Chapter 13. Development of Muscular, Strength, Endurance, and Flexibility

Transcription

1 Chapter 13 Development of Muscular, Strength, Endurance, and Flexibility

2 Types of Contractions Dynamic, Isotonic, or concentric Muscle shortens with varying tension while lifting constant load Isometric, or static Tension develops but there is no change in the length of the muscle Eccentric Muscle lengthens while contracting or developing tension Isokinetic Tension developed while shortening is maximal over the full range of motion

3 Isotonic Contraction Muscle does not exert same tension throughout range of motion (ROM) Tension depends on Length tension relationship Angle of pull on skeleton Speed of shortening Composition of muscle (Type I and II)

4 Length Tension Relationship Optimal overlap of myofilaments Maximal tension Opposite ends Too much overlap Actin out of range of crossbridges

5 Joint Angle Strength curve Varying amounts of force generated Due to biomechanical differences in joint angle Peak force occurs at o

6 Characteristics of Skeletal Muscle Type 1 Type 2a Type 2b Mito high hi/mod low Fatigue Resistance high hi/mod low Predominant energy system aerobic combination anaerobic Speed of shortening low intermediate low Capillary density high low low

7 Resistance Training

8 Resistance Training Neural and muscular factors contribute to strength gains Neural adaptations for short term gains Learning Coordination Ability to recruit prime movers Muscular adaptations for long term gains Increase in size of prime movers Hypertrophy

9 Neural Factors Kannus (1992) Trained limb vs untrained limb One arm is strength trained Some of the training effect is transferred to other arm Trained arm-strength gain related to muscle hypertrophy and activation of motor units Untrained arm-strength due solely to increased activation of motor units-neural factor

10 Neural adaptations EMG activity Enhanced ability to recruit motor units leads to increased force production rate of motor unit firing Firing rate controlled by CNS Larger MU have higher firing rates Motor unit firing rate can be enhanced by training explosively

11 Neural Adaptations Recruitment of high threshold MU MU differ in ease of recruitment Maximal force requires as many MU as possible High threshold units must be recruited during training in order to be used in performance Motor Unit coordination Motor unit synchronization Inhibition of golgi tendon organs Co-contraction of antagonists Helps in rapid cycling of extensor and flexor muscles

12 Muscular Adaptations Muscular Enlargement Type II can develop a bit more tension than I Strength training causes hypertrophy of both types, Type II changes more than I Alterations in fiber types rigorous exercise training alters fiber types Alters type IIb to type IIa These changes are small and are not complete transformation Capability for adaptive change-myoplasticity

13 Physiologic Changes Hypertrophy Number and size of myofibrils Increased amount of contractile protein Increased capillary density Increased amount/strength of connective tissues

14 Biochemical Changes Increases in PC, ATP, Glycogen Little change in ATP turnover enzymes Increases/no change in glycolytic enzymes Significant increases in Krebs cycle enzymes Decrease in density of mito due to increase in size of myofibrils Selective hypertrophy of Type II Shift from IIb to IIa with both strength and endurance training programs

15 Hypertrophy

16 Training Programs

17 Muscle Soreness Consequence of overexertion Acute Pain during and after activity persisting for several hours Delayed onset (DOMS) 24 to 48 hours Declines during next 5-7 days

18 Acute Soreness Pain during contraction Tension occludes blood flow in active muscles Ischemia Ischemia results in buildup of metabolic waste products Causing stimulation of pain receptors Pain relieved when contraction intensity is reduced or stops Waste products are removed

19 DOMS Why this occurs is not fully known Most theories acknowledge that eccentric action is primary cause Downhill running compared to level

20 DOMS 1. Mechanical Trauma Structural damage occurs in muscle fibers Damage to sarcolemma disrupts calcium homeostasis, resulting in necrosis Presence of cellular debris and immune cells leads to swelling and inflammation Responsible for pain in DOMS

21 DOMS 2. Ischemic Model Exercise (moderate) causes swelling in muscle tissue This increases tissue pressure Causing local ischemia Which causes pain and leads to tonic muscle constriction (spasm) Spasm causes additional swelling which perpetuates a cycle of swelling and ischemia Resulting in painful sensation-doms

22 Mechanical Trauma

23 Mechanical Trauma

24 Ischemic and Trauma Models

25 DOMS Misconception DOMS caused by lactic acid McArdle s syndrome Cannot use glycogen and do not produce La Still suffer from DOMS Eccentric contractions Produce lower lactic acid levels Results in more muscle soreness

26 Treatment Static stretching Thought to initiate myotatic reflex (by stimulation of GTO) which results in relaxation of the stretched muscle Research inconsistent that stretching reduces pain Acute exercise diminishes DOMS May be due to increased release of endorphins Anti-inflammatory drugs Best if taken before exercise