Ch 13 & 19 Physiology of Training & factors affecting performance

how free radicals contribute to muscular fatigue

1. Radicals can damage key contractile proteins (including myosin and troponin) -Damage to these muscle proteins reduces the Ca2+ sensitivity of myofilaments and limits the number of myosin cross-bridges bound to actin -When fewer cross-bridges between actin and myosin occur, muscle force production is reduced (i.e. fatigue occurs). 2. High radical production can depress the Na+/K+ pump activity in skeletal muscle. -This results in problems achieving fiber excitation-contraction coupling (impairing force production).

Aerobic Training-induced Changes: Capillary Density

A strong relationship exists between a person's VO2 max and the number of capillaries surrounding muscle fibers in a trained limb. Exercise-induced capillarization in the skeletal muscle is advantageous because diffusion distance for O2 and substrate delivery to muscle fibers is improved. Similarly, the diffusion distance for the removal of metabolic waste from the fiber is also decreased.

Aerobic Training-induced Changes: Mitochondria

Aerobic training can rapidly increase the mitochondrial density [of both subsarcolemmal and intermyofibrillar mitochondria (most common form)] in active skeletal muscle fibers. This can occur within the first 5 days of a training program Prolonged endurance training can typically increase muscle mitochondria by 50 - 100% in the first 6 weeks of training. The magnitude of the exercise-induced increase in mitochondria in muscle is dependent upon both the exercise intensity and duration

Aerobic Training-induced Changes: Antioxidant & Acid-Base Regulation

Although free radicals are produced during muscular action, endurance training can protect muscle fibers against free radical-mediated damage by increasing the levels of antioxidants within the trained musculature. Although endurance training at submaximal work rates does not increase muscle buffering capacity, regular endurance training results in less disruption of the blood pH during submaximal work. There is evidence that muscle buffering capacity can be increased by performing HIIT. Also, the lower amount of CHO that is used, the lower amount of pyruvate that is formed. The increase in mitochondria increases the chance that pyruvate will be taken up by the mitochondria for the Krebs Cycle, rather than being converted to lactate in the cytoplasm. Endurance training increases the number of "shuttles" used to transport electrons carried by NADH and FADH from the cytoplasm into the mitochondria -If the NADH formed in glycolysis is more quickly transported to the mitochondria, there will be less lactate and H+ formation

Peripheral Fatigue

Although there is evidence that the CNS is linked to fatigue, its contribution is estimated to be about 10% The vast majority of evidence points more towards the influence of peripheral fatigue, where neural, mechanical, or bioenergetic events can hamper muscle tension development It has been hypothesized that the sarcolemma might be the site of fatigue due to its inability to maintain Na+ and K+ concentrations during repeated stimulation. When the Na+/K+ pump cannot keep up, K+ accumulates outside the membrane and decreases inside the cell.

Satellite Cells

As muscle fibers increase in size in response to resistance training, these growing fibers add new nuclei (myonuclei) within the fiber. The source of these new myonuclei are the satellite cell, which is a type of adult stem cell located between the sarcolemma and the outer layer of connective tissue around the fiber. Resistance training activates these satellite cells to divide and fuse with the muscle fiber to increase the number of myonuclei.

Calcium Release

Calcium (Ca2+) can activate an important kinase called calmodulin-dependent kinase (CMDK). CMDK promotes the phosphorylation of various protein substrates. Once activated, CMDK can initiate a signaling cascade in muscle fibers that contributes to muscular adaptations to exercise training by activating proliferator-activated receptor gamma coactivator-1alpha (PGC-1alpha). PGC-1alpha is a key molecule activated by both HIIT and submaximal endurance exercise. Considered the master regulator of mitochondrial biogenesis in cells through assisting transcriptional activators (Olesen et al., 2010). Also regulates angiogenesis (formation of new capillaries), fast-to-slow fiber type shifts, and synthesis of antioxidant enzymes

Central Fatigue

Central fatigue implies that the central nervous system (CNS) would be implicated in fatigue. Either of the following could allude to central fatigue: Reduction in the number of functioning motor units involved in the activity. Reduction in motor unit firing frequency. Studies suggest that the upper limit of voluntary strength is "psychologically" set, given that certain motivational or arousal factors are needed to achieve a physiological limit Alterations in CNS "arousal" can facilitate motor unit recruitment to increase strength and alter the state of fatigue (Asmussen & Mazin, 1978). Excessive endurance exercise training (overtraining) has been associated with symptoms such as reduced performance capacity, prolonged fatigue, altered mood states, sleep disturbance, loss of appetite, and increased anxiety

Aerobic Training-induced Changes: Mitochondria (cont.)

Changes in citrate synthase (CS) activity (a marker of mitochondrial oxidative capacity) due to exercise programs differing in duration and intensity are shown below ch 13&19 pt 2 slide 3 Mitochondria in the working musculature are consuming the same number of O2 molecules/min. Because training results in an increase in the number of mitochondria in the muscle, how the ATP-producing chore is shared among the mitochondria differs between untrained and trained skeletal musculature. Also improves the rate of ADP transport into the mitochondria, resulting in a lower ADP concentration in the cytosol and less stimulation of anaerobic glycoloysis. A lower ADP concentration results in less phosphocreatine (PCr) depletion. The lower ADP concentration in the cell also results in less stimulation of anaerobic glycolysis, and therefore a reduced production of lactate and H+. The reduced stimulation of anaerobic glycolysis following endurance training results in less reliance on anaerobic glycolysis to provide ATP at the onset of exercise. The net result is a lower O2 deficit resulting in a faster rise in the O2 uptake curve at the onset of work, with less disruption of homeostasis.

Detraining

Compared to endurance training, the rate of detraining (i.e., loss of strength) after a resistance training program is much slower. Much of the loss of strength associated with detraining is associated with changes in the neural pathways. Also, regaining of dynamic muscular strength and a complete restoration of muscle fiber size back to peak training levels can occur very quickly.

Concurrent Aerobic & Strength Training (cont.)

Concurrent training studies where participants performed endurance training on > 2 days/week and > 30 min/day consistently concluded that concurrent training impairs strength gains and muscular hypertrophy compared to participants performing resistance training alone Successive bouts of either strength or endurance training can produce substantially lowered levels of muscle glycogen. -Therefore, resulting in low resting levels of muscle glycogen. Beginning a training session with low muscle glycogen can reduce the ability to perform subsequent resistance training sessions and impair the magnitude of the strength-training adaptations

Principles of Physical Training: Adaptation to Stress (cont.)

Each individual's body adapts to exercise differently. There tends to be a genetic cap on the maximal ability for the musculature to adapt to an exercise load. If from childhood you train the same way and put in the same amount of time as LeBron James, will you be just as good as he is?

Aerobic Training-induced Changes: Fuel Utilization

Endurance training results in a decreased use of CHO as fuel and an increase in fat metabolism during prolonged submaximal exercise. Together, these changes spare plasma glucose and increase the reliance on fat as a fuel source in skeletal muscle during exercise. Aerobic training increases the capacity to transport glucose into skeletal muscle fibers by increasing both the number of GLUT-4 glucose transporters and the ability of insulin to promote transport of glucose into the muscle. Consequently, trained individuals are better able to maintain blood glucose levels during prolonged exercise. Increases in mitochondria number elevate the enzymes involved in FFA beta-oxidation. -A high rate of beta-oxidation results in increased levels of citrate (first molecule in the Krebs cycle) in the muscle. -This is important because high citrate levels inhibit phosphofructokinase (PFK) (rate limiting enzyme in anaerobic glycolysis) which then as a result will reduce CHO metabolism. An increased reliance on FFA and less reliance on CHO metabolism during exercise leads to a better preservation of the limited muscle and liver glycogen stores.

Aerobic (Endurance) Training: Effects on Performance & Homeostasis

Endurance training results in: A more rapid transition from rest to steady-state exercise. A reduced reliance on the limited liver and muscle and glycogen stores. Numerous cardiovascular and thermoregulatory adaptations that assist in maintaining homeostasis. There is evidence that some improvements in performance occur rapidly and might precede structural or biochemical changes in skeletal muscle. This would suggest that initial metabolic adaptations to endurance training might consist of changes in the nervous system or neural hormonal adaptations, then followed by biochemical adaptations within muscle fibers. The typical changes include: -Increase in the percentage of Type I muscle fibers (i.e. fast-to-slow fiber type shift). -Increased capillary density. -Increases in the number of mitochondria within muscle fibers. Activation of three secondary signals (AMPK, CMDK, and p38) all promote mitochondrial biogenesis by activation of the master regulator, PGC-1α. -Enhanced ability to metabolize fat. -Improved muscle antioxidant capacity.

Training Programs & Changes in VO2 max

Endurance training that increase VO2 max typically involve dynamic exercise using large muscle mass (e.g., running, cycling, or swimming) for 20-60 min/session 3+ bouts/week at an intensity > 50% VO2 max. Endurance training programs of 2 - 3 months duration typically cause an increase in VO2 max between 15 - 20%, The range of improvements can be as low as 2 - 3% for those who start a program with a high VO2 max or as high as 50% for individuals with low initial VO2 max values. In addition, individuals with a low VO2 max prior to training can experience improvements with relatively low training intensities (40-50%) whereas individuals with a high VO2 max may require higher training intensities (>70% VO2 max)

Phosphate/Muscle Energy Levels

Exercise accelerates ATP consumption in the working muscle and increases the ratio of AMP/ATP in muscle fibers. This can initiate numerous downstream signaling events in skeletal muscle fibers. One of the most important signaling molecules in exercise-induced muscle adaptation is activation of a secondary messenger called 5'adenosine monophosphate activated protein kinase (AMPK). AMPK is linked to the control of muscle gene expression by activating transcription factors associated with FFA oxidation and mitochondrial biogenesis.

fatigue

Fatigue is defined as an inability to maintain power output or force during repeated muscular actions. The discussion of mechanisms by which fatigue occurs starts at the brain, where a variety of factors can influence the "will to win," and continues to the cross-bridges of the sarcomeres themselves.

Free Radical Production

Free radical production during exercise can activate nuclear factor kappa B (NFkB) and mitogen activated kinase p38 (p38). NFκB is an important transcriptional activator that plays a key role in the expression of several muscle proteins, including antioxidant enzymes that protect muscle fibers against exercise-induced oxidative stress. p38 is an intracellular kinase that plays a key signaling role in the production of new mitochondria.

Free Radical Production During Exercise

Free radicals are molecules that contain an unpaired electron in their outer orbital. This unpaired electron results in molecular instability. Therefore, radicals are highly reactive and capable of damaging proteins, lipids, and DNA in the cell (Halliwell & Gutteridge, 2007). Also called oxidative stress. Exercise induced oxidative damage is a key contributor to muscular fatigue during prolonged exercise of at least 30 minutes duration

Factors Limiting All-out Aerobic Performances: Intermediate-length (21 - 60 min)

In all-out performances lasting 21 - 60 minutes, the athlete will generally have to work at > 90% of VO2 max. A high VO2 max is certainly a pre-requisite to be an elite aerobic athlete, but other factors come into play once this time-point is reached. An individual who is considered an "economical" runner can move at a higher speed for the same amount of oxygen compared to a runner who is not as economical. Differences in running economy are due to biomechanical and/or bioenergetic factors The ability to run at a higher percentage of VO2 max is related to the concentration of lactate in the blood. Therefore, one of the best predictors of race pace is the lactate threshold. In this way, the VO2 max sets the "upper limit" for energy production in endurance performance, but is not the final predictor. A higher percentage of Type I muscle fibers is associated with both a greater lactate threshold and higher mechanical efficiency. Given the length of the activity, environmental factors (such as heat, humidity, and hydration status) play a role in the outcome of a race.

Hypertrophy vs. Hyperplasia (cont.)

In general, resistance training-induced increases in fiber size is a gradual process that takes as long as months - years of training to occur. There is some evidence that with HIIT, changes in muscle size may be detectable as soon as 3 weeks. Although resistance training increases the size of both fiber types, weight training elicits a much greater response in type II fibers. This is considered of great physiological significance because type II fibers can generate a greater force per cross-sectional area (CSA) than type I fibers. Resistance training-induced increases in muscle fiber CSA results from an increase in myofibrillar proteins (i.e., actin and myosin). This increase occurs due to the addition of sarcomeres in parallel to the existing sarcomeres, resulting in hypertrophy. The addition of additional contractile proteins increases the number of myosin cross-bridges in the fiber. This leads to a direct increase in the ability to generate a greater amount of force.

Factors Limiting All-out Aerobic Performances: Moderate-length (3 - 20 min

In moderate-length performances lasting 3 - 20 minutes, aerobic metabolism provides about 60 - 90% of the ATP. The factors limiting performance include: Cardiovascular system (delivers O2-rich blood to the muscles). Mitochondrial content of the muscles involved in the activity. Races lasting fewer than 20 min are typically run anywhere from 90 - 100% of maximal aerobic power, so the athlete with the higher VO2 max has a distinct advantage Because speed is often a pre-requisite for competitive performance in races lasting fewer than 20 min, Type IIa fibers (which are rich in mitochondria) are involved in supplying ATP (in addition to the already recruited Type I fibers). However, because Type IIx fibers are also recruited, lactate and H+ production are increased. H+ production would greatly hinder overall tension development.

Signaling Events Leading to Resistance Training-induced Growth

In order for muscle hypertrophy to occur, protein synthesis must exceed breakdown for several weeks to achieve any substantial muscular growth. Also, all essential amino acids must be present in the muscle in order for protein synthesis to occur. However, a single bout of resistance exercise can elevate the rate of muscle protein synthesis for up to 24 hours. This is considered transient, returning back to pre-exercise levels within 36 hours post-exercise (MacDougall et al., 1995; Tang et al., 2008). The primary signal for resistance exercise-induced protein synthesis is the mechanical stretch applied to a muscle during resistance training. This then triggers the secondary signal of IGF-1 synthesis and a cascade of downstream signaling events leading to increased protein synthesis.

Hypertrophy vs. Hyperplasia

In response to resistance training, skeletal muscles can increase their size by increasing the size of existing fibers (hypertrophy) or increasing their number of total fibers (hyperplasia) within the muscle. Whether resistance training promotes the generation of new muscle fibers in humans remains controversial. -Animal studies indicate that resistance training can promote an increased number of fibers in trained musculature -There are studies that both support and deny that this concept occurs in humans Current evidence indicates that even if hyperplasia does occur in response to strength training in humans, 90 - 95% of the increase in muscle size due to strength training is a direct result of muscle fiber hypertrophy.

Concurrent Aerobic & Strength Training (cont.)

In theory, concurrent resistance and endurance exercise bouts could result in impaired protein synthesis following resistance training exercise. The following is the proposed biochemical link to explain this theory: 1. Remember that resistance exercise training increases muscle contractile protein synthesis by activation of the IGF-1/Akt/mTOR signaling pathway. 2. In contrast, endurance exercise training increases AMPK activation and promotes mitochondrial biogenesis. Also, AMPK can activate a signaling molecule [tuberous sclerosis complex 1/2 (TSC 1/2)] that also inhibits mTOR activity. -Therefore, in theory, this would lead to an impairment of protein synthesis.

Training induced increase in FFA delivery to the muscle is accomplished by 3 training-induced adaptations

Increased capillary density which enhances the delivery of FFA to the muscle. Expanded ability to transport FFA across the sarcolemma. Improved capacity to move FFA from the cytoplasm into the mitochondria

Calcium Release (cont.)

Increases in cytosolic Ca2+ also activates calcineurin which participates in several adaptive responses in muscle. Including fiber growth/regeneration and the fast-to-slow fiber type transition that occurs as a result of endurance exercise training. Prolonged endurance exercise likely results in long periods of elevated Ca2+ levels in the muscle cytosol. Resistance exercise is only able to generate student cycles of high cytosolic Ca2+ levels It is reasonable to expect that exercise-induced differences in cytosolic Ca2+ levels between endurance and resistance exercise determine the downstream Ca2+-mediated signaling events leading to synthesis of specific muscle proteins.

Other Possible Alterations in Muscle

It appears whether resistance training improves muscle oxidative capacity (through an increase in capillarization) is dependent upon the duration of the training bout and the volume of exercise performed. Resistance training can improve the muscle's antioxidant capacity similar to endurance training. This should provide cellular protection against the potential oxidative damage associated with exercise-induced production of free radicals.

Overview of Training Physiology

It is clear that participation in regular endurance (aerobic) exercise increases the cardiovascular system's ability to deliver blood to the working muscles and increases the muscle's capacity to produce ATP aerobically. These parallel changes result in less disruption of the internal environment during exercise. Further, regular bouts of resistance exercise result in muscular adaptation that increases the muscle's ability to exert force and also improves performance in power events (e.g. weight lifting). In the coming lectures, we will discuss the physiological adaptations that occur in response to both endurance exercise training and resistance training. VO2 max is closely linked to the maximal capacity of the cardiovascular system to deliver blood to the working muscle. The ability to sustain long-term, submaximal exercise is linked more to the maintenance of muscle fiber homeostasis due to specific biochemical properties of the working muscles.

Factors Limiting All-out Anaerobic Performances: Short-term (10 - 180 sec)

Maximal performance in the 10 - 60-sec range are still predominantly anaerobic (> 70%), employing the high-force production ability of the type II fiber. Given that the ATP-PC system can supply ATP for only 10 - 14 seconds at a time, the vast majority of the ATP will be derived from anaerobic glycolysis. However, when a maximal performance is extended out further closer to 3 minutes (180 seconds), about 60% of the energy comes from aerobic metabolism.

Factors Limiting All-out Anaerobic Performances: Ultra Short-term (< 10 sec)

Maximal performance is limited by: 1. Fiber type distribution (type I vs. type II) 2. Number of muscle fibers recruited. Influenced by the level of motivation and arousal Optimal performance is affected greatly by skill and technique, which are dependent on skill development through practice. Also, energy release necessary for performance is primarily determined by the demand generated by neuromuscular drive, not by limitations in intramuscular energy supply

Neural adaptations

Most research point to neural adaptations playing the primary role of increases in strength in the short-term (8 - 20 weeks). These neural adaptations are considered to be related to: -Motor learning. -Muscular coordination. -Ability to recruit the primary muscles (i.e., prime movers). Neural adaptations in response to resistance training result in an improved ability to: -Recruit high-threshold motor units. -Alter motor neuron firing rates. -Enhance motor unit synchronization during a particular movement pattern. -Result in the removal of neural inhibition. Remember the role of the Golgi tendon organ (GTO)? -monitors force production in muscle

Muscular Fitness

Muscular strength: refers to the maximal force that a muscle or muscle group can generate and is commonly expressed as the one-repetition maximum (1-RM). 1-RM: the maximum load that can be moved through a full range of motion (ROM). Muscular endurance: refers to the ability to make repeated contractions against a submaximal load. Aging is associated with a decline in strength, with most of the decline occurring after the age of 50. The loss of strength is considered to be due, in part, to a loss of muscle mass (sarcopenia).

Cellular Changes & VO2 max

Numerous muscle receptors respond to chemical changes in the muscle, and these receptors provide information to the CNS regarding muscle work rate. The cardiorespiratory control center receives neural feedback from the working muscle resulting in output from the cardiorespiratory control center that increase both HR and pulmonary ventilation (Ve) As more motor units are recruited to develop the greater tension needed to accomplish a work task, larger physiological responses are required to sustain the metabolic rate of the muscles. Prior to endurance training, more mitochondria-poor muscle fibers must be recruited to carry out a workload at a given VO2. This results in a greater drive to the cardiorespiratory control centers, which causes a higher input to the SNS, leading to further increases in HR and increases Ve. For example, during an incremental exercise test, more and more muscle fibers are recruited to perform the exercise as workload increases. This generates a higher HR and increased VE in response to the work rate.

Peripheral Fatigue (cont.)

One of the beneficial effects of training is an increase in the capacity of the Na+/K+ pump, which may contribute to the maintenance of the Na+/K+ gradient and reduce the potential for fatigue through this mechanism (Fitts, 2006; Green, 2004). The cross-bridge's ability to "cycle" is important in continued tension development. Fatigue may be related, in part, to the effect of a high H+ concentration and the inability of the sarcoplasmic reticulum to rapidly take up Ca2+. The end result may be a longer relaxation time, which affects the rate of muscular action. When ATP-generating mechanisms cannot keep up with ATP usage, inorganic phosphate (Pi) begins to accumulate in the cell. An increase in Pi in the muscle has been shown to inhibit maximal force, and the higher the Pi concentration, the lower the force measured during recovery from fatigue. This Pi seems to act directly on the cross-bridges to reduce its binding to actin and also inhibits Ca2+ release from the sarcoplasmic reticulum.

Detraining

Plasma volume tends to decrease rapidly once the training stimulus is removed. A decrease in a-vO2 diff also tends to occur. This is associated with a decrease in the number of mitochondria, whereas capillary density remains unchanged. Detraining (from an aerobically trained state) leads to a transition of slow-to-fast fiber type. As few as 14 days of disrupted training can significantly impair submaximal exercise performance.

Stroke Volume Effect on VO2 max (cont.)

Prolonged endurance training (months to years) increases the size of the LV with little change in ventricular wall thickness. This increase in ventricular size will accommodate a larger EDV and therefore could be a factor in contributing to the training-induced increase in SV. The increase in resting SV in endurance-trained athletes is likely due to the increased EDV at rest that results from increased stretch of the myocardium because of the increased ventricular filling time associated with the slower HR rest that occurs following endurance training. After load refers to the peripheral resistance against which the ventricle is contracting as it tries to push blood into the aorta. This is important because when the heart contracts against a high peripheral resistance, SV will be reduced (compared to a lower peripheral resistance). Following an endurance training program, trained muscles offer less resistance to blood flow during maximal exercise due to a reduction in the sympathetic vasoconstrictor activity to the arterioles of the trained muscles.

Muscular Strength Training

Resistance training increases muscular strength by changes in both the nervous system and an increase in muscle mass. During longer term strength training programs, increases in muscle size plays a major role in strength development (typically after at least 8 weeks).

Resistance-training Induced Changes in Muscle Fiber Type

Strength training-induced shifts in muscle fiber types appear to be less prominent than the transformations seen with aerobic training. With resistance training, all of the change in fiber type is a shift from type IIx fibers to predominantly type IIa fibers. With no real changes elicited in the amount of type I fibers.

Detraining (cont.)

Studies reveal that after dynamic muscular strength has been increased by resistance training, a reduced frequency maintenance program of weight lifting can sustain strength. It has been shown that following a 12-week strength training period (consisting of 3 days/week of training), dynamic strength can be maintained by performing resistance training in as few as 1 bout/week for 12 weeks.

Principle of overload

an organ system (e.g. cardiovascular) must be exercised at a level beyond which it is accustomed in order to achieve a training adaptation.

Training Adaptations - Big Picture

The "stress" of exercise stimulates cell signaling pathways in contracting muscle fibers that "switch on" transcriptional activators. These are responsible for "turning on" specific genes to synthesize new proteins. A single bout of endurance exercise is insufficient to produce large changes in proteins within a muscle fiber. However, a single exercise session does promote transient disturbances in cellular homeostasis that, when repeated over time, result in the specific exercise-induced adaptations associated with long-term training Daily exercise has a cumulative effect, leading to a progressive increase in specific muscle proteins that improve muscle function.

regulation of muscle growth from resistance training

The IGF-1/Akt/mTOR signaling pathway plays a key role in regulation of muscle growth resulting from resistance training. 1. Contractile activity (i.e. muscle stretch) stimulates the production of IGF-1 from active muscle fibers. 2. IGF-1 then acts as an autocrine and paracrine signaling molecule, binding to its membrane receptor and initiating a cascade of molecular events to promote muscle protein synthesis. 3. The binding of IGF-1 to its receptor on the muscle membrane activates protein kinase B (Akt). 4. Akt then activates another kinase called mammalian target of rapamycin (mTOR). 5. mTOR then initiates a series of molecular events to increase protein synthesis by improving translation.

Muscular Fitness (cont.)

The age-related loss of muscle fibers appears to occur as an outcome of losing motor neurons. As a result, entire motor units are lost during the aging process. The remaining type I or type II muscle fibers then cluster in homogenous groups (in contrast to the heterogeneous distribution of fiber types typically seen in normal, healthy adults) (Deschenes, 2004; Hunter et al., 2004). Progressive resistance-training can lead to muscle hypertrophy and large improvements in strength in older individuals. Including those even into their 90's (Fiatarone et al., 1990; Fiatarone et al., 1994). Strength training for elderly individuals is important not only to carry out ADL's, but also for improved balance and reduced risk of falls

Aerobic Training-induced Changes: Muscle Fiber Type

The exercise-induced shift in muscle fiber type involves a reduction in the amount of fast myosin isoforms in the muscle and an increase in slow myosin isoforms. This is important because slow myosin isoforms have lower myosin ATPase activity but are able to perform more work with less ATP utilization. This fast-to-slow shift increases mechanical efficiency and can potentially improve endurance performance. However, most human and animal training studies indicate that although aerobic training promotes a fast-to-slow fiber shift in the active muscles, aerobic training does not result in a complete shift from fast fibers to slow fibers.

Training Programs & Changes in VO2 max (cont.)

The extremely high VO2 max values possessed by elite male and female endurance athletes are the genetic gift of a large cardiovascular capacity and high percentage of slow-twitch muscle fibers. Studies have concluded that heritability of VO2 max in the untrained state is approximately 50%. It is currently believed that the heritability of training gains in VO2 max is approximately 40%. Evidence points to differences in mitochondrial DNA as being important in both the individuals differences in initial (i.e. untrained) VO2 max and the training-induced improvements in VO2 max. Training-induced changes in VO2 max must be due to an increase in maximal cardiac output (Q) or an increase in the a-vO2 difference (a-vO2 diff). Or some combination of both. The Fick equation represents the relationship of the body's oxygen consumption (VO2), to the arterial-venous oxygen difference (a-vO2 diff) and cardiac output (Q). VO2 = Q x a-vO2 = (HR × SV) x a-vO2 Endurance training studies using young sedentary participants suggest that approximately half of the gains seen in VO2 max are due to increases in stroke volume (SV) and the other half to increased a-VO2 difference.

Signal Transduction Pathways

The four primary signals for muscle adaptation during exercise include: 1. Muscle stretch. 2. Increases in cellular Ca2+. 3. Elevated free radical production. 4. Decreases in muscle phosphate/energy stores.

Principles of Physical Training: Adaptation to Stress

The goal of any physical training is to produce long-term changes and improvements in the body's functioning in response to the physical stressor imposed on the body. Over time, immediate and short-term adjustments can translate into long-term changes and improvements.

a-vO2 diff Effect on VO2 max

The increased capacity of the muscle to extract O2 following training is primarily due to the increase in capillary division with an increase in mitochondrial number being of secondary importance. The increase in capillary density in trained muscle: Accommodates the increase in muscle blood flow during maximal exercise. Decreases the diffusion distance to the mitochondria. slows the rate of blood flow to allow more time for O2 diffusion from the capillary to the muscle fiber to occur. The increases in mitochondrial number following endurance training increase the muscle fiber's ability to consume O2 and also contribute to the expanded a-vO2 diff. The capacity of the mitochondria to use O2 exceeds the capability of the heart to deliver O2, making mitochondrial number not the key factor limiting VO2 max

Factors Limiting All-out Aerobic Performances: Long-term (1 - 4+ hours)

The longer the performance, the greater the chance that environmental factors will play a role in the outcome. In addition, for performances > 1 hour, the ability of the muscle and liver CHO stores to supply glucose may be challenged or exceeded. For the many endurance activities that are performed at higher exercise intensities (like marathon running), muscle fibers must have CHO to oxidize or performance will decline (by reducing intensity, thereby running pace). Glucose supplementation becomes increasingly important at this time-point.

peripheral fatigue (continued)

The mitochondrial content of Type IIa fibers is sensitive to endurance training, so that with detraining, more of the ATP supply would be provided by glycolysis. Leading to an increase in lactate production. If O2 delivery to this fiber type is decreased, or if the ability of the fiber to use O2 is decreased, tension development will decline, requiring Type IIx fiber recruitment to occur to maintain muscular tension. Type IIx fibers can generate the greatest amount of tension through anaerobic sources of energy, but it also fatigues quickly. These fibers are recruited at around 75% of VO2 max, adding to the tension developed from the other two fiber types. Making high-intensity exercise heavily dependent upon their ability to develop tension

Satellite Cells (cont.)

This is considered important in the attempt to keep a constant ratio between the number of myonuclei and the size of the fiber. The addition of new myonuclei appear to be a requirement to support the increased size and continued growth of muscle fibers in response to strength training. It appears that a single myonucleus can only manage a specific volume of muscle area. Therefore, as the muscle fiber increases in size, the addition of new myonuclei is required to manage the new growth.

too much or too little exercise

Too little amounts of exercise? Not enough stress on the body may show no effects on fitness. Too much exercise? Excessive amounts of exercise can be harmful, can cause injury and mess with your immune system.

Stroke Volume Effect on VO2 max

Training induced increases in maximal cardiac output are solely due to increases in SV. Exercise training does not increase HRmax(in fact, training typically results in a small decrease). Increases in SV are due to some combination of: -An increase in end diastolic volume (EDV) (also known as preload). -Increased cardiac contractility. -Decrease in total peripheral resistance (TPR) (also known as afterload). An increase in EDV results in stretch of the LV and a corresponding increase in cardiac contractility via the Frank-Starking mechanism. A primary mechanism is that plasma volume increases with endurance training and this contributes to augmented venous return and increased EDV.

Intermediate Length Performances (21 - 60 min) (cont.)

Ventilatory Equivalent for Oxygen (VE /VO2): measured in liters of air breathed per liter of O2 consumed per minute. Generally VE /VO2 remains relatively constant over a wide range of exercise levels. Ventilatory Threshold/Breakpoint: The point during intense exercise at which ventilation increases disproportionately to the oxygen consumption required. When work rate exceeds 55% to 70% VO2max, aerobic pathways can no longer meet the energy requirements of exercise so an increasing amount of energy must be derived from anaerobic glycolysis Remember that anaerobic glycolysis increases lactate levels (H+), which increase CO2 levels (buffering), which triggers increased ventilation. The ventilatory threshold tends to reflect/mirror the lactate threshold under most conditions, though the relationship is not always exact. Can be identified by noting a disproportionate increase in VE /VO2 without a simultaneous increase in the ventilatory equivalent for carbon dioxide (VE /VCO2).

Muscle (Mechanical) Stretch

When muscles contract, the mechanical force placed on the muscle fiber can trigger signaling processes to promote adaptation. Through activation of protein kinases and IGF signaling cascades The activation of these signaling pathways can then trigger secondary signaling pathways to turn on specific genes to express more protein. IGF-1/Akt/mTOR pathway In particular, the high levels of mechanical stretch that occur across the muscle membrane during resistance training appear to be a primary signal that promotes contractile protein synthesis, resulting in muscle hypertrophy.

Concurrent Aerobic & Strength Training

Whether aerobic and strength training interfere with the goals (and possible gains) of the other is a topic of controversy. Some research suggests that the effectiveness of concurrent training may depend on a variety of factors, such as the intensity, volume, and frequency of training As well as how the training modalities are integrated. Clearly, the frequency and intensity of training has an impact on the potential for one type of training to interfere with the other.

Overtraining

While a training overload is required to achieve improvements in performance, too much overload can result in an overtrained state. Defined as an accumulation of training stress that impairs an athlete's ability to perform training sessions and results in long-term decrements of performance. "Psychological staleness" May require several weeks or months of reduced or ceasing of training.

Cellular Changes & VO2 max (cont.)

With the increase in mitochondrial number following endurance training, this allows muscle tension to be maintained with fewer motor units involved in the activity. This reduced "feed forward" input from the higher brain centers results in lower SNS output, HR and ventilatory responses to exercise

peripheral fatigue (continued)

even with these mechanisms taking place and an intent of maximal effort, the cell does not run completely out of ATP (even in cases of extreme fatigue). Typically, the ATP concentration will only be allowed to fall to 70% of its pre-exercise level. The factors that cause fatigue also reduce the rate of ATP utilization faster than the rate of ATP generation so that ATP concentration is maintained. This is believed to be a protective function aimed at minimizing changes in cellular homeostasis with continued stimulation. Fatigue is directly associated with a mismatch between the rate at which the muscle uses ATP and the rate at which it can be supplied Up to about 40% of VO2 max, the Type I (slow-twitch) muscle fiber is recruited to provide development of tension (Sale, 1987). This fiber type is dependent on a continuous supply of blood to provide the needed O2 for the generation of ATP from CHO and fat. Any factor limiting the O2 supply to this fiber type (e.g. altitude, dehydration, blood loss, or anemia) would cause a reduction in tension development in these fibers and necessitate the recruitment of Type IIa fibers to generate muscle tension. Between 40-75% of VO2 max, Type IIa fibers (fast-twitch, fatigue-resistant) are recruited in addition to the Type I

Principle of progressive overload

the training principle that placing increasing amounts of stress on the body lead to adaptations that improve fitness. We can gradually build up our tolerance to exercise. Gradually increase the amount of time or exercises you do linearly.

The principle of specificity

the training principle that the body adapts to the particular type and amount of stress placed on it.

Principle of Reversibility

the training principle that the body will return to its original homeostatic state when amount of physical stress is removed for a specific time. "IF YOU DON'T USE IT, YOU WILL LOSE IT!" If you stop exercising completely, up to 50% of fitness improvements can be lost within weeks.