up in both running and walking -Can change size, number, type and isozyme profile -more complex movements lead to greater numbers of synaptic connections and more dendritic branching in the cerebral cortex, cerebellum. And basal ganglia creating a younger brain (which can do more complex movements more quickly) -The complexity is increased by complex, high intensity training, and may actually be reduced by slow, repetitive work. So be sure you add speed, power, and agility training to your routine Overtraining, over-reaching and staleness -over-reaching: an accumulation of training and/or non-training stress resulting in short-term decrement in performance capacity with or without related physiological and psychological signs and symptoms of overtraining in which restoration of performance capacity may take from several days to several weeks -overtraining: an accumulation of training and/or non-training stress resulting in a long-term decrement in performance capacity with or without overreaching and or related physiological and psychological signs and symptoms of overtraining in which restoration of performance capacity make take several weeks or months. -staleness: when the definitions of overtraining and overreaching are used as synonyms the terms staleness and overtraining syndrome are often used to indicate the state described as overtraining Types of overtraining -sympathetic form only (sprint, HIT): prolonged recovery, increase in RPE, increase in resting HR, sudden weight loss -Parasympathetic form only (endurance): unaffected recovery, mood swings (depression, irritability), decreased resting HR, no weight loss -symptoms of both: decreased performance, quick or chronic fatigue, sleep disruption -fatigue and apathy dominate in the parasympathetic type of overtraining which is typical for endurance sports -restlessness and hyperexcitability dominate in sympathetic type which is more typical in explosive sports or related to additional significant non-training stress factors. General adaptation syndrome is overlayed on super compensation curve -hansalier (psychologist) describes stress in terms of stages: alarm stage stress becomes a normal everyday activity so the body can adapt in resistance stage, but if the stress is driven to the point beyond what the body can handle, they enter the exhaustion stage (physical and mental) overreaching and overtraining in endurance athletes -without sufficient recovery, each time someone goes to train again, they get more and more overload (maladaptation). Happens during that session and also within weeks and even years of training Potential causes of overtraining -stress can lead to adaptation (proper application) or maladaptation (overreaching and overtraining) too high and intensity, too great a volume, too frequent, etc.) on a neuromuscular basis, could have to do with calcium in the sarcolemma -sympathetic overload has to do with beta adrenergic receptors which are responsible for circulating epinephrine -glycogen depletion, amino acid imbalance can reduce neurotransmitter in the brain and alter hormonal activity -sympathetic nervous system starts even right before a competition so with overtraining you are causing a downgrade of the typical sympathetic responses -psychological overload, altered hypothalamus and pituitary gland functioning -adrenal overload and decreased cortisol response Problems associated with the study of overtraining -different terms and definitions -no report or measure of performance -depending on the age and activity level of the person, what is considered overtraining may be different study looked at overreaching and overtraining in endurance athletes -in both cases as you move through a training protocol, an increase in volume causes a decrease in performance but an increase in intensity causes an increase in performance -decrease volume and increase intensity when nearing a competition Major physiological factors reported for endurance athletes include: -autonomic imbalance with reduced catecholamine response (blunted response to epinephrine and norepinepherine) -reduced vo2 max -reduced HR max (not resting only max) -increased NE with decreased adrenoreceptor response (with the same amount of NE release, there is less of a response because the receptors get downgraded) -reduced neuromuscular excitability (can be measured in the peripheral portion of the neuromuscular system from the spinal chord out) -increased adrenocorticotophic hormone with reduced cortisol release (stress hormone which should be going up during exercise) -impaired glycogenolysis, glycolysis, lipolysis, and HR response -reduced lactate response (bad because with more lactate it is an indication that glycolysis went up) -immune system repression overreaching and overtraining mistakes in strength and power -choice of exercise: are they all concentrating on a specific type of the body? Might overtrain a body part -order of exercise: does the activity take place in a specific muscle -intensity of exercise: usually looked at one dimensionally. EMG will be higher for explosive lifts -number of sets: has to do with volumetric load -amount of rest allowed between sets and exercises markers of overtraining -performance decline (number 1 marker. Problem is that once you see the decline you may already be too overtrained) -fatigue -mood disturbances -immune system -hormonal response -biochemical makers -cardiovascular response diagnosis of overtraining -SFMS questionnaire: standardized questionnaire of early clinical symptoms of the overtraining syndrome allowing the calculation of a score that may help to classify on a clinical basis sportsmen submitted to a heavy resistance training program -the score appears to be correlated with markers of muscular damage (CK, myosin) or neuroendocrine dysfunction (somatotropic axis) but also with some hematological markers like ferritin -the best hemorheogical correlate of fitness is a low hematocrit and the best hemorhelogical correlate of overtraining is increased plasma viscosity. Diagnosis of overtraining -performance: time to fatigue tests will most likely show greater changes in exercise capacity as a result of overreaching and overtraining. However, these test are accurate performance indicators. -the major problem in attempting to establish markers of overtraining is the failure of researchers to include the best accepted marker in the analysis: performance decrements -one of the best markers of performance is time to fatigue Relationship between training and performance -upside down U -undertraining then top is optimal and then overtraining -psychological disturbances such as increased irritability, loss of incentive, depression have been measured using the profile of mood state (POMS) questionnaire and associated with overtraining -biochemical markers include: 1) lactate: analyze changes in conjunction with performance. Alone it means nothing 2) CK: mirrors mechanical-muscular strain. More of a marker of extreme overtraining than general overtraining. Should be in heart or muscle and if it gets out it means there is damage to tissues which happens with extreme overtraining 3) Urea: marker of protein catabolism 4) Ammonia: byproduct of breakdown of amino acids 5) Iron: relates to reduction in oxygen carrying capacity of blood -validity of these variables is overestimated and cautious conclusion should be made -varies based on individuals so no absolute markers immune system -changes from intense training rather than from overtraining itself. Decreases in neutrophil, IgA, natural killer cells, and increase in upper respiratory infections -immune parameters may change in response to intensified training, independent of whether the training results in overreaching or overtraining -immunocompetance is best assessed by examining cell function as opposed to cell number -hormones: look at free testosterone/cortisol ratio. The plasma levels of free testosterone and cortisol may reflect the anabolic and catabolic activity in the tissue -a catabolic imbalance should be indicated by a decrease in the FTCR ratio and increased serum urea concentration reflecting increased proteolysis -criterion in long distance runners is a decrease in FTCR of more than 30% -free testosterone is anabolic -cortisol is catabolic -IGF1 and cortisol provide a more complete picture of the anabolic/catabolic status of the body in response to exercise -CRH induced pituitary release of ACTH in the corticotropin producing cells of the anterior pituitary gland increases with overtraining CV factors -looked at the factors in terms of biological interest and practicality -need to take markers like HR every day to have comparative data, easy marker since it is non-invasive, problem need detailed records every day -with EMG you look at change in frequency pattern of the muscle to look at fatigue. Not very helpful while the athlete is doing the sport because it changes -waste product buildup effects frequency in an EMG buildup -blood pressure is not a great marker and practicability is not good -taking blood is not a feasible method to see if an athlete is overtrained because it would be both time consuming and expensive Diagnosis tools -mood profile states always go down -RPE are major markers but need to be done pre and during -much more accurate measurement for people who are trained at doing the work -can be manipulated meaning people may not tell the truth about how they are feeling -a sport specific performance test is the gold standard for whether or not an individual is overtrained -the problem is we don’t need the gold standard to tell us if a person is overtrained, we need a marker that tells us if they are approaching over training. -how much of a drop do you see that has to do with over training and how much is just overreaching and when do you know when to begin taper. It is not very specific in this sense -creatine kinase and urea would be greater markers of damage as opposed to overtraining PERIODIZATION -The purposeful sequencing of different training units (long duration, medium duration and short-term training cycles and sessions) so that athletes can attain the desired state and planned results -Periodization has proven more effective than standard progressive resistance protocols for increasing strength and power. when looking at strength, power, etc you will not maximize gains without periodization -Optimal performance gains cannot occur unless periods of recovery are included in the training prescription, since the increases in intensity (load and speed) and volume (repetitions and sets) that induce training adaptations also cause reductions in performance due to fatigue and tissue damage . -Applying the proper patterns of work and recovery can reduce the incidence of overtraining syndrome, decrease injury levels , improve training efficiency and increase neuromuscular gains and exercise compliance through variations in training stimuli . -traditional theory shows: (i)a general elucidation of load and recovery in view of the supercompensation concept; (ii)general principles of periodized training; (iii) the hierarchy of periodized training cycles; (iv) proposed variations of the annual cycle. -Super compensation curve components: 1) stimulus: something that disturbs homeostasis to induce a change 2) fatigue or depletion stage: as someone is giving you an overload, that overload causes you to reduce performance (ex. Swim a mile and then do 100m you will be slow in the 100m because you are tired compared to if you had only done the 100m) 3) compensation/restitution: the stimulus is removed and there is an opportunity to recover in the compensation stage (ex. You swim a mile and wait a while and then do the 100m your machinery for recovery is working and you have given an outside stimulus to the body that tells it that it needs to prepare to improve function so that the activity will become more feasible). Improvements happen during the compensation stage 4) supercompensation/overcompensation: if you continue to give this overload in the proper technique, you won’t just get to baseline, your body would continue to recover and change its biochemical and structural machinery so it gets better at doing the specific activity related to that overload (form of training specificity) 5) involution/detraining: if you take the recovery period and stop training, you will become detrained and go back to baseline -There is a link between stress and the theory of periodization? Hans Selye’s stress syndrome known as the General Adaptation Syndrome or GAS. -the overlap seen in the GAS and supercompensation curve: -the thin line is GAS curve -thick curve is supercompensation curve 1) alarm stage which is the depletion stage in the supercompensation curve. Given a stimulus which will drive down performance and bring up endocrine markers of stress 2) resistance stage what we call compensation and supercompensation stage. Can develop a resistance to that overload and can supercompensate by responding to resist a particular stimulus and deal with the nature of that over load 3) exhaustion or prolonged fatigue can then result. added dashed line at bottom of supercompensation curve to represent prolonged fatigue and a measure of overtraining and salience -The fitness-fatigue model argues that different training stresses result in different physiological responses. -Training results in 2 after-effects, which can positively or negatively influence performance: 1) Fitness: Positive physiological response 2) Fatigue: Negative physiological response -overload makes you tired and as that overload is taken away, you recover -there are two models: pure fatigue model and 2 component model -2 component model: if I have a fatigue after effect (bottom line) but also after an entire training session there is a fitness after effect, the body brings you up to baseline but give you biological changes to make you more functional -if you add fitness and fatigue after effects you would come up with the supercompensation curve and this is why the curve has this shape -fatigue after effect: your body reacts to an overload because you are given more than your body can handle -insufficient overload wont give you the response you want -too much of a fatigue effect and don’t allow proper overload you will wind up at the bottom of the two green lines -if the curve does not dip down far enough (not enough fatigue) there will not be sufficient overload to generate a response so you will get minimal response -if you give too much overload you will become way too tired so the fatigue will bring you down -going too slow and too fast are both bad in different ways -how do you know when to taper? Need specific markers to know ii. Principles of Periodized Training a. Cyclic training 1. habitual rhythm of working days and vacation: can use normal vacation time as a rest period 2. the cyclical character of adaptation or periodical regeneration of adaptability: 3. the sharing of main tasks for development of general and sport specific motor abilities, 4. technical and tactical skills; and, 5. the competition schedule: natural dictated points that need to be targeted (competitions ranked by the coaches as to which are the most difficult vs which are not), training is dictated by NCAA and tell them when to train the athletes. if restrictions are removed everyone will do whatever they want and it will be unregulated. when you look at overall general ability (building up the persons background). Modify nature of training to get more sport specific. the competition schedule may be very different based on the amount of competitions in a short amount of time -should every single athlete have the same background work? No. -if you do not allow yourself sufficient recovery for this adaptation take place, you will not improve -the specificity of the background work is noteworthy -technical and tactical skills are one of the variables we play with for periodization ii. Principles of Periodized Training 1) unity of general and specialized preparation i.e. the importance of specific workloads during a long period of early season training, and the necessity of general conditioning workouts within the period of frequent competitions. need to apply the balance between intensity and frequency which is easier in the off season 2) Waveshape design of training workouts: This principle proclaimed the need to alternate days of high load and lower load, sequencing large, medium and small workloads which was expanded across months and years. daily undulating training: ex. Focus one day on power, one on hypertrophy and one on strength 3) Continuity principle: Breaks in training for recuperation and social needs should be thoroughly planned, whereas sporadic breaks should be totally excluded. Hierarchy of Periodized Training Cycles: 1) Multi year preparation: (years) long lasting systematic athlete training composed of 2 year or four year cycles 2) Macrocyle: (months) annual cycle with preparatory competition and transition periods. what do the different months look like within one year. Can apply the supercompensation curve over the whole macrocycle. Each macrocyle is made of a mesocycle. Preparatory period/Mesocycle 1 (1-4 weeks First Transition period/Mesocycle 2 (weeks - months)Competition period/Mesocycle 3Second Transition period (active rest)/Mesocycle 4 3) Mesocycle: (weeks) medium size training cycle composed of a number of microcycles 4) Microcycle: (days) small size training with a number of days that make up the mesocycle. There are types of microcyles that depends on adjustment, loading, impact, pre-competitive, competitive and restoration 5) Workout: (h/min) a single training session that is performed individually or within a group -if the workout is wrong it will affect the microcycle, mescocyle, then macrocycle -you need to start right at the workout level or you will mess up the hierarchy and lead to over training -there are variations of the traditional cycle model. different annual cycles -the number of peaks can differ -sometimes this doesn’t happen properly. It may move up and down due to insufficient recovery -so many peaks that you cant cycle correctly. Exists in many sports -there are major limitations of traditional periodization: 1) energy supply: lack of sufficient energy supply for concurrent performance of diversified workloads 2) cellular adaptation: training consequences such as mitochondrial biogenesis, synthesis of myofibril proteins, anaerobic enzymes presuppose separate pathways of biological adaption 3) post exercise recovery: because different physiological systems require different periods of recuperation, athletes do not get sufficient recovery 4) compatability of various workloads: exercises combining various modalities ofter interact negatively due to energy deficit, technical complexity, and or neuromuscular fatigue 5) mental concentration: performance of stressed workloads demands high levels of mental concentration that cannot be directed at many targets simultaneously 6) sufficiency of training stimuli for progress: sport specific programs of high level athletes demand high levels of mental concentration that cannot be directed at many target simultaneously 7) competitive activity: inability to provide multi peak preparation and successful performances during the entire annual cycle Factors Affecting the Revision of Traditional Periodization 1) An increase in the total number of competitions: correspondingly, their contribution to training stimuli has increased dramatically. 2) Financial motivation of top athletes, which became much stronger than previously. 3) Closer cooperation and sharing among world coaches, which led to enhancement of training quality and level of athletic performances. 4) The struggle against illegal pharmacological interventions, which affected and which led to the prevention of such harmful technologies in high-performance sport. 5) Implementation of advanced sport technologies and training methods such as monitoring of heart rate, blood lactate, movement rate, etc.; improvement of medical follow-up methods; and elaboration of advanced training equipment and new materials. -periodization charts in team sports: -phases across top and targets -metabolic conditioning tells you background built up and it should be specific to the sport -pre-season: 6-20 weeks is a long preseason but can work based on the nature of the sport involved -force velocity relationship taken into account are we focused on load or speed -vo2 max test: ml of oxygen used per kgbw per minute, so metabolic power test would be done -now that we are in season, there is more concentration on the movement patterns that make you successful in your sport -going high on the load you need to change the volume of the work -AR is active rest and PR is psychological recovery Types of periodization: 1) classic linear: • Characterized by high initial training volumes and low intensity, then volume decreases and intensity gradually increases. • Elicit peak performance of a distinct fitness variable (i.e. strength, RFD and/or power) for a precise and often narrow time window. • Superior to a nonperiodized RT program for increasing strength, power, motor performance and jumping ability. • It appear that longer training periods (>6months) may be necessary to underscore the benefits of periodized training. • Short-term both periodized and non periodized program are effective 2) undulating (non-linear): •Enables variation in intensity and volume within a cycle by rotating different protocols to train various components of neuromuscular performance (Strength, power, muscular endurance). •The use of heavy, moderate and light resistances may be systematically or randomly rotated over a training sequence. These training zones are varied on a training session, weekly or biweekly manner. •The order of the training zones occur randomly in this training model. The training zones are not necessarily sequentially performed so that the training intensity or volume follows a pattern of constantly increasing or decreasing over time. • Greater gains in strength compared to linear and non-periodized models • ex. One day hypertophy, one endurance, and one strength 3) block: Training Block refers to a training cycle of highly concentrated specialized workloads. Its general idea suggests the use and sequencing of specialized mesocycle-blocks, where highly concentrated training workloads are focused in a minimal number of motor and technical abilities. Concentration of training workloads (sufficient training stimuli to improve targeted abilities). Minimal number of target abilities within a single block. Consecutive development of many abilities. Use of specialized mesocycles-blocks to avoid negative load interactions. The method requires the systematization of the training means according to the intensity of their effect. They must also be ordered in groups of training means having different priorities 4) reverse -PAP has to do with a modification in ca sensitivity to displace myosin head to produce power more quickly -if you have a specific sport or athlete, when do you test the PAP? -what variables affect the PAP response? What lift/sport will you do and how will you do it. Why use one over the other? Specificity. Need to see which PAP will be good for that particular sport -the time is dependent on the level of competition -black performance line as you give heavy loads, performance will decline. We need a certain amount of time for restitution so we can then get supercompensation -interval training is a type of periodization -given a high intensity interval and not enough recovery, you will reduce your performance. Plan performance so you can stress overlo
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