metabolic system and exercise (continued) exs 558 lecture #5 september 28, 2005

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Metabolic System and Exercise (continued) EXS 558 Lecture #5 September 28, 2005

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Metabolic System and Exercise(continued)

EXS 558

Lecture #5

September 28, 2005

Review Questions #1

Which of the following is NOT an energy system used by the body to power physical activity?a.) glycolytic energy system

b.) cytoplasmic energy system

c.) oxidative energy system

d.) phosphagen energy system

Review Question #2

One mole of ATP stores ~12,000 calories of energy, BUT what is the true function of ATP?

The true function of ATP is for the TRANSFER of energy

Review Question #3

How quickly is your phosphocreatine (PC) stores depleted within your body during intense activity (sprinting)? Discuss the timing of PC resynthesis.

PC stores are depleted in 30 seconds and ½ of the PC stores can be recovered in 20-30 seconds but the remaining ½ may take up to 20 minutes to fully restore. Most, however, is restored within 3 minutes

Review Question #4

Which if the following is the process by which glycogen is synthesized from glucose to be stored in the liver?a.) glycolysis

b.) glycogenesis

c.) glycogenolysis

d.) glucolysis

Review Questions #5, 6

TRUE/FALSE Glycolysis, the breakdown of sugar, can be either

aerobic or anaerobic

TRUE/FALSE Glycolysis results in the production of 3 ATP

Review Question #7, 8

What is the consequence if glycolysis proceeds without the presence of oxygen?

And if oxygen is present?

The byproduct is lactic acid which can accumulate in the cell, and (1) interfere with the production of ATP and (2) hinder the binding of calcium to troponin

If oxygen is present then pyruvate is converted into acetyl-CoA and then integrated within Krebs Cycle.

Review Question #9

Oxidative capacity is determined by all of the following except?

a.) enduance training

b.) fiber-type composition and # of mitochondria

c.) oxygen availability and uptake in lungs

d.) phosphocreatine concentration

Review Question #10

What is the effect of high intensity training to the ATP-PC energy system?

No effect to the resting PC levels, but the activity of glycolytic enzymes can potentially be increased thus improving the efficiency of the energy system

Metabolic System and Exercise Adaptations – Endurance Effect

Capillary Density Myoglobin Content Mitochondrial Function and Content Oxidative Enzymes Glycolytic Enzymes (?)

Results in 2-fold ↑ in capacities to oxidize sugar and fat

Metabolic Adaptation to Endurance Training

Capillary Density Endurance trained athletes 5-10% higher than

compared to sedentary controls– Genetic predisposition?

Not really, a 15% ↑ in capillary content of skeletal muscle

Changes occur in a few weeks to months after an endurance program has started

Increase exchange of gases, heat, waste, and nutrients between muscle and blood

Myoglobin Content

Myoglobin = oxygen transport and storage protein of blood

Transfers oxygen from capillaries to the mitochondria Animal studies have shown ↑ myoglobin content but

human studies do not corroborate Role of myglobin in improving aerobic capactiy in

humans remains unclear

Mitochondrial Function and Content

Endurance training ↑ the size and # of mitochondria (Holloszy and Coyle,

1984)

Size increased 35% during a 27 week endurance training program in rats

Oxidative Enzymes

↑ concentration of enzymes associated with (1) Kreb’s Cycle, (2) electron transport chain, (3) activation, transport and β-oxidation of FFA

Better efficiency spares muscle glycogen and prevents buildup of lactic acid

Enzyme buildups increase at a greater rate in type II oxidative fibers (FOG)

Oxidative Enzymes (continued)

Succinate dehydrogenase (SDH) enzyme increases may be seen during the early phases of a training program (2x)

Plateau effect with a prolonged training program (after 4 months)

Poor correlation with maximal aerobic capacity (VO2 max)

Suggests that other factors may have a greater influence on improving aerobic capacity

↑ Oxidative enzyme concentrations may allow athletes to exercise at higher intensity than improving aerobic capactiy

SDH Effect

PLATEAU

Glycolytic Enzymes

Endurance training has NO effect on influencing [ ] of glycolytic enzymes

Effects of Detraining on Metabolic Enzymes

Rats: 15 weeks of endurance training results in twofold ↑ in cytochrome c, cistrase synthase and CoA transferase

After training stops, all enzyme activities return to baseline within 4-5 weeks

Humans: ↑ aerobic enzyme activity observed following 8-12 weeks endurance training, are returned to baseline within 6 weeks

Rate of detraining depends on duration of training program Human subjects who had trained for 6-20 years, asked to suspend

training for 12 weeks Show significant in ↓ aerobic enzyme activity, but still 50% greater

than sedentary controls

Circulating Lipid Use During Exercise

At rest plasma [FFA] 0.3 ≈ mmol/L ↓ in plasma [FFA] at onset of exercise,

followed by progressive ↑ as exercise continues (>20 min)– Initial ↓ in plasma [FFA] caused by imbalance

between uptake and release– ↑ Blood flow to muscle– Delay in lipolysis in adipocytes

Lipid Energy Sources During Exercise

Plasma chylomicrons minimal

Plasma VLDLs minimal

Plasma FFAs major source (from adipose), greatest reliance at low to moderate intensity (25-50% VO2 max)

Muscle FFAs major source, used increasingly as intensity exceeds 50% VO2 max

At high intensity (90% VO2 max) CHO used as primary energy source

Reliance Upon Lipids vs. CHO During Exercise

INTENSITY determines reliance upon fats as energy substrate

Low to moderate intensity (25-50% VO2 max): 50-70% energy supplied by fats, 5% by proteins, rest by CHO

60-65% and above VO2 max, reliance upon lipids generally ↓ while CHO reliance gradually ↑

At intensity of 85% VO2 max lipid contribution < 25%

Crossover Concept

Training

NO lactic acid buildup b/c of fat metabolism…good for athletes!

Causes for ↓ Fat Reliance at ↑ Intensities

↓ circulating FFA levels ↓ rate FFA release from adipocytes (inhibited by acidosis)

Inadequate transport of albumin ↓ rate of lipolysis of intramuscular TG stores ↓ uptake of circulating FFAs by muscle TRAINING can alter these!

Glycogen Sparing Effect

Training has no effect on total amount of energy required to perform a specific task

Training does allow greater reliance on fats to provide that energy

True of absolute work load OR relative work intensity

Endurance athletes use fats more effeciently at intensities > 50% VO2 max

Runners derive up to 75% of energy from fat when working at 70% VO2 max

Glycogen Sparing Effect (continued)

How does training allow greater reliance of fats and less on CHO? Mechanisms include:

↑ Mito density, ↑ oxidative enzyme capacity ↑ Capillary density (↑ oxygen delivery) Smaller changes in ATP and ADP ↓ Stimulation of hexokinase, PFK, and phosphorylase Maintain normal citrate levels more efficiently ↑ sensitivity of adipose to epinephrine (↑ lipolysis)

Glyocogen Sparing Effect (continued)

Appears that ↑ reliance upon fat directly related to ↑ use of intramuscular stores of triglycerides (TG)

Compare human subjects before and after 12 weeks endurance training program

After training– TG deposits in muscle twice as great– Intramuscular TG depletion twice as great

↑ use of intramuscular TG accounts for nearly all of “Glycogen Sparing Effect”

Respiratory Exchange Ratio (RER)

Used to measure the type of food source being metabolized to produce energy

RER = (V CO2)/ (V O2) The carbon and oxygen contents of glucose,

FFAs and amino acids differ

RER (continued)

Indirect Calorimetry– Assumes

the body’s O2 content remains constant

CO2 exchange in the lung proportional to its release from cells

– Fats = 0.71– CHO = 1.00

RESEARCH REVIEW

Substrate Oxidation, Obesity and Exercise TrainingBlank & Saris (2002)

Fatigue and its Causes

Phosphocreatine (PCr) depletion

Glycogen depletion (especially in activities lasting longer than 30 minutes)

Accumulation of lactate and H+ (especially in events shorter than 30 minutes)

Neuromuscular fatigue

Factors Influencing Energy Costs

Type of activity

Activity level

Sex

Age

Size, weight, and body composition

Intensity of the activity

Efficiency of movement

Duration of the activity

Muscle Glycogen & Exercise

Glyocogen During Running

Metabolic By-Products and Fatigue

Short duration activities depend on anaerobic glycolysis and produce lactate and H+.

Cells buffer H+ with bicarbonate (HCO3) to keep cell pH between 6.4 and 7.1.

When pH reaches 6.4, H+ levels stop any further glycolysis and result in exhaustion.

Intercellular pH lower than 6.9, however, slows glycolysis and ATP production.

Fatigue may result from a depletion of PC or glycogen, which then impairs ATP production.

The H+ generated by lactic acid causes fatigue in that it decreases muscle pH and impairs the cellular processes of energy production and muscle contraction.

Fatigue and Its Causes

Failure of neural transmission may cause some fatigue.

The central nervous system may also perceive fatigue as a protective mechanism.