overview of energy metabolism large nutrients digested into smaller, usable fuels –carbohydrates ...
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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
Energy Systems: Fuels
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 H H
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 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 H H
fatty acids
Energy Systems: Fuels
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)
Energy Systems: Fuels
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
ATP
PFK
4 ATP
pyruvate
lactate acetyl CoA
mitochondriamitochondria
glycogenolysis
sarcolemmasarcolemma
bloodblood
glycolysis
Overview of Glycolysis
ATP
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
high
low
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
ATP
PFK
mitochondriamitochondria
glycogen
sarcolemmasarcolemma
bloodblood
glycolysis+ insulin
+ insulin
Regulation during Rest
- insulin
glycogen synthase
glucose
ATP
ATP
4 ATP
pyruvate
Lactate + acetyl CoA
mitochondriamitochondria
glycogen
sarcolemmasarcolemma
bloodblood
glycolysis
Regulation during Exercise
phosphorylase
+Ca2+, EPI, Pi, ADP
+Ca2+, insulin
+Pi, ADP, EPI
FT ST
PFK
H+
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
chain
Overview of Aerobic Metabolism
Kreb’s cycle
(proteins)NADH
FADH2
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)
NAD
FAD
H+
H+
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
chain
Aerobic MetabolismOxidation Phosphorylation
Kreb’s cycle
Glycolysis (carbohydrates)
(proteins)
Beta Oxidation (fats)
NADH
FADH2
O2 H2O
ADP + Pi ATP
acetyl CoA
mitochondriamitochondria
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
2 --
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
VO2
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
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
VO2
Time
Resting energy requirementsEPOC
O2D
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
0.00
1.00
2.00
3.00
4.00
5.00
6.00
7.00
0 50 100 150 200 250 300 350 400
Power (W)
VO
2 (L
/min
)
0.60
0.70
0.80
0.90
1.00
1.10
1.20
1.30
1.40
RE
R
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
VO2
(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?
VO2
(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]
6
5
4
3
2
1
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
[La
] (m
mol
/L)
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)
Lac
tate
(m
mo
l/L)
Metabolic Fate of Lactate During Exercise
Lactate Shuttle
glucose
ATP
ATP
PFK
4 ATP
pyruvate
lactate acetyl CoA
mitochondriamitochondria
glycogen
sarcolemmasarcolemma
bloodblood
glycolysis
Metabolic fate of lactate during exercise
phosphorylase
+Ca2+, EPI, Pi, ADP
+Ca2+, insulin
+Pi, ADP, EPI
ST
Cori Cycle Liver converts La into glucose
Potential Energy in Lactate
Blood Glucose (C6)
Palmitic acid (C16)
Glycolysis/ oxidation
3 --
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
6
5
4
3
2
1
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:
ATP
PCr
pH
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
1
2
3
4
5
6
0 30 60 90 120 150 180
Time (min)
Glu
co
se
(m
M)
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)
Gly
cog
en
(m
mo
l/kg
)
athlete
untrained
slow
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