Neuromuscular Adaptations to Resistance Training

1. Neuromuscular Adaptations to Resistance Training KINE 433-504 Physiology of Exercise Fluckey JD TR 9:35-10:50a MBL.TAMU.EDU K_Shimkus@hlkn.tamu.edu

2. Muscular Strength • The maximal amount of force that a muscle or muscle group can generate • Absolute strength: Bench pressing 200lb is twice as strong as a person bench pressing 100lb • Relative strength: A 150lb person benching 200lb is relatively stronger than a 250lb person benching 200lb • Maximum strength is referred to as the 1-repetition maximum (1RM)

3. Muscular Power • Power= force * velocity • A person performing the same force faster is exerting more power • Power is the functional application of both strength and speed. It is the key component for most athletic performances • Effects of limb length on power • Speed is more difficult than force to alter

4. Muscular Endurance • A muscle’s ability to repeatedly develop and maintain force. • e.g. – pushups and situps • Can be tested as the number of repetitions completed at a identified % of the 1RM • Gains occur through adaptations in muscular strength and improvements in metabolic and cardiovascular function

5. Application It would be smart to identify what type of athletes would epitomize muscular power, and which athletes would prefer muscular endurance.

6. Resistance Training towards Strength, Power, Endurance • Principle of Progressive Overload • Principle of Specificity • Strength – high intensity, high volume • Power – high intensity, moderate - high volume with emphasis on speed • Endurance – lower intensity, lower volume, high no. of repetitions

7. Gains in Mass and/or Strength • Muscle mass is proportional to sheer force • i.e. a gain in muscle mass has a direct effect on gains in strength • But, you can have gains in strength WITHOUT gains in mass • Gains in muscle strength rely on more than muscle size • Studies with women who doubled their strength with no observable change in muscle size

8. Neural Control of Strength Gains • Initial gains in strength/power tend to be due to neural factors rather than muscular • Gains in strength in the first 8 weeks of training will result almost exclusively from neural adaptations

9. Synchronization & Improved Recruitment • Recall from Ch 2: the all-or-none principle, motor-unit recruitment, and EPSPs/IPSPs • Better synchronization of motor neurons increases signal velocity and strength, resulting in faster, more often, and more sustainable muscle contractions • Faster/more efficient recruitment for a given task • Not fully supported • Reduction of IPSPs

10. Autogenic (Neural) Inhibition • The inhibitory Golgi Tendon Organ • Training can gradually reduce or counteract these inhibitions, allowing the muscle to achieve greater force production • Explains how laboratory involuntary max effort forces are higher than voluntary, and superhuman feats of strength

11. Other factors • Reduction of coactivation • Less firing of the antagonist muscle • Improvements in rate coding • The motor-units ability to fire more often and lead to summation • Improvements at the NM Junction

12. Muscle Hypertrophy • Transient hypertrophy – the increase in muscle CSA due to fluid accumulation in the interstitial and intracellular spaces of the muscle • Occurs due to acute exercise, temporary • Fluid comes from blood plasma • Chronic hypertrophy – the increase in muscle size that occurs with long-term training, most often resistance • Due to an increase in myofibrils, myofilaments, sarcoplasm, and connective tissue

13. Training Styles’ Effect on Hypertrophy • 36 training sessions with subjects using either only concentric actions or only eccentric actions • Eccentric training increased fast-twitch fiber area by ~10-fold over increases from concentric training • What does that tell us? • Why might that occur with eccentric exercise?

14. Fiber Hypertrophy • Many believe that the number of muscle fibers per muscle are established at birth or shortly after • Believing that, muscle hypertrophy is due to an increase in fiber size, not muscle fiber number • Increases in myofibrils (actin and myosin), sacroplasm, and connective tissue • Larger fibers = larger CSA = more force

15. Will Type I Fibers Hypertrophy?

16. Hypertrophy & MPS • MPS – Muscle Protein Synthesis – the rate by which skeletal muscle is produced • MPB – Muscle Protein Breakdown – the rate by which skeletal muscle protein is converted into free amino acids and other products • MPT - Muscle Protein Turnover – the net between MPS and MPB

17. MPT Throughout the Day

18. Hypertrophy + Gender + Age • Males tend to build muscle in greater amounts due to endogenous testosterone, which promotes muscle growth • Men tend to build the most mass after puberty until old age, when testosterone is highest • Role of activity • 1cm2 CSA of 26 yr old male muscle generates the same relative force as the same CSA of a woman or older person

19. Fiber Hyperplasia • Studies on cats show fairly substantial evidence for an increase in the number of fibers with training • Not found in chickens, rats, mice, humans • Book’s example of human hyperplasia • In theory, a fiber could divide into two unique fibers • Claim satellite cells play a role

20. Satellite Cells for Hyperplasia

21. Satellite Cells for Hypertrophy

22. Myonuclear Domain Note: ‘fix’ myofiber number

23. Integration of Neural and Muscular Adaptations to Exercise • Initial gains (8 wks) are almost all neural • Long-term benefits are muscle size

24. Muscle Atrophy • As muscle grows to meet demands, it also breaks down when untaxed to become more efficient • Immobilization increases MPB and decreases MPS • Strength decreases are most dramatic in the first week, averaging 3-4% losses per day (does include neural losses of function) • Affects Type I more than II • Why? • Type I can convert to II

25. Methods to study Atrophy • Spaceflight analogs • Bedrest, casting, ULLS, HU • Animal techniques • Induce Sepsis, denervation • Other • Caloric restriction, nutrient deprivation

26. Cessation in Training • While training increases strength and muscle CSA, detraining decreases both • Men and women who detrained for 12 weeks after 10-18 of training lost 68% of their gains • The losses due to cessation of training are less substantial than losses due to immobilization

27. STRENGTH CHANGES IN WOMEN Strength trained for 20 weeks; then no training for 30-32 weeks; then retrained for 6 weeks

28. Maintenance of Strength/Mass • Muscle mass and strength can be maintained in people (less than elite) with a reduction in training (3 sessions/week to 1-2/week) • Intensity is the key component to maintenance

29. Alterations in Muscle Fiber Type • As discussed earlier, fiber types can change • Due to ‘rewiring’ of motor units • Enough training at either high intensity or chronic low intensity

30. Acute Muscle Soreness • Occurs during or immediately after exercise • Due to accumulation of end products of exercise (H+) and edema • Note- not lactic acid • Compartment syndrome • Alleviates within a few minutes to hours after cessation of exercise

31. DOMS • Delayed Onset Muscle Soreness is the pain that arises 12-48 hours after training has finished and persists for as long as 7 days • Due to actual damage, unlike acute soreness • Not fully understood, but all theories acknowledge eccentric contraction to play a big role • Downhill running

32. DOMS – Structural Damage • Breakdown of Myosin-Actin connections • Tearing of the Z disks • Rupturing of the sarcolemma • Leaking of calcium, myoglobin, metabolic enzymes Sarcomeres

33. Inflammatory Reaction • May be a tie to white blood cells and their activity to DOMS, as WBC counts are higher after activities tied to DOMS • Injured muscle initiates an inflammatory process • Neutrophils release cytokines which attract and activate other inflammatory cells, as well as release oxygen free radicals • Macrophages enter muscle and remove debris to allow for rebuilding

34. Armstrong’s Mechanisms of DOMS • High tension in the muscle contribues to structural damage to the cell and its membrane • Cell membrane damage disturbs the calcium balance of the cell, triggering necrosis (cell death) 48h post-exercise • Products of macrophage activity and muscle leakage accumulates and stimulates nerve endings and pain receptors • Also could explain edema as a factor

35. How DOMS affects Performance • Immediate short term is an inability to synthesis gylcogen to replenish energy stores • 50% strength loss • Failure in E-C coupling predominates short-term • Loss of contractile PRO could take weeks to recover

36. Reducing Muscle Injury w Reduce eccentric component of muscle action during early training w Start training at a low intensity, increasing gradually or w Begin with a high-intensity, exhaustive bout of eccentric-action exercise to cause much soreness initially, but decrease future pain Over-the-counter anti-inflammatory drugs (e.g., aspirin) have not been shown to be effective in alleviating DOMS, although there is some disagreement on this issue.

37. Exercise-Associated Muscle Cramps (EAMCs) • Can occur during exercise, immediately after, or hours later while asleep • A painful, sporadic, involuntary contraction of a portion or entirety of a muscle • May result from: • Electrolyte imbalance, which affects body fluids • Sustained α-motor neuron activity, which occurs due to loss of control at the spinal level • Causes an increase in spindle activity and GTO activity decrease

38. Resistance Training in Sport • Gaining strength, power, or endurance simply for the sake of increases may not improve athletic performance • Sometimes, overdevelopment may hinder an athlete, especially when they train for adaptations counterintuitive to their sport

39. Determining Muscle Mass - Myostatin • Myostatin is a protein that negatively regulates muscle mass • Higher amounts of myostatin = _______________

40. Other cases of Myostatin Knockdown http://videos.mlive.com/chronicle/2009/01/liam_hoekstra_all_muscle.html