Adaptations to Anaerobic Training Programs PDF
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Samford University
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This document provides an overview of the adaptations to anaerobic training programs. It covers a range of topics, such as acute and chronic responses, muscle adaptations, and neural adaptations, all the way through to detraining and overtraining. The document includes detailed information on concepts within exercise physiology.
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Adaptations to Anaerobic Training Programs Terminology Acute responses – How the body systems respond to meet the demands of the exercise stress Chronic adaptations – Repeated exposures of the exercise stressors lead to positive changes in structure and functi...
Adaptations to Anaerobic Training Programs Terminology Acute responses – How the body systems respond to meet the demands of the exercise stress Chronic adaptations – Repeated exposures of the exercise stressors lead to positive changes in structure and function of the systems the boy to Changes to naclapt to the stress on the body and changes in cncitomy physiology Anaerobic Training L Doesn't need oxygen Type of training stresses the anaerobic energy systems – ATP-PC – Glycolytic High-intensity, intermittent exercise bouts: – Resistance training – Plyometrics – Sprint training – Agility training – High-intensity intervals of improvements Everyone can make some type the most improvements the Fastest untrained AthletesCan make - ROM around muscle Bodybuilders could have affected ROM be such large amounts of muscle mass - How does training improve performance? the body would change Put Stress on the body so Adaptation – Change in structure or function that results in an improved ability to respond to a stressor and maintain homeostasis The actual amount going down is not Adaptations to training can occur through the neuromuscular, musculoskeletal, metabolic, endocrine, cardiorespiratory systems. Measuring Neuromuscular Activity Electromyography (EMG) – Measurement of the electrical activity of skeletal muscle – Surface EMG and intramuscular EMG of Higher degree EMG with heavier load units Cycle through motor EMG does tell us: – Amplitude of electrical activity – Muscle activation (i.e., % of MVIC) EMG does NOT tell us: – Which motor units are being recruited – Force production Neuromuscular Responses What are typical responses to activity? – Motor unit recruitment → Henneman’s size principle – Rate coding – Excitation-contraction coupling – Proprioception: GTO & muscle spindles – Stretch-shortening cycle Neural/muscular components Neural Adaptations Chronic anaerobic training augments neural drive – Increased agonist recruitment Only 71% of motor units activated during maximal efforts in untrained individuals. (Adams et al., 1993) – Increased firing frequency Action potentials overlap allowing for summation of force production AbilitySo Send Easter Signals – More synchronous recruitment Synchronized recruitment to pull heavy weight Important for timing of force production & RFD – Reduced inhibitory mechanisms Constitutes many of the early adaptations leading to performance enhancement but slows down the more advanced become you Neural Adaptations Motor unit recruitment – Better at recruiting high threshold units – Once recruited, less activation required – Selective recruitment Mechanism of post-activation potentiation (PAP) Important for RFD One the muscle is activated once its easier after Increases in muscle size will decrease activation at the same force requirement force requires (The same for the same movement less activation Neural Adaptations Neuromuscular Junction – Increased end plate surface area – Increased acetylcholine receptors Neuromuscular Reflex Potentiation – 19% - 55% increase stretch-reflex (Aagaard et al., 2000) – Increased RFD Neural Adaptations Cross-education effect – Increased neural adaptations to the non-exercised, contralateral limb – Average increase in contralateral strength by 8% – Implications for injury rehabilitation Bilateral deficit – Force produced bilaterally is lower than the sum of forces produced unilaterally – Occurs in untrained individuals and can be improved with bilateral training – Bilateral facilitation – more force bilaterally than sum of unilateral forces Decreased antagonist co-contraction We would decrease antagonist output – Higher activation of antagonist in untrained individuals, especially with complex movements Joint stability and reduce injury risk – Training decreases antagonist activation Muscular Adaptations Increased CSA Atropy a pry Stuys the same – Muscle hypertrophy – ↑ net accretion of contractile proteins and noncontractile proteins (i.e., titin) – Increase in number of myofibrils – Increased sarcoplasmic content What about hyperplasia? hyperplasia discussion The number of muscle Fiber Hypertrophy : Growth of the musch more nuclei = more muscle growth a Muscular Adaptations Resistance training-most Stimulus for growth What stimulates hypertrophy? – Process of synthesizing new muscle proteins – Mechanical tension stimulates anabolic pathways How does the muscle experience tension? – Synthesis rates elevated up to 48 hrs after resistance training Time decreases with advanced trainees – Exercise-induced muscle damage? Is it necessary or even beneficial? - No Not all inflammation is back Due to the of muscle theory premony it is easier back to where - get off before they left their muscher atrophied Training Status and MPS Untrained Trained Damas et al., 2015 EIMD and Hypertrophy Damas et al., 2017 I muscle increase arm = Moment increased Increases in moment arm of muscle Muscular Adaptations Fiber Type Transitions – Muscle fibers are typed on a continuum from most to least oxidative – I → Ic → IIc → IIac → IIa → IIax → IIx – Type of training can shift fibers along the continuum Primarily due to a shift in their form of ATPase – Training makes fibers more oxidative – Likely to occur in the early stages of training – Unlikely to shift to and from Type I to Type II Muscular Adaptations Structural and Architectural Changes – Increased pennation angle Increases force production capacity Allows for greater CSA – Increased fascicle length Increases contraction velocity Muscular Adaptations Increased sarcoplasmic reticulum and T-tubule density – Enhanced calcium release Reduced mitochondrial and capillary density – Mitochondria and capillaries may stay the same or slightly increase – Disproportionate to increase to fiber size Increased buffering capacity – Ability to tolerate H+ accumulation – Improves muscular endurance and delayed fatigue onset Increased substrate storage – Increased ATP, PC, and glycogen stores Connective Tissue Adaptations Mechanical loading and bone growth – Osteoblasts secrete proteins (i.e. collagen) – Proteins become mineralized to form hard outer surface of bone – Increased bone mineral density (BMD) – Time course for bone adaptations is long (> 6 months) Minimal essential strain (MES) – Threshold stimulus required to stimulate new bone formation – 1/10th force required to fracture a bone – Increases diameter of bone increases surface area of which force is distributed and reduces the mechanical stress Bone can now handle more Stress Connective Tissue Adaptations System to decrease chance of Astropinia Load up Skeletal Training principles for increasing bone strength – An increase in muscle strength will result in greater stress on the bone – Specificity of loading – mechanical stress is placed on the specific structures – Structural exercises – multi-joint exercises that load the spine and hip Allow for greater loading than single-joint movements High impact ballistic exercises can be beneficial – Progressive overload to continue bone adaptations – Young bone may be more responsive than mature bone Peak bone mass in early adulthood associated with bone mass later in life – Beneficial for minimizing stress fractures and bone-related conditions Connective Tissue Adaptations Tendons, ligaments, and fascia – Collagen fibers form the structure of connective tissue – Collagen strength comes from cross-linking adjacent collagen molecules – Collagen bundles form longitudinally to form: Tendons – connect muscle to bone Ligaments – connect bone to bone Fascia – sheets of connective tissue branching in many directions Connective Tissue Adaptations Tendons, ligaments, and fascia – Small number of active cells in tendons and ligaments – Very low blood supply Slow recovery from injury – Tissue contain elastic fibers (elastin) to allow for slight stretch during motion - Poor vascular Connective Tissue Adaptations - Yields structural changes Adaptations to tendons, ligaments, and fascia – Degree of adaptation determined by exercise intensity – Sites of connective tissue adaptation Junctions between tendon/ligament and bone surface Body of the tendon/ligament Fascial network – Increased strength resulting from: Increased collagen fibril diameter Greater number of collagen cross-links Increase number of collagen fibrils Increase in packing density of collagen fibrils – Increased tendon stiffness increases force transmission Heavy loads needed to increase tendon stiffness Connective Tissue Adaptations Bad vascularization around cartilage Adaptations to cartilage – Dense connective tissue with considerable force absorbing capacity Hyaline cartilage – found on articulating surfaces of bones Fibrous cartilage – found in between intervertebral discs and junction of tendons and bones – Main functions: Smooth joint articulating surface Force absorption for joints Attachment of connective tissue to skeleton – Lacks blood supply and must receive nutrients from synovial fluid fluid Walking helps with synovial joint Endocrine Responses and Adaptations Acute Responses – Increased concentrations of testosterone, GH, and cortisol following resistance training Magnitude based on amount of muscle activated, intensity, and rest periods – IGF-1 can be released in skeletal muscle in response to mechanical loading – Catecholamines released to meet demands of exercise bout: ↑ regulate force production ↑ muscle contraction rate ↑ energy availability augment other hormones Endocrine Responses and Adaptations Chronic Adaptations – Chronic changes in resting hormone concentrations following resistance training is unlikely Resting concentrations more reflective of the current training stress imposed – Androgen receptor content upregulated within 48-72 hrs. after training – Chronic elevations in anabolic hormones may be counterproductive long-term Down-regulation of receptors Cardiorespiratory Responses and Adaptations Acute Cardiovascular Responses – Cardiovascular demands increase during exercise: ↑ Heart rate ↑ Stroke volume ↑ Blood pressure ↑ O2 uptake – Blood pressure highest during the concentric phase of the lift Does not result in chronic high blood pressure – Blood flow decreased to active muscle during an exercise set Contraction occludes capillary flow Acute lack of blood flow causes potent anabolic stimulus Reactive hyperemia Cardiorespiratory Responses and Adaptations Chronic Cardiovascular Adaptations – Resting HR – no change or decreased (4 – 13%) – Blood pressure – slight decrease (2 – 4%) – Cholesterol unchanged or slightly improved ↓ Total and LDL; ↑ HDL – Hypertrophy of left ventricular wall No change in LV volume – Cardiovascular response is reduced at a given absolute intensity or workload Cardiorespiratory Responses and Adaptations Ventilatory Responses and Adaptations – Ventilation rate does not limit anaerobic exercise performance – Minimal improvements experienced with anaerobic exercise – Increased tidal volume and breathing frequency with maximal exercise carlig both freshing Y resistana Don ↑ in the same Session Does concurrent training negatively affect anaerobic training adaptations? Combining Aerobic and Anaerobic Training Interference Effect – Aerobic training MAY negatively affect anaerobic performance Power and speed more affected than strength – Anaerobic training does not appear to negatively affect aerobic power – Highly dependent on volume, frequency, and intensity – Sequence of training is also important – Concurrent training → greater risk of overtraining 6hrs apart same Session low volume/high volume Overtraining Accumulation of training stress resulting in long-term decrements in performance and maladaptation Types: – Sympathetic OTS Increased sympathetic activity at rest – Parasympathetic OTS Increased parasympathetic activity at rest and during exercise Suppression of many physiological systems Overtraining Overreaching – Short-term decrement in performance as a result of excessive overload – Non-functional overreaching – Functional overreaching Overload and taper Detraining Principle of reversibility – Rate of decay differs among abilities “Muscle memory”