BS2014 - Muscle adaptations to exercise

Physiological mechanisms for hypertrophy

• repeated microtrauma to muscle fibres

• accumulation of anabolic signals (e.g. from hormones like testosterone, growth hormone, and IGF-1)

• consistent protein synthesis exceeding protein break

Gains of muscle strength due to neural control

• changes in motor unit recruitment

• increased neural drive

Benefits of synchronous motor unit recruitment

• more forceful contraction

• increased rate of force development

• increased capacity to exert steady state forces

Increased neural drive

• increased motor unit recruitment during maximal contraction

• increased frequency of neural discharge (rate coding)

Autogenic inhibition

action of the Golgi tendon organ to inhibit muscle contraction to prevent too much force being exerted on a muscle to prevent injury

Golgi tendon organ

proprioceptors between the muscle and tendon which detects changes in muscle tension

Effect of training on autogenic inhibition

increases the threshold at which the Golgi tendon is activated, allowing for more force to pass through the muscle before the inhibitory mechanism kicks in

Autogenic inhibition mechanism

• afferent nerves (on the Golgi tendon) have stretch-sensitive ion channels within them

• when force is exerted, the tendon is deformed, changing its shape and stretching the collagen elements

• changing the shape and length of the afferent fibres

• stimulation of the Golgi tendon organ signals back to the spinal cord

• leads to inhibitory reflex stopping contraction

• activation of antagonist muscle occurs to further inhibit contraction

Hypertrophy

increase in the volume or mass of muscle fibres without an increase in cell number

Muscle protein synthesis stimuli

• feeding

• exercise

Molecules in feeding that activate protein synthesis

• insulin

• branched chain amino acids — leucine, isoleucine and valine

Master regulator of cell growth

mTOR

Insulin-induced protein synthesis

• eating triggers insulin secretion into bloodstream

• insulin binds to receptors in muscle cell

• activates Akt which activates mTOR

• mTOR starts mRNA transcription and translation

Amino acid-induced protein synthesis

• eating causes breakdown of proteins into amino acids

• leucine enters the cell through an amino acid transporter

• leucine directly activates mTOR

• increase in transcription and translation

Exercise-induced protein synthesis

• exercise

• increases levels of phosphatidic acid

• direct activation of mTOR

• increased transcription and translation

Skeletal muscle adaptations to endurance exercise

• hypertrophy of type I fibres

• angiogenesis — synthesis of more capillaries to supply each fibre with more blood (area specific)

• increase in myoglobin content → increases oxidative capacity

• fat oxidation

• increase in mitochondrial density

• increase in mitochondrial oxidative enzyme capacity

• mitochondrial biogenesis

Mitochondrial biogenesis

production of new mitochondria

Benefits of mitochondrial biogenesis

• increase in oxidative capacity

• increases endurance performance

Mitochondrial oxidative enzymes

• citrate synthase

• succinate dehydrogenase

Role of mitochondrial oxidative enzymes in aerobic metabolism

ATP synthesis

Main master regulator for mitochondrial biogenesis

PGC-1α

Factors increasing transcription rates

• calcium signalling during exercise increases PGC-1α

• shift in AMP:ATP ratio (during exercise)→ increase in AMPK → increases in PGC-1α

PGC-1α-induced mitochondrial biogenesis

PGC-1α signals downstream to other transcription factors such as NRF-1/2 and TFAM which starts the process of mitochondrial DNA replication

Fatigue

the failure to maintain the required force and power output for the performance that you want to produce

Central fatigue

fatigue of: the brain, spinal cord, peripheral nerve

Peripheral fatigue

fatigue of: muscle sarcolemma, t-tubules, Ca²⁺ release, actin-myosin interaction, cross-bridge cycling, force/power output

Product inhibition

product of an enzyme reaction inhibits its production

Contribution of reduced muscle pH to fatigue

• reduced activity to glycolytic enzymes

• interference with contractile process

• stimulation of nerve endings

Major cause of fatigue in high intensity exercise

inorganic phosphate

iP+ in the development of fatigue

• phosphocreatine → creatine + iP+

• iP+ enters SR

• iP+ combines with Ca²⁺ forming calcium phoshpate precipitate

• sequesters calcium away from being released

• less calcium release from next action potential → weaker muscle contraction

Role of ADP in the development of fatigue

• ATP → ADP + H⁺

• ADP has been shown to slow cross-bridge cycling rate

• slower detachment of myosin from actin — ADP competes with ATP to rebind to myosin head

• ultimately reduces the speed of skeletal muscle shortening

• contribute to the development of fatigue

Energy sources for oxidative metabolism

• muscle glycogen

• liver glycogen

• adipose tissue

• blood glucose

Main determinant for substrate use

exercise intensity

Substrate use changes as exercise intensity increases

• at rest — predominantly plasma FFA for ATP synthesis

• in light exercise — predominantly plasma FFA + muscle triglycerides + plasma glucose

• in moderate exercise — big input from fat stores and increased input from muscle glycogen stores

• in intense exercise — predominantly muscle glycogen and plasma glucose + less contribution from fat stores

Why are fat sources less useful in intense exercise

takes a long time to mobilise fat stores

Exercise duration and substrate use

• start with heavy reliance upon muscle glycogen

• between hour 1&2 stores will deplete → switch to fat stores

• fat stores produce energy much slower than glycogen/glucose stores