Physiology of Training Homeostatic Variables Purpose of Training
Physiology of Training
Homeostatic Variables
Purpose of Training • Exercise disrupts homeostasis • Training reduces the disruption • Reduced disruption of homeostasis results in improved performance
Principles • Overload • Specificity • Reversibility
Overload and Reversibility • a system or tissue must be stressed with a workload which it is unaccustomed – can be intensity, duration or frequency • this stress results in adaptation • Reversibility is the converse – once the overload stimulus is removed, the adaptation is lost
Specificity • the training effect is specific to the – tissue or system stressed (eg. Arms do not adapt to cycling stimulus) – the mode of stress imposed (eg. Strength training does not result in endurance adaptations) – eg. Run training vs. Cycle training and LT (58% & 20% vs. 39% alone)
Research Designs • Cross-sectional – take samples of populations ie. Cardiac patients, normal sedentary & elite athletes – disadvantage - black box • Longitudinal – changes over time ie. VO 2 max improvements in cardiac patients after 1 year of endurance training – advantage - can find mechanisms for differences between groups, but expensive
VO 2 max • ability of the cardiovascular system to deliver blood (oxygen) to a large muscle mass involved in dynamic work and the ability of the muscle mass to utilize the oxygen • how does training affect VO 2 max?
Improvements in VO 2 max • training must involve – large muscle groups in dynamic exercise – 20 - 60 minutes in duration – 3 -5 times per week – 50 - 85% VO 2 max
Law of Initial Values • training programs of 3 months duration can increase VO 2 max ~15 % on average • values may be as low as 2 -3 % or as high as 50 % • persons with low initial values will realize greatest improvements • persons with high initial values will realize smallest improvements
Genetics and VO 2 max • genetics are thought to account for 40 -66 % of one’s VO 2 max • you can blame your parents for not being able to win the Olympic marathon, but you can’t blame them for not being able to run one
Contributions to Improved VO 2 max • VO 2 max = HRmax x SVmax x (a-v. O 2 diff)max • We know that max HR cannot be changed significantly • What will be the most important contributor to improved VO 2 max?
Insert Table 13. 2 & 13. 3
Factors Increasing Stroke Volume
End Diastolic Volume • endurance training increases left ventricle size with no increase in wall thickness (volume overload vs. pressure overload) • plasma volume increases contribute to increased filling volume • bradychardia increases filling time • Frank-Starling says increased stretch means increased stroke volume
Cardiac Contractility • strength of the cardiac muscle (ventricle) contraction • contractility does increase in response to sympathetic stimulation • not a large contributor to adaptation as sedentary individuals already have high ejection fraction
Afterload • amount of resistance offered as ventricle forces blood into the aorta • if force of contraction does not change, but peripheral resistance (afterload) decreases, stroke volume will increase • trained muscles offer less resistance to blood flow than untrained during maximal work
Afterload cont’d • MAP = Q x TPR • decrease in peripheral resistance balances the increase in cardiac output to maintain homeostatic blood pressure • vasoconstriction is decreased in the trained exercising muscles • this is possible due to the increased cardiac output (two legged exercise) – willy nilly vasodilation is dangerous
Arteriovenous Difference • comprises 50% of improvement in VO 2 max during extended training programs • not due to increases in Hb content • not due to increases in PO 2 saturation • must be due to decrease in mixed venous O 2 content – increased O 2 extraction due to capillary density
Increased Capillary Density • accommodates increased muscle blood flow due to cardiac output • decreases diffusion distance to individual cells and hence mitochondria • slows rate of blood flow to allow more time for diffusion (transit time)
Factors Contributing to Improved VO 2 max
insert fig 13. 4
Detraining • decreased VO 2 max after detraining is result of – first decreased stroke volume – second decreased oxygen extraction
Time-course of changes with detraining
Changes in Citrate Synthase Activity
Endurance Training Effects
Maintenance of Homeostasis • more rapid transition from rest to steady state • reduced reliance on limited liver and glycogen stores • cardiovascular adaptations that are more capable of maintaining homeostatic conditions
Adaptations • neural – Central Command – Respiratory and Circulatory Control centers • neural-hormone - reduced catecholamines (sympathetic) response to submaximal workload • biochemical - mitochondrial enzymes (citrate synthase) • structural - contractile proteins
Note: • performance improvements - the ability to sustain submaximal work is reliant more on adaptations (biochemical and structural) in skeletal muscle; as opposed to small increases in VO 2 max
Skeletal Muscle Adaptations • increased number of mitochondria (up to 4 times in type II) • increased capillary density – increased Krebs cycle enzymes – increased ß-oxidation enzymes – increased electron transport chain (ETC) enzymes
Cont’d • improved shuttle which moves NADH from glycolysis to mitochondria • change in LDH which converts lactate to pyruvate and vice versa
Training/Detraining Adaptations in Mitochondial Content
Biochemical Adaptations and O 2 Deficit • ATP > ADP + Pi by muscle contraction (crossbridges) is stimulus for ATP producing systems – 1 st - ATP-PC – 2 nd - glycolysis – 3 rd - Krebs oxidative • oxidative metabolism primary system during steady state • increased mitochondria due to training adaptation means…. . .
Mitochondrial Number and Changes in [ADP]
During Steady State. . . • O 2 consumption shared between mitochondria as opposed to only 1 • it takes a smaller change in [ADP] to stimulate mitochondria to take-up O 2 • oxidative metabolism will be activated earlier, reducing the O 2 deficit • therefore - less PC depletion, less glycogen depletion, less lactate production
Endurance Training Reduces O 2 Deficit
Biochemical Adaptations and Blood Glucose • increased FFA transport into muscle – at same [FFA] transport into cell is increased post-training
• increased movement of FFA from cytoplasm to mitochondria – carnitine transports FFA and carnitine transferase facilitates the transport – more mitochondria results in more surface area which exposes more carnitine transferase – FFA can be transported at a greater rate across the mitochondrial membrane
• increased FFA oxidation – increased mitochondrial number means increased enzymes involved in ßoxidation – results in more acetyl-co. A (breakdown product of FFA) and formation of citrate (first compound in Krebs cycle) – increased citrate inhibits glycolysis
Increased Mitochondrial Number, Increased FFA Utilization, Spared Gycogen
Biochemical Adaptations and Blood p. H • [pyruvate] + [NADH] <=LDH=> [lactate] + [NAD+] • ^ mitochondrial number lowers pyruvate formation (reduced glycolysis) • ^ likelihood pyruvate will be oxidized (^ mitochondria)
• ^ shuttling of NADH into mitochondria (less for lactate production) • change in LDH (5 isoforms – change to low affinity for pyruvate (like the heart)
Increased Mitochondria and Maintenance of Blood p. H
Biochemical Adaptations and Lactate • lactate accumulation is balance between formation and removal – lactate can rise either by increased production or decreased clearance • due to increaed a-vo 2 difference less blood need to go to working muscles at given workload • more blood can go to liver for Cori cycle (less sympathetic stimulation as well) • also, the LDH change results in less production
- Slides: 45