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Lecture 10

Lecture 10 (revised).docx

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Kinesiology&Physical Education
EDKP 395
Russell T Hepple

12/8/2012 7:26:00 PM Overload  Training effect occrurs when a system is exercised at a level BEYOND WHICH ITS NORMALLY ACCUSTOMED  Way in which you overload is specific to type of motor unit recruitment o Intensity o Frequency o Duration  Different definition when dealing with elite athletes vs those who are focused on maintaining health Specificity  Training effect is specific to o Muscle fibers involved  If doing slow moving long distance running you will train the type I fibers, BUT won’t get any adaptations in type II within the same muscle o Energy system involved  Aerobic vs anaerobic  Mitochondrial/capillary adaptations to endurance  Contractile protein adaptations to resistive weight training o Velocity of contraction o Type of contraction  Eccentric, concentric, isometric  Important for overload  Also refers to the types of adaptations occurring o Endurance: primary adaptations in caps/mito- to increase aerobic capacity o Resistance: increase quantitiy of contractile proteins caps/mito can be reduced  Comes down to: which motor unit is being recruited and how o Makes it easier to predict outcomes when you know which muscle group you want to train and what fibers to stress Reversibility  Gains lost when overload is removed  Gains that you get will be lost when you stop doing the exercise o Time for regression differs with type of exercise 12/8/2012 7:26:00 PM VO2max: how much O2 can you breathe in and supply (delivery) to muscle and how much can the muscle use (metabolism)  Delivery (SV) and metabolism are responsible for the expression of VO2mac  AKA Maximal aerobic power During exercise PO2 is very high, but not a lot is being taken up  Stimulation of angiogenisis to inc. capillarization to allow for increased amount of O2 available to muscle Training to increase VO2max  Large muscle groups, dynamic activity  20-60- min  3-5 days/week  50-85% VO2max Expected increases in VO2max  Average: 15-20%  2-3%: those with high initial VO2max o requires intensity >70%  up to 50% for those with initially low values of VO2max o intensity 40-50% VO2max Genetic predisposition  Accounts for 50% of VO2max value o Prereq. For very high VO2max  Affects the sensitivity of the individual to the effect of a training program Why does crosscountry have the highest amount?  Most amount of muscle mass involved: large mass = greater O2 consumption due to higher amount of working fibers Cycle ergometer vs treadmill  Higher VO2max on cycle b/c of SPECIFICITY o Mode of exercise: those who are unaccustomed to exercise mode will have a harder time performing, i.e. lower VO2max  Lack of transfer is related to the muscle fibers that are recruited for each mode Heritage family study  Study the role of genotype in cardiovascular, metabolic, hormonal responses to exercise training  Results: o Heritability of VO2max is 50% (previously mentioned) o Large variation in change in Vo2max w/ training  Average improvement: 15-20%  Ranged from no improvement to 50% increase  Heritability of change in VO2max is 47% o 21 genes play a role in change in VO2max with training  shows that types of adaptations are dependant on the type of exercise used 12/8/2012 7:26:00 PM Calculation  VO2max: HRmax x SVmax X (a-vO2)max o Notes CO = HRmax x SVmax Difference in VO2max in different populations  Primlariy due to difference in SVmax Improvements in VO2max  50% inc. SV 50% inc. a-vO2 o b/c with endurance training HR typically decreases  shorter duration training (4mo) o increase in SV> a-vO2  Longer duration (28mo) o Increase in a-vO2 > SV Changes occur rapidly  Within 6 days of training o 11% inc. plasma volume o 7% inc. VO2max o 10% inc. SV due to inc. in EDV Stroke volume (EDV – ESV)  Increase max. SV via o Increase Preload (EDV) (increases size of left ventricle- NOT the thickness)  Inc. plasma volume  Most significant/important factor to increasing VO2max  Allows for an increased amount of blood to work with o Training has the same effects of blood doping: alteration of RBC production allowing for inc. carrying capacity for O2  Venous return  Vasodilation  Afterload  Muscle pump effect  Most substantial contribution o With more training comes more muscle, with more muscle comes more of an ability to help with pumping blood  Ventricular volume  Modest changes (not as important) o Decrease Afterload (TPR) afterload= peripheral resistance the ventricles are contracting against  Dec. arterial constriction  Less vascoconstriction due to override via accumulation of metabolites  Maintenance of energy state is the most important regulator of muscle function  Max BF w/o change in MAP  Decrease in resistances parallels the increase in maximal CO  Inc. maximal muscle BF w/ no change in MAP  Due to a reduction in SNS vasocontriction activity to arterioles of train muscle at same time CO inc. o Inc. contractility (inc. myocardial contractility)  these changes occur in the central aspect (heart) o Some changes seen in periphery (muscle) but not to the same extent A-VO2 Difference  Inc. muscle BF o Dec. SNS vasoconstriction  Improved ability of muscle to extract O2 from blood (inc. A-VO2 diff) o Inc. capillary density  Slows rate of RBC flux through muscle and increases time for O2 off-loading  Increases SA for gas exchange  more important than mitochondrial adaptations o Inc. mitochondrial volume  Creates good diffusion gradient  increases ability to off load and extract O2  Ability to extract O2 from blood exceeds the body’s ability to deliver it not the limiting factors of VO2  There are always 2 sides to adapataions  delivery and supply  usage Effects 12/8/2012 7:26:00 PM Maintenance of Homeostasis  More rapid transition from rest to steady-state o Able to switch from anaerobic to aerobic processes easier/faster  Related to metabolic changes in muscle  Reduced reliance on glycogen stores o Mechanisms for aerobic ATP production are more efficient o Primary energy source you will use is glycose and glycogen  Cardiovascular thermoregulatory adaptations o Supply and useage is improved but vascularization changes and improvements in cardiovascular delivery are improving heat exchange and removal  Heat can be limiting factor too high, you shut down  Ability to remove heat and maintain core temp. is important  Sweat efficiently & more via increase BF to skin  Note: replenish water to maintain plasma volume  Due to neural and hormonal adaptations  Due to structural and biochemical changes in muscle Endurance training increases mitochondrial content in skeletal muscle fibers  2 locations of mitochondria o Subsarcolemmal are located below sarcolemma  Maintains RMP of membrane which is essential to facilitating exercise endurace o Intermyofibrillar located around contractile proteins  Increased delivery of ATP to muscle  Density increases quickly o Can increase 50-100% within first 6 weeks  Depends on initial fitness level o Depends on intensity and duration o Results in increased endurance performance  due to changes in muscle metabolism, more so than increase in VO2  paralleled increase in the caps w/ inc in mitochondrial density/number w/ endurance training  Mitochondrial number (volume/density) and performance o [ADP] stimulates mitochondrial ATP production  Increased mitochondrial volume after training reduces the amount of ADP required to increase ATP production via mitochondrial respiration and therefore VO2  We need both inc. in mitochondrial number and [ADP] to get changes in VO2  ADP is an important factor governing ATP production and stimulus for change  Lower [ADP] = less stimulation for glycolysis  Note: ADP stimulates metabolic function, ATP inhibits it o O2 deficit lower following training  Same VO2 at a lower [ADP] oxidative phosphorylation activated much earlier, less reliance on anaerobic methods  Energy requirements can be met by oxidative ATP production at the onset of exercise  Faster rise in VO2 curve, and steady state is reached earlier
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