1 / 59

Maximizing Muscle Strength Gains in Resistance Training

Learn the mechanisms behind muscle strength gain through resistance training. Understand neural adaptations, motor unit recruitment, hypertrophy, and fiber hyperplasia. Discover how resistance training can enhance muscle performance effectively.

capriceg
Download Presentation

Maximizing Muscle Strength Gains in Resistance Training

An Image/Link below is provided (as is) to download presentation Download Policy: Content on the Website is provided to you AS IS for your information and personal use and may not be sold / licensed / shared on other websites without getting consent from its author. Content is provided to you AS IS for your information and personal use only. Download presentation by click this link. While downloading, if for some reason you are not able to download a presentation, the publisher may have deleted the file from their server. During download, if you can't get a presentation, the file might be deleted by the publisher.

E N D

Presentation Transcript

  1. Chapter 10 • Adaptations to Resistance Training

  2. Chapter 10 Overview • Resistance training: gains in muscular fitness • Mechanisms of muscle strength gain • Muscle soreness • Resistance training for special populations

  3. Resistance Training: Introduction • Resistance training yields substantial strength gains via neuromuscular changes • Important for overall fitness and health • Critical for athletic training programs

  4. Resistance Training: Gains in Muscular Fitness • After 3 to 6 months of resistance training • 25 to 100% strength gain • Learn to more effectively produce force • Learn to produce true maximal movement • Strength gains similar as a percent of initial strength • Young men experience greatest absolute gains versus young women, older men, children • Due to incredible muscle plasticity

  5. Mechanisms of Muscle Strength Gain • Hypertrophy versus atrophy –  Muscle size   muscle strength –  Muscle size   muscle strength • But association more complex than that • Strength gains result from –  Muscle size • Altered neural control

  6. Figure 10.1a

  7. Figure 10.1b

  8. Figure 10.1c

  9. Mechanisms of Muscle Strength Gain:Neural Control • Strength gain cannot occur without neural adaptations via plasticity • Strength gain can occur without hypertrophy • Property of motor system, not just muscle • Motor unit recruitment, stimulation frequency, other neural factors essential

  10. Mechanisms of Muscle Strength Gain:Motor Unit Recruitment • Normally motor units recruited asynchronously • Synchronous recruitment  strength gains • Facilitates contraction • May produce more forceful contraction • Improves rate of force development –  Capability to exert steady forces • Resistance training  synchronous recruitment

  11. Mechanisms of Muscle Strength Gain:Motor Unit Recruitment • Strength gains may also result from greater motor unit recruitment –  Neural drive during maximal contraction –  Frequency of neural discharge (rate coding) –  Inhibitory impulses • Likely that some combination of improved motor unit synchronization and motor unit recruitment  strength gains

  12. Mechanisms of Muscle Strength Gain:Motor Unit Rate Coding • Limited evidence suggests rate coding increases with resistance training, especially rapid movement, ballistic-type training

  13. Mechanisms of Muscle Strength Gain:Autogenic Inhibition • Normal intrinsic inhibitory mechanisms • Golgi tendon organs • Inhibit muscle contraction if tendon tension too high • Prevent damage to bones and tendons • Training can  inhibitory impulses • Muscle can generate more force • May also explain superhuman feats of strength

  14. Mechanisms of Muscle Strength Gain:Other Neural Factors • Coactivation of agonists, antagonists • Normally antagonists oppose agonist force • Reduced coactivation may strength gain • Morphology of neuromuscular junction

  15. Mechanisms of Muscle Strength Gain:Muscle Hypertrophy • Hypertrophy: increase in muscle size • Transient hypertrophy (after exercise bout) • Due to edema formation from plasma fluid • Disappears within hours • Chronic hypertrophy (long term) • Reflects actual structural change in muscle • Fiber hypertrophy, fiber hyperplasia, or both

  16. Figure 10.2a

  17. Figure 10.2b

  18. Mechanisms of Muscle Strength Gain:Chronic Muscle Hypertrophy • Maximized by • High-velocity eccentric training • Disrupts sarcomere Z-lines (protein remodeling) • Concentric training may limit muscle hypertrophy, strength gains

  19. Mechanisms of Muscle Strength Gain:Fiber Hypertrophy • More myofibrils • More actin, myosin filaments • More sarcoplasm • More connective tissue

  20. Mechanisms of Muscle Strength Gain:Fiber Hypertrophy • Resistance training   protein synthesis • Muscle protein content always changing • During exercise: synthesis , degradation  • After exercise: synthesis , degradation  • Testosterone facilitates fiber hypertrophy • Natural anabolic steroid hormone • Synthetic anabolic steroids  large increases in muscle mass

  21. Mechanisms of Muscle Strength Gain:Fiber Hyperplasia • Cats • Intense strength training  fiber splitting • Each half grows to size of parent fiber • Chickens, mice, rats • Intense strength training  only fiber hypertrophy • But difference may be due to training regimen

  22. Figure 10.3

  23. Figure 10.4

  24. Mechanisms of Muscle Strength Gain:Fiber Hyperplasia • Humans • Most hypertrophy due to fiber hypertrophy • Fiber hyperplasia also contributes • Fiber hypertrophy versus fiber hyperplasia may depend on resistance training intensity/load • Higher intensity  (type II) fiber hypertrophy • Fiber hyperplasia may only occur in certain individuals under certain conditions

  25. Mechanisms of Muscle Strength Gain:Fiber Hyperplasia • Can occur through fiber splitting • Also occurs through satellite cells • Myogenic stem cells • Involved in skeletal muscle regeneration • Activated by stretch, injury • After activation, cells proliferate, migrate, fuse

  26. Figure 10.5

  27. Mechanisms of Muscle Strength Gain:Neural Activation + Hypertrophy • Short-term  in muscle strength • Substantial  in 1RM • Due to  voluntary neural activation • Neural factors critical in first 8 to 10 weeks • Long-term  in muscle strength • Associated with significant fiber hypertrophy • Net  protein synthesis takes time to occur • Hypertrophy major factor after first 10 weeks

  28. Mechanisms of Muscle Strength Gain:Atrophy and Inactivity • Reduction or cessation of activity  major change in muscle structure and function • Limb immobilization studies • Detraining studies

  29. Mechanisms of Muscle Strength Gain:Immobilization • Major changes after 6 h • Lack of muscle use  reduced rate of protein synthesis • Initiates process of muscle atrophy • First week: strength loss of 3 to 4% per day –  Size/atrophy –  Neuromuscular activity • (Reversible) effects on types I and II fibers • Cross-sectional area  cell contents degenerate • Type I affected more than type II

  30. Mechanisms of Muscle Strength Gain:Detraining • Leads to  in 1RM • Strength losses can be regained (~6 weeks) • New 1RM matches or exceeds old 1RM • Once training goal met, maintenance resistance program prevents detraining • Maintain strength and 1RM • Reduce training frequency

  31. Figure 10.6a

  32. Figure 10.6b

  33. Figure 10.6c

  34. Figure 10.7

  35. Mechanisms of Muscle Strength Gain:Fiber Type Alterations • Training regimen may not outright change fiber type, but • Type II fibers become more oxidative with aerobic training • Type I fibers become more anaerobic with anaerobic training • Fiber type conversion possible under certain conditions • Cross-innervation • Chronic low-frequency stimulation • High-intensity treadmill or resistance training

  36. Mechanisms of Muscle Strength Gain:Fiber Type Alterations • Type IIx  type IIa transition common • 20 weeks of heavy resistance training program showed • Static strength, cross-sectional area  • Percent type IIx , percent type IIa  • Other studies show type I  type IIa with high-intensity resistance work + short-interval speed work

  37. Muscle Soreness • From exhaustive or high-intensity exercise, especially the first time performing a new exercise • Can be felt anytime • Acute soreness during, immediately after exercise • Delayed-onset soreness one to two days later

  38. Muscle Soreness:Acute Muscle Soreness • During, immediately after exercise bout • Accumulation of metabolic by-products (H+) • Tissue edema (plasma fluid into interstitial space) • Edema  acute muscle swelling • Disappears within minutes to hours

  39. Muscle Soreness:DOMS • DOMS: delayed-onset muscle soreness • 1 to 2 days after exercise bout • Type 1 muscle strain • Ranges from stiffness to severe, restrictive pain • Major cause: eccentric contractions • Example: Level run pain < downhill run pain • Not caused by  blood lactate concentrations

  40. Muscle Soreness:DOMS Structural Damage • Indicated by muscle enzymes in blood • Suggests structural damage to muscle membrane • Concentrations  2 to 10 times after heavy training • Index of degree of muscle breakdown • Onset of muscle soreness parallels onset of  muscle enzymes in blood

  41. Muscle Soreness:DOMS Structural Damage • Sarcomere Z-disks: anchoring points of contact for contractile proteins • Transmit force when muscle fibers contract • Z-disk, myofilament damage after eccentric work • Physical muscle damage  DOMS pain • Fiber damage and blood enzyme changes may occur without causing pain • Muscle damage also precipitates muscle hypertrophy

  42. Figure 10.8

  43. Figure 10.9a

  44. Figure 10.9b

  45. Muscle Soreness:DOMS and Inflammation • White blood cells defend body against foreign materials and pathogens • White blood cell count  as soreness  • Connection between inflammation and soreness? • Muscle damage  inflammation  pain • Damaged muscle cells attract neutrophils • Neutrophils release attractant chemicals, radicals • Released substances stimulate pain nerves • Macrophages remove cell debris

  46. Muscle Soreness:Sequence of Events in DOMS 1. High tension in muscle  structural damage to muscle, cell membrane 2. Membrane damage disturbs Ca2+ homeostasis in injured fiber • Inhibits cellular respiration • Activates enzymes that degrade Z-disks (continued)

  47. Muscle Soreness:Sequence of Events in DOMS (continued) 3. After few hours, circulating neutrophils 4. Products of macrophage activity, intracellular contents accumulate • Histamine, kinins, K+ • Stimulate pain in free nerve endings • Worse with eccentric exercise

  48. Muscle Soreness:Sequence of Events in DOMS • Damage to muscle fiber, plasmalemma sets up chain of events • Release of intracellular proteins • Increase in muscle protein turnover • Damage and repair processes involve buildup of intra- and extracellular molecules • Precise causes of skeletal muscle damage and repair still poorly understood

  49. Muscle Soreness:DOMS and Performance • DOMS   muscle force generation • Loss of strength from three factors • Physical disruption of muscle (see figures 10.8, 10.9) • Failure in excitation-contraction coupling (appears to be most important) • Loss of contractile protein

  50. Figure 10.10

More Related