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KIN 2CC3 > MT1 > Flashcards

MT1 Flashcards

1
Q

overview of energy systems in body

A
  1. skeletal muscle sets the demand for O2 and fuels, produces fuel by-products and heat
  2. heart and circulation transport fuels, by-products, and wastes
  3. lungs obtain O2 and expel CO2 into external environment
  4. supply tissues such as liver glycogen and adipose tissue provide fuels
  5. removal tissues such as kidneys, liver, and lymphatic system remove by-products (wastes) and heat from circulation
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2
Q

bioenergetics: E transfer
1. bioenergetics def
2. 1st law of thermodynamics
3. in body
4. equivalent exchange

A
  1. E transfer through chem rxns in living tissue
  2. E cannot be created or destroyed, only transferred, deltaE = usable/free E + non-usable E (heat)
  3. E in fuels (macronutrients) transformed into ATP, ATP breakdown provides E for physiological function (chem, mech, or electric E; most lost as heat)
  4. to produce a certain amount of E for work (changing substrate from A to B) req equivalent input of E in form of fuel
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3
Q

ATP
1. E transfer using ATP
2. fuel sources to regenerate ATP
3. use of fuel sources
4. storing ATP?

A
  1. ATP comp adenine and 3 phosphate group (E bond) bonded to ribose have; ideally both P-P bonds broken for complete combustion of fuel to max E transfer but not always possible bc limited by the type of fuel
  2. carbohydrate, PRO, lipid, Pcr
  3. depend on exercise intensity and duration and diet
  4. little storage, ATP v. big, 1 kg consumed/hour at rest increase x100 during exercise
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4
Q

Bioenergetics: chem rxns
1. def enzymes
2. Factors affecting enzyme activity

A
  1. molecules increase rate of rxn w/o being used up in rxn, lower activation E and do not alter free E change (change in E required for substrate > product)
  2. Substrate concentration increases rate of reaction up until vmax when all available enzymes have bound to substrate (saturated), simulators/inhibitors bind to enzyme allosteric sites to change the enzyme shape to be more/less compatible with substrate thus increase/decrease speed of rxn, speed of rxn increase with temperature up until point of denaturation, highest at optimal pH
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5
Q

5 things to consider for supplements

A

dose, purity, digestion (breakdown in body), circulating conc (will it affect conc in body), effect on target tissue (will it produce effect on performance)

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6
Q

Major fuels and locations

A
  1. carbs: glucose in blood, glycogen in muscle cytosol and liver
  2. lipids: FA in blood, TG in the muscle cytosol and adipose tissue
  3. other: phosphagen in muscle cytosol and AA in body
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7
Q

phosphagen sys
1. location
2. chem process
3. purpose

A
  1. phosphagen breakdown in muscle cytosol, anaerobic, modulated by substrate-product conc
  2. uses one Pcr phosphate (abt the same amount of E as P-P bond of ATP) to replenish one ATP
  3. buffer decrease in ATP during high-intensity exercise and changes in workload (interval training and rest-to-work transition)
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8
Q

glycolytic sys
1. location
2. chem process
3. importance of lactate
4. purpose

A
  1. glycolytic sys in muscle cytosol, anaerobic
  2. glucose transpoted into cell from blood, glycolysis of glucose into glucose 6-phosphate by hexokinase, requires one ATP
  3. glycogenolysis of glycogen into glucose 1-phosphate by glucose phosphorylase entering at level of glucose 6-phosphate
  4. one ATP used by phosphofructokinase (PFK), produces 4 ATP via substrate-level phosphorylation (directly form ATP anaerobically), 2 NADH+, 2 H+ and 2 pyruvate
  5. net total 2 ATP from glucose, 3 from glycolysis
  6. if demand by ADP is high enough, O2 is available, pyruvate converted to acetyl CoA by pyruvate dehydrogenase in mitochondria for oxidative metabolism, not enough pyruvate clearance (glycolysis rate > oxidative) pyruvate converted to lactate by lactate dehydrogenase, producing NAD+ to continue glycolysis and gen H+ which inhibit enzyme activity (metabolism) and decrease CBC (contraction)
  7. used during intense exercise and workload transition
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9
Q
  1. ATP supply v. demand
  2. rate and duration
A
  1. supplied by phosphogen, glycolytic, and oxidative sys; demand set by Ca2+ ATPase (Ca2+ for CBC), myosin ATPase (CBC), and Na+/K+ ATPase (maintain ion gradient for signal of contraction)
  2. demand not equal supply, if diseased or inactive, oxidative sys compromised since less mitochondira thus rely more on anaerobic sys
  3. faster rate of ATP provision, shorter the duration
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10
Q

oxidative metabolism overview
1. location
2. overview
3. three essential steps
4. purpose

A
  1. in the mitochondria
  2. aerobic limited by mitochondrial capacity, complete combustion of glucose, glycogen, lipids, and AA into CO2 and H2O to release all E
  3. formation of acetyl CoA (CHO, fat, AA); oxidation of acetyl CoA during Krebs Cycle to reduce coenzyme (produce NADH and FADH2); formation of ATP in ETC by oxidizing coenzyme (reforming NAD+ and FAD)
  4. steady state exercise and rest, longer duration than 2 mins
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11
Q

oxidative metabolism: chem process and measures of mitochondria markers

A
  1. formation of acetyl CoA: pyruvate dehydrogenase on inner mitochondrial membrane transports pyruvate into the mitochondria and converts it into acetyl CoA, producing CO2 and NADH (x2)
  2. Krebs Cycle: citrate synthase combine acetyl CoA (2C) with oxaloacetate (4C) to form citrate (6C), citrate gets rearranged, forming 1 FADH2, 3 NADH, 1 ATP (via SLP), 2 CO2 into oxaloacetate (x2)
  3. ETC: series of redox rxn, e- passed as H+, in matrix NADH ox at complex I to re NAD+, pump 2 H+ into intermembrane space for each complex I, III, and IV, FADH2 ox at complex 2 to re FAD, pump 2 H+ for each III and IV est Electrochem grad; five pairs of 2H+ pass through ATP synthase to restore Electrochem grad, forming 1 ATP per pair by ox O2 to re H2O via cytochrome oxidase (x2)
  4. cytochrome oxidase and citrate synthase, measure of mitochondrial capacity
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12
Q

lipid catabolism: process

A
  1. FA mobilization: TG undergoes lipolysis, converted into 3 FAs and glycerol by hormone sensitive lipase (HSL); glycerol converted in liver to glucose via gluconeogenesis to support brain func during prolonged starvation, FA transported by albumin through blood to be catabolized for E in muscle
  2. FA uptaken to muscle cytosol from blood via FA transporter (limits the speed of fat metabolism), requiring 2 ATP and 1 CoA to form active fatty acyl-CoA, uptaken by carnitine palmitoyl transferase into mitochondrial matrix (reg fat oxidation, insulin increases CPT activity)
  3. Each beta oxidation cycle breaks 2C chains off of fatty acyl-CoA and produces 1 FADH2 and 1 NADH, using one CoA to produce acetyl CoA and the cycle repeats until the last 4C is broken into 2 acetyl CoA
  4. mitochondria oxidation: the acetyl CoAs enter TCA, NADH and FADH2 enter ETC
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13
Q

E provision summary: which is the better sys?
1. ATP/s
2. ATP/unit substrate
3. usable capacity

A
  1. phosphagen: 10 ATP/s, 1 ATP/ unit substrate, produce ATP fast for high intensity but only lasts <=15 s
  2. glycolytic: 5 ATP/s, 2 (glucose) or 3 (glycogen) ATP/unit substrate, high intensity use for <= 60 s
  3. CHO oxidative: 2.5 ATP/s, 38-39 ATP/unit substrate, low intensity lasting 90 mins, capacity of 2500 kcal, 6.3 ATP/O2 allows for higher intensity than fat
  4. fat oxidative: 1.5 ATP/s, 129 ATP/unit substrate, low intensity for days, unlimited storage, 5.7 ATP/O2 low intensity
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14
Q

Protein metabolism:
1. why is PRO different from carbs or lipids?
2. process
3. BCAA supplementation
4. gluconeogenesis

A
  1. has amino group with nitrogen, making it great for building structures but hard to remove from body in natural form NH3
  2. most AA in blood are broken down in the liver and converted to urea to be excreted in urine by the kidneys; branched-chain AA (LEU, ILE, and VAL) in blood are transported into skeletal muscle are deaminated, producing NH3 and BCOAs, BCOAs converted to pyruvate and acetyl CoA, small amount of NH3 allowed in blood, convert to GLN and ALA, transport through blood to the liver, converted to urea
  3. increase blood NH3 and ALA and GLN, leucine acts as an activator in protein synthesis for hypertrophy
  4. the formation of glucose from metabolic intermediates, actively occurring during exercise, lactate, alanine, and glycerol transported through blood to liver, converted to glucose; train to enhance lactate circulation to gen glucose and reduce pH deviations in muscle
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15
Q

metabolism during exercise:
1. key signals of reg E provision
2. relative E contribution during maximal exercise

A
  1. ATP/ADP ratio, Ca2+, hormones
  2. <2 mins mostly anaerobic (<15 mostly phosphogen, >15 glycolytic), at 2 mins 50/50, >2 mins mostly aerobic
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16
Q

anaerobic exercise response
1. Wingate test
2. effect of intense exercise on metabolite concentration
3. determining total anaerobic E from biopsies

A
  1. 30 sec maximal exercise bike ride measuring PP, mean P, and fatigue index, estimate metabolite concentration
  2. ATP stays relatively the same bc replenished, PCr decrease rapidly to replenish ATP, muscle lactate concentration increase greatly then slowing down as venous lactate increases due to lactate exportation into blood to increase muscle pH
  3. phosphagen sys measure change in Pcr, ATP yield based on 1 Pcr:1 ATP; glycolytic sys measure change in lactate, 1 lactate: 1.5 ATP
17
Q

aerobic exercise response
1. calorimetry
2. determining fuel use and respiratory exchange ratio
3. RER assumptions and limitations

A
  1. quantify E production in body, direct based on measure of heat production due to complete combustion of fuels, 1 kcal = increase 1 deg C of 1 kg water; indirect based on measure of O2 use, 1 L O2 uptake approx 5 kcal (depending on fuel)
  2. RER is ratio CO2 produced to O2 consumed (VCO2/VO2), O2 req for combusting food is constant but differs b/w CHO (RER 1.0) and fat (RER 0.7); value of RER is a combo of CHO and fat, allowing accurate fuel consumption
  3. assume no PRO contribution and under steady state oxidative conditions, limited by hyperventilation which blows off CO2 not from aerobic exercise and not a good measure for intense (anerobic comp) exercise
18
Q

O2 uptake at rest:
1. def
2. *Vo2
3. average VO2

A
  1. rate of O2 used by body at rest
  2. volume of O2 consumed/min, * refers to rate, L or mL/min is abs, ml/kg/min is relative; abs VO2 increases with body size bc need more ATP, relative increases slightly with higher skeletal muscle mass (body comp)
  3. 0.2-0.3 L/min or 250 mL/min; 3.5 mL O2/kg/min (1 metabolic equivalent); expressing as 1 MET allows for easy comp
19
Q

O2 uptake maximal exercise
1. VO2max and sig
2. determinants of VO2max
3. VO2max test

A
  1. maximal rate of O2 consumption (oxidative metabolism) by the body; good indicator of metabolic disease and mortality, higher than 1 MET indicates lower respectability to all diseases
  2. ability of the CR sys to deliver O2 to muscle and mitochondrial ability to use O2 in muscle
  3. progressive increase in workload until Vo2 (L/min) plateaus at max (primary criteria); not everyone can reach plateau therefore determine VO2peak through secondary criteria reaching max HR (220-age), x8 resting blood lactate indicate maxed out oxidative metabolism from reliance on anaerobic, or voluntary exhaustion, RER > 1.1
20
Q

VO2max typical values
1. sedentary
2. active
3. well-trained
4. elite

A
  1. F 2.0, M 3.0 L/min; F 33, M 38 mL/kg/min
  2. F 2.5, M 4.0 L/min; F 42, M 50 mL/kg/min
  3. F 3.0, M 4.5 L/min; F 50, M 56 mL/kg/min
  4. F 4.0, M 6.0 L/min; F 67, M 75 mL/kg/min
21
Q

rest-work transition and O2 uptake

A
  1. increasing intensity (working at higher VO2) results in delay O2 uptake before oxi catches up to higher rate, supply E through non-oxi to meet demand
  2. The greater the increase in intensity, the greater the reliance on non-oxi
  3. training to increase mitochondrial capacity to turn on oxi faster reduces reliance on non-oxi
22
Q

lactate threshold
1. def
2. blood lactate and measuring lactate threshold
3. muscle lactate
4. factors affecting muscle lactate

A
  1. exercise intensity at which there is abrupt increase in blood lactate, reflects ability to sustain oxi since reliance on non-oxi indicates non-steady state
  2. measurement (mmol/L) of lactate threshold is protocol dependent, avg lactate threshold occurs at 60% VO2max
  3. at 50% VO2 max increases rapidly before reaching new steady-state (when oxi sys adjusted to higher rate), past 100% higher lactate accumulation, no longer able to reach steady state
  4. O2 availability, enzyme activity (amt LDH and PDH/LDH ratio), fibre type (type II produce more lactate), muscle lactate transports, SNS activity increase lactate

KIN 2CC3 (3 decks)

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