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73 Cards in this Set
- Front
- Back
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Euglycemia
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90-108 mg/dL, 5-6 mM
(Post-Absorptive) |
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Hypoglycemia
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< 65 mg/dL, 3.5 mM
(Fasting, Diabetics) Exhibits central fatigue (brain, not muscle) |
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Hyperglycemia
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> 126 mg/dL, 7 mM
(Post-Prandial, Diabetics) |
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Insulin / Glucagon & Exercise
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- Intensity-INDEPENDENT
(Secretion dictated by [blood glucose]) *At high intensities, increase catecholamines = no insulin |
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Catecholamines & Exercise
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- Dynamic exercise (vs. static) releases more catch.
- Intensity-DEPENDENT increase - Duration-DEPENDENT increase (glycogen depleted, increased glucose uptake) - Inverse response w/ [glucose] - Rapid decrease post-exercise to recover - No gender differences - Decreased catech. release w/ age (adrenal atrophy) |
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Cortisol & Exercise
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- Increased release > 60% VO2max
- Duration-DEPENDENT increase (15 min delay) - Stimulates liver glucose output - Inhibits inflammation - Circadian rhythm: highest in morning - CHO ingestion: decreased/blunted response - Dehydration: increased levels (stressful) - Repeated exercise bouts: increased levels * Greater for endurance exercise (vs. resistance) |
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Growth Hormone & Exercise
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- Intensity-DEPENDENT increase (> females)
- Duration-DEPENDENT increase (> males, 15 min delay) - Mode-DEPENDENT --> Sprint = greatest absolute amount --> Endurance = more total release |
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Duration-Dependent Hormone Release
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1) Catecholamines
2) Cortisol 3) Growth Hormone |
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Intensity-Dependent Hormone Release
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1) Catecholamines
2) Growth Hormones |
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α-1 Adrenergic Receptor
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G-q allosteric stimulator of Phospholipase-C
-Expressed in vascular smooth muscle & liver Liver: -Liver glycogenolysis -Increased glycogen phosphorylase Smooth Muscle: -Increase Ca2+ -Vasoconstriction -Increased contraction & BP (increased blood flow back to heart) |
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α-2 Adrenergic Receptor
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G-i inhibitor of adenylate cyclase
-Expressed in β-islet cells of pancreas & vascular smooth muscle Pancreas: -Inhibit insulin release -Decreased adenylate cyclase activity = Decreased cAMP levels |
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β Adrenergic Receptors
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G-s stimulates adenylate cyclase
β-1: Expressed in heart (epinephrine) β-2: Expressed in vascular smooth & skeletal muscle & liver *cAMP an allosteric stimulator of PKA β-1: - Increased heart rate β-2: - Stimulate TG hydrolysis - Stimulate muscle glycogenolysis - Vasodilation - Lungs = bronchodilation - Increased Liver glycogenolysis **Epi stronger affinity for β-2 in vasculature, but more total α-1 receptors |
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Liver Glucose Output
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Glycogenolysis: Increases w/ exercise duration, followed by decrease (fuel for brain, then depleted stores)
Gluconeogenesis: Increases during long durations (due to depleted glycogen stores) [precursors take awhile to become available] Total glucose output: Decreases when [glycogen] decreases |
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Gluconeogenic Precursors
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1) Glycerol --> DHAP (Glycolysis)
2) Pyruvate --> OAA 3) Lactate --> Pyruvate --> OAA 4) Alanine --> Pyruvate --> OAA 5) Aspartate --> OAA (Aminotransferase) |
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Glucose Rate of Appearance
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AKA rate of glycogenolysis & gluconeogenesis
-Intensity-dependent increase in Glucose R-a (Catechol. stimulates liver glycogenolysis) -Duration-dependent increase in Glucose R-a during mod. intensity exer. -Rapid decrease @ end of exercise (no more energy demand, decreased catech.) |
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Non-Regulated Glucose Uptake Transporters
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GLUT-1: RBC, nervous system, SM & adipose tissue @ rest
GLUT-2: Liver, pancreas, kidney |
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Regulated Glucose Uptake Transporters
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GLUT-4: SM & adipose tissue
*Insulin & exercise stimulate GLUT4 translocation (additive effect on uptake) |
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Glycolytic Flux
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-Measures the rate of appearance of pyruvate
-Dependent on cell energy demand (@rest vs. exercise) @rest: glucose uptake-dependent Exercise: glycogenolysis-dependent *Loosely regulated* |
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Rapid Glycolysis
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-Independent of [O2] (anaerobic exercise)
- NAD+ reduction rate > NADH oxidation rate -Increase in lactate -Increase glucagon stimulation of gluconeogenesis (and from catecholamine & cortisol release) |
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Lactate as Fuel
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- Restores NAD+ gluconeogenic precursor
- LDH the highest glycolytic Vmax - Produced @ rest and during MC (FA oxidation inhibited) - Excess Glucose = Increased La+ = Glycogen synth. - Oxidized in the mitochondria |
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Cori Cycle
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- Helps maintain blood glucose during exercise
- Anaerobic glycolysis in SM increases blood lactate - Gluconeogenesis in liver increases blood glucose *Epi/Norepi stimulate gluconeogenesis during exercise (increased muscle glycogenolysis = increased La+ --> enters cycle) |
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Lactate & Catecholamines
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- Lactate infusion decreases catech. secretion during mod. intensity exercise
--> Slowed glycogenolysis --> Good for trained populations: less fatigue at end of exercise bout |
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Glucose Homeostasis During Exercise
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1) Increased glucose uptake (GLUT-4 in liver)
2) Decreased blood glucose & insulin secretion 3) Decresed glucose uptake by non-active tissues (AT, liver, kidney) 4) Increased catechol/glucagon/GH secretion 5) Increased glycogenolysis & gluconeogenesis 6) Increased cortisol secretion 7) Increased TG hydrolysis (glycerol a gluconeogenic precursor) 8) Decreased liver/muscle glycogen 9) Cessation of exercise |
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CHO Ingestion During Exercise
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- Increased blood glucose
- Increased insulin secretion, decreased epinephrine - Greater reliance on CHO = decreased TG hydrolysis, FA uptake & oxidation - Spares liver glycogen for the brain *No effect on muscle glycogenolysis *Only effective for durations 60min+ |
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Low [glycogen] and CHO Metabolism during Exercise
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- Decreased muscle glycogenolysis
- Increased plasma FA oxidation - Decreased time-to-fatigue = Decreased performance *Delays central fatigue (brain), not muscle fatigue |
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High-Fat Diet and CHO Metabolism during Exercise
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- Decreased muscle glycogenolysis
- No change in plasma glucose oxidation - Increased catecholamine response (stressful condition) - Increased TG hydrolysis & FA oxidation - Additive effect on glycogen sparing w/ training |
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Lipid Mobilization
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With epinephrine binding to β-2 receptor, PKA phosphorylates perilipin --> Hydrolysis enzymes able to bind, TG hydrolysis occurs
ATGL: Important for rest HSL: Important for exercise |
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TG Hydrolysis & Adipose Tissue FA Output
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- Increased w/ catecholamine release
- Increased w/ exercise duration (Longer duration = lower intensity = more fat utilization) |
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Reesterification & Adipose Tissue FA Output
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- FFA converted to TG in AT
- Decreases w/ exercise duration (Longer duration = need to hydrolyze TGs, not store) |
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Blood Flow & Adipose Tissue FA Output
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- Low-Mod Intensity: β-2 = Vasodilation promotes blood delivery to SM
*High intensity: β-2 saturated, α-1=Vasoconstriction - Decreased blood flow to AT |
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Total FA Output
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- Increase w/ duration
- Decrease w/ intensity - Increase @ end of exercise bout - Increased blood flow to adipocytes |
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IMTG Hydrolysis
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- Local effect
- Rate = Rate of appearance of glycerol - Lacks perilipin (enzymes can freely access TG = decreased regulation) - Doesn't respond to epinephrine & lipase activity in muscle - Increased Ca2+ modifies PKC which modifies ERK1/2 which activates HSL |
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Plasma FA Availability
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Increased intensity increases glycerol appearance, then plateaus due to vasoconstriction
Appearance of FA decreases w/ increased intensity |
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ERK1/2 & FA Uptake (Turcotte 2005)
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-PD98059 inhibits ERK1/2
@ Mod. Intensity Exercise: - Decreased ERK1/2 phosphorylation - Decreased FA Uptake - No change in AMPK activity AMPK --> ERK1/2 --> FA Uptake |
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AMPK & FA Uptake (Raney 2005)
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AICAR stimulates AMPK
(Increased ZMP --> Analog of AMP --> Increased AMPK) - Increased FA Uptake w/ AICAR - @ Low intensities, AMPK not involved Therefore, no raise in AMP levels to activate AMPK @ low intensity exercise |
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Exercise Intensity & FA Uptake (Raney & Turcotte 2006)
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@ Low intensity: Increased FA Uptake w/ Increased intensity, Increased AMPK activity
@ High intensity: ↓ FA Uptake, Decreased AMPK activity ERK1/2 not dictating at high intensities, intensity-dependent increase |
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CaMKII & FA Uptake (Raney & Turcotte 2008)
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KN92 = Inactive inhibitor of CaMKII
KN93 = Active inhibitor of CaMKII Caffeine mimics Ca2+ release during MC - ↑ FA Uptake w/ caffeine → ↑ Cytosolic Ca²⁺ but no stimulation of CaMKII w/ KN93 ∴ CaMKII involved in Ca²⁺-dependent FA Uptake - Exercise = ↑ CaMKII activity - MC ↑ ERK1/2 phosphorylation, but no ∆ w/ caffeine [ERK1/2 Ca²⁺-independent] - With mod. intensity & MC, there are both Ca²⁺-dependent and -independent signaling pathways Dependent: ↑CaMKII → ↑ AMPK → ↑ FA Uptake Independent: ↑AMPK → ↑ ERK1/2 → ↑ FA Uptake |
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FA Oxidation & Exercise Intensity (Raney & Turcotte 2006)
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- At high intensities, decrease in FA oxidation (↑ CHO utilization)
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FA Oxidation & AMPK (Raney 2005)
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( )
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Lipid Metabolism & Gender
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- > IMTG utilization in women for acute bout
- Women burn more fat than men in acute bout - Higher [epi] in men - Training = no effect on gender diffs. - Estrogen ↑ FA oxidation by activating AMPK |
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Lipid Metabolism & Exercise Recovery
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- IMTG a big energy source during recovery
- ↓ Muscle glycogenolysis - ↑ Glycogen synthesis |
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Lipid Metabolism & a Low-Fat Diet
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- Slower recovery
- ↓ IMTG storage - No ∆ in glucose or FA uptake - ↓ Total FA oxidation - ↑ Muscle glycogen oxidation * Increased reliance on glycogen (esp. in women) = fatigue sooner |
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Enzymes in the PDH Complex
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1) Pyruvate Dehydrogenase
2) Dihydrolipoyl Transacetylase 3) Dihydrolipoyl Dehydrogenase When PDH phosphorylated, reaction to form Acetyl CoA inhibited |
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Limitations to Glucose-FA Cycle
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In Heart/Diaphragm:
- High fat = ↓ pyruvate production, ↑ G6P, ↓ Glucose uptake (agrees w/ cycle) In SM: - High fat ≠ ↑ Citrate or G6P, ↓ % Glucose oxidized ∴ Glucose availability may be more important Prolonged high fat = ↓ [GLUT4] |
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Limitations to Reverse Glucose-FA Cycle
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In Rodents:
- High Glucose + Insulin = ↑ [malonyl CoA], ↓ FA oxidation In Humans: -High Glucose + insulin ≠ ↑ [malonyl CoA] ∴ malonyl CoA not the sole regulator |
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Ketone Bodies
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- During fasted/low-CHO state, liver converts FAs for fuel
Favoring formation: - β-oxidation rate > use of acetyl CoA - Low OAA levels Oxidized in muscle, nerves, brain 3 forms: 1) Acetoacetate 2) β-Hydroxybutyrate 3) Acetone |
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FA Activation of PPARα
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aka Peroxisome Proliferator Activated Receptor-α
Deficiency → - Liver TG accumulation --> Insulin Resistance (IR) - ↑ Glycolysis & glucose oxidation Overexpression → - ↑ FA uptake & oxidation - ↑ TG accumation --> IR |
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Protein Synthesis
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Transcription Translation w/ mRNA on ribosomes
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Protein Synthesis & Exercise
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- ↑ AMPK activity = ↓ synthesis by over 50% (high AMP)
- ↑ Synthesis post-resistance exercise independent of feeding - ↑ Synthesis post-aerobic exercise dependent on CHO-protein intake |
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Proteolysis
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Ubiquitination: Ubiquitin bines to proteosomes, frees AAs
-Hydrolysis by proteosomes & proteases *Cortisol ↑ Ubiquitin *Insulin ↓ Ubiquitin ∴ ↑ proteosome transcription |
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Synthesis vs. Proteolysis Balance
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Resistance Exercise:
- No diff. @ rest or mod. intensity - Synthesis > Proteolysis @ high intensities Endurance Exercise: - No diff. @ rest - @ Mod. intensity, no ∆ synth, ↑ proteolysis - @ High intensity, ↓ synth. relative to rest, ↑ proteolysis (cortisol released) * AA availability increases protein synthesis * AA avail. + CHO = ↑↑ protein synth. |
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Amino Acid Deamination
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- Conversion of AAs to ammonia, which is converted to urea
- Occurs in mito. matrix of liver |
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Amino Acid Transamination
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- Transfer of amine groups from one molecule to another
AA + α-Ketoglutarate ←aminotransferase→ Glutamate + Keto Acid |
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Glucose-Glutamine Cycle
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Occurs in Kidney
Glutamine → Glutamate → Glucose |
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Glucose-Alanine Cycle
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Occurs in Liver
Alanine → Pyruvate → Glucose |
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Oxidative Deamination
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Removal of an amine group in the mito. matrix of the liver
Glutamate ←Glutamate Dehydrogenase → α-KG From L to R: ↑ w/ high ADP:ATP or GDP:GTP ratio From R to L: ↑ w/ high levels of Krebs intermediates ↑ w/ high NADH:NAD⁺ ratio |
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Muscle Hypertrophy
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- Result of increased protein synthesis
- ↑ IGF-1 w/ GH binding to cytokine receptors in liver → satellite cell proliferation = ↑ DNA content - Ca²⁺/calmodulin-stimulated transcription factors - GH plays minor role in healthy adults |
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Hypertrophy & Ischemia
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- Ischemia ↑ GH secretion post-exercise
(Similar responses bet. low intensity + ischemia & high intensity) - Increases hypertrophic response to exercise |
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Gender Differences in Protein Metabolism
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- Men have > leucine oxidation during exercise (enhanced w/ β-adrenergic blockade)
--> Why men need to consume more AA - Women have > adipose tissue β-adrenergic sensitivity |
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Insulin & Training
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↑ [GLUT4] transcription
↑ PI3K activity ↑ Insulin sensitivity ↓ Insulin secretion Elevated [ ] during exercise ↓ Muscle glycogen degradation |
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Glucagon & Training
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- Lower [ ] during exercise (↑ reliance on fat, no glycogenolysis b/c blood glucose maintained)
- ↑ HGP (hepatic glucose production) w/ physiological [glucagon] @ rest, during exer. - Increased glucagon sensitivity in adipocytes= ↑ receptor density ↑ receptor affinity |
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Catecholamines & Training
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- No effect on resting [ ]
- ↓ secretion during low-mod int. exercise (using fat, more efficient, not stressful) - > secretion during high int. exercise (use CHO) - "Sports adrenal medulla" - No ∆s in women - No ∆s w/ resistance training |
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Sports Adrenal Medulla
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Hypertrophy of the adrenal gland w/ training
> Anaerobic training effects |
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cAMP Cascade & Training
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- ↑ Hepatic glucagon receptors
- ↑ β-adrenergic receptors (bind to catech.) → Liver - increased glycogenolysis → SM - increases muscle glycogenolysis → AT - ↑ TG hydrolysis - ↑ sensitivity to β₂-adrenergic receptors on smooth muscle (vasodilation = ↑ blood flow to AT to pick up FAs released) |
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Cortisol & Training
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- No ∆ @ rest
- Secretion during exercise: ↓ @ same absolute intensity = @ same relative intensity ↑ @ supramax intensity HPA Adaptation: - During exercise = ↑ cortisol w/ duration, no ∆ sensitivity - Post exercise = ↓ sensitivity, ↑ protein synth. w/ GH |
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Overtraining Syndrome
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Poor performance for 6+ weeks
Diagnosed based on plasma ACTH/cortisol levels - ↑ cytokine transcription (inhibition of enzyme that inhibits cortisol) |
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Hypoglycemia-associated Autonomic Failure (HAAF)
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Antecedent hypoglycemia ↓ the counterregulatory response
- ↓ Glucagon, ACTH, epinephrine, cortisol secretion (body wants to adapt to lower glycemic levels) - Exaggerated hypoglycemia - ↓ Threshold for neurogenic/neuroglycopenic symptoms (--> Diabetic coma) |
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Growth Hormone & Training
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- ↑ 24 release
- ↑ exercise response (ONLY if above La+ threshold) - Doesn't apply to resistance training - ↑ [IGF-1] = ↑ hypertrophy response |
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CHO Metabolism & Training
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- Increased PDH activity @ high intensities
- La+ decreases if PDH activity increases |
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Lactate Clearance & Training
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With training, lactate clears faster, appearance same (decreased threshold for OBLA)
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FA Metabolism & Training
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- ↑ FABPpm (helps w/ LCFA uptake)
- ↑ mitochondrial density (more oxidative enzymes) - ↑ muscle HSL activity (use more IMTGs) - ↑ FA uptake & oxidation |
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Limitations & Explanations for Energy Efficiency
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MORE O₂ NEEDED TO PRODUCE ATP W/ LIPIDS THAN W/ CHO
but - Lipids have a higher ATP generating capacity - No real diff. in relative energy output (2.7 vs. 2.3) Mechanisms: - Carnitine depletion (shuttles lipids to mito. matrix) - Acetyl CoA + carnitine → acetyl-carnitine + CoA (build up from rapid glycolysis drives run forward) (↑ PDH activity facilitates CHO metab) - ↓ cytosolic pH (inhibits CPT-1 activity) - Mito. [ADP] (limiting factor, forced to use cytosolic glycolysis) |
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Limiting Factors for Aerobic Energy Production
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- O₂ Availability: Differences in altitude training (more La⁺ @ sea level)
- Rate of acetyl CoA oxidation: anaerobic glycolysis doesn't use acetyl CoA (only glucose used as substrate) [PDH inhibited in the mitochondria] |
