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How do skeletal myofibers have adaptive potential? (2 categories)
What affects their phenotypic profile? (5)
Muscle is highly adaptive in both metabolic and contractile senses.
Phenotypic profile is affected by: (1) innervation/neuromuscular activity (2) exercise training (3) mechanical loading/unloading (4) aging (5) hormones
What are key metabolic features of muscle? (4)
- 1. Metabolic plasticity
- 2. Mitochondrial enrichment
- 3. Major site of GLUT 4
- 4. Special muscle version of metabolic enzymes
Disadvantage of aerobic pathway? (1)
Disadvantage of anaerobic pathway? (2)
Aerobic pathway requires O2.
Anaerobic pathway can lead to buildup of lactate and produces net 2 ATP vs. net 38 ATP
What are the 3 energy systems that support exercise? When does each start and how long does it last?
- 1. Immediate (ATP-CP) system - starts at t =0, depletes by 45s
- 2. Short-term glycolytic system - begins at 10 s, peaks from 30s to 3 min until aerobic system can catch up
- 3. Long-term aerobic system - begins growing at 10 s and hits its peak at 10 min.
What is creatine phosphate for?
Buffering limited ATP supply within muscle during exercise. When low ATP, CP can donate P to 2 ADP to create 1 ATP and 1 AMP.
What is energy intensity proportional to? Where the anaerobic threshold and what happens there? What is VO2 max?
Anaerobic threshold is where VO2 max levels out. After anaerobic threshold, lactate production increases exponentially.
VO2 Max is the maximum capacity of an individual to transport and use glucose at 100% intensity.
What is one benefit of using lots of glucose during heavy exercise?
Most reducing equivalents are NADH that enter through complex 1, providing the full ATP capacity.
What happens to glucose during exercise? (3)
What's another helpful tissue? Why?
- 1. Muscle begins glycogneolysis, but at this moment, glucose --> glycolysis, TCA, ETC plays a big role.
- 2. Blood glucose is maintained via hepatic glycogenolysis & gluconeogenesis
- 3. Muscle cannot do GNG, but can provide lactate & alanine as GNG substrates.
- Other helpful tissues: ADIPOSE (epinephrine --> HSL --> lipolysis --> FFAs & glycerol for GNG).
What are the metabolic characteristics of different fiber types? Mitochondrial density, oxidative enzymes, glycolytic enzymes, insulin sensitivity, and force-fatigue?
How does glycogen deplete in relation to exercise intensity? Carboloading?
The more intense the workout, the faster glycogen depletes. Determines whether you should carboload or not.
What does it mean that fatty acids burn in a carb flame?
Basically, must have carbs to oxidize FAs. Even if you have acetyl CoA from FA oxidation, you must have OAA, as well, which is a byproduct of pyruvate which comes from glucose.
Reaction that form intermediates of a metabolic pathway (i.e. TCA cycle)
What factors determine which substrates will be utilized? Name these 3 factors
- Mode (fiber recruitment) - type of exercise. Different fiber types have differnet metabolic needs.
intensity & duration = total workload.
Which substrate is used more with high intensity exercise? What about longer exercise durations - Why? What is the limiting factor for long-term exercise?
Glucose. Plasma FFAs, while muscle glycogen & serum glucose used decreases to conserve plasma glucose.
Blood glucose levels for the brain.
How does the muscle switch from glucose to fatty acid substrate use?
1. Increasing [citrate] activates production of acetyl CoA via ATP citrate lyase.
2. Citrate activates ACC --> malonyl CoA (key player in liver and muscle in determining substrate selection).
3. Malonyl COA will inhibit CPT-1 blocking B-oxidation. If there's a lot of glucose, there will be a lot of malonyl CoA production and B-oxidation will be shut down.
4. Due to AMP:ATP increase, AMPK will decrease ACC, lifting block on CPT-1 enhancing B-oxidation.
How does the body allow for glucose sparing during exercise? (3)
B-oxidation can produce more Acetyl CoA than TCA can handle.
Acetyl CoA then inhibits PDH --> leading to no glucose oxidation.
Anaplerotic rxns (those that form int of pathway) fill TCA cycle and FA oxidation allows for glucose sparing.
What happens to substrate utilization when you train? What % of subtrate used at rest is fat?
TAG vs. FFA vs. Carbs?
Shifts metabolic crosssover point to the right (once you pass this point, you start producing lots of lactate)
Increased glucose sparing and delay in anaerobic threshold (production of lactate).
At rest, 60% of substrate use is fat.
You increase TAG use, decrease FFA use and carb use.
What is beneficial about having lipid stores in muscle? What is paradoxical about this?
What's the take home message?
You have a local source of lipids to spare glucose - don't have to wait for hormonal signals to activate lipolysis.
Many metabolic disorders are associated with lipid droplet accumulation in muscle which leads to insulin resistance.
Having lipid droplets accumulate in muscle isn't pathological
What signaling pathways are involved in muscle adaptation to exercise?
Change in AMP:ATP (AMPK) and CA2+ signaling
AMPK regulates transcription factors like PPARg and PPARa, allowing long-term regulation via gene transcription.
What are training-induced adaptations in skeletal muscle? What three things happen to intermediate fibers?
Increased capacity for oxidative ATP production & to use FA substrates.
Training allows adaptive intermediate fibers to become red/type I/oxidative (low force, fatigue resistant)
Fiber type shift, angiogenesis, and fiber hypertrophy
What is PPARg Coactivate 1a (PgC1a)'s role in mitochondrial biogenesis and muscle energy metabolism?
Activates 4 things
PGC1a interacts with, NRF (nuclear respiratory factor -mitobiogenesis), and ERRa (oxidative phosphorylation), and MEF2 (glucose metabolism) PPARg - adipogenesis
What role does skeletla muscle play in whole body lipid/glucose homeostasis? 7 total, but 3 important ones.
- 1.Accounts for large portin of total energy expenditure - protects against nutrient-incduced metabolic stress.
- 2. Key site of whole-body lipid oxidation and insulin-stimulated glucose disposal (~80%)
- 3. Key site of serm lipid clearance (FFAs, VLDL-TAG< Chylomicron TAG)
- 4. Major site of energy dysregulatino associated with obesity, insulin resistance, and T2D & metabolic syndrome
- 5. Physical activity impacts lipid metabolism during & after exercise. Leads to high level of FA oxidation in fasting state and high level of glucose oxidation in fed state, whereas T2D and obesity make G/FA ratio stay the same despite meal6. Exercise stimulates glucose transport via insulin-indep mechanism (Contraction stimulates GLUT 4 translocation too via Ca2+ and AMPK)
- 7. Exercise enhances insulin sensitivity. (via AMPK <--AMP:ATP <--muscles)
Can you gain the benefits of exercise without doing the work? (Can we increase AMPK and PPAR activity)
Difficult bc rates of respiration is coupled to ATP demand - difficult to trick the system.
Also, you will have increased membrane potential and more reactive oxidative species.
Increased expression of PGC1-1 increased mitochondria, ATP production, fat oxidation, and exercise indurance - but more susceptible to insulin resistance!!!
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