Metabolic adaptations to training

1. Metabolic adaptations to training

2. 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

3. 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

4. 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

5. 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

6. Intramuscular fuel stores 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

7. 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

8. 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

9. 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

10. 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

12. 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

13. 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

14. 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

15. 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

16. 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

17. 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

18. 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

19. 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