overview of energy metabolism large nutrients digested into smaller, usable fuels –carbohydrates ...

Overview of Energy Metabolism large nutrients digested into smaller, usable

fuels– carbohydrates glucose– fats (triglycerides) fatty acids– proteins amino acids

blood delivers fuels to muscle which transforms them into ATP (adenosine triphosphate)

ATP is the universal “currency” used by tissues for energy needs

food + O2 ATP + CO2 + H2O + heat

Energy Systems: Fuels

primary form is glucose transported to muscle (and other

tissues) via blood stored in liver and muscle as glycogen ATP produced more quickly from CHO

than from fats or proteins CHO stores can be depleted

Carbohydrates

Fats (triglycerides)

glycerol

H H H H H H H H H H H H H H H

~C—C—C—C—C —C —C —C —C —C —C —C —C —C —C —COOH

H H H H H H H H H H H H H

~C—C—C==C—C —C —C —C —C —C —C —C —C —C —C —COOH

fatty acids

stored in adipose tissue and in muscle muscle uses fatty acids for fuel produce ATP more slowly than CHO during rest, provides >½ the ATP, but

little during intense exercise fat stores not depletable

Fats (triglycerides)

split into amino acids in gut, absorbed, and transported by blood

1º role is providing building blocks for metabolic functions and tissue building

provides 5-15% of fuel for ATP production

Proteins

Adenosine Triphosphate (ATP)

Overview of Energy Metabolism

muscles have small ATP storage capacity 3 energy systems produce ATP

– aerobic – 1º system for endurance events– anaerobic – 1º system for speed events– “immediate” – 1º system for power events

systems may work simultaneously– depends upon exercise intensity and duration

Maximal Power and Capacityof Energy Systems

System Max Power (kcalmin-1)

Max Capacity (kcal)

Immediate 36 11

Anaerobic 16 15

Aerobic 10 unlimited

Interaction of Energy Systems

Aerobic system takes 2-3 min to fully activate

Anaerobic glycolysis takes ~5 s to fully activate

Immediate system can provide ATP immediately

Anaerobic ATP Contribution During 30-s Sprint

At the beginning of a 100-m sprint (first 3 s), what energy system(s) is(are) being used?

a. Aerobic

b. Anaerobic

c. Immediate

d. Only anaerobic and immediate

e. All three systems

Describe the changing contributions of the aerobic and anaerobic energy systems at the onset of exercise.

Provide a rationale for your response.

Immediate Energy Sources

ATPase

ATP ADP + Pi

creatine kinase

PCr + ADP ATP + Cr

adenylate kinase

ADP + ADP ATP + AMP

Changes in [ATP] and [PCr] during sprint exercise

Glycolysis

glucose

pyruvate

lactate acetyl CoA

mitochondriamitochondria

glycogenolysis

sarcolemmasarcolemma

bloodblood

glycolysis

Overview of Glycolysis

At exercise onset, how are intracellular concentrations of ATP, ADP, Pi, and Ca2+ affected?

a. Increased

b. Decreased

c. No change

At onset of exercise, changes in energy charge stimulation of energy metabolism

These factors stimulate PFK and phosphorylase

[ATP] [ADP][Pi]

Intracellular concentrations of ATP, ADP, and Pi

Muscle Glycogen

Formed by glucose molecules linked together

Glycogenolysis• regulated by phosphorylase

by EPI, Ca2+, Pi, – by ATP, H+, insulin

Glycogenesis• regulated by glycogen synthase• activated when phosphorylase is inactive

Regulation of Glycolysis

energy charge is primary regulator PFK (phosphofructokinase) primary

rate-limiting enzyme

Stimulators Inhibitors

Pi ATP

ADP PCr temperature insulin

EPI H+

glucose

glycogen

bloodblood

glycolysis+ insulin

+ insulin

Regulation during Rest

- insulin

glycogen synthase

glucose

pyruvate

Lactate + acetyl CoA

glycogen

bloodblood

glycolysis

Regulation during Exercise

phosphorylase

+Ca2+, EPI, Pi, ADP

+Ca2+, insulin

+Pi, ADP, EPI

Why is muscle glycogen preferable over blood glucose or fatty acid metabolism

during high-intensity exercise?

Why is there little lactate produced during low-to-moderate intensity exercise?

1. Explain why glycogen is preferred over glucose as a substrate during high-intensity exercise.

2. At the onset of exercise, describe metabolic changes in muscle that serve to stimulate glycolysis and glycogenolysis.

3. Discuss how these mechanisms work to slow metabolism at the cessation of exercise.

4. FT fibers have greater glycolytic capacity than do ST fibers. Describe metabolic differences between the fiber types. Include differences in CHO use, rate of ATP synthesis, and lactate production.

5. Discuss how these metabolic differences are beneficial in light of the motor unit recruitment pattern.

electron transport

Overview of Aerobic Metabolism

Kreb’s cycle

(proteins)NADH

O2 H2O

ADP + Pi ATP

acetyl CoA

1. Preparation for entry into Kreb’s cycle

2. Removal of “energized” electrons

3. 1º ATP synthesis; Oxidation-phosphorylation

mitochondria

Beta Oxidation (fats)

Glycolysis (carbohydrates)

Mitochondria

not a bean shape, rather a long reticulum aerobic metabolism of CHO, fats, and

proteins occur entirely in mitochondria all substrates formed into acetyl

Coenzyme A before entering Kreb’s cycle

Kreb’s Cycle(Citric Acid Cycle)

primary function is to reduce NAD+ and FAD acetyl CoA (C2) combines with a C4

molecule forming a C6 molecule C6 molecule is partially degraded back to a

C4 molecule each loss of C gives off a CO2

Glycolysis takes place in the

a. Sarcoplasm

b. Mitochondria

Oxidative metabolism (i.e. Kreb’s cycle and ETC) takes place in the

a. Sarcoplasm

b. mitochondria

The CO2 that is ventilated off during rest OR exercise is produced in

a. Glycolysis

b. Kreb’s cycle

c. Mitochondria

d. all of the above

e. both b and c

Kreb’s Cycle(source of CO2)

Pyruvate (C3)

electron transport

Aerobic MetabolismOxidation Phosphorylation

Kreb’s cycle

Glycolysis (carbohydrates)

(proteins)

Beta Oxidation (fats)

O2 H2O

ADP + Pi ATP

acetyl CoA

oxidation

phosphorylation

Electron Transport Chain (ETC)Oxidative Phosphorylation

Oxidation NADH and FADH2 transfer electrons to ETC final acceptor of electrons is O2

Phosphorylation energy generated by oxidation used to

resynthesize ATP– 3 ATP from each NADH– 2 ATP from each FADH2

Explain the primary function of the Kreb’s cycle and the ETC.

Lipid Metabolism

1. lipolysis triglycerides broken down to release free fatty acids (FFA)

2. FFA diffuse into blood and are transported to muscle via albumin

3. FFA are transported into muscle and translocated into mitochondria

4. -oxidation cleaves off 2-carbon molecules and forms acetyl CoA

5. acetyl CoA enters Kreb’s cycle

Beta-oxidation is to fat metabolism as _______ is to carbohydrate metabolism.

a. Kreb’s cycle

b. Lipolysis

c. Glycolysis

d. Glucose transport

Energy (ATP) Production

Blood Glucose (C6)

Palmitic acid (C16)

Glycolysis/ oxidation

Kreb's Cycle 2 8

Electron Transport Chain

32-34 121

Total 36-38 129

Regulation of Aerobic Metabolism

mitochondrial energy charge primary regulator

How does the onset of exercise serve to stimulate/inhibit the aerobic system?

Compare/discuss the rates of CHO and fat aerobic metabolism. Which substrate would be favored during high-intensity exercise? Explain.

Discuss why fat metabolism is preferable over CHO metabolism during prolonged exercise.

Exercise Energy Metabolism During Exercise

At onset of exercise, three systems are used continuously, though contribution of the three systems change with time.

What energy system(s) are being used during a 100-m sprint? What is the primary system?

What energy system(s) is(are) being used during a marathon?

How does the contribution of the various energy systems change during a 1-mile race in which the runner sprints to the finish?

What is the function or purpose of the immediate energy system?

Measuring Energy Utilization

Indirect Calorimetry food + O2 CO2 + H2O + energy (ATP)

rate of O2 utilization (in mitochondria) = VO2

VO2 usually expressed as (ml•kg-1•min -1):

mL of O2 consumed

per kg body weight

per min

Indirect Calorimetry

Measurement of O2 Consumption (VO2)Determined by:

– differences in O2% and CO2% between ambient air and expired air, and

– rate that air is breathed

O2% CO2%

Ambient Air 20.9% 0.0%

Expired Air ~16% ~4%

Relationship of VO2 to Exercise Intensity

Exercise Intensitylow high

VO2max

Maximal Aerobic Power (VO2max)

VO2 increases linearly with exercise intensity

A point is reached in which VO2 will not get any higher in spite in increasing work load

– VO2max (VO2peak)

– How could one exercise at higher intensity without further increase in VO2?

Exercise intensity often expressed as % of VO2max

– e.g. exercise intensity was at 60% of VO2max

Which of the following does NOT describe VO2?

a. Energy expenditure

b. Rate of oxygen consumption

c. Rate of metabolism

d. Amount of air inhaled

e. All of the above describe VO2

a. is linearly related to exercise intensity.

b. increases at the same proportion with equal increases in exercise intensity.

c. is the rate of ATP produced by the immediate, glycolytic, and aerobic energy systems.

VO2max

a. is the maximal rate of O2 that can be used by mitochondria.

b. represents the maximal rate at which one can exercise.

c. represents the maximal power that can be achieved by oxidative phosphorylation

d. rate of O2 used for any exercise intensity

O2 Deficit and EPOC

Resting energy requirementsEPOC

exercise recovery

1º Mechanisms of O2 deficit contribution of PCr contribution of anaerobic glycolysis

1º Mechanisms of EPOC replenishment of PCr replenishment of (myoglobin) O2 stores

The O2 deficit

a. occurs at the onset of exercise.

b. occurs with an increase of exercise intensity.

c. represents aerobic energy production.

d. all of the above are correct

e. only a and b are correct

The O2 deficit

a. represents ATP synthesized only by glycolysis.

b. would be smaller if mitochondria would become active more quickly.

Provide an explanation of an O2 deficit at the onset of exercise.

Provide an explanation for the initial 3-4 min of EPOC during exercise recovery.

Energy systems: fuel storage capacity Total

amount (g) Total energy

(kcal) Carbohydrates

blood glucose 15 62 muscle glycogen 250 1,025 liver glycogen 110 451

Fat subcutaneous 7,800 71,000 intramuscular 161 1,465

Substrate Utilization During Exercise

CHO preferred during high-intensity exercise

reliance on fat increases during prolonged exercise

Type of fuel utilization affected by exercise intensity and duration

Effects of Exercise Intensity

Effects of Exercise Duration

Coyle et al., JAP, 1986

Determining substrate contribution:respiratory exchange ratio (RER)

RER = VCO2 / VO2

reflects ratio of CHO and fat metabolism– 100% CHO metabolism, RER = 1.0

» e.g. glucose 6 CO2 / 6 O2 = 1.0

– 100% fat metabolism, RER = 0.7» e.g. palmitic acid 16 CO2 / 23 O2 = 0.7

– 1:1 CHO to fat ratio, RER = 0.83– assumes (incorrectly) no protein is used

VO 2 and RER response to incremental cycling

0 50 100 150 200 250 300 350 400

Power (W)

If RER was high (>0.96), thena. mostly CHO was being used for fuel.

b. exercise intensity was high.

c. the subject thought the exercise intensity was hard.

d. muscle glycogen was the primary fuel being used.

e. all of the above are correct

During prolonged exercise,a. RER increases.

b. muscle glycogen stores decrease.

c. there is an increased reliance on CHO for fuel.

d. none of the above are correct

Discussion Questions

1. Discuss what VO2 represents. Does VO2 always represent the total energy expenditure? Explain.

2. Describe the VO2 response to exercise intensity. Be specific.

3. What energy systems were being used from 0-2 min? Provide evidence from the data to support your answer.

4. Explain how the energy systems were being controlled (i.e., How did the systems “know” to increase ATP production at exercise onset or with a change in intensity?).

5. Describe the change in substrate utilization with exercise intensity. Provide evidence from the data to support your answer

Acute Effects of Exercise

(mlkg-1min-1)

RER Blood [lactate] (mmolL-1)

25.6 0.83 1.4

29.8 0.86 1.4

34.9 0.88 1.7

40.1 0.93 2.9

45.3 0.96 4.2

From the data above, a. each stage was similar in intensity.b. each stage decreased in intensity.c. each stage increased in intensity.

What evidence can you provide to support your response?

(mlkg-1min-1)

RER Blood [lactate] (mmolL-1)

25.6 0.83 1.4

29.8 0.86 1.4

34.9 0.88 1.7

40.1 0.93 2.9

45.3 0.96 4.2

From the data above, a. the relative contribution of CHOs in the early stages was less than

in the later stages.b. more FT fibers were being recruited in the later stages than in the

early stages.c. the later stages were more difficult to perform than the early

stages.d. all of the above are correct

What evidence can you provide to support your response?

Why does blood lactate increase during heavy exercise?

lactate appearance exceeds lactate removal

evidence does not point to muscle hypoxia

FT recruitment epinephrine release

Effects of epinephrine (EPI) on metabolism

glycogenolysis glycolysis inhibits lipolysis

Acute Effects of Exercise

Effects of Intensity curvilinear response of blood [La] curvilinear response of epinephrine (EPI)

Blood [La]

(mmol/L)

20 40 60 80 100

Intensity (% of VO2max)

Blood [EPI]

Lactate Threshold

Blood [La] represents difference in La appearance (production) and removal

La threshold – point at which blood [La] begins rapidly rising above resting levels

occurs at ~60% of VO2max

– trained individuals have a higher LT

Intensity (% of VO2max)

0 50 100

The lactate threshold occurred at a. 50 W

b. 75 W

c. 100 W

d. 125 W

e. 150 W

0 25 50 75 100 125 150Power (W)

Metabolic Fate of Lactate During Exercise

Lactate Shuttle

glucose

pyruvate

lactate acetyl CoA

glycogen

bloodblood

glycolysis

Metabolic fate of lactate during exercise

phosphorylase

+Ca2+, EPI, Pi, ADP

+Ca2+, insulin

+Pi, ADP, EPI

Cori Cycle Liver converts La into glucose

Potential Energy in Lactate

Blood Glucose (C6)

Palmitic acid (C16)

Glycolysis/ oxidation

Kreb's Cycle 2 8

Electron Transport Chain

32-34 121

Total 37-39 129

Accumulation of blood La related to onset of fatigue and performance

One with a high VO2max has greater capacity for muscles to utilize oxygen

Endurance athletes have higher VO2max

How can an athlete with a lower VO2max beat someone in an endurance event

who has a higher VO2max?

Comparison of La Thresholds

Blood La (mmol/L)

5 6 7 8 9 10

Running Velocity (mph)

VO2max = 50 ml/kg/min

VO2max = 55 ml/kg/min

Speed at lactate threshold better predictor of endurance performance than VO2max

Metabolic Responses to Exercise

During exercise, the primary way that lactate is removed from the blood is

a. oxidation by FT fibers.

b. oxidation by heart muscle.

c. oxidation by liver.

d. conversion to blood glucose.

e. oxidation by ST fibers.

The lactate threshold occurs becausea. More lactate is produced than is removed.

b. Recruitment of FT fibers.

c. Release of epinephrine.

d. All of the above are correct

e. Only b and c are correct

Effects of Exercise Intensity

Work (W)

VO2 (ml/kg/min)

HR (bpm)

RER RPE (6-20)

Lactate (mmol/L)

50 20.5 112 0.90 11 1.22

100 25.9 121 0.90 12 1.59

150 33.1 143 0.96 13 1.78

200 38.4 161 0.97 15 2.46

250 48.3 174 1.01 17 3.58

300 54.3 182 1.07 19 6.09

Kolkhorst et al., unpublished data

Effects of Access Fat Conversion Activity Bar

30 min 60 min 90 min 120 min VO2

31.0 31.1 31.7 32.4

(ml/kg/min) 31.7 31.8 31.8 32.3

Lactate

0.55 0.56

(mmol/L) 0.80 0.52

RER 0.85 0.82 0.82 0.81

0.85 0.84 0.82 0.81

Glycerol

0.29 0.36

(mmol/L) 0.21 0.34

Glucose

5.40 5.12

(mmol/L) 5.44 4.91

Control trial in black; Access Bar trial in blue. Kolkhorst et al., 1999

What do you think we concluded about the effectiveness of the Access bar for increasing fat use during exercise?

1. It was effective.2. It was ineffective.3. The evidence was contradicting, thus we could not arrive at a

conclusion.

Fatigue

Inability to maintain desired work output force output slowed force development slowed relaxation

Potential Sites of Fatigue

CNS Motor neuron

sarcolemmaT-tubule

SR–Ca2+ release

Actin-myosin interaction

ATP availability

Central FatigueCentral Fatigue

Peripheral FatiguePeripheral Fatigue

Effect of central fatigue on motor unit recruitment

Peripheral Causes of Fatigue during High-Intensity Exercise

Is it:

Metabolic Changes During Exercise

Rest Fatigue

[ATP] 25 17

[ADP] 3 4

[PCr] 85 5

[Pi] 5 90

[H+] 0.1 M 1.0 M

Values expressed as mmol•kg-1 DW

Peripheral FatigueSubstrate Depletion

less ATP synthesized with onset of fatigue rate of ATP hydrolysis is in fatigue exhaustive exercise depletes total muscle [ATP]

to only ~70% of resting values not thought to be a cause of fatigue

Does ATP depletion cause fatigue?

Decline of force output and [PCr]

with exercise

Stimulation at 20 and 50 Hz

= force

= [PCr]i

= [ATP]i

Δ = [La]i

= [IMP]i

closed = 20 Hz open = 50 Hz

Peripheral FatigueSubstrate Depletion

PCr is nearly depleted within 10-15 s Decline in [PCr] and force not parallel

Creatine supplementation studies suggest: 10-30% in resting [PCr] no benefit to single bout exercises delay of fatigue during repeated bouts more rapid resynthesis of PCr between bouts

Does PCr depletion cause fatigue?

Peripheral FatigueProduct Accumulation

affinity of troponin for Ca2+

tension development by cross bridges rates of glycolysis and glycogenolysis rate of ATP hydrolysis bicarbonate loading improves performance of brief

duration (1-10 min) recovery of muscle pH faster than force

– pH recovers in ~30 min– force recovery takes > 1 hour– thus, other mechanisms must be involved

Accumulation of H+ in muscle:

Effect of active recovery on blood lactate removal

Peripheral FatigueProduct Accumulation

[Pi]i during exercise

[Pi]i decreases force developed by cross bridge

Pi taken up by SR and slows Ca2+ release

Accumulation of Pi in muscle:

Westerblad & Allen, J Physiol 1993

Phase I Phase II Phase III

Tension and Ca2+ Transients During Fatigue and Recovery

Lee et al., 1991

Peripheral Fatigue Conclusions

numerous factors cause fatigue factors causing fatigue vary by intensity and

duration early in high-intensity exercise, 1° factor is [H+]

and [Pi]i

during late high-intensity exercise, 1° factor is Ca2+ release

Inadequate ATP availability is a likely cause of muscular fatigue

a. True

b. False

The primary cause of fatigue is thought to be

a. inadequate ATP.

b. buildup of H+.

c. inadequate PCr.

d. inadequate Ca2+ release from SR.

Peripheral Causes of Fatigue during Prolonged Exercise

Substrate depletion?

0 30 60 90 120 150 180

Time (min)

athlete

untrained

Blood glucose response to prolonged exercise to exhaustion

Muscle glycogen depletion during prolonged exercise

020406080

100120

0 30 60 90 120 150 180

Time (min)

athlete

untrained

Effects of CHO feeding during exercise on maintenance of blood glucose and and exercise duration

Top figure: Trained cyclists exercised at 70% of VO2max until exhaustion. Notice that there was still muscle glycogen available at exhaustion.

Bottom figure: On a later trial, subjects were given CHO every 20 min. At exhaustion, blood [glucose] had not dropped.

Coyle et al., JAP, 1986

Training Adaptations

Metabolic Adaptations to Endurance Training

mitochondrial enzymes nc - anaerobic enzymes

mitochondria nc - ATP-PCr enzymes capillary density nc - buffering capacity myoglobin nc - fiber type muscle glycogen

La threshold curve is shifted to the right—WHY?

Endurance training adaptation of La threshold

Blood [La]

Running Velocity

post-training

lactate production lactate removal

pre-training

1995 Marathon Training Data (females)

VO2 Pre-training Post-training 5 mph 30.7 29.8 7 mph 35.5 34.6

RER 5 mph 0.92 0.88* 7 mph 0.95 0.92*

Blood [lactate] 5 mph 1.83 1.51* 7 mph 2.39 1.77*

VO2max 54.4 58.5* HRmax 206 198*

* less than Pre-training value (p < .05)

Metabolic Adaptations to Speed Training

ATP-PCr enzymes nc/ - aerobic enzymes

glycolytic enzymes nc/ - VO2max

buffering capacity

Untrained Anaerobically Trained

Aerobically Trained

Aerobic enzymes Oxidative system

Mitochondrial volume

2.15 --- 8.00*

SDH 8.1 8.0 20.8* MDH 45.5 46.0 65.5 * Carnitine

transferase 1.5 1.5 2.3 *

Anaerobic enzymes ATP-PCr system

ATP 3.0 --- 6.0 * PCr 11.0 --- 18.0 * Creatine kinase 609 702 * 589 Myokinase 309 350 * 297

Glycolytic system Phosphorylase 5.3 5.8 3.7 * PFK 19.9 29.2 * 18.9 LDH 766 811 621

Muscle buffering capacity

30 60* 30

Muscle glycogen 85 --- 120 *

Metabolic Training Adaptations

Quiz 41. incremental; of VO2, RER & [La]2. b3. CHOs are primary substrate4. b5. muscle glycogen6. b7. d8. c9. d10. e11. fat use; post-training RER was

12. ß oxidation enzymes13. endurance; aerobic enzymes;

n/c in buffering capacity 14. occurred at faster speed15. e16. a17. provides fuel and spares

glycogen for ST fibers yes; maintains blood glucose

18. Yes; helps maintain blood [glucose]

19. your opinion, but based on current evidence

20. close relationship between Ca2+ release and force

Exam 2 – Thu, Oct 19

You’ll need a narrow (red) ParSCORE sheet Exam is 60 questions

– I will be present to begin exam at 7:30 am—You may begin at any time.

Study with classmates!!!– Work to understand the material, not memorize it

Visit with me to clarify questions/problems

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