Physiology of Training

1. Physiology of Training Powers CH 13

2. Principles of Training Overload Stimulus beyond what tissue is accustomed Intensity, duration, frequency of training Specificity Muscle fiber type(s) recruited Principal energy system involved (aerobic v. anaerobic) Velocity of contraction (Vmax) Type of contraction (concentric, eccentric, isometric) Specific Adaptations = �Training Effect� Aerobic training = capillary and mitochondrial adaptations Power training = increase in contractile proteins

3. Cardio-Respiratory Adaptations

4. Endurance Training and VO2 Max Programs that enhance VO2 Max: Involve large muscle mass / dynamic exercise (running, cycling, swimming, XC skiing) 20-60 min. per session 3-5x per week Intensity @ 50 � 85% VO2 Max Capacity for improvement: Large genetic component (differences in mitochondrial DNA explain much of individual differences in VO2 Max) Largest gains experienced by those with low initial values

5. VO2 Max and Cardiac Output Increases in VO2 Max with endurance training: 50% of increase due to SV 50% of increase due to O2 extraction (A-VO2 diff) Greater capillary density and increased # of mitochondria in trained muscle ( maximal ex. ventilation) Increase in Max HR has less influence on VO2 Max

6. Influences on Stroke Volume Influences on increased EDV: Increased ventricular size Increased venous return (�preload�) Increased myocardial contractility Decreased peripheral resistance to blood flow out of heart (�afterload�) With endurance training: peripheral resistance = CO (arterial BP remains unchanged)

7. Detraining and VO2 Max Weeks 1 and 2 Decrease in SV due to decrease in plasma volume Weeks 3 � 7 Decrease in A-VO2 difference (due to decrease in # of mitochondria more than decrease in capillary density) Mitochondria number doubles in muscle cell after 5 weeks of training 1 week of inactivity (detraining) = loss of 50% of that gained in 5 weeks of training 3-4 weeks of retraining needed to reach former levels

8. Biochemical Adaptations and O2 Deficit ATP converted to ADP + P allows x-bridges to form ADP concentration in cell cytoplasm is stimulus for ATP-producing systems to kick in: Phosphagen system (initially) Glycolysis Mitochondrial oxidative phosphorylation (provides ATP aerobically in Steady State exercise) Endurance Training Effect Increases in mitochondria #, oxidative enzymes, and # of capillaries in muscle fiber (�shared� chore of ATP production)

9. Biochemical Adaptations and O2 Deficit More mitochondria = �shared� chore in ATP production Less change required in ADP concentration to stimulate mitochondria to take up O2 (fewer mitochondria to do work requires higher ADP concentration to stimulate mitochondria) Since less change in ADP concentration is needed to stimulate mitochondria to work, rising ADP levels at onset of work will cause earlier activation of oxidative phosphorylation This causes faster rise in O2 uptake curve at exercise onset and shorter time to steady state VO2 � resulting in lower O2 deficit, less creatine phosphate depletion, and less lactate and H+ formation. Mitochondria = money ADP concentration = hunger �Think about the price of a snack � either I am very hungry (high adp concentration) or I have plenty of money (increased mitochondria #), but if I am not that hungry and short on $$, I�ll wait to find it cheaper somewhere else (glycolysis or phosphagen systems) however, they are fatigable and are like driving around looking for cheaper snacks and spending all of your money in gas trying to find a better price.Mitochondria = money ADP concentration = hunger �Think about the price of a snack � either I am very hungry (high adp concentration) or I have plenty of money (increased mitochondria #), but if I am not that hungry and short on $$, I�ll wait to find it cheaper somewhere else (glycolysis or phosphagen systems) however, they are fatigable and are like driving around looking for cheaper snacks and spending all of your money in gas trying to find a better price.

10. Biochemical Adaptations and Plasma Glucose Concentrations Combination of increased capillary density and # of mitochondria per muscle fiber enhances: Transport of FFA into muscle Transport of FFA from cytoplasm into mitochondria Greater activity of enzyme carnitine transferase Mitochondrial oxidation of FFA Increased rate of formation of acetyl CoA from FFA for oxidation in Krebs Cycle

11. Biochemical Adaptations, Blood pH and Lactate Removal Mitochondrial adaptations result in: Smaller O2 deficit due to more rapid increase in O2 uptake at onset of work Increase in fat metabolism (muscle glycogen / blood glucose sparing) Reduction in lactate and H+ formation Increase in lactate removal

12. Bone and Connective Tissue Adaptations

13. Bone Adaptation Mechanical loading stimulus affecting bone growth: Magnitude of load (greater intensity = greater stimulus for bone growth) Rate of loading (higher rates of contraction / high-power activities = greater stimulus) Direction of forces (alteration of normal bone loading pattern = greater stimulus) Types of loading: Compression Tension Shear Bending Torsion

14. Forces Acting on Bone / Joint Bones accustomed to normal forces (force parallel to long axis) and handles rapid rate of loading due to brittle nature of cortex Cortical bone can withstand high levels of weight bearing or muscle tension in the longitudinal direction before failure (Fx)

15. Forces Acting on Bone Trabecular (spongy) bone Scaffolding arrangement Bone weight reduction Adaptive to multi-directional stress

16. Bone Integrity Bone is adaptive material sensitive to disuse, immobilization, vigorous activity Wolff�s Law � change in bone�s internal architecture in response to loading Bone resorption � osteoclasts Bone deposition - osteoblasts

17. Physical Activity and Bone Remodeling Cyclic loading MES ( ~ 1/10 force required to Fx bone) Increase in appositional (x-sectional) growth Wolff�s Law SAID principle Sharpey�s fibers (kinetic chain)

18. Ligaments and Tendons Connect bone-to-bone (L) or muscle-to-bone (T) Viscoelastic Collagen and elastin fibers Tensile strength related to x-sectional area Become stiffer with cyclic loading Fail under rapid stretch

19. Articular cartilage High water content Stiff but compressible shock absorption Lubricates joint surfaces via secretion of synovial fluid

20. Joint Degeneration Degenerative Joint Disease Avascular Necrosis

21. Muscular Adaptations

22. Muscular Adaptations Muscle strength Maximal force a muscle (group) can generate (1RM) Power F x D / t (W/t) Muscle endurance Repeated contractions against submaximal load

23. Muscular Adaptations to Resistance Training Hypertrophy Increase in synthesis of contractile proteins w/in myofibril Increase in # of myofibrils w/in ms fiber (new myofilaments added to external layers of myofibril � Hyperplasia??) Increase in x-sectional area of ms fiber = increase in force development Fiber-type Response Greater increases in size of Type II (fast twitch) fibers # of fast twitch fibers relative to slow twitch may indicate ultimate potential for hypertrophy Neural Adaptations Primary catalyst for strength gains early (1st month) resistance training Detraining Strength decreases occur at faster rate than muscle atrophy Decreases in 1st month of detraining connected w/ loss of neural adapt.

24. Muscular Adaptations to Endurance Training Fiber-type Response Selective recruitment of Type I (slow twitch) fibers (sustain low intensity / high volume exercise) Conversion of Type IIx to Type IIa (glyc-oxidative) to enhance endurance) Increased training intensity causes increase in fast twitch fiber recruitment Hypertrophy Less capacity for hypertrophy in slow twitch fibers principally recruited for endurance events Energy Production Increase in mitochondria size and # Increased myoglobin levels for O2 transport w/in cell??

25. Muscular Adaptations Concurrent performance of intense endurance and resistance training can result in decreased strength gains Concurrent resistance (strength) training does not hinder (and may enhance) endurance capacity Anaerobic training may = enhanced aerobic performance Aerobic training does not = enhanced anaerobic performance

26. Hormonal Adaptations

27. Hormonal Interactions with Muscle Hormonal mechanisms mediate changes in the metabolic and cellular processes of muscle as a result of resistance training Muscle Remodeling: Disruption / damage of muscle fibers Inflammatory response Hormonal interactions New protein synthesis (contractile and non-contractile proteins)

28. Adaptations to Resistance Training Increase in muscle contractile proteins (A & M) Synthesis of non-contractile proteins (laid down 1st to provide structural integrity and orientation of contractile elements within sarcomere) Protein metabolism Type II fibers depend on dramatic increase in protein synthesis to maintain hypertrophy Type I fibers depend on protein degradation reduction