Physio Lec 7 Muscle Fiber Ex 1

Front 1

Creatine phosphate

Back 1

Creatine phophokinase is linked to the M-line. This is a one step reaction that can give the muscle ATP very quickly

Front 2

Myokinase

Back 2

another one step fast reaction. This enzyme/reaxtion is only found in muscles. Takes two ADP molecules. Transfers the phosphate from one to the other.

Front 3

AMP has been shown to have a number of important functions in muscle.

Back 3

1. Allosteric activator of glycolysis
2. Interacts with AMP activated protein Kinase activated by AMP. This enzyme initiates a phophorylation cascade that alters gene transcription.

Front 4

Glycolysis

Back 4

the oxidation of glucose. Glucose can come from the blood stream on stored glycogen in skeletal muscle and liver (via glycogenolysis).

Front 5

Glucose from blood stream is imported into skeletal muscle via

Back 5

GLUT 1
transporter.

Front 6

CC GLUT 1 transporter is stimulated by insulin. Diabetic patients have lost of this stimulation. Interestingly, in muscle GLUT 1 is

Back 6

also stimulated by metabolic bi-products of exercise (insulin independent stimulation of GLUT 1). THUS, in diabetics it is important to have an exercise regimen to maintain glucose homeostasis.

Front 7

*Oxidative phosphorylationtai—

Back 7

*Oxidative phosphorylation—slower but high energy. Not to know in detail Produces 36 ATP glucose molecules.

Front 8

Fatty Acids--can also enter the TCA cycle via

Back 8

the TCA cycle via Beta Oxidation. Fats take from blood. Stored as TAGS or used as FA.

Front 9

Creatine Pathway
rate
capacity
atp/glucose

Back 9

-very fast
-very limited
-0

Front 10

Anaerobic Glycolysis
rate
capacity
ATP/ glucose

Back 10

fast
-limited
-2-3

Front 11

Aerobic/glycolysys/OX pHOS
RATE
CAPACITY
ATP/GLUCOSE

Back 11

Slow
unlimited
36

Front 12

The relation between rate and capacity is

Back 12

inverse because the faster the rate the slowe the capacity (as in amount of ATP the system can produce)

Front 13

McArdle’s Disease

Back 13

: Also known as Glycogen Storage Disease
Type V (GSDV). Caused by mutation of the Myophosphorylase gene. Most
common of muscle metabolic studies

Front 14

Symptoms of McArdles

Back 14

Myalgia=muscle pain
Exercise intolerance
rhabdomyiosis:muscle breakdown...elelvated serum CK and myoglobinuria

Front 15

CPT II Deficiency

Back 15

Caused by mutation of Carnitine PalmitoylTransferse II
gene. Range of symptomology depends on degree to which CPT II activity
is affected. The myopathic forms is the least severe and most common
defect of muscle lipid metabolism.

Front 16

CPTII Deficiency symptoms

Back 16

Myalgia = Muscle Pain
Exercise-Associated muscle weakness
Rhabdomyolysis = Muscle Breakdown
: Elevated serum CK and Myoglobinuria

Front 17

VO2 Max is

Back 17

the maximum capacity of an individual's body to transport and use oxygen during increasing workloads. It serves to represent a person’s fitness because as training occurs VO2 Max increases.

Front 18

In other words, as exercise workload is increasing the ability to use oxygen for ATP production (via the ETC—electron transport chain) is about to reach it’s maximum production capacity and plateau meaning:

Back 18

at a certain point you can only produce so much ATP and though your workload is increasing your amount of ATP production is steady

Front 19

when a steady production of ATP is reached (VO2 Max,

Back 19

to meet the demands of the exercising body, ATP starts being produced from other sources. So, while some mitochondria are producing ATP via oxidative phosphorylation other enzymes in the sarcoplasma (cytoplasm of muscle fibers) will begin producing ATP via the lactate system; anaerobic threshold

Front 20

Anaerobic threshold

Back 20

the point where lactate build up in the blood stream becomes exponential

Front 21

It is always important to remember that the lactate pathway (via glycolysis) and oxidative phosphorylation are always occurring simultaneously. However, in a working muscle when VO2 Max has been reached

Back 21

other enzymes in the sarcoplasm realize there is a greater demand for ATP production and start producing ATP and lactate

Front 22

have probably noticed that with training it take longer to reach VO2 Max that is because

Back 22

there are certain adaptation that lead to an increase in VO2 Max.

Front 23

what are the ada[tations that lead to an increase in VO2 max

Back 23

Slow twitch fiber diameter
VO2 Max and Oxidative capacity
Capillary density
Enzymes of fat metabolism
Myoglobin
TCA Cycle enzymes
Mitochondrial density

Front 24

Slow twitch fiber diameter

Back 24

Increase in type I fiber (slow twitch) diameter.

Front 25

Type I fibers (slow twitch) have a high capacity for

Back 25

oxidative phosphorylation, how ATP is used produced via oxygen utilization. Therefore an increase in these fibers means a greater capacity to produce ATP via oxidative phosphorylation, thus the VO2 Max plateau will take longer to be reached.

Front 26

Capillary density

Back 26

the more capillaries the greater the efficiency of oxygen unloading to muscle fibers.

Front 27

Enzymes of Fat Metabolism

Back 27

remember that through these enzymes fatty acids can be converted into Acetly-CoA® that enters the TCA cycle® which then enters the ETC to produce ATP via oxygen utilization.

Front 28

Myoglobin

Back 28

has a higher affinity (ability to bind) to oxygen. Thus, it is present in muscles to transport oxygen. This is what gives muscles its red color.

Front 29

• TCA Cycle enzymes

Back 29

the more enzymes for TCA cycle the more fuel for the ETC

Front 30

Mitochondrial density

Back 30

an increase of mitochondria leads to an increase in TCA cycle and ETC enzymes. Thus, greater capacity to produce ATP longer and increasing the VO2 Max

Front 31

Type I fibers

Back 31

twitch fibers are lighter staining relative to types IIA and IIB. However, when staining for oxidative enzymes both type I and IIA stain intensely

Front 32

Type II

Back 32

fast twitch red fibers. These are red because they have a higher myoglobin content when compared to type IIB. Notice an even more intense red stain when stained for oxidative enzymes like succinate dehydrogenase

Front 33

The higher myoglobin content gives IIA

Back 33

a longer fatigue resistance relative to type IIB because myoglobin has a high oxygen affinity and can deliver more to the tissues

Front 34

Type IIB

Back 34

fast twitch white fibers. In comparison to IIA fibers, type IIB don’t have a myoglobin content. It is myoglobin that gives off the red pigment

Front 35

Type IIB
Glycolytic activity
xidative activity

Back 35

V. High
Low

Front 36

tYPE IIB
MHC-ATPase Twitch Speed
Fatigue Resistance
Activity Profile

Back 36

High
Low
Short term phasic

Front 37

Type IIA
Glycolytic activity
Oxidative activity

Back 37

high
V. high

Front 38

Type IIA
MHC-ATPase Twitch Speed
Fatigue Resistance
Activity Profile

Back 38

High
moderate
sustained phasic

Front 39

Type I

Glycolytic activity
xidative activity

Back 39

Low
High

Front 40

Type I
MHC-ATPase Twitch Speed
Fatigue Resistance
Activity Profile

Back 40

Low
V. High
Sustained Tonic

Front 41

transitioning from fast to slow twitch.

Back 41

Imposibble to do regardless of how much we exercise, nerve innvervation must change. So an increase in any particular type of fiber in a muscle means that the innvervation is changing

Front 42

composition as a
result of training. The response to training is use specific. Activated motor
units respond to endurance training by

Back 42

increasing oxidative capacity

Front 43

motor units activated by strength training respond by

Back 43

hypertrophy and increased glycolytic capacity

Front 44

Strength training does not increase

Back 44

the myofiber number (hyperplasia

Front 45

Learning/coordination (Typing, darts) major adaptive response

Back 45

Central Nervous System
Motor Unit Recruitment Patterns
notice that muscle fiber types are not the main focus here. Instead, it is motor unit recruitment pattern. Remember that motor unit recruitment follow the size principle—meaning smaller motor units are recruited first and larger ones are recruited last. Thus, the adaptive response is to recruit smaller motor units for controlling these fine movements

Front 46

Endurance Exercise (Marathon Running) major adaptive response

Back 46

Increased oxidative capacity
Limited Myofiber Hypertrophy
will see in increase in Type I fibers, due to the enhanced oxidative capacity. Meaning, that fibers will change into slow twitch fibers. Limited fiber hypertrophy will occur, thus these muscles tend to be more slender

Front 47

Strenght exercise (weight lifting) major adaptive response

Back 47

Hypertrophy of Myofibers
Enhanced Glycolytic Capacity
will see in increase in Type IIB and IIA fibers, due to the enhanced glycolytic capacity. Meaning that slow twitch fibers will change into fast twitch.

Front 48

, which is a increase in number of fibers, does not occur in

Back 48

adult life.

Front 49

marathon runners are tall and skinny because they increase

Back 49

type I fibers and have limited myofiber hypertrophy.

Front 50

Soccer players—who run for long periods of time, yet do mostly in sprinting and kicking (i.e. higher resistance than a slow steady run (marathoners) have

Back 50

broad muscular legs because they increase their type IIB (mostly) and Type IIA fibers and have muscle hypertrophy

Front 51

Fatigue is the use dependent decrease in

Back 51

the force production by motor units

Front 52

General fatigue

Back 52

is a state of disturbed homeostasis involving multiple systems

Front 53

cellular fatigue

Back 53

is specific to motor units and myofibers

Front 54

Rapid fatigue

Back 54

is associated with high intensity exercise, fatigue of type IIB units

Front 55

Slow fatigue

Back 55

is associated with endurance exercise, involves glycogen depletion

Front 56

Sites of cellular fatigue

Back 56

Sarcolemmal Excitability
E/C Coupling
Myofilament Ca2+ sensitivity
Energy metabolism

Front 57

Fatigue has nothing to do with ATP depletion rather

Back 57

it has to do with energy metabolism. INCREASE in lactate and phosphate

Front 58

Increase of lactate during fatigue leads to

Back 58

decrease in pH. The muscle becomes acidic and this decrease in pH has profound effects on the Ca++ sensitivity of the myofilaments. So decrease in Ca++ leads to decrease in Ca++ sensitivity

Front 59

excitation contraction (E/C) coupling is affected by cellular fatigue

Back 59

Ca++ release from Sarcoplasmic reticulum fails, due to high amount of phosphate in the muscle. This phosphate forms precipitates in the sarcoplasmic reticulum and the Ca++ can’t be released anymore.
TAKE HOME: fatigue not due to ATP depletion, but potentially regulated by elevations of phosphate and lactate affect those different sites.

Front 60

In a whole muscle response to fatigue, the individual type fibers responses are

Back 60

that IIB type muscles fail quickly. Delayed failure in IIA and no visual failure in Type I.