metabolic system and exercise (continued) exs 558 lecture #5 september 28, 2005
Post on 21-Dec-2015
213 views
TRANSCRIPT
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
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%
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
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
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.