Week 6 - Recovery and Rest Lecture Notes PDF

RECOVERY WEEK 6   GAS  Metabolic recovery  Neurological recovery AGENDA  Mechanical recovery  Active recovery  Fascia  Other tools  How do we recover?  FIRST – we must understand wh...

RECOVERY WEEK 6   GAS  Metabolic recovery  Neurological recovery AGENDA  Mechanical recovery  Active recovery  Fascia  Other tools  How do we recover?  FIRST – we must understand what we need to recover/replenish RECOVERY What happens when we exercise?  Neurological  Metabolic  Tissue   Vigorous exercise alters a muscle’s chemistry.  For a muscle to return to its pre-exercise state the following must occur;  Oxygen reserves (stored in myoglobin) must THE SCIENCE… be replenished  Accumulated lactic acid must be reconverted to pyruvic acid  Glycogen stores must be replaced  ATP and creatine phosphate reserves must be resynthesized. *The goal is to achieve an optimal balance between training and recovery in order to prevent maladaptation to accumulated psychological and physiological stresses induced by the training load. WHAT HAPPENS DURING EXERCISE?  Muscle damage  Nervous system fatigue  Depletion of neurotransmitters (ACH)  Creatine, glycogen, oxygen  A training session initiates the alarm phase  Metabolic TRAINING Substrates – glycogen, ATP-CP By products – hydrogen ions, lactate SESSION  Neurological Neurotransmitters – serotonin, dopamine, acetylcholine  Mechanical Skeletal tissue damage – sarcolemma, contractile proteins, connective tissue  G.A.S GENERAL ADAPTATION SYNDROME  The harder the workout (more depletion of substrates/neurotransmit ters/hydration) the longer it will take to replenish   Carbohydrates are stored as glycogen in the liver and muscle tissue  Glucose will circulate through the blood (blood glucose)  Blood glucose is necessary to supply METABOLIC  the brain During exercise – muscles deplete the stored glycogen to produce muscle contraction  As levels decrease, glucose gets pulled from the blood.  As blood glucose drops, liver glycogen breaks down GLUCOSE REGULATION During Exercise: Muscle uptake of blood glucose increases. As blood glucose levels drop, we release glucagon to mobilize stored glucose from the liver. When we consume glucose: We increase the blood glucose We store it in the liver and muscles, Any excess glucose is stored as fat. Anaerobic and aerobic metabolism both require glucose in order to create energy (ATP). To ensure adequate glucose is available: both muscle and liver stores must be replenished post- exercise. In addition, pre-exercise carbohydrate consumption is required to top up liver and blood glucose stores.  METABOLIC RECOVERY  Glycogen – replenished through CHO  WHERE:  1. Muscle glycogen 2. blood glucose 3. liver glycogen  Eat CHOs – goes into the blood – to muscles and/or liver.  If you don’t replenish all these sites you can not recovery optimally. Muscle’s and brain will not perform well.  WHEN:  1. during 2. immediately post-exercise 3. post-exercise  HOW MUCH:  1.2 grams of CHO/kg of body mass/ hour  to be consumed at 15-30 minute intervals immediately post exercise.  Hydration – necessary for dissipating body heat, transporting nutrients through the blood and removing metabolic waste.   “CNS fatigue from prolonged endurance exercise (ex: high intensity exercise, max speed workouts, explosive jumping) occurs when the by-products of high intensity exercise buildup to a point where the CNS impulses NEUROLOGICAL are handicapped” – Charlie Francis Training System  Recovery from CNS work requires 48 hours before participating in similar work load. In this time, proper recovery strategies can help restore homeostasis. NEUROLOGICAL  Fatigue results from depleted energy stores in the muscles or accumulating metabolites in the muscle cells.  Leads to failure of neural transmission outside the muscle cell within the nervous system.  Neural transmission:  the process where signaling molecules (neurotransmitters) are released by a neuron (pre-synaptic neuron) and bind to and activate the receptors of another neuron.  CNS fatigue can also lead to an increase in perceived effort and eventually and inability to produce high quality muscular power.  NEUROLOGICAL RECOVERY  Key Transmitters:  Serotonin – Increases during exercise. Low levels are associated with lethargy and loss of motor drive, depression.  Dopamine – dopamine is released with exercise. When its present it can increase neural drive and motivation.  Acetylcholine – decreases during exercise. Necessary for temperature regulation and facilitates muscle contraction.  Sleep!  HGH (human growth hormone) - released during deep sleep. HGH stimulates muscle repair and growth, bone building and fat burning.  Sleep deprivation can:  slow muscle recovery, alter mood, increase cortisol (stress hormone), decrease glycogen synthesis and increase RPE.  During REM phase of sleep acetylcholine is replenished.  Non-REM sleep important for re-sensitizing serotonin receptors.   Skeletal tissue damage – damage to the sarcolemma, contractile proteins and connective tissues.  Until repair is completed the MECHANICAL muscles will be unable to generate peak force.  The muscle damage impairs transport of the blood glucose into the muscle cells and therefore leads to a decreased capacity to replenish the glycogen stores.  Muscle damage = soreness and pain MECHANICAL RECOVERY  CHO + protein is necessary for synthesis of muscle glycogen  Muscle adaptations to exercise induced muscle damage are dependent on a positive protein balance  Massage/Stretching  Cold water immersion  Metabolic Glycogen EAT ATP-CP By-products Neurological Serotonin SLEEP Dopamine EAT Acetylcholine Mechanical Skeletal muscle tissue EAT TREAT SLEEP RECOVERY RECAP  Passive Active recovery Requires recovery little active involvement from Requires action from the participant ie: the participant ie: massage Foam rolling, stretching, exercise, eating/ drinking, sleeping RECOVERY   Massage  Stretching MODALITIES   Active recovery Cold water immersion  Fascial mobilization/release  MASSAGE  DOMS is induced by muscle damage  Massage can improve muscle blood flow and reduce muscle edema  Improvement in perceived fatigue  Decrease in creatine kinase concentration (reduction in muscle damage = faster recovery after exercise) STRETCHING **not many studies to provide a positive change in recovery with stretching!!   AR has a positive effect on DOMS but may only be significant during a short period after exercise.  The impact of AR on CK concentration in the ACTIVE blood may depend on the duration of the treatment. RECOVERY  The significant effect of AR may be explained through enhanced blood flow in muscle tissue, which facilitates the removal of metabolic waste and may contribute to a reduction in muscle lesions and pain.   Immersion in cold water is shown to aid in lessening muscle fatigue and soreness.  The exact mechanisms are not well understood.  It causes peripheral vasoconstriction which COLD WATER aids in mitigating the inflammatory response. IMMERSION  The added hydrostatic pressure is thought to aid in increasing the osmotic gradient and allow for better ‘flushing’ of the metabolic by products. * Some studies say CWI can impair maximal hypertrophy, so depending on your goal in training CWI may not be an ideal way to recover. FASCIAL NETWORKS GIMMICKY MODALITIES  Foam roller  Taping  Cupping  Compression garments  Massage gun