Bioenergetics pt 1
Ca2+, EPI
What is the inhibitor of cytochrome c oxidase?
ATP
What are the ketogenic and branched-chain amino acids?
Ketogenic - leucine, lysine, tryptophan, alanine, and tyrosine
BCAA- Leucine, isoleucine, valine
What conditions are needed / do not allow us to obtain steady state?
What does it take to not get us to get into steady state?
Too humid, too hot, exercise maximally
Submaximal
Cool/ dry environment
Explain the differences between homeostasis, dynamic constancy, and steady state
Homeostasis - relatively constant & normal internal environment during resting condtions
Dynamic constancy – a physiological variable that fluctuates between highs and lows but maintains a relatively constant mean (trend) – exercise and rest
ex: Fluctuations of SBP /DBP
Steady-state – physiological variable remaining relatively constant despite exercise
the physiological variable is constant and unchanging.
What are the stimulators of PFK-1?
ADP, AMP, Pi
What are the simulators of ICDH?
Ca2+, ADP, NAD+
Which of the following best describes substrate/fuel utilization in the transition from moderate-intensity to high-intensity exercise?
All the above
What is oxygen deficit? What causes this?
What are examples of a high gain and low gain control system?
High Gain -
High gain – greater control over maintaining homeostasis / HIGH ABILITY TO DETECT DEVIATION
Examples: temperature / pH – it takes a lot to change temperature / pH – deviate a little bit but not much
Low Gain - HR/BP
Explain the two mechanisms that allow glycolysis to continue. Be sure to discuss the limited pool of NAD+ in the cytosol, the enzyme that catalyzes the reaction reducing pyruvate to lactate, and the enzyme that catalyzes the reaction oxidizing glyceraldehyde-3-phosphate (G-3-P) to 1,3 Bisphosphoglycerate (1,3 BPG).
1. malate aspartate shuttle – MDH oxidizes OAA to malate and in the process of oxidizing NADH to NAD+
2. Oxidizing pyruvate to lactate, in the process of oxidizing NADH to NAD+ to be recycled back into the cytosol
What are the stimulators of HSL?
cAMP,
cAMP stimulators: glucagon, growth hormone
Explain the fast and slow components of EPOC
Fast component (2-3 minutes post-exercise)– 1. Replenish ATP stores, 2. Replenish phosphocreatine stores (3ish minutes), 3. Reoxygenate hemoglobin 4. re-oxygenate myoglobin
Slow component (greater than 3 minutes) –1. increased HR (need to come down), 2. increased BP 3. increased body temp 4. circulating EPI/NEPI (catecholamines – technically dopamine too) 5. lactate oxidation (slow twitch muscle and heart love lactate) back to pyruvate 6. glycogen resynthesis 7. Ion imbalance (Na+/K+/ Ca2+) ca/ATPase – get back to resting membrane potential -70mV, decreases vo2 8. muscle tissue repair 9. increased respiratory rate 10. cori cycle
*EPOC tells us when our body is at rest
In your own words explain what the training effect is and its relation to O2 kinetics in trained and untrained mitochondria
What are the differences between adaptation, acclimation, and acclimatization?
Adaptation refers to a change in the structure and function of a cells, tissues, organs or an organ system that results in an improved ability to maintain homeostasis as well as attain steady state
Acclimatization - adaptation to external, natural (temp, altitude) – improve plasma volume inn heat/humid
Cold – don’t typically adapt bc of clothing – BUT we can adapt to sleep in cold via brown fat
Acclimation – adaptation to external laboratory-induced – chamber adjust temp, humidity, altitude
How many NADH and FADH are produced in glycolysis, glycogenolysis, pyruvate to acetyl-CoA, the Krebs cycle, and beta-oxidation?
Glycolysis – 2 NADH – G3-3-PDH; No FADH
Glycogenolysis- 2 NADH – G3-3-PDH; No FADH
Pyruvate to acetyl-CoA – 2 NADH
Krebs – 3 NADH, 1 FADH
NADH:
Isocitrate DH
Alpha-keto DH
Malate DH
FADH: succinate DH
Beta-oxidation – 1 NADH, 1 FADH
How many ATP are consumed and produced in glycolysis, glycogenolysis, and the Krebs cycle via substrate phosphorylation?
1 consumed hexokinase and 1 PFK – glycolysis
Produce 2- phosphoglycerate kinase
2 pyruvate kinase
Glycolygenolis – 1 consumed at PFK
Produce 2- phosphoglycerate kinase
2 pyruvate kinase
Krebs – don’t consume any
1 ATP - succinyl CoA synthetase
Started with glucose or glycogen – 2 ATP
Explain why an endurance exercise-trained individual will have a smaller oxygen deficit at the onset of exercise than an untrained individual
Trained individuals have a greater mitochondrial density and more efficient oxidative enzymes
How does this translate to a smaller O2 deficit?
Explain how an endurance athlete can help prevent himself of herself from ‘hitting the wall’ during a long race such as a marathon. In your answer explain what causes a person to ‘hit the wall’ and also explain why ‘fats burn in the flames of carboydrates’. (10 points
An endurance athlete will ‘hit the wall’ when he or she depletes their glycogen stores. Once an athlete hits the wall, he or she can no longer maintain exercise intensity. This occurs because ‘fats burn in the flames of carbohydrates’. The term ‘fats burn in the flames of carbohydrates’ refers to the requirement of carbohydrate metabolism to provide Krebs cycle intermediates which prime the Krebs cycle, allowing for ATP from fat to be produced more efficiently.
Explain how lactate production occurs and why it is a good thing.
Overproduction of NADH causes an increase in lactate
•need to oxidize NADH (by oxidizing pyruvate to lactate) to NAD+
NAD+ can be recycled back through G-3-PDH to allow glycolysis to continue & to synthesize ATP between 10 sec-2 min of exercise or until AEROBIC metabolism can kick in
How many ATP are produced when glycogen goes through glycogenolysis? Must show the total calculation
33
How many ATP are produced from a 12-C molecule?
Rounds: n/2-1
12/2-1 = 5 rounds
5 * (1 NADH) * (2.5ATP/NADH) = 12.5
5 * (1 FADH) * (1.5 ATP/NADH) = 7.5
Acetyl coA = n/2
12/ 2 = 6 acetyl CoA
6 acetyl coA * (3 NADH/ acetyl coA) * (2.5 ATP/NADH) = 45
6 acetyl coA * (1 FADH/acetyl coA) * (1.5 ATP/ FADH) = 9 ATP
6 acetyl CoA * (1 GTP/acetyl CoA) * (1 ATP/GTP) = 6 ATP
12.5+7.5+45+9+6 -2(activation of acyl CoA) = 78 ATP/ 12-C molecule
Explain the differences in their oxygen kinetics at the start of exercise and post-exercise. Please be sure to include the components of their recovery
Kimberly has an increase in mitochondrial capacity, enzymes, and greater ADP sensitivity to activate cytochrome c oxidase, less O2 deficit
Kimberly has a greater number of glycolytic, and oxidative enzymes, an adaptive ability to recover
The higher the intensity, the greater the O2 deficit – the more we have to rely on immediate energy system/ glycolysis
How ATP supply and demand change at the onset of exercise? How does the deficit occur?
At the onset of exercise, ATP demand and ATP supply increase in a square-wave fashion – steady frequency between time/ ATP use
ATP SUPPLY = DEMAND
O2 deficit = difference between ATP supply in a square wave fashion and ATP from VO2 which occurs in a mono-exponential fashion
*ATP supply from the Oxidative system (VO2) increases in a mono-exponential fashion
Explain the Chemiosmotic hypothesis and how many protons are pumped at each complex and whether NADH or FADH is involved
NADH + H+ transfers its electrons through complex I & III , pumps 4 H+
NADH - 2H+ from complex IV
UBIQUINONE – carries electrons to complex III (4+H+), 0 H+ ARE pumped at complex II
Complex II – succinate to fumarate – succinate dehydrogenase – 2 H+, electrons are MOVED to complex III
FAHD2 – complex III (4H+), and IV (2H+)
Cytochrome c oxidase carries electrons from III to IV
Complex V – ATP synthase – the protons are pumped back into the inner membrane space, the generating power to ATP synthase