S2 Bsf Exam 5: Energy Metabolism

Front 1

What are the main energy stores in the body

Back 1

glycogen & lipids
(protein only in malnutrition)

Front 2

(Liver/Muscle) stores 8% of body weight in glycogen. Glycogen is available for use for the body

Back 2

Liver


(muscle stores 2% muscle weight, for muscle use ONLY, bc muscle lacks G-6-Pase)

Front 3

(Liver/Muscle) takes up glucose and stores it as glycogen under the influence of insulin

Back 3

Liver


(insulin does NOT have an affect on muscle)

Front 4

Although protein is NOT a primary fuel store, it can be oxidized to CO2 & converted to _____ or ______ for energy

Back 4

glycogen or triacylglycerol (TAG)



(AAs--> glucose & fat)

Front 5

_________ provides the most energy

How is it stored?

Back 5

Lipids

stored in non-aqueous adipocytes

Front 6

Describe the 2nd law of thermodynamics

Back 6

dE= dG = TdS

energy glucose = energy stored as glycogen + energy lost as heat

* chemical rxn results in loss of energy to drive metabolism

(1st law: energy in = energy out

Front 7

Besides glycogen, glucose can also be converted to what 2 things?

Back 7

pyruvate (--> lactate)
&
fat (via FA synthesis)

Front 8

T/F
Fat can be converted to glucose

Back 8

FALSE

fat is either stored or oxidized (beta-ox) for energy

Front 9

Beta-oxidation breaks down fat. ____ carbons are lost each cycle. Where do these carbons go?

Back 9

2 carbons

go to TCA cycle, leave body as CO2

Front 10

What are the 3 major organs that utilize glucose (from food)?

What is its fate in each?

Back 10

Liver: glucose--> glycogen & FA

Muscle: glucose--> glycogen & AA

Adipocytes: glucose--> G-3-P

Front 11

Effect of increased insulin & decreased glucagon on 3 major organs

Back 11

Liver: glycogen breakdown inhibited, glucose uptake & storage as glycogen increased, glucose converted to FA & exported as TAGs & VLDLs

Muscle: increased glucose--> glycogen (glycogen synthase) & increased oxidation (via pyruvate dehydrogenase)

Adipose: glucose uptake (GLUT-4) & conversion to G-3-P, TAGs hydrolyzed to FA (via lipoprotein lipase (LPL)) & taken in, FA + G3P--> TAG & stored

*enzymes stimulated by insulin
*ANABOLIC effects

Front 12

The ___________ has relatively constant uptake of glucose via insulin-independent GLUT-1

Back 12

brain


* individual neurons uptake via insulin-independent GLUT-3

Front 13

How is fat taken into the body from food?

Back 13

fat binds to chylomicron in intestine-->
chylomicron enter blood stream-->
chylomicron hydrolyzed to FA via LPL-->
FA is re-esterfied (combined w/ G3P) in adipocyte-->
stored as TAG

Front 14

Insulin stimulates _____ & ______ leading to fat storage

Insulin inhibits ________ suppressing stored TAG hydrolysis (fat breakdown)

Back 14

stimulates LPL (TAG hydrolysis, allows fat uptake) & GLUT-4 (allows glucose uptake)

inhibits hormone sensitive lipase (prevents breakdown of TAGs stored in adipocytes)

Front 15

What 2 major organs utilize AAs (from food)?

what is its fate in each?

Back 15

Muscle: branched AAs (Leu, Ile, Val)--> muscle protein

Liver: gluconeogenic AAs (Ala & Glu)--> glycogen

Front 16

Epinephrine & Glucagon have an (anabolic/catabolic) effect on glycogen

Back 16

CATABOLIC

glycogen-- (glycogenolysis)--> glucose

(via glycogen phosphorylase in muscle)
(via G6Pase in liver, only liver glucose goes to rest of body*)

Front 17

What are the affects of Epi & GH on adipocytes?

Back 17

*catabolic

activate hormone sensitive lipase (bc low insulin), allows TAG in adipocyte to be hydrolyzed-->
FA & glycerol released into blood--->
FA--beta-ox-->Acyl-CoA--TCA--> ATP/ energy

Front 18

What are the final ATP yields from oxidative phosphorylation (TCA)

Back 18

NADH--> 2.5 ATP
FADH2--> 1.5 ATP


(if not all pyruvate--> TCA, will become lactate)

Front 19

In muscle, Epi & glucagon also promote ___________, producing ATP & lactate

Back 19

glycolysis

Front 20

In liver, Epi & glucagon also promote ______________ via glycerol (from adipocytes) & AAs

Back 20

gluconeogenesis

Front 21

Type (I/IIb) muscle fiber:
Few fibers w/ moderate diameter
Low force w/ high excitability
Slow conduction w/ moderate contraction
Oxidative metabolism
Low fatigability

Back 21

Type I


(Type IIb is opposite w/ glycolytic metabolism, Type IIa is in between the two)

Front 22

What 2 things determine the force of muscle contraction?

Back 22

1. number of motor units recruited
2. frequency of motor unit firing

*firing pattern of alpha motor neuron determines contractile & metabolic properties of muscles

Front 23

(Endurance/Strength) training leads to greater ox capacity of muscle fibers, increased O2 delivery, capillary supply, & mitochondrial content, reduced fatigue, and small fiber diameter

Back 23

Endurance training

(strength training leads to great force & contractile speed via increased amount of contractile protein)
*training type changes muscle composition*

Front 24

3 muscle energy sources utilized during exercise

How long does each source last?

Back 24

1. ATP & PCr- 20 sec or less

2. Muscle glycogen- 60-90 secs

3. Oxidation of glucose & FA- longer than 2 min

Front 25

Describe how ATP & PCr are used as an energy source

Back 25

PCr + ADP (stored) <----> ATP (usable energy)
via creatine kinase (both ways)

(when ATP is used for energy, ADP is produced. PCr (creatine phosphate) is stored in muscle)

Front 26

As ATP & PCr are used up, what accumulates in the muscle sarcoplasm?

What does this accumulation lead to?

Back 26

P, ADP, lactate, & H+

impairs Ca pump at SR, reducing electrochemical gradient & impairing Ca release from SR (for contraction)

Front 27

Lactate is produces from incomplete breakdown of glucose (too much pyruvate). How does lactate lead to muscle fatigue?

Back 27

protons (low pH) produced w/ lactate restrict muscle performance by inhibiting;
myosin ATPase (reducing contraction velocity)
binding of Ca to troponin c (limiting cross-bridge)
Na-K pump (limiting depolarization)
PFK (limiting glycolysis)

Front 28

During the first 2 seconds of exercise all the _____ already present in the muscle is used. What type of energy use is this?

Back 28

ATP

anaerobic

Front 29

From 2-20 secs remaining _____ & _____ are used.

This is also ______________

Back 29

ATP & PC

anaerobic

Front 30

From 20-120 secs ______________, in addition to ATP & PC are used.

This is both anaerobic & ___________ energy use

Back 30

muscle glycogen


glycolytic

Front 31

From 120-240 secs __________ & muscle glycogen are used to supply energy

This is both anaerobic & ___________

Back 31

lactic acid


aerobic

Front 32

From 240 secs on, ______ & muscle glycogen are used to supply energy

At this point energy use is _________ only

Back 32

FAs


aerobic

Front 33

Give the progressive order for threshold reaching :
lactic acid system
aerobic system
ATP store
ATP-PC system

Back 33

ATP stored--> (2 sec)
ATP-PC system--> (10 sec)
Lactic acid system--> (1 min)
Aerobic system

* all begin to be used at onset of energy, but are exhausted at diff thresholds

Front 34

The anaerobic glycolytic system is dependent on O2 delivery & glycolytic reliance (glucose breakdown)

What is its limitation?

Back 34

lactate threshold

Front 35

The aerobic system is dependent on glycogen/fat/protein & O2 (oxidative metabolism)

What is its limitation?

Back 35

glycogen depletion (hitting the wall)



(*no lactate accumulation in aerobic system)

Front 36

After the first few minutes, VO2 remains at a steady state (50-75% max) in (anaerobic/aerobic) system

Back 36

aerobic

Front 37

After exercise has ended, HR & Ventilation remain elevated, but _____ falls rapidly. What does this lead to?

Back 37

VO2

leads to "oxygen debt" in muscles
= excess post-exercise O2 consumption--> lactate production (anaerobic metabolism)

(will eventually refuel muscle O2, lactic acid will be present in muscle)

Front 38

In addition to lactic acid fatigue, muscle fatigue can also occur from CNS. Describe CNS fatigue.

Back 38

altered input from muscle sensory fibers-->
reduced excitatory input to motor control centers & spinal cord-->
altered excitability of alpha & gamma motor neurons

Front 39

High frequency fatigue occurs in type (I/II) muscle

How does this fatigue occur?

Back 39

type II

AP moves Na in & K out (too fast)-->
Na-K ATPase cannot restore potential-->
Potential becomes more + -->
inactivates voltage gated Na channels-->
impaired excitability w/o Na = fatigue

Front 40

Low frequency fatigue occurs in type (I/II) muscle

How does this fatigue occur?

Back 40

type I

Decreased Ca release from SR-->
Ca cannot saturate Troponin C-->
Troponin C prevents myosin & actin binding-->
prevents cross-bridge AP tetanus = fatigue

Front 41

How does aerobic training lead to prolonged glycogen depletion?

Back 41

increases mitochondria, oxidative enxymes, capillary density
= more O2 & better FA oxidation (in mito) to produce ATP
(utilize stored glycogen after FA, prolong depletion)

Front 42

Endurance training results in decreased sensitivity to ________ during exercise

This decreases __________ (enzymes) & favors _____ use for energy

Back 42

insulin


decreases glycolysis (decrease rate-limiting enzymes) & favors FA use (increases mitochondrial enzymes)

Front 43

The most efficient diet after 2 hr workout is _____________

This diet prior to workout also allows a longer duration before exhaustion

Back 43

high carb

Front 44

Early strength gain in resistance training is due to (muscle/neural) factors

Describe how

Back 44

neural

more fibers are coordinated to motor units & cross bridges are synchronized

Front 45

Later strength gain in resistance training is due to (muscle/neural) factors

Describe how

Back 45

muscle

increased fiber size/muscle mass, increased anaerobic capacity, glycolytic enzymes, & phosphagens (to make PCr)
*remember strength training favors anerobic/glycolysis for energy

Front 46

Fiber (hypertrophy/hyperplasia) is the major mechanism for strength increase

Explain the diff btwn the two

Back 46

hypertrophy!

hyperplasia= new fibers made (DOESNT occur)
hypertrophy= enlargement of fibers

Front 47

What causes Delayed onset muscle soreness (DOMS)?

What does DOMS lead to?

Back 47

causes:
out of shape
sacrolemmal or structural damage
metabolite accumulation

leads to:
resistance to future damage/soreness