Chapter 13

mitochondria in response to endurance training

mitochondrial content increases quickly; improves a muscle fiber's capacity to oxidize both carbohydrate and fat and produce ATP aerobically; can increase 50 to 100 percent within first six weeks.

selective requirements

rapid changes in direction of force; explosive/ballistic muscle actions such as plyometric, speed, power, and agility training; benefit high-velocity and powerful movements in which time of force production is vital to success

lactate threshold

reached at higher percent of VO2 max; lactate production decreases and lactate clearance increases; allows high intensity without lactate accumulation

the central nervous system might adapt by

recruiting some motor units not in consecutive order and by preferential recruitment of fast twitch fiber first to help with greater production of power or speed in a movement

fiber hypertrophy

refers to muscular enlargement from an increase in the cross sectional area of the existing fibers

Increased EMG activity

reflects an increase in neural activation; results from increased numbers of active motor units, increased motor unit firing rates or motor unit synchronization

trained muscles and carbohydrate

trained muscle exhibits enhanced capacity to oxidize carbohydrates during maximal exercise

myostatin

a gene that inhibits muscle growth; if you inhibit it muscles can grow

Neural mechanisms responsible for the adaptations in strength and power observed with resistance training

1. Increased central nervous system activation 2. Increased synchronous recruitment of motor units 3. greater motor units recruitment 4. selective recruitment 5. reduction in inhibitory impulses

reduction of carbohydrate as fuel and the increase of fatty acid oxidation in submaximal exercise results from three combined effects

1. decreased muscle glycogen use 2. reduced glucose production 3. reduced use of plasma-borne glucose

resistance training studies

alter the activity of about seventy genes responding to the mechanical loading prior to hypertrophy

fiber type transition

although proportions of type i and type ii fibers are genetically determined, muscle fiber subtype transitions occur during resistance training

Golgi Tendon Organ

conveys information regarding muscle tension to CNS; amount of stretch increases with increased muscle tension; activation results in reflex relaxation of muscle

GTO

defensive mechanism to prevent damage to bones and tendon; cause agonist muscle relaxation if tendon tension is too high

motor units

defined as a motor neuron and the muscle fiber it innervates; composed exclusively of slow oxidative, fast oxidative glycolytic, or fast glycolytic fibers

increased myoblobin effect on glycogen

enhanced capacity for glucose storage as glycogen; higher muscle glycogen content at rest (2.5 times compared to pre-training)

late phase of strength gain

increase in muscle size (hypertrophy) is responsible for most of the strength gain past four to eight weeks

Late phase of strength gain

increase in muscle size via muscle protein accretion is responsible for most adaptation. occurs after 4 to 8 weeks of training

accumulation of glucose-6-phosphate

inhibits hexokinase and glycogen phosphorylase; leads to slower rate of glycogenolysis and glycolysis; results in sparing of muscle and liver glycogen

accumulation of citrate

inhibits phosphofructokinase

increased acetyl-CoA

inhibits pyruvate dehydrogenase

process of training induced muscle adaptation

muscle contraction activated primary and secondary messengers; reults in expression of genes and synthesis of proteins; peaks in 4 to 8 hours, back to baseline in 24 hours;

early phase of strength gain:

neural factors predominate for increases in strength and power; intial four to eight weeks of training

increased flexibility from resistance exercises

primarily if the individual has poor flexibility to begin with; the combination of resistance training and stretching appears to be the most effective method to improve flexibility with increasing muscle mass

PGC-1-alpha gene

specifically responsible for mitochondria biogenesis; allows us to increase the number of mitochondria in our muscle; if there is an increase of this genes expression, there will be an increase of mitochondria and aerobic performance

unilateral training

strength training that's only in one limb results in an increase in strength in the untrained (contralateral)limb up to 22 %, with average increases of 8 percent

fiber type formation

the Type IIx (anaerobic fibers) will transform into a type II fiber types that will be able to do more aerobic exercise (type IIa)

Effects of mitochondria and capillaries on FFA and glucose utilization

the combination of the increase in the density of capillaries and the number of mitochondria per muscle fiber increases the capacity to transport FFA from the plasma to cytoplasm to mitochondria

enhanced motor performance

the magnitude of change is based on the specificity of the exercises or modalities perfomed; resistance training has shown to increase vertical jump, spint speed, tennis serve velocity, and kicking performance

increased synchronouse recruitment of motor units

typically fire asynchronously; training results in greater synchronization; firing of two or more motor units at a fixed time intervals

neural activity increases in the primary motor cortex

when level of force developed increases and when new exercises or movements are being learned

resistance training and cardiac hypertrophy

works to increase the heart size by primarily increasing the thickness of the myocardial wall

Time frame for resistance training/strength gain

1. Early phase of strength gain 2. Late phase of strength gain

lower oxygen deficit induced by training allows

1. less lactate and H+ formation 2. less PC depletion

mitosis of the muscle fiber

each half then increases to the size of the parent fiber; may contribute to resistance training-induced increases in muscle hypertrophy; has been shown in lab animals; show in cats and birds, not mice and rats; mixed evidence in human studies; 90 to 95 % of muscle enlargement due to hypertrophy

type I fibers

have large quantities of myoglobin; gives them a red appearance

Other modifications of lipid relative to carbs caused by exercise by endurance training

increased mobilization or free release of free fatty acids from the adipose tissue, greater utilization of the intramuscular triglyceride, and increase in the capacity/contribution of muscle to take up and oxidize lipids

reason more mitochondria result in less carb breakdown

more mitochondria means more Krebs cycle; the first product of the Krebs cycle is citrate, which inhibits glycolysis's PFK. Since PFk is inhibited there is less glycolysis going on and therefore less carbs being broken down

lifting light weights optimally cannot maximally recruit all available motor units during an exercise

motor unit recruitment is intensity dependent; heavy resistance training program ( greater than 80 to 85 % of 1 rep max) is required to maximally recruit type II motor units

Mitochondrial number and performance

oxygen deficit is reduced following training; energy requirement can be met by oxidative ATP production at the onset of exercise; faster rise in VO2 curve, and steady state is reached earlier

Satellite cells

play role in muscle growth and repair by increasing the number of nuclei in the muscle fiber

aerobic training effects on myoglobin

shown to increase muscle myoglobin content by 75 to 80 percent in animal studies (rodents not humans)

motor units are recruited according to the size principle

smaller motor units are recruited first during activities that requires low force output; as the need for for production increases, larger motor units are recruited; before a high-threshold motor unit is recruited, all of the motor units below it are recruited sequentially

greater motor unit recruitment

voluntary activation of motor units; untrained individuals have limited ability to maximally recruit motor units, especially fast twitch units; MRI study show only 71 % of muscle tissue was activated during maximal effort in untrained persons; training can reduce deficit

fiber hypertrophy involves both

1. an increase in the synthesis of the contractile proteins actin and myosin within the myofibril (adding more sacromeres) 2. an increase in the number of myofibrils within a muscle fiber

Lower RER in response to exercise by endurance training

Decreased RER at both absolute and relative submaximal intensity; increased dependent on fat and decreased dependent on glucose

experts believe that gradual resistance training reduces

GTO sensitivity (inhibitory impulses) which enables muscle to generate more force from trained muscles independent of increases in muscle mass

proprioreceptors located at muscle-tendon junction

Golgi Tendon Organ is a protective device to make sure we don't produce too much force output and end up tearing a muscle or damaging a tendon

Cardiovascular adaptations at rest

HR and BP: no change or small decrease Stroke Volume: no change or small increase Blood lipid profile: no change or small increase (for HDL-C) or small decrease (for LDL-C)

Electromyography (EMG)

Records and quantifies electrical activity in the muscle fibers of activated motor units

if after endurance training, there is an increase in mitochondria size and count, would we expect to see and increase or decrease in the Phosphofructokinase and Citrate Synthanase?

There would be a decrease in Phosphofructokinase and an increase in Citrate Synthase because more mitochondria means more mitochondrial enzymes will be activated. PFK is not in the mitochondria, it's in the cytoplasm. Citrate Synthase, associated with the Kreb's Cycle, is found in the mitochondria.

improved Acid-base balance during exercise

due to a decrease of H+ ion formation from decreased lactic acid

descending corticospinal (or pyrimidal) tracts

a large collection of axons linking the cerebral cortex to the spinal cord; characterized by neurons in the brain (primarily in the motor areas) forming synapses with other nerves that eventually make their way down the spinal cord to the exact anterior root of exit for innervation originates from these descending corticospinal tracts

increased strength in the untrained limb

accompanied by greater EMG; central neural adaptation accounts for the strength gain (known as cross education)

4-week resistance training program

after four weeks, the amount of EMG activity is greater for a given resistance lifted compared to baseline; greater neural drive with training apparently mediated the strength adaptations; early phase improvements in strength gain not accounted for increased muscle size; studies concluded that increase in neural drive to a muscle results in greater strength

mTor signaling enzyme

becomes elevated after resistance training; every time this signaling enzyme is increased there is increased protein synthesis and therefore muscle hypertrophy

Cardiovascular adaptations to resistance exercise

chronic resistance training reduces the cardiovascular response to an acute bout of resistance exercise of a given absolute intensity or workload; HR and BP: small decrease

neural adaptation

complex and typically occurs before structural changes in skeletal muscle

resistance training yield substantial strength/power gains via neuromuscular changes

critical for exercise training programs; resistance training is important for overall fitness and health, not just for athletes

myonuclear domain

cytoplasm surrounding each nucleus; each nucleus can support a limited myonuclear domain; more nuclei allow for greater protein synthesis; series of intracellular signaling processes take place that regulate gene expression and subsequent protein expression

synchronous recruitment leads to strength gains

facilitates contraction; may produce more forceful contraction; improves rate of force development; increases capability to exert steady forces

myoglobin

facilitates the diffusion of oxygen from the blood into the skeletal muscles

force on joint

forces should be exerted throughout the full range of motion of a joint; vary exercise selection to change the distribution of the force vectors to continually present a unique stimulus

alpha-two = slow twitch fibers (type I)

has the smallest size of motor neurons; innervates a cluster of less than or equal to 300 muscle fibers; low excitation thresholds; slow conduction velocities; recruited at low workloads

connective tissue

havy loading is vital for connective tissue changes (tendons, ligaments, and fascia) especially bone (it takes atleast six months)

maximal oxygen consumption (VO2max) in response to resistance training

heavy resistance training does not significantly affect aerobic capacity unless the individual is initially deconditioned; the exception is in relatively untrained people, who can experience increases in VO2max ranging from five percent to eight percent as a result of resistance training; circuit training and programs using high volume and short rest periods (30 sec or less) have been shown to improve VO2max

increased power from resistance exercises

heavy resistance training with slow velocities of movement leads primarily to improvements in maximal strength; power training increases force output at higher velocities and rate of force development; peak power output is maximized during the jump squat with loads corresponding to thirty percent to sixty percent of squat one rep max; for the upper body, peak power output can be maximized during the ballistic bench press throw using loads corresponding to forty-six to sixty-two percent of one rep max bench press

triglyceride content

higher intramuscular triglyceride content in trained individuals compared with untrained controls

Other muscle adaptations that occur with endurance training

higher muscle and liver glycogen as well as intramuscular triglyceride content, increase in size and number of mitochondria, and increased oxidative enzyme activity

increased muscular strength from resistance exercises

if you take an untrained person and introduce them to a training program, they'll show a faster increase in gains than if you were to show an elite athlete to a new program; heavier loads are most effective for fiber recruitment; the effects of training are related to the type of exercise used, its intensity, and its volume

Fiber hyperplasia

increase in the number of muscle fibers via longitudinal fiber splitting (new fiber development; basically mitosis of the muscle fiber)

mitochondrial oxidation of FFA

increased enzymes of beta oxidation and increased krebs cycle and rate of acetyl-CoA formation

improved capacity to take up FFA into the muscle cell from the plasma/circulation

increased fatty acid binding protein and fatty acid translocase; increased capillary density

increased ability to transport FFA from the cytoplasm to the mitochondria

increased mitochondrial number and carnitine transferase

improved body composition

increases in lean tissue mass, daily metabolic rate and energy expenditure during exercise are outcomes of resistance training; resistance training solely can increase fat-free mass and reduce body fat by one percent to nine percent; largest increases in FFM area little greater than 3 kg (6.6 lbs) in about ten weeks of drug-free resistance training

skeletal muscle adapts to resistance training primarily by

increasing its size, facilitating fiber type transitions, and enhancing its biochemical and ultra-structural components; changes results in enhanced muscular strength, power, and muscular endurance

resistance training may elicit adaptations along the neuromuscular chain by

initiating in the higher brain centers and continuing down to the level of individuals muscle fibers

up-regulation of factors such as myogenin and myoD

involved with muscle regenerations (myogenesis) and down-regulation of inhibitory growth factors (myostatin)

alpha-one = Fast twitch fibers (Type II)

largest cell body; innervates a cluster of greater than or equal to 300 muscle fibers

Early phase of strength gain

neural factors predominate for increases in strength and power; occurs in the initial 4 to 8 weeks of training

Reduced utilization of muscle glycogen and blood glucose in response to exercise by endurance training

one metabolic consequence is glycogen sparing; a slower rate of utilization of muscle glycogen and enhanced reliance on fat as a fuel source at a given exercise intensity; reduces extent of liver glycogenolysis and contributes to the better maintenance of blood glucose homeostasis during prolong exercise; includes low to moderate exercise intensities; at high intensities you would still have to use carb regardless of your fitness level

changes to skeletal muscle following endurance training

presents a greater surface area for exchange between muscle fiber and blood, increases the length of time available for diffusion of oxygen from capillary to fiber to occur, and increased capacity for delivering oxygen, glucose, and FFa to active muscle tissues/higher oxygen extraction

transcriptional activators

responsible for turning on specific genes to synthesize new proteins; gene activation results in transcription of messenger RNA which contains the genetic information for a specific protein's amino acid sequence; the newly synthesized mRNA leaves the nucleus and travels to the ribosome where the mRNA message is translated into a specific protein.

much of the early gain in strength

result of learning how to more effectively produce force and produce a true maximal movement, such as moving a barbell from the chest to a fully extended position in the bench press.

major training adaptation

shift from type IIx to (the more oxidative) type IIa fiber type; means that a shift of the type of myosin adenosine triphosphatase (ATPase) isoform content and heavy chains takes place during training; still powerful but more oxidative and fatigue resisstant with training; transition causes more force to be produced over time; less extent than endurance training

capillary change due to endurance training

there is an increased number of capillaries per muscle fiber and capillary density

Muscular hypertrophy that occurs with endurance training

there is selective hypertrophy of type I fibers

increased oxidation of lipid relative to carbohydrates in response to exercise by endurance training

with training the body can use more fats and rely less on carbohydrates at low to moderate exercise intensities; untrained people have to rely more on carbs than trained people