Exercise Physiology-Chapter 13

expected increase in VO2 max after a 20 week program

average increase was 15-20%

some results of the heritage family study

-heritability of VO2 max is 50%
- large variation in change in Vo2 max with training; some people don't response to exercise 7 some people hyper respond to exercise
-21 genes play a role change in VO2 max with training

calculation of Vo2 max

-product of maximal cardiac output and arteriovenous difference
-VO2 max= HR x SV max X (a-VO2) max

factors increasing SV

-stroke volume at rest is a lot higher in training individual. Stroke volume is also higher at sub-maximal and maximal activity in a trained individual
-preload
-afterload (TPR)
-contractility

afterload (TPR) (factor increasing SV)

goes down; decrease in arteriole constriction, so you have less that the ventricles have to fight against to get blood out, and more blood flow to the muscle

contractility (factor increasing SV) 3 other effects of contractility

-after training your heart will contract w/ more force effecting
1) plasma volume: effect of training: total blood volume is 5L, after training it can go up to 5.7 L
Hematocrit is about 45% after training it drops to about 42%
2) filling time and venous r

increase arteriovenous O2 difference cause

-increased muscle blood flow, decreases in SNS nervous constriction
-improved ability of the muscle to extract oxygen from the blood

why can you extract more oxygen from the blood? (2 adaptations)

1) with training you have an increase in capillary density-so you have more capillaries which slows down oxygen exchange. More capillaries is like taking a highway with a bunch of off shoots that are smaller- so it starts to slow down. This gives more tim

factors causing increased Vo2 max

look at slide 12

effects of endurance training on maintenance of homeostasis

1) more rapid transition from rest to steady-state: takes 3 minutes to reach steady state, with training you get there quicker
2) reduced reliance on glycogen stores: you use more fats-preserve glycogen
3) cardiovascular and thermoregulatory adaptations
4

endurance training-induced changes in fiber type and capillarity (2)

1) fast to slow shift in muscle fiber type-muscle is more efficient (IIx goes to IIa). This happens by a reduction of fast myosin and an increased production of slow myosin. This is dictated by genes, nucleus, and proteins that are produced. The extent of

endurance training increases mitochondrial content in skeletal muscle fibers. What is the mitochondria in the muscle

-subsarcolemmal
-intermyofibrillar
-mitochondrial content increases quickly
-results in increased endurance performance because muscle metabolism has been changed as a function of training
-the ability to use oxygen and produce ATP is dependent on the num

time course of training/detraining in mitochondrial changes

-double mitochondria content in 5 weeks going from untrained to trained

what is responsible for oxidative metabolism in mitochondria?

oxidative enzymes- these carry out oxidative metabolism

what are the enzymes involved in oxidative metabolism in the mitochondria?

-citrate synthase: beginning of kreb cycle, if oxidative metabolism is ramped up then the activity of that enzyme is amped up
-SDH: electron transport chain, index of aerobic capacity
* these are both impacted a lot by endurance training

mitochondrial number and ADP concentration needed to increase VO2

-squirt ADP on mitochondria stimulates mitochondria to start consuming oxygen because ADP is the substrate for ATP, the mitochondria makes ATP oxydatively. If you give it the substrate it will consumes oxygen to make ATP.
-100 units of ADP will stimulate

changes in citrate synthase activity with exercise

-enzymes in mitochondria are responsible for aerobic metabolism. Citrate synthase is an enzyme used a lot as an indirect indicator of aerobic metabolism. If you are more active this activity goes up.

type IIa (red gastrocnemius)

-goes up as a function of intensity and duration, but its not intensity dependent. All VO2 max percentages do basically the same thing

type IIx (white gastrocnemius)

-its intensity and duration dependent. The percentage of VO2 max is a factor of citrate synthase activity

why the difference in fiber types?

-slow muscles are already oxidative and they are already on. Your white muscles or fast twitch muscles you have to call on to get activity. As you increase intensity you call on more white fibers

biochemical adaptations and plasma glucose concentration

1) increased utilization of fat and sparing of plasma glucose and muscle glycogen
2) transport of FFA into the muscle
3) transport of FFA from the cytoplasm to the mitochondria
4) mitochondrial oxidation of FFA

increased utilization of fat and sparing of plasma glucose and muscle glycogen

-having more mitochondria makes use able to utilize fats rather than carbs

transport of FFA into the muscle: 2 factors

1) increased capillary density- allows you to transport more FFA into the muscle
2) you produce FABP (fatty acid binding protein) and fatty acid translocase- trans locates fat from outside of the cell to inside the cell (type of protein)

transport of FFa from the cytoplasm to the mitochondria

-we can metabolize anything aerobically. The only thing we can metabolize anaerobically is carbohydrates

increased capillary density=

slower blood flow in muscle and increased FFA transporters, increased upter of FFA, FFA utilization, and spares plasma glucose

increased mitochondrial number=

increased fatty acid cycle enzymes and carnitine transferase, increased FFA utilization, and spares plasma glucose

CAT

involved in trans locating fats from cytosol into cell; mitochondrial protein. This increases activity and amount of enzyme.

citrate does what to carbohydrate metabolism

-it is a negative inhibitor, so you use more fat instead of carbs to save for later when you really need them

endurance training improves muscle antioxidant capacity

-free radicals are produced by contracting muscles
-training increased endogenous antioxidants

exercise training improves acid-base balance during exercise: lactate production during exercise

-->(LDH-A)
pyruvate+NADH-->lactate +NAD
<--(LDH-B)

exercise training improves acid-base balance during exercise: training adaptation (3)

1) increased mitochodnrial #
2) increased NADH shuttles
3) change in LDH type

lactate threshold

-physiological marker that is closely associated w/ endurance performance. The higher the threshold the better you can perform in an endurance event. The threshold is shifted to the right as a function of training

what is responsible for lactate threshold shift?

-NADH shuttles: saturate shuttles
-LDH has two genes: LDH A and LDH B
* as a function of endurance training threshold gets higher, so we use more lactate in the krebs cycle

increased mitochondrial # and blood pH

figure 13.7

lactate removal

we're better at removing lactate; when we workout blood flow increases to working tissue, as a function of training at the same absolute workload you have a decrease blood flow to working muscle and increase blood flow to liver and other unworking areas,

training adaptation-big picture

-endurance and resistance exercise increase specific muscle proteins. Endurance training increases proteins that are more mitochondrial related

process of training-induced muscle adaptation (2)

1) muscle contraction activates primary and secondary messengers
2) results in expression of genes and syntheses of proteins

mRNA and protein changes in response to exercise. What are the two phases of protein synthesis?

1) transcription-DNA mRNA
2) translation-mRNA to protein

mRNA and protein changes in response to exercise

following exercise you have an upregulation of protein synthesis so you have more transcription, once it turns on it builds up then turns off and goes away. Muscle protein levels for these three proteins rise over time. The message can go away because the

primary signals for muscle adaptation

-mechanical stretch
-calcium
-free radicals
-phosphate/muscle energy levels
*primary signals lead to adaptations
*effect depends on exercise stimulus

secondary muscles in skeletal muscle

1) AMPK
2) PGC-1a
3) Calcineruin
4)IGF-1/AKT/mTOR
5)NFkB

AMPK

glucose uptake, fatty acid oxidation, and mitochondrial biogenesis

PGC-1a

-increased in capillaries, mitochondria, and antioxidant enzymes
-activated by p38 and CaMK

Calcineurin

fiber growth, fast-to-slow fiber type change

IGF-1/AKT/mTOR

muscle growth from resistance training

NFkB

antioxidant enzymes

exercise induced signaling

figure 13.9

links between muscle and systemic physiology

biochemical adaptations to training influence the physiological response to exercise

links between muscle and systemic physiology due to :

-reduction in "feedback" from muscle chemoreceptors
-reduced number of motor units recruited
* demonstrated in one-leg training studies
*as a function of training you don't have as hard as SNS response
*post training your heart rate response and ventilato

lack of transfer training effect

*one left training isolates whats in the peripheral muscle
*the one leg acted like nothing happened to it. Demonstrating that an exercise training regimen elicits a pattern of local changes w/in the trained muscle only. Something that happened in the musc

peripheral changes

changes in muscle-are just as important as cardiovascular changes that happen with the muscle

peripheral and central control of cardiorespiratory responses

-peripheral feedback from working muscles: group II and group IV nerve fibers
-central command: motor cortex, cerebellum, basal ganglia
*in order to workout at a given submaximal workload you need a certain number of motor units to meet the tension or for

group III afferents are? Group IV afferents are?

mechanoreceptors--III
chemoreceptors-IV

prior to training you have a lot of what kind of mitochondria motor units

-mitochondria poor motor units, so you have a higher drive from the CNS that is going to go to cardiorespiratory sensors. More mitochondria=more central drive, so you don't have to recruit as many motor units

peripheral control of heart rate, ventilation, and blood flow

figure 13.11 and figure 13.12

detraining and changes in VO2 max and cardiovascular variables

-rapid decrease in VO2 max if you don't do anything. VO2 max is going down because Q and Q is due to decrease in SV. Early changes are due to SV, later changes are due to AVo2 difference. We're not getting blood to the muscles as well at first and we're n

time course of training/detraining mitochondrial changes

*50% of gains in mitochondrial are lost in one week of detraining and about 90% in two weeks
*retraining does come back somewhat quickly

resistance training improves

antioxidant capacity: 100% increase in two antioxidant enzymes