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Lecture 11

Lecture 11 (revised).docx

25 Pages
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Department
Kinesiology&Physical Education
Course Code
EDKP 395
Professor
Russell T Hepple

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12/12/2012 9:08:00 AM Peripheral and Central control of Cardiorespiratory responses  Peripheral feedback from working muscle o Group III & IV nerve fibers  Responsive to tension, temperature, chemical changes  Mechano/metaboreceptors  Feed into cardiovascular control center  Central command o Motor cortex, cerebellum, basal ganglia  Recruitment of muscle fibers  Stimulates cardiorespiratory control center Peripheral control of HR, ventilation and BF Information from working fibers with either have 1 of 2 effects at the level of the spinal cord  Positive  Inhibitory  regulated in parallel lines (occur at same time  very efficient) During activation of muscle (ex. beginning of contractions)  Activation of motor cortex, cerebellum, basal ganglia o Motor recruitment increases to match the work rate  Inc. VO2 (i.e. delivery & supply of O2 to muscles) to match the work being done o Co-activation of cardiorespiratory control centers  Increases HR/ventilation linearly to work rate  Decreases BF to visercal organs inc. BF to exercising muscles Summary  Biochemical changes in muscle due to endurance training influence the physiological response to exercise  Reduction in “feedback” from chemoreceptors in trained muscle and a decreased need to recruit motor units to accomplish an exercise tasks results in reduced SNS, HR, ventilation responses to submax. Exercise In Endurance Exercise 12/12/2012 9:08:00 AM Detraining and VO2max  Rapid decrease in VO2max o ~8% in 12 days o 20% after 84 days  initial dec. (12 days) due to decrease in SV  due to dec. in plasma volume  later decrease due to dec. A-VO2max Detraining occurs faster than retraining: lose mitochondrial adaptations within first 1- takes about 4-5 weeks to regain those adaptations  Decrease SVmax o Rapid loss of plasma volume- most important factor for the decrease in VO2max w/ detraining  Dec. Max A-VO2 difference o Decrease # mitochdonria  Decreased oxidative capacity of muscle  Dec. type IIa fibers, inc. IIx & IIa/IIx hybrid fibers Note with training you get an increase in I fibers o Note: if we increase the rate at which O2 is delivered, we will get a decrease in A-VO2 diff: less time RBC spend in caps for gas exchange  AVo2 difference : DECLINES  Biggest decrease in o SVmax o CO doesn’t decrease to same extent b/c HR is elevated  Increase in HR o To compensate for the dec. in SV  Max HR lower in long term endurance athletes too high HR will leave inefficient time for filling of ventricles  With a slightly lower HR you can maximize SV response  12/12/2012 9:08:00 AM Retraining and VO2 max  Muscle mitochondrial adapt quickly to training o Double within 5 weeks  Mitochondrial adaptations lost quickly with detraining o Loss of 50% training gain within 1 week detraining o Majority of adapatations lost within 2 weeks  Requires 3-4 weeks of retraining to regain mitochondrial adaptations  retraining response is quicker than the detraining response o Muscle memory: phenomenon where a formerly trained athletes who became sedentary for a couple months can get their stride back quickly  Epigenetics: have the DNA/genome that is fixed throughout life where DNA is packed with histoproteins  Don’t know for sure if this is the reason  mitocondrail context at 5-6 weeks o doubles with training, and will remain high if training is continued  in order to get further adaptations, must change exercise stimulus o Training stops: fast decline in adaptations  Retraining can help regain adaptations at a faster rate then they disappeared Summary  After stoppage of exercise training, VO2max begins to decline quickly  Decrease in VO2max with cessation of training is due to both a decrease in SVmax and decrease in O2 extraction (a-vO2 diff) o Reverse of what happens with training  Exercise performance during submax exercise tasks also declines rapidly following detraining o Due primarily to a decline in the number of mitochondria in muscle fibers Fibers/Neural/Cap&Mito Changes 12/12/2012 9:08:00 AM Physiological responses  Muscular strength o Max. force a muscle or muscle group can generate  1 RM  Muscular endurance o Ability to make repeated contractions against a submax load  Strength training o Percent gain inversely proportional to initial strength  Genetic limitation to gains in strength  The lower initial values will experience a greater increase o High resistance training (2-10 RM)  Gains in strength o Low resistnace training (20+ RM)  Gains in endurance Changes in Nervous system  Neural adaptations responsible for early gains in strength o Initial 8-20 weeks  No visible changes in muscle itself  Adaptations include o Increased ability to recruit motor units o Altered motor neuron firing rates o Enhanced motor unit synchronization o Removal of neural inhibition  Decrease in co-activation of antagonist muscle Gap in hypertrophy even though there is an increase in strength  NERUAL ADAPTATIONS Changes in Skeletal muscle size  Hyperplasia o Increase in muscle fiber number o Mixed evidence in human studies o Not a great contributor  90-95% muscle enlargement due to hypertrophy  Hypertrophy o Enlargement of both type I and II fibers  Greater degree of hypertrophy in II fibers o Hypertrophy causes  Increased myofibrillar proteins  Increased number of cross-bridges  Increased ability to generate force o Type of activity effects type of hypertrophy  Endurance athletes: increased hypertrophy in type I fibers  Resistance: hypertrophy in all fibers Changes in Muscle fiber type  Fast-slow twitch shift o From IIx  IIa  5-11% change follow 20weeks training  occurs b/c IIa express some characteristics of IIx  lesser extent than endurance training o w/ endurance training: more of a shift from IIx-IIa  some shift to Ia but not a lot  NO increase in type I fibers w/ resistance training Resistance and Oxidative capacity (mitochondrial content)/Capillary number  Conflicting results o Some show decrease or no change in mitochondrial content  Some show small increase o Some show small increase in capillary number  Others show small decrease  Reasons for conflicting results o Different frequency/duration of training o Long=term, high volume training can improve oxidative capacity of muscle Resitance training improve muscle antioxidant enzyme activity  Resistance training improve antioxidant capacity o 100% increase in 2 antioxidant enzymes  Limited evidence o Long term benefits are unclear Summary  Increases in strength due to short-term (8-20 weeks) are due to the results of changes in the nervous system, whereas gains in strength during long term training are due to an increase in the size of the muscle  Current evidence remains equivocal whether hyperplasia occur in humans. Even if it does, 90-95% of the increase in muscle size following resistance training occurs due to an increase in muscle hypertrophy not hyperplasia o Typically: the number of muscle fibers you have a birth are the max amount you will have  Prolonged periods of resistance training can promote a shift in muscle fiber types o Most of the training induced shift is the conversion of type IIx to IIa  Not change in number of I fibers  Whether resistance training increases muscle oxidative properties depend on the nature of training stimulus o Long term- high volume resistance training can improve muscle oxidative capacity and increase the number of capillaries around the trained fibers  Resistance training improve anti
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