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 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

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. 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

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 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

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 Blood volumeIncreased Stroke volumeIncreased Heart rateDecreased at rest (and submaximal exercise) Cardiac outputIncreased Blood flow (distribution)Increase in flow capacity, reduced heterogeneity Oxygen extractionIncreased ability to extract Arterial blood pressureReduced blood pressures at any submaximal workload VentilationIncreased ability to sustain high ventilatory rates

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 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

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 –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