Metabolic adaptations to training

Principles of training

• General principles– Overload

• Increased frequency, duration or intensity of exercise

– Typically, mode specific

– Specificity• Adaptations occur in the

specific muscles engaged– Adaptations occur in response to

specific mode of exercise

– Individual responses vary• Genetics• Willpower

– Transient• Changes are reversible

– Overtraining

Adaptations to endurance training

• Endurance training– Typical

• 50-80% VO2max• 30-90 minutes• 5-7 days/wk

– ATP supply must meet ATP demand

• If not, fatigue

Muscle adaptation to endurance training

Hypertrophy of type 1 fibers

Increased capillary volume

Increased myoglobin content (?)

Increased mitochondrial volume

Reduced heterogeneity of blood flow

Increased sensitivity of mitochondria

Reduced reliance on non-oxidative metabolism

Increased stores of muscle glycogen

Increased ability to uptake and utilize lipids

Fiber type composition• Effects of endurance training

– Type 1 fiber % increases• Costill et al. showed that type 1 fiber

% increased from– Untrained: 58%

– Trained: 62%

– Elite: 79%

– Type 1 fiber X-sectional area increased

• ~30% in elite runners– Thus, >80% of the muscle volume was

occupied by type 1 fibers

• Not so in trained runners– Thus, some of these adaptations may be

genetic or require a long time

Muscle capillary density• Endurance training

– Increases capillary density by a variety of measures• No. of caps/fiber• No of caps per fiber volume

– This improves• Oxygen delivery• By-product removal• How?

– Relationship between cardiac output, capillary density and capillary transit time• TT = instantaneous volume/instantaneous flow• Rest

– Volume: 75 ml

– Flow: 85 ml/s

– TT: ~0.9 seconds

• Exercise– Volume: 175 ml

– Flow: 650 ml/s

– TT: ~0.27s

•

•Muscle glycogen content•Increased insulin sensitivity after training

•Increased GLUT-4 concentration

•Glycogen synthase activity is elevated after training

•Increase in hexokinase activity following training

Intramuscular fuel stores

Muscle mitochondrial density and oxidative enzyme activity

• Training increases mitochondrial volume

– Enzymes of TCA cycle• Activity is increased (30-100%)

– Enzymes of ETC• Activity is increased (30-100%)

– Allows faster adjustment to a new workload– Increased ability to utilize oxidative

metabolism– Faster recovery– These adaptations occur in both type 1 and

2 fibers

Metabolic response adaptations

• Following training– Increased

enzymes of fatty acid uptake and utilization

• Allows greater uptake of fats and allows them to make a greater contribution at any given workload

Lower RER and RQ at a given exercise intensity

Reduced rate of muscle glycogen utilization at a given intensity

Reduced utilization of blood glucose

Reduced accumulation of muscle/blood lactate

Increased utilization of fat at any given intensity

Increased utilization of intramuscular triglycerides (?)

Reduced rate of liver glycogenolysis

Metabolic adaptations• Less disturbance to ATP

homeostasis during exercise following training

– Smaller rise in ADP and Pi– Less formation of AMP– Less IMP and ammonia– Slowed glycogenolysis/glycolysis

• This would allow greater fat utilization at the same absolute workload

Physiological adaptations• VO2 = HR x SV x (a-

vO2 diff)• Stroke volume

– Increased ventricular volume

– Greater end diastolic volume

– Enhanced contractility

• Oxygen carrying capacity

– CaO2 = 1.34*[Hb]*(%sat) + PaO2*(0.003)

– [Hb] actually falls or doesn’t change with training (Why?)

– Is this beneficial?• Lower viscosity• Reduced resistance to

flow

Blood volume Increased

Stroke volume Increased

Heart rate Decreased at rest (and submaximal exercise)

Cardiac output Increased

Blood flow (distribution) Increase in flow capacity, reduced heterogeneity

Oxygen extraction Increased ability to extract

Arterial blood pressure Reduced blood pressures at any submaximal workload

Ventilation Increased ability to sustain high ventilatory rates

Time course of training/detraining• Training adaptations

– Determined by Load• Lode = intensity x duration x

frequency

– Specific to the muscles used

– Takes weeks to months to manifest

• Some evidence of improved “metabolic coupling” after 5-7 days of training

• Some evidence that mitochondrial protein synthesis is upregulated

– HIIT• Seems to provide the

greatest stimulus to mitochondrial volume

– Long, slow distance• Increases cardiovascular

function and fluid balance

Detraining• Seems to follow the

same time course as adaptations to training

• This follows the logic of Cram and Taylor and their theory of symorphosis

Hormonal adaptations to training• In general,

– Hormonal response to exercise are attenuated after training

• Catecholamines, cortisol, glucagon and growth hormone all reduced during submaximal work in trained

• Insulin is the exception– Tends to be higher in trained

– Seems to be mode specific– Why do we see these hormonal

adaptations?• Overall stress of the exercise is less

– Reduced Cortisol, reduced catecholamines, reduced HR

– Implications• Lower catecholamine

– Reduced rate of glycogenolysis

• Lower catecholamines and elevated insulin

– Reduced rate of liver glycogenolysis

– Reduced rate of lipolysis

– Tissue responsiveness• Same effect in some tissues if

concentration is down, but sensitivity is up

• Would make the system more responsive

Adaptation to sprint and strength training

• Sprint training– Affects mostly the ATP-PCr and

anaerobic energy systems– Increased ATP, PCr and

glycogen concentrations• ATP and PCr, Likely the result of

relative increase in type II fiber area

– Enzyme activity• PFK increased• LDH increased• Adenylate kinase increased

– Increased lactate levels after training

• Improved buffering capacity– Increased bicarbonate

– Increased transport of lactate and hydrogen ions

• Improved pain tolerance

Hypertrophy of muscle fibers

Increased muscle X-sectional area

Increased phosphocreatine and glycogen content

Increased glycolytic capacity

Increased strength/anaerobic work capacity

Decreased mitochondrial volume (?)

Imncreased muscle buffering capacity

Muscular adaptations to training• Stimuli? Mechanisms?

– Myosin seems to be the key– Stimuli

• Mechanical– Stretch-contraction cycling

• Metabolic– Genes

– Fast twitch appears to be the default

• Immobilization causes a shift to type II fiber type

• Training stimulus required to shift to type I

– Transduction of mechanical forces• Occurs through the cytoskeleton

– Directly– Stretch activated ion channels– Stretch induced alterations in certain molecules

(e.g. adenylate cylcase)

• Induces– Altered gene expression– Changes in protein synthesis/degradation

– Mitochondrial biogenesis• Increased by increased metabolic flux

– Increased cycling through the pathways with associated changes in metabolites

– Increased ADP/ATP, Cr/PCr

Immunosuppression/overtraining• Athletes seem to be more

susceptible to infection– Depressed immune system?

• Immune system– White blood cells

• Decreased by repeated bouts of intense training (why?)

– Increased stress hormones– Reduced glutamine levels

– Acute exercise response• Mimics infection

– Increase in circulating white blood cells– Tumor necrosis factor– Interleukins– C-reactive protein– Activated complement– Hormonal response

» Increased catecholamines» Cortisol» GH» Prolactin (all immunomodulatory effects)

– Recovery• NK activity falls • Lymphocytes fall• T-lymphocyte helper/suppressor ratio falls

– “Open window” for infection after exercise

Immunosuppression/overtraining• Reduced immune function

with heavy training– Cumulative effects of hard

training and elevated stress hormones

– Insufficient time for the immune system to recover

– Fall in plasma glutamine• Essential for white blood cells

– Cell division

– Antibody production

– Bacteriophage activity

• Exercise– Increased release of glutamine from

muscle

– Increased glutamine requirement by other organs

– Decrease in plasma glutamine levels

Overtraining

• Overtraining– Underperformance despite

continued or increased training– Training too hard, too often, with

insufficient rest between bouts– Pathophysiology

• Muscle soreness/weakness• Hormonal/haematological changes• Mood swings• Depression• Loss of appetite/diarrhea• Persistent viral infection

– May cause drop in glutamine

– Low carb diets, infection, fasting, physical trauma also can cause a fall in glutamine levels