Training for Performance

P38

Mitogen activated kinase that plays a key role in the production of new mitochondria by activating PGC-1 alpha - Activated by increase in free radicals Activated during endurance exercise

CAMK (calmodulin-dependent kinase)

Vital kinase that contributes to activation of PGC-1 alpha - Activated by endurance training Primary upstream signal for activation is increased cytosolic calcium levels

Primary Signals

- Increased Ca2+ - Increased AMP/ATP - Increased free radicals

Responses to Exercise-Induced Signaling Events

1) Fast to slow fiber type shift - Caused by calcineurin and PGC-1 alpha 2) Mitochondrial biogenesis - Caused by PGC-1 alpha (primarily), CaMK, AMPK, and p38 3) Antioxidant enzyme synthesis - Caused by PGC-1 alpha and NFkB

Summary of Factors Causing Increased VO2max With Endurance Training

1) Increased maximal cardiac output - Caused by increase in SV -- Result of increased preload and decreased afterload 2) Increased atriovenous difference - Caused by increase in capillaries and mitochondria - Caused by increase in muscle blood flow A decrease in SNS activity to working muscle contributes to increase in blood flow and decreased after load

AMPK

Activated during high-intensity interval training and sub maximal endurance exercise training due to changes in muscle fiber phosphate/energy levels - Kinase that regulates numerous muscle signaling processes leading to adaptation in response to endurance training (activated by increase in AMP/ATP ratio) Stimulates glucose uptake and fatty acid oxidation during exercise Linked to the control of muscle gene expression by activating transcription factors associated with fatty acid oxidation and mitochondrial biogenesis Can inhibit components of the IGF pathway

Free Radicals

Activates NFkB and mitogen-activated kinase p38

Calcium

Activates calmodulin-dependent kinase - Promotes phosphorylation of various protein substates - Initiates a signaling cascade in muscle fibers that contributes to muscle adaptation to exercise training Calcium is released from sarcoplasmic reticulum when stimulated - Level of free calcium in the muscle cytosol is determined by the mode, intensity, and volume of exercise - Prolonged endurance exercise results in long periods of elevated calcium (important role in adaptations to endurance training) Causes increase in - Calcineurin - CAMK

Mitochondria

At the onset of exercise, ATP is converted to ADP and Pi in the muscle fibers to develop tension Increase in ADP concentration in the cytoplasm is immediate stimulus for ATP-producing systems to meet the ATP demands of the cross-bridges Increased mitochondrial content in muscle fibers from endurance training affects oxygen uptake responses at the onset of sub maximal steady state work - Steady state VO2 in sub maximal work is not affected by endurance training (mitochondria in the working muscles consume the same number of oxygen molecules per minute) - Because training increases the number of mitochondria in the muscle, the ATP producing chore is shared among the mitochondria differently - Causes the rate of ADP transportation into the mitochondria to double, so the ADP concentration in cytosol increases only half as much (because of the additional mitochondria) - This lower concentration of ADP in the cytosol results in less phosphocreatine depletion and less stimulation glycolysis, and thus reduces production of H+ Reduced stimulation of glycolysis due to lower ADP and higher PC concentrations results in less reliance on anaerobic glycolysis to provide ATP at the onset of exercise and faster oxygen uptake - Results in: - Lower oxygen deficit - Less depletion of PC - Reduction in lactate and H+ formation Results in faster rise in oxygen uptake curve at onset of work, less disruption of homeostasis, and reduces the O2 deficit

PGC-1 Alpha (peroxisome proliferator-activatd receptor-gamma coactivater 1 alpha)

Considered the master regulator of mitochondrial biogenesis in cells - Activated by both high intensity interval training and sub maximal endurance exercise (and activated by increases in CaMK, AMPK, and p38) Assists transcriptional activators that promote mitochondrial biogenesis in skeletal muscle following endurance training Also regulates: - Formation of new capillaries (angiogenesis) - Fast-to-slow muscle fiber type shift - Synthesis of antioxidant enzymes Primary upstream molecules: all of them

Aging, Strength, and Training

Decline in strength after 50 1) Loss of muscle mass (sarcopenia) - Loss of both type I and II fibers - Atrophy of type II fibers - Loss of intramuscular fat and CT 2) Loss of motor units 3) Reorganization fo motor units 4) Also associated with NSAID use Progressive resistance training: - Causes muscle hypertrophy and strength gains - Important for activities of daily living, balance, and reduced risk of falls

Reversibility

Describes the temporary nature of a training effect; adaptations are lost when the training stops Fitness gains by exercising at an overload are quickly lost when training is stopped and the overload is removed

The HERITAGE Family Study

Designed to study the role of genotype in cardiovascular, metabolic, and hormonal responses to exercise and training Some results: 1) Heritability of VO2max among sedentary adults is about 50% - 50% of the VO2max in untrained subjects can be explained by genetic differences 2) Large variation in change in VO2max with training - Genetics also plays large role in the training-induced improvements in VO2max - Average improvement 15-20% - Ranged from no improvement to 50% increase - Heritability of change in VO2max is 47% Those individuals with genetics for a high VO2max in the untrained state and the genetic background to be a "high responder" to an endurance training stimulus have the potential to achieve a VO2max required to successfully comet in endurance events at the olympic level 3) 21 genes play a role in change in VO2max (adaptations) with training

Endurance Training and Fat Metabolism

Endurance training increases fat metabolism during exercise: 1) Increased capillary density enhances delivery of FFA to the muscle - Slows rate of blood flow past cell membrane, allowing more time for FFA to be transported into the cell 2) Expanded ability to transport FFA across the sarcolemma - Caused by increase in both fatty acid binding protein and fatty acid translocase that transport the fatty acids from outside to inside the sarcolemma 3) Improved capacity to move FFA from the cytoplasm into the mitochondria - Carnitine (CPT-I) and FAT work to increase FFA entry into the cell - Increase in # of mitochondria increases the SA of the mitochondrial membranes and the amount of FAT and CPT-I so that FFA can be transported at a faster rate to the mitochondria for oxidation Also increases muscle's ability to metabolize fat by increasing the number of mitochondria in the muscle fiber - Increase in mitochondria number also increases the number of enzymes involved in fatty-acid beta oxidation - Increases rate at which acetyl-cow molecules are formed form FFA for entry to the Krebs cycle - Increases citrate levels, which inhibit PFK (rate limiting enzyme in glycolysis) to reduce carbohydrate metabolism to preserve muscle and liver glycogen stores

Endurance Training to Increase VO2mac

Endurance training programs that increase VO2max involve: - Dynamic activity using large muscle groups (i.e. running, cycling, swimming) - 20-60 min, 3-5x per week 50-85% VO2max Expected increases in VO2max - Average increase is 15-20% after training for 2-3 months duration - 2-3% increase in those with high initial VO2max (requires intensity of >70% VO2max) - Up to 50% in those with low initial VO2max (experience greater improvement with relatively low training intensities; requires intensity of only 40-50% of VO2max) Genetic Predisposition - Accounts for about 50% of VO2max - Prerequisite for very high VO2max Magnitude of improvement in VO2max response to exercise training is also genetically determined - Heritability of training gains in VO2max is 47% - Those who show high magnitudes of improvement (40-50%) are referred to as high responders Difference in mitochondrial DNA is important for individual differences in initial (unattained) VO2max and the training induced improvements in VO2max

Effect of Mitochondria and Capillaries on Free-Fatty Acid and Glucose Utilization

Endurance training results in a decreased use of plasma glucose (carbohydrate) as fuel and an increase in fat metabolism during prolonged sub maximal exercise - Spares plasma glucose and increases reliance on fat as a fuel source in skeletal muscle Increase in capillary density causes slower blood flow in muscle and increased FFA transporters - Increases uptake of FFA Increased mitochondria number increases fatty acid cycle (beta oxidation) enzymes and carnitine transferase - Increases FFA utilization Increased FFA utilization spares plasma glucose

Endurance Training and Plasma Glucose

Endurance training results in decreased utilization of plasma glucose during prolonged submax exercise Increases the capacity to transport glucose into skeletal muscle fibers by increasing the number of GLUT4 glucose transporters and availability of insulin to promote transport of glucose into the muscle - Surprising that training results in decreased reliance on arbs as energy source during prolonged submax exercise Uptake and oxidation of glucose from the blood during submax exercise is decreased int rained individuals - Trained also better able to maintain blood glucose

Lack of Transfer of Training Effect

Exercise-induced adaptations in skeletal muscle are related to lower heart rate, ventilation,and catecholamine responses measured during sub maximal work following an endurance training program Heart rate, ventilation, blood lactate, and plasma caecholamine responses all decrease throughout a training program when a specific muscle group is worked When training another part of the body however, these responses are now elicited - i.e. not transfer of training from one leg to another if only work one separately Heart rate, ventilation, lactate, and plasma catecholamine responses to prolonged submax exercise are determined not by the specific adaptation of each organ or system, but by the training state of the muscle groups engaged in the exercise - Reduction of afferent feedback from chemoreceptors in the trained muscle and a decreased need to recruit motor units to accomplish an exercise task results in reduced sympathetic nervous system, heart rate, and ventilation responses to sub maximal exercise

Primary Signal Transduction Pathways in Skeletal Muscle

Exercise-induced muscle adaptations occurs due to the coordination between primary and secondary signaling pathways in muscle fibers to increase the expression of certain genes for increased protein synthesis Four primary signals for muscle adaptation during exercise includes: - Muscle stretch - Calcium (via calmodulin-dependent kinase) - Free Radicals - Phosphate/muscle energy levels (AMP/ATP ratio activates AMPK) These primary signals lead to adaptations by activating secondary messengers to promote gene expression and increase protein synthesis - Lead to adaptation of increased protein synthesis Exercise-induced adaptations in skeletal muscle fibers depends on exercise stimulus - Intensity and duration - Resistance vs. endurance training; endurance training promotes metabolic adaptations (i.e. increased mitochondrial volume) with little change in muscle fiber size, resistance training is vise versa

High VO2max of Endurance Athletes

Extremely high VO2max values are the result of genetic gift of a large cardiovascular capacity and high percentage of slow muscle fibers - Heritability of VO2max in the untrained state is approximately 50%

Factors Increasing Stroke Volume Summary

Factors that cause an increase in stroke volume from training include: 1) Increased contractility 2) Increased end diastolic volume ("preload") - Caused by: - Increase in plasma volume (primarily) - Increase in filling time and venous return - Increased ventricular volume 3) Decrease in the total peripheral resistance ("after load")

Endurance Training-Induced Changes in Fiber Type and Capillarity

Fast-to-slow shift in muscle fiber type - Reduction in fast myosin isoforms in the muscle - Increase in slow myosin isoforms in the muscle - Extent of change determined by duration of training and genetics Slow myosin isoforms have lower myosin ATPase activity but are able to perform more work with less ATP utilization (are more efficient) i.e. the number of type I (slow) fibers in leg muscles of distance runners is correlated to the number of years of training Although endurance training promotes a fast-to-slow diver shift in active muscles, this shift does not result in a complete shift from fast fibers to slow fibers Increase number of Capillaries - Enhanced diffusion of oxygen (reduces the distance for diffusion) - Increased removal of wastes

Secondary Signals

Following initiation of the primary signal, additional (secondary) signaling pathways are activated to mediate the exercise-induced signal to promote muscle adaptation (either directly or indirectly by increasing gene expression of specific muscle proteins) Secondary signaling molecules include: - Increased calcineurin - Increased CaMK - Increased AMPK - Increased p38 - Increased NFkB - Increased PGC-1 alpha

Endurance Training Improves Muscle Antioxidant Capacity

Free radicals are produced by contracting muscles - Can damage muscle contractile protein Antioxidants neutralize radicals and protect against radical-mediated injury Training increases endogenous antioxidants (those produces within the cells of the body) in the trained muscles - Protects against oxidative damage and fatigue

Detraining and Submaximal Exercise

Inactivity not only influences VO2max, but also decreases sub maximal endurance performance As feew as 14 days of disrupted training (detraining) can significantly impair submacimal exercise performance - Primarily due to decrease in msucle mitochondria While muscle mitochondriaa increase extremely quickly at onset of training (doubles in about 5 weeks), only one week of detraining results in loss of about 50% of gains during the 5 weeks of training

Increased End Diastolic Volume

Increase in EDV results in stretch of the left ventricle and a corresponding increase in cardiac contractility via the Frank-Starling mechanism (increase strength of ventricular contraction) Increase in EDV as a result of endurance training: 1) Increase plasma volume is a primary mechanism - Contributes to augmented venous return and increased EDV - Quick increases in VO2max are likely the result of increase in stroke volume due to increase in EDV 2) Prolonged endurance training increases size of left ventricle with little change of wall thickness - Accommodates a higher EDV Increased stroke volume at rest in addition to during maximal exercise - Results from increased stretch of the myocardium because of the increased ventricular filling time associated with slower resting heart rate that follows endurance training

Signaling Events Leading to Resistance Training-Induced Muscular Growth

Increase in muscle fiber size aoccurs when the rate or protein synthesis in muscle fibers is greater than the rate of protein breakdown - Muscular hypertrophy is therefore a slow process because protein synthesis must exceed breakdown for several weeks ofr significant muscular growth Single bout of resistance exercise increases rate of muscle protein synthesis for up to 24 hours - Increases rate of muscle protein synthesis by 50% 4 hours after - Increases rate by 100% at 24 hours after - Increase in protein synthesis is not permanent, returns to resting keels by 36 hrs Changes in protein synthesis dye to an increase in the amount of protein synthesized per molecule of mRNA rather than simply an increase in total mRNA - Resistance exercise therefore promotes muscle protein synthesis by improving translational efficiency

Endurance Training Increases Mitochondrial Content in Skeletal Muscle Fibers

Mitochondrial content increases quickly - Depends on intensity and duration of training - Can increase 50-100% within 6 weeks Results in increased endurance performance - Due to changes in muscle metabolism

Increased Mitochondrial Number and Blood pH Summary

Increase in number of mitochondria: 1) Increases FFA oxidation and decreases PFK activity 2) Decreases pyruvate formation - Increased H4 form of LDH 3) Decreases lactate and H+ formation 4) Blood pH is maintained Increase in number of mitochondria: 1) Increases mitochondrial uptake of pyruvate and NADH 2) Decreases lactate and H+ formation 3) Blood pH is maintained

Phosphate/Muscle Energy Levels

Increased AMP to ATP ratio in the muscle fibers caused by increased ATP consumption during exercise causes activation of AMPK

Specificity

Indicates that the adaptation of a tissue is dependent on the type of training undertaken Training effect is specific to: - Muscle fibers involved - Energy system involved (aerobic vs anaerobic)/types of fibers recruited - Velocity of contraction - Type of contraction (eccentric, concentric, isometric) i.e. if person participates in low intensity distance running program that utilizes slow twitch muscle fibers, there is little or no training effect occurring in fast-twitch fibers in the same muscle i.e. muscle hypertrophy with heavy resistance training i.e. increase in mitochondria with endurance training

Range of VO2max Values in the Population

Males always have a higher VO2max than females - Exception: severe pulmonary disease patients Cross country skiers have the highest VO2max 1) Cross country skiers: - M = 84 - F = 72 2) Distance runners: - M = 83 - F = 62 3) Sedentary young: - M = 45 - F = 38 4) Sedentary middle age: - M = 35 - F = 30 5) Post myocardial infarction pts: - M = 22 - F = 18 6) Severe pulmonary disease pts: - M = 13 - F = 13

VO2max

Maximal oxygen uptake (aka maximal aerobic power) is the measure of the maximal capacity of the body to transport and use oxygen during dynamic exercise using large muscle groups

Exercise Training Improves Acid-Base Balance During Exercise

Muscle buffering capacity at sub maximal work can be increased by performing high-intensity interval training - Endurance trained muscles produce less lactate and H+ 1) Increased mitochondrial number (reduces pyruvate) - Lower ADP concentration in cytosol prevents the activation of PFK at onset of work - Increased capacity to use fat as fuel spares need for carbohydrate oxidation during prolonged work - Results in less carbohydrate utilization, so less pyruvate is formed - Also increases the chance that pyruvate will be taken up by the mitochondria for oxidation in the Krebs cycle 2) Increased NADH shuttles to transport electrons associated with NADH from the cytoplasm to the mitochondrion (reduces lactic acid formation) - Less NADH available for lactic acid formation 3) Change in the type of LDH present in the muscle cell (reduces lactic acid formation) - 5 isozymes of LDH; the H4 or heart form of LDH has a low affinity of the available pyruvate - Results in less lactic acid formation and increases likelihood of uptake of pyruvate but the mitochondria more likely

Retraining and VO2max

Muscle mitochondria adapt quickly to training - Doubles within 5 wks of training Mitochondrial adaptations lost quickly with detraining - Loss of 50% of training gain within 1 wk of detraining - Majority of of adaptation lost in 2 wks Requires 3-4 wks of retraining to regain mitochondrial adaptations

Resistance Training-Induced Changes in the Nervous System

Neural adaptations are primarily responsible for early gains in strength Adaptations incude: - Increased ability to recruit motor units - Altered motor neuron firing rates - Enhanced motor unit synchronization - Removal of neural inhibition In contrast to endurance training, resistance training-induced changes in the nervous system can be transferred to the non-trained limb to cause increase in strength - i.e. when one arm is exposed to resistance truing, a portion of the training effect is transferred to the other arm - strength gain in untrained arm due solely to neural adaptation

Resistance Training-Induced Hypertrophy and Myonuclei Increase

Number of myonuclei increases Myofiber size also increases (Myofiber CSA)

Mechanisms for the Impairment of Strength Development

Overtraining - No direct evidence Neural factors - Impaired motor unit recruitment - Only limited evidence Low muscle glycogen content - Due to successive bouts of endurance exercise -- Reduces intensity of subsequent resistance training Depressed protein synthesis following resistance exercise training - Resistance training increases muscle contractile synthesis by activation of the IGF-1/Akt/mTOR singling pathway; endurance training increases AMPK activation an promotes mitochondrial biogenesis - Endurance training adaptations interfere with protein synthesis via inhibition of mTOR; AMPK causes TSC1/2, which inhibits mTOR activity and impairs protein synthesis

Mechanical Stretch

Passive stretching can stimulate activation of protein kinases and insulin-like growth factor signaling cascades High levels of mechanical stretch that occurs during resistance resistance training appears to be a primary signal that promotes contractile protein synthesis, resulting in muscle hypertrophy

Calciuneruin

Phosphatase that participates in fiber growth/regeneration, fast-to-slow fiber type transition - Activated by endurance training Primary upstream signal for activation is increased cytosolic calcium levels

Concurrent Strength and Endurance Training

Potential for interference of adaptations - Endurance training increases mitochondrial protein - Strength training increases contractile protein - Depends on intensity, volume, and frequency of training Studies report that combining strength and endurance gaining impairs strength gains and muscular hypertrophy - Depends on intensity, volume, and frequency of training

Resistance Training-Induced Signaling Events

Primary signal for resistance induced protein synthesis: - Increase in mechanical stretch (force) to the muscle Secondary signals - Increase in IGF-1, Akt (activated by IGF-1), and mTOR (activated by Akt) - mTOR finally promotes protein synthesis by increasing translation and building more proteins; a single bout can increase protein synthesis 50-100% Responses: 1) Muscle hypertrophy: increased cross-sectional area of fibers 2) Increased number of myonuclei in each fiber - Comes from satellite cells (adult stem cell located between the sarcolemma and outer layer of CT/basal lamina around the fiber) - Additional myonuclei required for continued muscle adaptations (essential for optimal fiber hypertrophy in response to resistance training)

Overload

Principle of training describing the need to increase the load (intensity) of exercise beyond the level to which an organ system or tissue is accustomed in order to cause a further adaptation to the system - Training effect occurs when a system is exercised at a level beyond which it is normally accustomed in terms of intensity, duration, or frequency Systems/tissues gradually adapt to the overload over time, so a pattern of progressively overloading a system is necessary to cause improved function over time Variables that can be manipulated to cause overload include - Intensity - Duration - Frequency (days per week)

Hypertrophy

Refers to an enlargement in the cross-sectional area of both type I and II fibers (aka fiber hypertrophy) - Primary means of increasing muscle size during long-term strength training In general is a gradual process that takes months to years of training - With high intensity resistance training, changes in muscle six detectable by 3 weeks Greater degree of hypertrophy in type II fibers (generate greater specific force or force per cross-sectional area) Increase in fiber cross-sectional area results from: - Increase in myofibrillar proteins (actin and myosin filaments due to the addition of sarcomeres in parallel to the existing sarcomeres to cause muscle fiber hypertrophy) - Increase in number of cross-bridges (by addition of more contractile proteins) - Increased ability to generate force

Hyperplasia

Refers to an increase in the total number of muscle fibers within a specific muscle Mixed evidence in human studies - 90-95% of muscle enlargement due to hypertrophy and not hyperplasia

Afterload

Refers to the peripheral resistance against which the ventricle is contracting to push blood into the aorta When the heart contracts against a high peripheral resistance, stroke volume will be reduced Decreased in after-load is due to decrease in arteriolar constriction in the trained muscles, which is needed to accept the increase in maximal muscle blood flow Trained muscles offer less resistance to blood flow during maximal exercise due to reduction in the sympathetic vasoconstrictor activity to the arterioles of the trained muscles - Decrease in resistance parallels increased maximal cardiac output so that mean arterial blood pressure remains unchanged during exercise

Cardiac Contractility

Refers to the strength of the cardiac muscle contraction when the fiber length (EDV), afterload (peripheral resistance) and heart rate remain constant High intensity exercise training increases cardiac pumping ability by increasing the force of ventricular contraction Endurance exercise trainng incases left ventricular twist mechanics to incerease stroke volume

mRNA and Protein Changes in Response to Exercise

Regardless of whether a training program is endurance or resistance exercise, the exercise-induced adaptation that occurs in muscle fibers is the result of an increase in the amount of specific proteins - Specific types of proteins contained in a muscle fiber determine the muscle characteristics and its ability to perform specific types of exercise Muscle contraction during a training session generates a signal that promotes muscle adaptation by increasing primary and secondary messengers - Messengers initiate coordinated signaling events, resulting in increased expression of specific genes and the synthesis of specific proteins A bout of exercise generates a transient increase in e quantity of specific mRNAs, which typically peak during the first 4-8 hours post-exercise and returns to basal levels within 24 hours - mRNA levels for specific muscle preens increase at different rates and peak at varying times - Exercise induced increase in mRNA results in increased synthesis of specific muscle proteins Exercise repeated on a daily basis has a cumulative effect, leading to progressive increase in specific muscle preens that improve muscle function - Explains why maintaining constant level of fitness requires regular bouts of exercise Training induced increases in muscle proteins is a gradual process, with large increases in muscle protein levels during the first weeks followed by a slower rate of protein accumulation as training progresses

Resistance Training and Satellite Cells

Resistance training activates satellite cells to divide and fuse with the adjacent muscle fiber to increase the number of nuclei in the fiber Increase in the number of muonuclei in growing fibers results in a constant ratio between the number of myonuclei and the size of the fiber - Required for continued muscle adaptations (i.e. hypertrophy) in order to manage new muscle fiber growth These myonuclei are required to maintain the high level of translational capacity required to synthesize muscle proteins at a high rate following a strength training session - A specific myonucleus can only manage a specific volume of muscle area) Removal of satellite cells from skeletal muscle limits the fiber's ability to grow in response to overload

Mechanisms Responsible for Resistance Training- Induced Increases in Strength

Resistance training increases muscular strength by changes in both the nervous system and an increase in muscle mass In training studies of short duration (8-20 wks): neural adaptations relayed to learning, coordination, and ability to recruit the primary muscles play a major role in strength gains In training studies of long-term duration: increase in muscle size plays the major role in strength development

Physiological Effects of Strength Training

Similar to VO2max: Percent gain inversely proportional to initial strength - Genetic limitation to gains in strength (variability in responses) High resistance (2-10 RM) training - Gains in strength Low resistance training (20+ RM) - Gains in endurance

Detraining Following Strength Training

Stoppage of resistance training results in a loss of muscular strength and in muscle atrophy - Compared to the are of detraining following endure Slow decrease in strength - 31% decrease in strength following 30 wks detraining - Associated with small decreases in fiber size or atrophy (2% decrease type I, 10% decrease type IIa, and 13% decrease type IIx) - Indicates that loss of dynamic strength is due primarily to nervous system changes Implies that resistance induced muscular adaptations (i.e. dynamic strength and muscle hypertrophy) can be retained for relatively long periods due ing detraining Retraining results in rapid regain of strength and muscle size - Within 6 wks after resuming training: complete restoration of all muscle fiber sizes and rapid regain of strength - Can maintain strength with reduced training for up to 12 wks

Muscular Endurance

The ability to make repeated contractions against a sub maximal load

Stroke Volume

The amount of blood ejected from the heart with each beat and is equal to the difference between EDV and ESV All training induced increases in maximal cardiac output are the result of increase in stroke volume - Months of endurance training can cause a small decrease in maximal heart rate

Resistance Training-Induced Changes in the Skeletal Muscle Size

The amount of force produced by a muscle is directly linked to the amount of actin and myosin within the muscle fibers - The more myosin attached to actin n a cross-bridges for a power stroke, the more force produced In response to resistance training, skeletal muscles can increase their size by increasing the size of existing fibers (hypertrophy) or by increasing their number of total fibers (hyperplasia)

Muscular Strength

The maximal force that a muscle or muscle group can generate - Commonly expressed as the one repetition maximum (1-RM): the maximal load that cn be moved through a full range of motion

Atriovenous O2 Difference

Training-induced increase in a-vO2 difference is due to increased O2 extraction from the blood Increase in muscle blood flow - Decreased SNS vasoconstriction Improved ability of the muscle to extract oxygen from the blood due to: 1) Increases capillary density (slows blood flow through the muscle, decreases diffusion distance to the mitochondria, accommodates the increase in blood flow during maximal exercise) - primary reason 2) Increase in mitochondrial number - Increases the muscle fibers's ability to consume oxygen

NFkB

Transcriptional activator activated by free radicals in contracting muscles Promotes expression of several antioxidant enzymes that protect muscle fibers against free radical-mediated injury

Calculation of VO2max

VO2max is the product of maximal cardiac output and atriovenous difference - Studies indicate that endurance exercise training improves VO2max by increasing both maximal cardiac output and the atriovenous difference (the factor that accounts for most of the change however depends on duration of the program) Fick equation: VO2max = HR max x SV max x (Av-O2)max - Av-O2 differnce is a measure of how much oxygen is removed from arterial blood and used by the tissues Differences in VO2max in different populations - Primarily due to differences in SV max Improvements in VO2max - About 50% increase due to SV and and atriovenous difference in sedentary individuals The size of the contribution of each factor in training induced improvements in VO2max varies as a function of training duration - Shorter duration training (about 4 months): increase in SV > increase in atriovenous difference - Longer duration training (about 28 months): increase in atriovenous difference > increase in SV Training induced increase in SV is solely responsible for the exercise-induced increase in maximal cardiac output

Detraining and VO2max

When endurance training is stopped: Rapid decrease in VO2max - Decreases 8% within 12 days - Decreases 20% after 84 days Decresae in SV max - Rapid loss of plasma volume Decrease in maximal atriovenous difference - Decerase in mitochondria (capillary density remained the same) - Decrease in oxidative capacity of muscle (due to decrease in type IIa fibers and increase in type IIx fibers); slow to fast fiber type shift Initial decrease (12 days) due to decrease in SVmax - a-vO2 difference stays constant - HR max increases again Later decrease due to decrease in max atriovenous difference

Lactate Production During Exercise

pyruvate + NADH -(LDH)-> lactate + NAD Lactate formation occurs when there is accumulation of NADH and pyruvate in the cytoplasm where lactate dehydrogenase is present