Endurance athlete Flashcards
What boundary of energy production is used in endurance events?
CHO and glycolysis and so exercise is limited by the levels of glycogen as high rates of glycolysis deplete this
What enhances oxidative metabolism in endurance events?
Facilitation of oxygen delivery. The diffusion distances of the myofibrils are reduced.
What is the mitochondria involved in?
Involved in Ca2+ control, cell signaling, apoptosis and ATP production
What are the features of the outer mitochondrial membrane?
- Contains roughly equal proportions of proteins and lipids
- Contains porins: channel-forming proteins allowing free diffusion of small ions and molecules (up to 10 kD)
- Relatively permeable
What are the features of the inner mitochondrial membrane?
- High protein content (~ 80%)
- The density of the extensive cristae reflects respiratory activity of the cell
- Freely permeable to O2, CO2 and H2O
- Impermeable to most other ions and metabolites, thus requiring specific transporters or carriers, thus ion gradients are maintained across the inner membrane
What is VO2max?
Maximum oxygen uptake (VO2max) is the upper limit of oxygen transport and utilisation attainable in any individual
What size capacity for oxidative metabolism is required to minimise endurance performance?
High
How many H+ are required to generate 1ATP?
4
What is the ATP yield of NADH and FADH?
1 NADH yields 2.5 ATP (10 / 4)
1 FADH2 yields 1.5 ATP (6 / 4)
What is running speed correlated too?
VO2 max and lactate threshold
What determines the limit between moderate intensity and heavy intensity exercise?
Lactate threshold
What is the total yield from complete oxidation of glucose?
32 (30 depends on whether the electrons associated with the cytoplasmic NADH are shuttled into the mitochondrion on the malate-aspartate shuttle (5 ATP) or the a-glycerophosphate shuttle (3 ATP))
What is the overall reaction for oxidative phosphorylation with NADH as the electron source?
O2 + 2 NADH + 2 H+ + 5 ADP + 5 Pi –> 2 NAD+ + 5 ATP + 2 H2O *
What are the controlling/ limiting factors of oxidative phosphorylation?
- Oxygen availability
- Phosphorylation potential [ATP] / [ADP] · [Pi]
- Oxidation reduction (redox) potential [NADH] / [NAD+]
What is the maximal forward flux of oxidative phosphorylation dependent on?
1.Biochemical factors that limit the rate of substrate availability ([NADH], [ADP], [Pi]) e.g. Glycolyitic activity, TCA cycle activity, or NADH shuttles:
non-O2-dependent factors
2.O2 transport factors that limit the rate of oxygen delivery to the mitochondria. These include convective O2 transport in the blood and diffusive O2 transport between the capillary and the mitochondria:
O2-dependent factors
Both O2-dependent and -independent factors are influenced by muscle fibre type because, compared to type II, type I fibres have:
Greater oxidative enzyme activity Greater M-A shuttle activity SS and IMF mitochondrial expression Myoglobin content More capillaries Smaller area Shorter O2-diffusion distances
What percentage changes do we see from pre training?
VO2max = 16% LT = 30% Capillary density = 20% Fibre area = 20% Succinate dehydrogenase (SDH) activity= 40% Cytochrome c activity = 40%
Is it the delivery or the utilization that limits VO2max?
Over the first few weeks the intramuscular processes are increasing at a rate similar to the rate of VO2max increase with O2 delivery changing a much smaller degree over the same time. It takes longer for oxygen delivery to increase compared to utilisation
What happens to LT in hypoxic and hyperoxic conditions in trained and untrained individuals?
It decreases in hypoxic and increased in hyperoxic in endurance athletes
It decreases in hypoxic and stays the same in hyperoxic in untrained individuals
This may reflect that VO2max and LT in untrained subjects is limited muscle O2 utilisation, but that O2 delivery is the limiting factor in trained athletes
In all subjects hypoxia reduces LT, but hyperoxia only increases LT in some
This may reflect a limitation of mitochondrial NADH oxidation, causing an increase in cytosolic redox potential and increasing [lactate]/[pyruvate] (L/P)
What does it mean that ATP remains constant during endurance exercise?
Most of the control of VO2 by the phosphorylation potential ([ATP] / [ADP] · [Pi]) is exerted through changes in [ADP]
[ADP] is buffered through the creatine kinase reaction
therefore, (when intracellular pH is constant)
What control does Phosphorylation potential: [ATP] / [ADP] · [Pi]
Appears to exert a tight control over oxidative phosphorylation in vivo during endurance exercise, at least in healthy subjects when NADH and O2 are in abundance
However, under some conditions either O2 or NADH (or both) can become limited
What is the TCA cycle regulated by?
Substrate availability
Allosteric factors
Product inhibition
Competitive feedback inhibition by intermediates further along the cycle
Availability of Acetyl CoA
regulated by pyruvate dehydrogenase (PDH)
Availability of oxidised reducing equivalents
NAD+ for the three dehydrogenase reactions
Isocitrate dehydrogenase (ICD)
a-ketogluterate dehydrogenase (a-KD)
Malate dehydrogenase (MDH)
FAD for one dehydrogenase reaction
Succinate dehydorgenase (SDH)
Allosteric control of 3 non-equilibrium reactions
ICD, a-KD, and Citrate synthase (CS)
What does NADH drive from?
- Cytosolic NADH shuttled into the mitochondrion (supplies electrons to FAD if a-glycerophosphate shuttle is used)
- Tricarboxylic acid (TCA) cycle (supplies electrons to FAD in succinate dehydrogenase)
What changes are seen in a Cycle ergometry to exhaustion at 70% VO2max?
Fumarate, Malate, succinate, isocitrate, citrate and Oxaloactetate all increase from rest to 5 mins but then progressively fall
2-oxogluterate (a-ketogluterate) falls immediately
Oxaloactetate falls below resting levels by exhaustion
What happens during endurance exercise to reactants on span I (right hand side) compared too span II?
Throughout endurance exercise reactants on the ‘right hand side’ (span I) of the TCA cycle are maintained at much lower levels than span II reactants
Span I= Cit, Iso, 2OG
Span II= Suc, Fum, Mal. Oxa
In addition, it has been suggested that TCA cycle flux may exceed PDH activity at the limit of tolerance during high intensity exercise
This might contribute to the reduction in span I intermediates at the tolerable limit of endurance exercise
What does endurance exercise require?
Endurance exercise requires the limited muscle glycogen stores to be maximised by a high reliance on oxidative energy provision, however, the response time for oxidative phoshporylation is relatively slow compared to the other energy systems
What is seen following exercise training?
Following exercise training oxidative energy provision is maximised by increases in mitochondrial density, oxidative enzymes, capillarity, and myoglobin
What are sensitive to limitations in O2 delivery?
VO2max and LT are sensitive to limitations in O2 delivery
Where is control of oxidative phosphorylation predominantly exerted?
through the phoshphoryaltion potential, but may be limited by mitochondrial O2 and NADH availability
