Exercise Physiology Class Notes PDF

EIMD and Recovery ​ Periodization ○​ Exercise is STRESS ○​ One bout of exercise or stress results in smaller but longer lasting gain in fitness and a larger but shorter lasting increase in muscle fatigue ​ EIMD ○​ Exercise Induced Muscle damage wil...

EIMD and Recovery ​ Periodization ○​ Exercise is STRESS ○​ One bout of exercise or stress results in smaller but longer lasting gain in fitness and a larger but shorter lasting increase in muscle fatigue ​ EIMD ○​ Exercise Induced Muscle damage will occur when activity is high relative to capacity ○​ Exercise has an eccentric bias ​ Why is it important to understand? ○​ 3 major problems can occur when fatigue is not taken into consideration ​ injury ​ Drop out ​ Halt in progression ​ 4 Initial Stages of EIMD ○​ Initial ​ Mechanical: High tension ​ Damage to force bearing and force generating structures ​ Damage to sarcolemma ○​ Mechanical disruption and calcium entry ○​ Phospholipase A2 ○​ Calcium entry through stretch activated channels ​ Damage to SR ​ Damage to myofibrillar structures ​ Inital events in EIMD ​ Metabolic events: ○​ High temp ○​ Insufficient ATP production ○​ Free radical production ○​ Lowered pH ○​ Autogenic ​ Calcium activated proteases cause damage ​ Phospholipase A2 causes damage ​ Arachidonic acid used to synthesize leukotrienes and PGs ​ Lysophospholipids are involved in immune response ​ Mitochondrial Ca accumulation ​ Lysosomal Protease ​ Free radicals ○​ Phagocytic ​ ○​ Regenerative ​ EIMD and Recovery Questions  1.​ What is the relationship between exercise and stress? How does it impact fitness and fatigue? a.​ Exercise causes stress, stress impacts fitness negatively if not properly recovered, stress would increase fatigue 2.​ Why is understanding the Exercise-Induced Muscle Damage (EIMD) cycle important in training programs? a.​ If EIMD is not taken into account, it could increase the risk of injury, player drop out, or halt progression 3.​ What type of exercise causes the most muscle damage, and why? a.​ Anaerobic exercise causes a higher amount of muscle damage because it is creating bigger muscle tears in tissue 4.​ What are the three major problems caused by EIMD in training programs? a.​ 5.​ What are the four stages of the EIMD cycle, and what happens in each stage? 6.​ What mechanical and metabolic events occur during the initial phase Chapter 1: Structure and function of exercising muscle ​ Anatomy of skeletal muscle ○​ Entire muscle ​ Surrounded by epimysium ​ Made of many bundles ○​ Fasciculi ​ Surrounded by perimysium ​ Made of individual muscle cells (fibers) ○​ Muscle fiber ​ Surrounded by endomysium ​ Made of myofibrils divided into sarcomeres ○​ Plasmalemma (cell membrane) ​ Fuses with tendon ​ Conducts action potentials ​ Maintains pH, transports nutrients ○​ Satellite cells ​ Involved in muscle growth and development ​ Aids response to injury, immobilization, training ○​ Sarcoplasm ​ Serves as cytoplasm of muscle cell ​ Has unique features: glycogen storage, myoglobin ○​ Transverse tubules (T-tubules) ​ Serve as extension as plasmalemma ​ Carry action potential deep into muscle fiber ○​ Sarcoplasmic Reticulum (SR): Ca^2+ storage ​ Myofibrils and Sarcomeres ○​ Myofibrils ​ Muscle -> fascilculi->muscle fiber-> myofibril  ​ Hundreds to thousands per muscle fiber ○​ Sarcomeres ​ Basic contractile element of skeletal muscle ​ End to end for full myofibril length ​ Distinctive striped appearance ​ A bands- dark stripes ​ I bands- light stripe ​ H zone- middle of the A band ​ M line- middle of the H zone ​ Common boundary structure Z Disk ○​ Sarcomere protein filaments ​ Muscle contraction ​ Actin (Thin Filaments) ​ Show up lighter under microscope ​ I-band contains only actin filaments ​ Composed of three proteins ○​ Actin: contains myosin-binding site ○​ Tropomyosin: covers active site at rest ○​ Troponin (anchored to actin): moves tropomyosin ​ Anchored to Z disk ​ Equally spaced out by titan ​ Nebulin is an anchoring protein ​ Myosin (Thick Filaments) ​ Show up darker under a microscope ​ A band contains both actin and myosin ​ H zone contains only myosin filaments ​ Two intertwined filaments ​ Globular heads ○​ Protrude 360 degrees from thick filament axis ○​ Will interact with actin filaments for contraction ​ Titan as stabilizer ​ Titan (Third Myofilament) ​ Acts like a spring (stiffness increases with muscle activation and force development ○​ Extends from Z disk to M band ○​ Ca2+ binds to titan, increasing muscle force when stretched ○​ Addressed by “winding filament theory” ​ Stabilizes sarcomeres and centers myosin ​ Prevents overstretching ○​ Motor Units ​ Motor units ​ Consist of a single a-motor neuron + all fibers it intervenes ​ More operating motor units = more contractile force  ​ Neuromuscular junction ​ Consists of a synapsis of a-motor neuron and muscle fibers ​ Serves as a site between neuron and muscle Slide 18-50 ○​ Generation of Force ​ Motor unit recruitment ​ Type 2 motor units = more force ​ Type 1 motor units = less force ​ Fewer small fibers versus more large fibers ​ Frequency of stimulation (rate coding) ​ Twitch ​ Summation ​ Tetanus ​ Length-tension relation ​ Optimal sarcomere length equals optimal overlap ​ If too short or too stretched, little to no force develops ​ Speed-force relation ​ Concentric: maximal force development decreases at higher speeds ​ Eccentric: Maximal force development increases at higher speed Chapt 11 Adaptations to Resistance Training ​ Resistance training: Introduction ○​ Substantial strength gains via neuromuscular changes ○​ Important for overall fitness and health ○​ Critical for athletic training programs ​ Gains in Muscular Fitness ○​ After 3-6 months of resistance training ​ 25- 100% strength gain ​ Better force production ​ Ability to produce true maximal movement ○​ Similar strength gains as percentage of initial strength ​ But greater absolute gains for young men than for young women, older men, or children ​ Due to incredible muscle plasticity ​ Mechanisms of strength gains ○​ Hypertrophy vs atrophy ​ Increase in muscle size -> increase in muscle strength ​ Decrease in muscle size -> decrease in muscle strength ○​ Sources of strength gains ​ Increase in muscle size ​ Altered neural control ○​ Neural control ​ Strength gain cannot occur without neural adaptations via plasticity  ​ Strength gain can occur without hypertrophy ​ Strength is the property of the motor system, not just of muscle ​ Essential elements include motor unit recruitment, stimulation frequency, and other neutral factors ​ Motor units normally recruited asynchronously ​ Synchronous recruitment -> strength gains ​ Facilitates contraction ​ May produce more forceful contraction ​ Improve rate of force development ​ Improves capability to exert steady forces ​ Resistance training -> synchronous recruitment ​ Strength gains may also result from greater motor unit recruitment ​ increased neural drive during maximal contraction ​ Increased frequency of neural discharge (rate coding) ​ Decreased inhibitory impulses ​ Likely that combination of improved motor unit synchronization and motor unit recruitment leads to strength gains ○​ Motor unit rate coding ​ Limited evidence suggests that rate coding increasing with resistance training, especially rapid-movement, ballistic type training ○​ Autogenic Inhibition ​ Normal intrinsic inhibitory mechanisms ​ example : Golgi tendon organs ​ Inhibit muscle contraction if tendon tension too high ​ Prevent damage to bones and tendons ​ Inhibitory impulses decrease by training ​ Muscles can generate more force ​ May also explain superhuman feats of strength ○​ Other Neural Factors ​ Coactivation of agonists, antagonists ​ Normally antagonists oppose agonist force ​ Reduced coactivation may -> strength gain ​ Morphology of neuromuscular junction ○​ Muscle Hypertrophy ​ Hypertrophy: increase in muscle size ​ Transient hypertrophy (after exercise bout) ​ Due to edema formation from plasma fluid ​ Gone within hours ○​ Chronic Muscle Hypertrophy ​ Structural change in muscle ​ Fiber hypertrophy, fiber hyperplasia, or both  ​ Maximized by high velocity eccentric training, which disrupts sarcomere Z-line ​ Concentric training may limit muscle hypertrophy, strength gains ​ Stimulated by intensities as low as 30% 1RM and as high as 90% ​ Caused by both high rep (low load) and low red (high load) training ○​ Fiber Hypertrophy ​ More myofibrils ​ More actin, myosin filaments ​ More sarcoplasm ​ More connective tissue ​ Resistance training -> increased protein synthesis ○​ Muscle content always changing ○​ During exercise: ​ Decrease in synthesis ​ Increase in degradation ○​ After exercise ○​ Increase in synthesis ○​ Decrease in degradation ○​ Hormones and hypertrophy ​ Fiber hypertrophy facilitated by testosterone ○​ Natural anabolic steroid hormone ○​ Synthetic anabolic steroids -> large increases in muscle mass ​ Growth hormone ​ Insulin-like growth factor ​ Elevated post exercise levels not required for anabolism and strength ○​ Fiber Hyperplasia ​ Cats ​ Intense strength training produces fiber splitting ​ Each half grows to size of parent fiber ​ Chickens, mice, rats ​ Intense strength training produces only fiber hypertrophy ​ But difference may be due to training regimen ​ Humans ​ Most hypertrophy is due to fiber hypertrophy ​ Fiber hyperplasia also contributes ​ Fiber hypertrophy versus fiber hyperplasia may depend on resistance training intensity or load ​ Higher intensity causes (type II) fiber hypertrophy  ​ Fiber hyperplasia may occur only in certain individuals under certain conditions ​ Can occur through fiber slitting ​ Also occurs through satellite cells ​ Myogenic stem cells involved in skeletal muscle regeneration ​ Activated by stretch, injury ​ After activation: proliferate, migrate, fuse ○​ Neural Activation and Hypertrophy ​ Short-term increase in muscle strength ​ Substantial increase in 1RM ​ Due to increase in voluntary neural activation ​ Neural factors critical in first 8-10 weeks ​ Long-term increase in muscle strength ​ Associated with significant fiber hypertrophy ​ Net increase protein synthesis requiring time to occur ​ Hypertrophy major factor after first 10 weeks ○​ Atrophy and Inactivity ​ Reduction or cessation of activity -> major change in muscle structure and function ​ Limb immobilization studies ​ Detraining studies ○​ Immobilization ​ Major changes after 6 h ​ Lack of muscle use -> reduced protein synthesis ​ Initiates process of muscle atrophy ​ First week: Strength loss of 3-4% per day ​ Decrease in size (atrophy) ​ Neuromuscular activity ​ (Reversible) effects on type I and II fibers ​ Cross-sectional area decrease, cell contents degenerate ​ Type I is affected more than type II ○​ Detraining ​ Leads to decrease in 1RM ​ Loss strength can be regained (about 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 ○​ Fiber Type Alterations ​ Training regimen may outright change fiber type, but… ​ Type II fibers more oxidative with aerobic training ​ Type I fibers more anaerobic with anaerobic training  ​ Fiber type conversion is possible under certain conditions ​ Cross-innervation ​ Chronic low frequency stimulation ​ High-intensity treadmill or resistance training ​ Type IIx -> type IIa transition common ​ 20- week heavy resistance training program ​ Static strength, cross sectional area increase ​ Percentage type IIx decrease, percentage type IIa increase ​ Other studies: type I -> type IIa with high-intensity resistance work + short-interval speed work ○​ Interaction Between Resistance Training and Diet ​ Resistance training increases protein synthesis ​ Consume 20 to 25g protein after resistance exercise for muscle growth ​ Consume 1.6 to 1.7g protein per kg body weight per day to increase muscle mass ​ Small doses (20g) every 2 to 3 hours are recommended for protein synthesis ​ Larger doses (20-25g) recommended immediately after resistance training ○​ Protein synthesis ​ Repeated muscle stretch -> increase IGF-1 ​ Increase IGF-1 -> increase mTOR ​ Integrates input from insulin , growth factor, amino acids ​ Dictates transcription of mRNA ​ Synthesizes ribosomes ​ Stimulated by insulin ​ Translation ​ Amino acid converted into protein via mRNA ○​ Special populations: Age ​ Children and Adolescents ​ Myth: Resistance training is unsafe due to growth plate, hormonal changes ​ Truth: It is safe with proper safeguards ​ Children can give both strength and muscle mass ​ Elderly persons ​ Helps restore age-related loss of muscle mass ​ Improves quality of life and health ​ Helps prevent falls ○​ Strength Training in Older Adults ​ Increases in strength dependent primarily on neural adaptations ​ No difference across sex or race ​ Same response as in younger but blunted ​ Decreased mTOR signaling response  ​ Small increases in myofibrillar protein and muscle size ​ 25-50g protein necessary to stimulate protein synthesis ○​ Resistance Training for Sport ​ Training is not worth it beyond the basic strength, power, and endurance needs of the chosen sport ​ Training costs valuable time ​ Training results should be tested with sport-specific performance metrics Pre-class questions 2/10 1.​ List the steps involved in E-coupling a.​ Depolarization of plasma membrane in the T tubular system by an action potential b.​ Depolarization signal gets sent through the sarcoplasmic reticulum membrane c.​ The Sarcoplasmic reticulum releases Calcium causing a change in shape d.​ The change in shape of the troponin removes tropomyosin from its blocking position on the actin filament e.​ Myosin heads attach to actin, generating force and tension in the muscle f.​ The muscle contracts 2.​ List the steps involved in the sliding filament theory a.​ Nerve impulses are sent to the neuromuscular junction, causing calcium release in the sarcoplasmic reticulum b.​ The calcium binds to troponin, cause tropomyosin to shift, exposing actin binding sites c.​ Myosin attaches to actin, forming cross bridges d.​ Power stroke happens, pulling actin filament towards the M-line e.​ ATP binds to myosin, causing it to detach from actin f.​ Calcium is reabsorbed and the cycle repeats