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. VO2max improvements in cardiac patients after 1 year of endurance training –advantage - can find mechanisms for differences between groups, but expensive

VO2max 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 VO2max?

Improvements in VO2max training must involve –large muscle groups in dynamic exercise – minutes in duration –3-5 times per week – % VO2max

Law of Initial Values training programs of 3 months duration can increase VO2max ~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 VO2max genetics are thought to account for % of one’s VO2max 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 VO2max VO2max = HRmax x SVmax x (a-vO2 diff)max We know that max HR cannot be changed significantly What will be the most important contributor to improved VO2max?

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 VO2max during extended training programs not due to increases in Hb content not due to increases in PO2 saturation must be due to decrease in mixed venous O2 content –increased O2 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 VO2max

insert fig 13.4

Detraining decreased VO2max 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 VO2max

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 O2 Deficit ATP > ADP + Pi by muscle contraction (cross- bridges) is stimulus for ATP producing systems –1st - ATP-PC –2nd - glycolysis –3rd - 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... O2 consumption shared between mitochondria as opposed to only 1 it takes a smaller change in [ADP] to stimulate mitochondria to take-up O2 oxidative metabolism will be activated earlier, reducing the O2 deficit therefore - less PC depletion, less glycogen depletion, less lactate production

Endurance Training Reduces O2 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 ß- oxidation –results in more acetyl-coA (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 pH [pyruvate] + [NADH] [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 pH

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-vo2difference 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