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Biomed > physiology S2 Y1 > Flashcards

physiology S2 Y1 Flashcards

1
Q

What happens when upper limit of exercise is reached?

A

Slowing, skill and coordination deteriorates

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2
Q

What happens when glucose reacts with oxygen?

A

Activation is overcome by enzymes and body heat - the energy is then conserved within activated molecules

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3
Q

5 energy yielding pathways in exercise and amount of time they supply energy for exercise?

A
  1. ATP –> ADP + Pi (1-2 seconds)
  2. Phosphagen system: PCr + ADP –> ATP + Cr (10-15 seconds)
  3. Glycolysis (15 seconds - 3-5 minutes)
  4. Krebs cycle (CAC) (2-3 minutes onwards)
  5. Oxidative phosphorylation (“ “)
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4
Q

What limits ATP synthesis?

A

Substrate

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5
Q

Phosphagen system:
- What does phosphocreatine (PCr) act as?
- What does PCr do?

A
  • Energy reservoir
  • Recycles ATP for further muscle contractions
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6
Q

Glycolysis:
- Reaction?
- What temporarily accepts H?
- What is yielded?
- Difference between lactate and lactic acid?

A
  • Glucose into pyruvate or lactate
  • NAD
  • 2 ATP
  • Lactate has COO- group, lactic acid has COOH
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7
Q

Krebs cycle:
- What can it fuel indefinitely?
- What is released?

A
  • Low-intensity exercise
  • CO2, H, H+, NADH, FADH2, 2 ATP
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8
Q

Electron transport chain:
- What provide H+ and e-?
- What creates conc. gradient for electrons to move from complex to complex?
- How does it generate energy?

A
  • FADH2 and NADH
  • Active pumping of H+
  • Electric potential is a form of stored energy
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9
Q

Different ways pyruvate is generated? (3)

A
  1. Fats –> glycerol +fatty acids –> Beta-oxidation –> pyruvate
  2. Carbohydrates –> glucose –> glycolysis –> pyruvate
  3. Protein –> amino acids –> deamination –> pyrvuate
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10
Q

Why does sprinting rapidly decrease power output?

A
  • ATP is used in 2b and 2a muscle fibres, PCr depletes, lactate accumulates
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11
Q

How is sprinting performance improved?

A

Creatine supplementation - increase Cr in muscles so PCr depletion is delayed, increases rate of ATP and PCr re-synthesis, lowers lactate and dependence on glycolysis reduces, increases work output

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12
Q

What happens if someone exercises a part of their body for a prolonged period after not exercising it regularly?

A

High lactate, lower muscle pH, greater K+ release, poorer performance than regular exersisers

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13
Q

Running:
- % aerobic, % anaerobic for 1.5km?
- How is oxygen liberated calculated?
- How is oxygen debt calculated?

A
  • 70-80, 20-30
  • = VO2max x minutes
  • = oxygen required - oxygen liberated
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14
Q

How can middle-distance performance be improved + how? (2)

A
  1. Carbohydrate supplementation - improves performance time, increases work output BUT increases lactate
  2. Bicarbonate supplementation - increases intracellular pH, H+ then leaves muscle cells faster
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15
Q

What does intracellular acidification cause?

A

Reduced sensitivity of contractile apparatus to Ca2+

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16
Q

How does substrate use vary with exercise intensity?

A

Blood glucose and muscle glycogen used more at higher intensity, fat used at lower exercise

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17
Q
  • What is carbohydrate loading?
  • 4 results?
A
  • Athletes eating carbs before/during exercise to delay use of other fuel sources
    1. Plasma glucose spared
    2. Less fat oxidised
    3. Less protein oxidised
    4. Exercise intensity maintained
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18
Q

Why do glycolytic intermediates have at least one ionised phosphate group?

A

To keep them in the cytosol (highly ionised groups cannot bypass membrane)

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19
Q

What is substrate-level phosphorylation?

A

ADP phosphorylated by substrate

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20
Q

Lactate:
- How is it formed?
- 2 pathways it can follow during lactate shuttling?
- What is it used in the liver for?

A
  • Pyruvate gaining 2 H atoms from NADH and H+
  • Enters bloodstream or converted back to pyruvate
  • As a precursor for glucose formation
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21
Q

2 types of proteins for ETC?

A
  1. Those that mediate the series of reactions that cause transfer of hydrogen ions to oxygen (can be cytochromes)
  2. Those that couple the energy released by these reactions with the synthesis of ATP
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22
Q

End product of ETC?

A

Water

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23
Q

Why does FADH2 contribute less to chemiosmosis than NADH?

A

Enters ETC later on

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24
Q

What product from triglyceride hydrolysis is used to synthesise glucose?

A

Glycerol

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25
Q

Where is fat mostly stored?

A

Adipocytes that form adipose tissue

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26
Q

Does fat produce high or low levels of ATP?

A

High (an 18C saturated fatty acid forms 146 ATP)

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27
Q

2 fates of amino acids?

A
  1. Oxidative deamination = NH2 removed and replaced with oxygen (forms keto acid and NH3+)
  2. Transamination = amino group transferred to keto acid
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28
Q

2 fates of keto acids?

A
  1. Metabolised to form CO2 + ATP
  2. Used as intermediate to form glucose
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29
Q

4 functions of endocrine system releasing hormones?

A
  1. Regulates metabolism
  2. Regulates balance of ions, water and nutrients in the blood stream
  3. Stress response
  4. Regulates growth, development and reproduction
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30
Q

What do almost all tissues secrete?

A

Biologically active substances

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31
Q

How are most endocrine glands connected?

A

Functionally (not anatomically)

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32
Q

Why can some glands secrete many hormones?

A

Contain multiple cell types that secrete different hormones

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33
Q

3 major hormone classes?

A
  1. Amine hormones
  2. Peptide and protein hormones
  3. Steroid hormones
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34
Q

What does the chemical structure of a hormone influence?

A

Its transportation in the blood

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35
Q

Amine hormones:
- What are they derived from?
- 3 examples?

A
  • Tyrosine
  • Thyroid hormones, adrenaline/noradrenaline, dopamine (last 2 are catecholamines)
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36
Q

Peptide and protein hormones:
- Abundant?
- 3 steps of production?

A
  • Yes (e.g. insulin, glucagon)
    1. Synthesised as protein prohormones by ribosomes in endocrine cells
    2. Packaged into secretory vesicles and cleaved into peptides (activated)
    3. Stored in cells until secretion when cells are stimulated
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37
Q

Steroid hormones:
- Derived from?
- Where are they produced?
- Main characteristic?

A
  • Cholesterol
  • Adrenal cortex and gonads – 1,25 - dihydroxyvitamin D is from kidneys though
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38
Q

What is the effect of a hormone dependent on?

A

Hormone concentration in the blood

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39
Q

4 factors hormone concentration in the blood depends on?

A
  1. Secretion from endocrine gland
  2. Metabolism and excretion of hormones (mostly metabolised in liver + kidneys)
  3. How they circulate in blood (free or bound to plasma proteins), plasma volume changes and blood redistribution during exercise
  4. Binding to target cells to produce a response
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40
Q

3 inputs that control hormone secretion?

A
  1. Humoral (ions, nutrients)
  2. Neural (neurotransmitters)
  3. Hormonal stimulation
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41
Q

What are tropic hormones?

A

Hormones that induce secretion of other hormones

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42
Q
  • 2 factors that affect hormone transport in the blood?
  • How is it different between protein/peptide hormones and steroid+thyroid hormones?
A
  • Chemical composition and water solubility
  • Protein/peptide = water-soluble, dissolved in plasma – fast acting, short half life, rapidly eliminated
    Steroid+thyroid = lipid-soluble, transported bound to plasma transport proteins –slower action, long half life, slow elimination
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43
Q

What does intracrine mean?

A

Hormone action inside cell

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44
Q

What does autocrine mean?

A

Hormone action from cell on itself

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45
Q

What does paracrine mean?

A

Hormone action on neighbouring cells

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46
Q

What does endocrine mean?

A

Hormone action from endocrine glands to distant cells

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47
Q

What does neuroendocrine mean?

A

Neurons secrete hormones and affect distant cells

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48
Q

Where are specific receptors in tissues?

A

In or on target cells

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49
Q

What does location of specific receptors on/in target cells depend on?

A

Water solubility of hormone (if soluble the receptor will be in the cytoplasm, if it is insoluble then it enters with a carrier protein and the receptor is in the nucleus)

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50
Q

Why is the number of hormone receptors always limited?

A

So that the hormone action reaches a saturation point

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51
Q

Difference between high and low affinity ligands?

A

High affinity for strong bonds, low form weak

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52
Q

What could the number of receptors be regulated by?

A

Availability of hormone in blood plasma (down-regulation = low conc.+low number of receptors, up-regulation = high conc. + increased number of receptors)

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53
Q

4 types of endocrine diseases?

A
  1. Hyposecretion (too little hormone secreted)
  2. Hypersecretion (too much hormone secreted - usually caused by endocrine tumour)
  3. Hyporesponsiveness (reduced responsiveness of target cells to physiological hormone levels)
  4. Hyperresponsiveness (increased responsiveness of target cells
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54
Q

What kind of hormones does the hypothalamus release many of?

A

Tropic hormones

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55
Q

Posterior pituitary gland:
- What hormones does it secrete?
- 2 hormones it secretes + what they do?

A
  • Ones synthesised in the hypothalamus
  • Oxytocin (involved in milk ejection and emotional bonding) and ADH (involved in regulation of water balance and osmolarity)
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56
Q

Anterior pituitary gland:
- What do FSH and LH impact?
- What does growth hormone impact?
- What does TSH impact?
- What does prolastin impact?
- What does ACTH impact?

A
  • Gonads (germ cell development, hormone secretion)
  • Liver and other cells, tissues and organs (secrete GF-1, protein synthesis, carbs/lipids metabolism)
  • Thyroid (secretes thyroxine and triiodothyronine)
  • Breasts (development, milk production)
  • Adrenal cortex (secretes cortisol)
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57
Q

Endocrine growth control:
- What determines growth?
- What can stimulate growth?
- Hormones involved in growth?

A
  • Genetics, but environment too
  • Exercise
  • Growth hormones, insulin-like growth factors, insulin, thyroid hormones, sex hormones, cortisol
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58
Q

Growth hormone:
- 3 things it stimulates?
- 4 things it affects the growth and function of?
- When is its release stimulated?
- What increases release?
- What is it opposite in effect to?

A
  • Postnatal growth, liver to secrete insulin-like growth factor 1, protein synthesis
  • Muscle, liver, adipose and bones
  • During exercise which stimulates muscle growth via IGF-1 release
  • Younger age during exercise and endurance
  • Insulin
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59
Q

How does endocrine system respond to stress?

A
  • Increased cortisol and adrenaline secretion
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60
Q

8 steps of cortisol response to chronic stress mechanism?

A
  1. Neural inputs
  2. Increased corticotropin-releasing hormone (CRH) from hypothalamus
  3. Increased plasma CRH
  4. Increased ACTH secretion from anterior pituitary
  5. Increased plasma ACTH
  6. Increased cortisol secretion from adrenal cortex
  7. Increased plasma cortisol
  8. Target cells respond to cortisol
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61
Q

What does increased cortisol act as?

A

End-product inhibitor

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62
Q

What does cortisol permit action of?

A

Epinephrine and norepinephrine on muscles and blood vessels

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63
Q

What does cortisol promote in liver?

A

Glucose synthesis during LT fasting and exercise

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64
Q

What does cortisol increase in adipose tissue?

A

Lipolysis

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65
Q

What cellular concentrations are maintained by cortisol?

A

Metabolic enzymes required to produce glucose and fatty acids between meals

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66
Q

What events that are associated with the inflammatory response are decreased by cortisol?

A

Capillary permeability and production of prostaglandins

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67
Q

What cycle does cortisol follow?

A

Diurnal

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68
Q

Why does cortisol work in synergy with other hormones?

A

To increase supply of energy to working muscle

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69
Q

What individuals have the highest cortisol levels?

A

Elite endurance athletes

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70
Q

What kind of response does catecholamine have to stress?

A

A fast fight or flight response or stimuli mediated by adrenaline and noradrenaline

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71
Q

4 results of catecholamine response to stress?

A
  1. Increased availability of energy (glucose and lipids) in the blood
  2. Increased heart rate, breathing rate and cell metabolism
  3. Dilation of major blood vessels and constriction of peripheral capillary
  4. Pupil dilation
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72
Q

What is the main catecholamine secreted by medulla?

A

Adrenaline

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73
Q

What is noradrenaline and what releases it?

A

A hormone and precursor of adrenaline, mainly released by adrenergic neurons of sympathetic nervous system

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74
Q

What do adrenaline and noradrenaline bind?

A

Alpha and beta-adrenergic receptors and cell membranes

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75
Q
  • 2 effects of adrenaline?
  • 5 effects of noradrenaline?
    AND RECEPTOR USED FOR THE EFFECT
A
  • Increased heart rate and blood pressure (beta 1), peripheral vasoconstriction (alpha 1)
  • 2 shown above, increased lipid breakdown (beta 2), coronary and bronchial dilation (beta 2), glycogen into glucose (beta 2)
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76
Q

What are the exocrine parts of the pancreas for?

A

Secretion of pancreatic enzymes for food digestion in duodenum

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77
Q
  • What is the endocrine part of the pancreas?
  • 5 parts and what they secrete?
A
  • Islets of langerhans
    1. Alpha cells, glucagon
    2. Beta cells, insulin
    3. Delta cells, somatostatin
    4. F cells, pancreatic polypeptide
    5. Gamma cells, ghrelin
      ALPHA= 10%, BETA = 80%
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78
Q

5 ways insulin decreases blood glucose?

A
  1. Increasing glucose uptake and storage in adipose and muscle tissues
  2. Increases glucose uptake and storage of glycogen in liver
  3. Decreases hepatic glucose production
  4. Increases amino acid uptake and protein synthesis
  5. Decreases lipolysis in adipose tissue
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79
Q

How does glucagon raise glucose levels?

A

Acts on liver to promote glycogenolysis and gluconeogenesis

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80
Q

How is glucose metabolism regulated during exercise (glucagon, adrenaline/noradrenaline, cortisol, growth hormone and insulin involved)?

A

Glucagon, adrenaline and noradrenaline- increase to promote glycogenolysis

Cortisol - increases to promote protein catabolism for later gluconeogenesis

Growth hormone - increases to increase fatty acid oxidation, lipolysis and gluconeogenesis

Insulin - decreases to lower glucose storage

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81
Q

How does diabetes disrupt glucose homeostasis?

A

Type 1 - destruction of beta cells of pancreas, no insulin secreted
Type 2 - action of insulin impaired (insulin resistance)

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82
Q

Equation for VI?

A

(Fraction of expired nitrogen x VE) / fraction of inspired nitrogen

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83
Q

Equation for inspired volume of O2 (IVO2)?

A

IVO2 = VI x (FIO2 / 100)

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84
Q

Equation for expired volume of O2 (EVO2)?

A

EVO2 = VE x (FEO2 / 100)

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85
Q

Equation for VO2 consumption?

A

IVO2 - EVO2

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86
Q

Equation for VCO2 consumption?

A

EVCO2 - IVCO2

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87
Q

Equation for RER?

A

VCO2 / VO2

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88
Q

Check sheet for how to calculate glucose and fat oxidised

A
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89
Q

4 main processes of gastrointestinal system?

A

Digestion, absorption, secretion, motility

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90
Q

6 components of gastrointestinal tract? 4 accessory organs?

A

Mouth, pharynx, oesophagus, stomach, small and large intestines
Salivary glands, yes, gallbladder, exocrine pancreas

91
Q

4 parts of gastrointestinal wall?

A

Mucosa, submucosa, muscularis externa, serosa

92
Q

Mucosa:
- What lines it and surrounds the lumen?
- 2 hormonal cells?
- What is the loose connective tissue?
- What is the layer of smooth muscle?

A
  • Epithelium
  • Endocrine cells (hormones for brain), exocrine cells (hormones for intestines)
  • Lamina propia
  • Muscularis mucosa
93
Q

Submucosa:
- What vessels penetrate layers above and below?
- What is the submucosal plexus?

A
  • Blood and lymphatic
  • Network of neurons to control muscle
94
Q

Muscularis externa:
- Role?
- How is myentric plexus innervated?
- Purpose of longitudinal muscle?

A
  • Circular muscle to narrow lumen via contraction
  • From autonomic nervous system (also connected to submucosal plexus)
  • Shortens tract when it contracts
95
Q

Serosa:
- What is it?
- Role?

A
  • Connective tissue surrounding outer surface of tract
  • Sheets of connective tissue connect it to the abdominal wall to hold GI tract in place
96
Q

What is the cephalic phase of digestion?

A

Brain anticipates food, saliva increases (parasympathetic), stimulation of gastric juice and insulin secretion

97
Q

Stage of digestion in the mouth?

A

Mechanical breakdown and mixing with saliva, chemical digestion of carbohydrates initiated using salivary amylase, antibacterial

98
Q

4 components of saliva for digestion?

A
  1. Bicarbonate = neutralises acids
  2. Mucus = lubricates + protects from abrasion
  3. Salivary amylase = CHO breakdown and starch hydrolysis
  4. Lysozyme = destroys certain bacteria to prevent tooth decay
99
Q

Role of pharynx?

A

Food to oesophagus

100
Q

Role of oesophagus?

A

Food to stomach

101
Q

Role of epiglottis?

A

Prevents food entering trachea

102
Q

Where are sphincters and what are they for?

A

Bottom of oesophagus to stop air and stomach contents entering oesophagus

103
Q

What is peristalsis?

A

Progressive muscular contraction and lumen compression to force food along to stomach

104
Q

What happens when peristalsis cannot move large food bolus?

A

Secondary peristalsis (repeated waves of compression)

105
Q

Role of stomach in digestion and 3 components?

A

Mechanical breakdown of food and mixing to form chyme
1. HCl (kill bacteria)
2. Pepsin (begins protein digestion)
3. Gastric lipase

106
Q

4 roles of small intestine in digestion?

A
  1. Chemical digestion of all nutrients using pancreatic and brush bored enzymes
  2. Absorption of water, ions, vitamins and digestive-end products
  3. Hormone secretion
  4. Secretion of bicarbonate-rich fluid
107
Q

3 roles of colon?

A
  1. Ion and water absorption
  2. Conversion of chyme to faeces
  3. Faeces storage
108
Q

Role of rectum?

A

Stores faeces

109
Q

Why does stomach have gastric pits?

A

To increase the surface area

110
Q

Role of parietal cells in stomach?

A

Have intrinsic factor for vitamin B12 absorption

111
Q

Role of chief cells in stomach?

A

Secrete inactive pepsinogen that is activated by acid

112
Q

Role of enteroendocrine cells in stomach?

A

Secrete gastrin

113
Q

Role of entero-chromaffin-like cells in stomach?

A

Release histamine

114
Q

Role of D cells in stomach?

A

Secrete somatostatin and important for H+ secretion

115
Q
  • 3 parts of HCl production?
  • What does potentiation mean?
A
    1. Enteric neurons release acetylcholine to stimulate parietal cells
      1. G cells secrete gastrin to stimulate ECL cells to produce histamine which stimulates parietal cells
      2. BUT somatostatin stops HCl production by inhibiting parietal, ECL and G cells
  • Action of 3 substances is greater than individual effects
116
Q

What is pepsinogen changed into in the stomach?

117
Q

How does the stomach mix the contents?

A

Clenches at top and bottom

118
Q

How does the stomach halt starch digestion?

A

Denatures salivary amylase

119
Q

3 things the stomach absorbs?

A

B12, alcohol and caffeine

120
Q

What increase the surface area of the intestines?

121
Q

3 things the pancreas secretes?

A

Pancreatic juice (bicarbonate), proteases and pancreatic lipase

122
Q

Role of gall bladder?

A

Storage and concentration of bile

123
Q

Enzyme and its role released from salivary glands?

A

Amylase = initial starch digestion

124
Q

3 enzymes/juices and their role released from gastric glands?

A
  1. HCl = protein denaturation, acidification of pepsin, pepsinogen activation
  2. Pepsin (secreted as pepsinogen) = initial protein digestion
  3. Gastric lipase = lipid hydrolysis in stomach
125
Q

Juice and its role released from small intestinal wall?

A

Succus entericus = dilution and lubrication

126
Q

2 juices released from gall bladder and their roles?

A
  1. Bile = chyme neutralisation
  2. Bile salts = fat emulsification
127
Q

3 enzymes/juice released from exocrine pancreas and their roles?

A
  1. Pancreatic juice = chyme neutralisation
  2. Pancreatic lipase = triaglycerol hydrolysis
  3. Proteases = protein digestion to oligopeptides and free amino acids
128
Q

2 enzymes of the brush border membrane and their roles?

A
  1. Disaccharidases = disaccharide hydrolysis
  2. Peptidases = hydrolysis of peptides to di/tripeptides
129
Q

Role of the liver in digestion?

A

Secretes bile and processes absorbed nutrients

130
Q

Bile:
- 3 components for digestion?
- 3 parts removed from blood?

A
  • Bile salts, phospholipids, HCO3-
  • Cholesterol, bile pigments, trace metals
131
Q

What transporter moves glucose from intestinal lumen into intestinal cells?

A

SGLT1 (sodium dependent)

132
Q

What transporter transports glucose from intestinal cells into the bloodstream?

133
Q

Why does fructose use GLUT5 in and GLUT2 out?

A

Allows more carbohydrate into the bloodstream as SGLT1 becomes saturated fast alone

134
Q

What does ingesting fructose and glucose allow?

A

Greater power output

135
Q

What is the incretin effect?

A

Stimulation of insulin secretion during digestion (greater than if glucose is injected)

136
Q

2 incretin hormones and what stimulates and secretes them and their roles?

A
  1. GIP = stimulated by nutrients in small intestine, secreted by K-cells in duodenum and jejenum, stimulates insulin secretion
  2. GLP-1 = stimulated by nutrients in small intestine, secreted by L-cells in ileum, promotes insulin release, inhibits glucagon release, delays gastric emptying, suppresses appetite and energy intake
137
Q

How is fat digested?

A

As lipids are insoluble in water, lipase can only act on the surface of droplets SO bile salts emulsify fats (into micelles) to increase surface area so lipase can act more greatly

138
Q

What is there between micelles and fatty acids?

A

Equilibrium

139
Q

7 steps of fat digestion?

A
  1. Emulsified
  2. Hydrolysed by lipase
  3. Temporarily stored as micelles
  4. Transported into epithelial cells
  5. Re-esterified to TAG
  6. Packaged as chylomicrons
  7. Enters lymphatic system and then general circulation
140
Q

4 steps of protein absorption?

A
  1. Pancreatic proteases and peptidases break down proteins into small peptides and amino acids
  2. These then hijack H+ and Na+ channels to enter intestinal epithelial cells
  3. Peptidases convert any small peptides into amino acids
  4. Amino acid transporters then transport the amino acids into the interstitial fluid
141
Q

How is food moved through the small intestine?

A

Through segmentation (and a bit of peristalsis) = rhythmic contraction and relaxation of longitudinal muscles to mix and move material

142
Q

What is the gastroileal reflex?

A

Segmentation increases in the ileum with gastric emptying and as most of meal is absorbed segmentation is replaced with peristalsis in small intestine

143
Q

What is the migrating myoelectric complex (MMC)?

A

Movement of undigested material into the large intestine to prevent bacteria staying in small intestine too long

144
Q

Large intestine:
- Why is fluid absorbed?
- Role of ileocecal sphincter?

A
  • To concentrate faeces
  • Opens to allow chyme through when ileum contracts, closes when large intestine distends
145
Q

Gastrin:
- Site of production?
- Stimulus for secretion?
- Receptor/site of action?
- Major function?

A
  • G cells (primarily), duodenum/colon/pancrease to lesser extent
  • Food ingestion
  • CCK2 receptor on fundic enterochromaffin-like cells + gastric parietal cells
  • Stimulates gastric acid secretion and epithelial cell proliferation + role in iron homeostasis
146
Q

Ghrelin:
- Site of production?
- Stimulus for secretion?
- Receptor/site of action?
- Major function?

A
  • P/D1 endocrine cells of oxyntic mucosa
  • Fasting or before a meal
  • Growth hormone secretagogue receptor-1a (CNS) or receptor on vagal afferents innervating stomach (PNS)
  • Orexigenic effect on appetite, stimulates gastric emptying, acid secretion, MMC, protects against gastric stress, increases growth hormone release
147
Q

Leptin:
- Site of production?
- Stimulus for secretion?
- Receptor/site of action?
- Major function?

A
  • Chief cells and endocrine P cells
  • Food ingestion, vagal nerve stimulation, CCK and secretin
  • Leptin receptor Ob-R on gastric vagal afferents
  • Anorexigenic effect on appetite, stimulates CCK and GLP-1 secretion, modulates intestinal nutrient absorption
148
Q

Somatostatin:
- Site of production?
- Stimulus for secretion?
- Receptor/site of action?
- Major function?

A
  • Enteroendocrine D cells in antral and fundic mucosa of stomach
  • Intraluminal nutrients and acid, adrenergic stimulation, CCK and gastrin
  • Somatostatin receptor on GI tract and in pancrease
  • Inhibits gastric acid secretion and endocrine + exocrine pancreatic secretion
149
Q

Secretin:
- Site of production?
- Stimulus for secretion?
- Receptor/site of action?
- Major function?

A
  • In small instestine and enteroendocrine S cells of duodenal mucosa
  • Acididc chyme from stomach, digested fat and protein
  • Secretin receptor on basolateral membrane of ductal and centroacinar cells of pancreas, epithelial cells of large intrahepatic bile duct units and in kidney
  • Stimulates alkaline secretion from pancrease and biliary ductular systems, inhibits gastric motility + acid secretion, role in osmoregulation
150
Q

GIP:
- Site of production?
- Stimulus for secretion?
- Receptor/site of action?
- Major function?

A
  • Enteroendocrine K cells of duodenum
  • Food ingestion
  • GIP receptor on endocrine pancreas
  • Incretin hormone
151
Q

CCK:
- Site of production?
- Stimulus for secretion?
- Receptor/site of action?
- Major function?

A
  • Enteroendocrine I cells of duodenum and jejunum
  • Food ingestion
  • CCK1 on vagal afferents, stomach, small intestine, pancreas and gall bladder
  • Reduces feeding, inhibits gastric emptying + acid secretion, stimulates gall bladder contraction and pancreatic digestive enzyme secretion
152
Q

Motilin:
- Site of production?
- Stimulus for secretion?
- Receptor/site of action?
- Major function?

A
  • Enteroendorcine M cells of small intestine
  • Interdigestive fasting period
  • Motilin receptor on nerves and muscle of GI tract
  • Induces phase III contraction of MMC
153
Q

PYY:
- Site of production?
- Stimulus for secretion?
- Receptor/site of action?
- Major function?

A
  • Enteroendocrine M cells of small intestine
  • Food ingestion
  • Y receptor subtypes long GI tract, in pancreas and the CNS
  • Reduces food intake, inhibits gastric emptying and secretion, suppresses intestinal motility and electrolyte secretion and inhibits pancreatic secretion
154
Q

GLP-1:
- Site of production?
- Stimulus for secretion?
- Receptor/site of action?
- Major function?

A
  • Enteroendocrine L cells of jejunum, ileum and colon
  • Food ingestion and bile acids acting on TGR5
  • GLP-1 receptor
  • Incretin hormone, inhibits glucagon secretion
155
Q

GLP-2:
- Site of production?
- Stimulus for secretion?
- Receptor/site of action?
- Major function?

A
  • Enteroendocrine L cells of jejenum, ileum and colon
  • Co-secreted with GLP-1 in response to nutrient ingestion
  • GLP-2 receptor
  • Stimulates cell growth in gut mucosa and stops apoptosis, inhibits gastric emptying and acid secretion, enhances intestinal nutrient absorption and blood flow
156
Q

OXM:
- Site of production?
- Stimulus for secretion?
- Receptor/site of action?
- Major function?

A
  • Enteroendocrine L cells of jejenum, ileum and colon
  • Food ingestion
  • GLP-1 and glucagon recptors
  • Reduces food intake, reduces gastric acid and exocrine pancreatic secretion, potentiates glucose-stimulated insulin secretion
157
Q

FGF19:
- Site of production?
- Stimulus for secretion?
- Receptor/site of action?
- Major function?

A
  • Ileal enterocytes
  • Bile acids acting on FXR
  • Heteromeric receptor in liver
  • Suppresses bile acid synthesis, stimulates hepatic protein synthesis and glycogenesis, suppresses gluconeogenesis
158
Q

What is CICO?

A

Calories in, calories out

159
Q

What is a calorie?

A

The energy required to raise 1g of water by 1 degrees celsius

160
Q

What are calories in?

A

Macronutrients we derive our energy from (protein, fat, carbs, alcohol)

161
Q

What are calories out?

A

Energy expenditure = resting metabolic rate, diet induced thermogenesis (or TEF or SDA), physical activity energy expenditure

162
Q

What is diet induced thermogenesis?

A

Energy used for food processing (8-10% energy)

163
Q

What are nutrients?

A

Any chemical substance the body needs to sustain life (water is most important at first if deprived of all nutrients)

164
Q
  • What is digested?
  • What is absorbed and transported?
  • What is stored?
A
  • Protein, carbs, fat
  • Amino acids, sugars, fatty acids
  • Protein, glycogen, triglcerides
165
Q

Relationship between amino acids and sugars?

A

Can be interconverted

166
Q

Relationship between sugars and fatty acids?

A

Sugars can be converted into fatty acids (BUT NOT BACK)

167
Q

RQ for macronutrients?

A

Protein = 0.8, fat = 0.7, carbs = 1.0

168
Q

What is ghrelin?

A

Orexigenic hormone for appetite (makes you eat more) that can be acylated (active, episodic) or deacylated (inactive, stable) – gradual response to fasting that is stimulated by glucagon and noradrenaline

169
Q

What rapidly inhibits ghrelin?

170
Q

Hormones the pancreas releases to impact blood glucose?

A

Insulin, amylin and pancreatic polypeptide

171
Q

What hormone does the duodenum/jejunum release and why?

A

Cholecystokinin (CCK) – rapid response during feeding, sensitive to organ stretch, protein and fat, makes us feel full

172
Q

Hormones released by large/small intestines?

A
  1. Peptide tyrosin(e) - delayed response (15-120 mins after food), limits refeeding
  2. Oxyntomodulin
  3. Glucagon-like peptide-1 - incretin hormone, stimulates insulin secretion
173
Q

Why is the energy available from food not equal to the energy absorbed?

A

Some energy not accessible or passes through

174
Q

Why do carbohydrate reserves go up and down every day?

A

Act as a regulator of appetite and affected by food intake

175
Q

Characteristics of fat reserves?

A

Larger and impact appetite less

176
Q

2 adipokines?

A
  1. Adiponectin = increases with health, regulates glucose levels and lipid metabolism
  2. Leptin = higher when obese, delayed/tonic response, helps maintain weight
177
Q

3 components of energy expenditure?

A
  1. Basal metabolic rate
  2. Dietary induced thermogenesis/thermic effect of food
  3. Physical activity
178
Q

What does body mass dictate?

A

Basal metabolic rate (higher mass = higher BMR)

179
Q

How to measure metabolic rate?

A

Direct calorimetry - chamber with controlled air entry and a water jacket
(total heat loss is equal to rate of energy utilisation when body temperature is constant)

180
Q

How does direct calorimetry work?

A

Water and air leaving has a temperature directly proportional to the energy used

181
Q

4 limitations of direct calorimetry?

A
  1. Cannot monitor rapid changes (not all the heat produced during exercise is immediately liberated)
  2. Only good at rest (limits responses)
  3. Any exercise would generate friction (produces heat)
  4. Cannot determine which fuel is used
182
Q

What is the alternative for direct calorimetry?

A

Indirect calorimetry (uses gas exchange e.g. Douglas Bag/ventilated hood)

183
Q
  • How can BMR be predicted?
  • Disadvantage?
A
  • Using age, weight and height in the Schofield/Harris-Benedict equations
  • Does not take body composition into account
184
Q
  • What is an advantage of indirect calorimetry?
  • Consideration?
A
  • Can measure physical activity
  • Temporal
185
Q

What is steady state?

A

When oxygen uptake is constant during exercise

186
Q
  • What is room/whole body calorimetry?
  • Limitation?
A
  • Type of indirect calorimetry that monitors gas exchange over 24+ hour time frames
  • Cannot take representative behaviours into account
187
Q
  • How can energy expenditure be measured in free living conditions?
  • Limitations?
A
  • Portable indirect calorimetry
  • Very expensive, inconvenient, alters behavious, cannot be worn for extended time periods
188
Q

What is doubly-labelled water and how is it used?

A
  • Use of heavy isotopes of H (2H) and O (18O) and the difference in the rate of loss is used to calculate CO2 production
189
Q

Why is 18O lost quicker than 2H?

A

Lost in CO2 and H2O

190
Q

4 limitations of doubly-labelled water?

A
  1. High cost of equipment + specialised staff
  2. Assumes RER/RQ is 0.8 or 0.85
  3. No information on components of energy expenditure
  4. No information on pattern/intensity
191
Q

Activity diaries and recall questionnaires for assessment of physical activity energy expenditure:
- What is used?
- How is energy expenditure found?
- Advantage?
- Limitations?

A
  • Activity score or MET value (1 MET = BMR) and is a compendium of physical activities
  • Multiplication of METs by time
  • Increases comparability of results
  • Little inforomation, laborious, subjective, easy for individuals to not write everything down
192
Q

Pedometers and accelerometry:
- Advantages?
- Disadvantages?

A
  • Removes subjective/self-reported element, predicts energy expenditure well during ambulatory activities (walking, running)
  • Overlooks activities like cycling
193
Q

Heart rate monitor:
- What is it based on?
- Advantage?
- Disadvantage?

A
  • Linear relationship between HR and energy expenditure
  • Captures activites accelerometry misses
  • Influenced by stress
194
Q

How do multi-sensor physical activity monitors work?

A

Combines inputs to find energy expenditure

195
Q

Why is actiheart good?

A

Combines heart rate and accelerometry to be more precise

196
Q

4 ways of measuring body composition?

A
  1. BMI
  2. MRI
  3. Hip-waist ratio
  4. Underwater weighing
197
Q

What does an oral glucose tolerance test show?

A

If vigorous exercise occurs everyday, overfeeding will not change body mass

198
Q

Equation for RER?

199
Q

What does exercise maintain?

A

Healthy adipose gene expression (even during adipose expansion)

200
Q

What is de novo lipogenesis?

A

Endogenous pathway that converts excess dietary starch, sugar, protein and alcohol into specific fatty acids

201
Q

How does long-term inactivity affect blood sugar levels?

A

Increases them even if food intake is reduced to avoid weight gain

202
Q

When VO2max increase?

A

With training (increases linearly with intense training) – standardised endurance training can be heritable

203
Q

Why is capillary density 2-3 times greater in trained athletes?

A

To increase blood flow to the muscle

204
Q

How do mitochondria adapt to changes in exercise?

A

Increases and decreases in training change it drastically (e.g. 1 week off will decrease mitochondrial ability until training resumes and they increase over time)

205
Q

What do mitochondria adapt in accordance to?

A

Exercise volume (mostly intensity though)

206
Q

Why are mitochondria essential for skeletal muscle fat oxidation?

A

Surround fat and the lipid droplets from the fat enter the mitochondria and are oxidised

207
Q

Why is increased capacity for fat oxidation good?

A

Can spare glycogen stores

208
Q

What do steroids increase?

A

Muscle cell width and myonuclei

209
Q

Why is the impact of steroids still seen even if they aren’t being taken anymore?

A

The individual will still have higher increases of myonuclei and muscle cell width during training than unexposed individuals

210
Q

What does ketone monoester ingestion increase?

A

Post-exercise erythropoietin concentrations in healthy men (increases haemoglobin mass which increases O2)

211
Q

How does SNPs affect drug efficacy?

A

Decrease it

212
Q

Sickle cell disease:
- What is it?
- Symptoms?
- What causes it?

A
  • Inherited blood disease with abnormal haemoglobin structure
  • Pain, anaemia, swelling
  • SNP whereby glutamate is substituted for valine to create 2 abnormal copies of beta-globin gene
213
Q

How can sickle cell disease be beneficial?

A

Can help in defence against malaria as porous membrane of sickle cells will leak the nutrients the parasites need –> faulty cells are eliminated and parasite will be destroyed at the same time

214
Q

Sports performance is composed of genetic and environmental factors, how does genetics contribute?

A
  1. Hereditary factor
  2. Trainability is never a product of a single gene
  3. Genetic predisposition
215
Q

Gene for sprinting?

A

Alpha actinin 3 = role is fast-muscle fibre function

216
Q

Gene for mountaineering and endurance?

A

Angiotensin converting enzyme (ACE)

217
Q

Gene for marathon running?

A

Peroxisome proliferator-activated receptor delta

218
Q

Gene for cycling?

A

Muscle-specific creatine kinase = improves VO2max

219
Q

Gene for weight-lifting?

A

Myostatin = without it there is large muscle development

220
Q

Alpha-actinin 3:
- What is it known as?
- Major structural component of?
- Where is it expressed?
- Why do 16% of population have a deficiency?

A
  • Speed gene
  • Z line
  • Type 2 fibres (responsible for forceful contraction at high velocity)
  • Common polymorphism where 577th amino acid is converted to STOP
221
Q

What does myostatin do?

A

Inhibits muscle cell growth (so without it reduced body fat and increased muscle size is a result)

222
Q

Why is gene doping inhibited?

A

It is impossible to detect

Biomed (9 decks)

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