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Exercise Science and Health > Exam 2 > Flashcards

Exam 2 Flashcards

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1
Q

Why is blood glucose control important?

A

short term problems of uncontrolled blood sugar levels: hypoglycemia, hyperglycemia, diabetic ketoacidosis

longterm problems: damage to the vessels of heart, kidneys, eyes, and nerves

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2
Q

What is the negative effect of too little blood glucose?

A

Hypoglycemia (glucose level below 70); occurs when someone eats too little food, takes too much insulin/diabetes medication or is more physically active that usual

can happen suddenly, or without any warning

Shaking, fast heartbeat, sweating, dizziness, anxiousness, hunger, vision problems are some symptoms

diabetics should always carry a quick acting source of sugar in case they take too much insulin/become hypoglycemic

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3
Q

What is the negative effect of too much blood glucose

A

Hyperglycemia (glucose levels above 180); occurs when there’s not enough insulin in the body, if you miss taking diabetic medication, eat too much, or don’t get enough exercise

Diabetics are at risk if their diet and activity level is not balanced with food intake

Extreme thirts, frequent urination, dry skin, hunger, blurred vision, dorwsiness, slow healing wounds

stress can increase blood glucose

can result in ketoacidosis (diabetic coma)

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4
Q

WHen blood glucose increases does insulin increase or decrease?

A

insulin increases when blood sugar is high because the pancreas releases insulin to help cells absorb glucose from the bloodstream to lower blood sugar levels (in healthy, non-diabetics).

In diabetics, insulin injections are needed to absorb the glucose.

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5
Q

What happens to fat uptake in adipose tissue when insulin increases?

A

there is an increase in fat uptake because the insulin brings sugar out of the bloodstream and into the cells for storage

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6
Q

What happens to fat uptake in adipose tissue when insulin decreases?

A

there is a decrease in fat uptake because insulin isn’t active and the body will soon start releasing fats as spare blood glucose to get energy to the organs FAST

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7
Q

What happens to fat release when insulin decreases?

A

fat is released when insulin decreases because the body doesn’t have enough energy to function; fight or flight response with increased epinephrine occurs to process glucose QUICKLY

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8
Q

What happens to fat release when insulin increases?

A

fat is stored when insulin increases because there’s enough glucose to fulfill the body’s energy requirement

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9
Q

What happens to protein synthesis when blood insulin is high?

A

High Insulin = High Protein Synthesis

because energy is readily available through glucose, we dont’t need to resort to FFA release

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10
Q

What happens to protein synthesis when blood insulin is low?

A

Low insulin = High Protein Breakdown

because FFA help with created ATP through glucagon and epinephrine

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11
Q

When does gluconeogenesis occur?

A

Low blood glucose = gluconeogenesis

occcurs in the liver: synthesized from pyruvate, lactacte, glycerol (non-carb substrates)

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12
Q

Where is glycogen stored?

A

liver and muscle celss

glycogen is the storage form of glucose

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13
Q

When does glycogenolysis occur?

A

Converting glycogen into glucose

it occurs in the liver and muscle cells in response to hormonal and neural signals (stimulated by epinephrine and is regulated hormonally by glucagon and insulin)

occurs during periods of fasting and in skeletal muscle during active exercise

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14
Q

What is the effect of epinephrine on blood glucose? on adipose tissue fat release/uptake?

A
  • Epinephrine breaks down glycogen into glucose quickly
  • increases liver output for blood glucose
  • increases the release of fat from fat stores (spare blood glucose)
  • process when glucose is needed QUICKLY
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15
Q

Type I vs Type II diabetes

Type of Disorder

A

Type I: autoimmune disorder

Type II: Metabolic disorder

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16
Q

Type I vs Type II diabetes

Insulin level

A

Type I: Hypoinsulinemia

Type II: Hyperinsulinemia

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17
Q

Type I vs Type II diabetes

Age of Onset

A

Type I: predominantly in youth

Type II: predominantly after age 40

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18
Q

Type I vs Type II diabetes

Genetic Component

A

Type I: weak

Type II: strong

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19
Q

Type I vs Type II diabetes

Proportion of diabetes patients

A

Type I: 5-10%

Type II: 90-95%

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20
Q

Type I vs Type II diabetes

Insulin depndence

A

Type I: permanent

Type II: permanent only in subset of patients

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21
Q

Type I vs Type II diabetes

Insulin Resistance

A

Type I: low

Type II: High

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22
Q

Type I vs Type II diabetes

Onset

A

Type I: acute and potentially severe

Type II: Mostly mild, insidious

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23
Q

Type I vs Type II diabetes

Other

A

Type I: Often normal body weight (or thin/wasted)

Type II: frequently linked to obesity

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24
Q

What happens to the cells responsible for releasing insulin in type I diabetics?

A

pacreatic beta cells (responsible for releasing insulin) are mistakenly recognized as ‘foreign; by the immune system and are selectively destroyed

these beta cells are erased from the body, and circulating insulin levels in the blood dramatically decrease or disappear.

Insulin injections are necessary to stay alive

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25
Q

What happens to insulin levels in type II diabetics?

A

levels are normal, high or decreased (elevated most common)

Insulin is produced, but not used effectively

Either the pacreatic Bcells dysfunction (gradually fail to adequately produce insulin in response to circulating levls of glucose in the blood) or insulin resistance in which insulin-sensitive tissues become desensitized to insulin

Treatment: diet, exercise, and oral medication

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26
Q

Why are type II diabetics obese while type I are normal or wasted?

A

Type II: glucose can’t be utilized because of insulin insensitivity, so glucose is stored as fat

Type I: No insulin, so proteins are used as fuel via the breakdown of adipose tissue

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27
Q

How does diet and exercise effect Type I diabetes?

A

exercise helps improve insulin insensitivity, so not as much insulin would be needed to conteract eating CHO.

Exercise can also help avoid long term complications. Type I do not need to diet as much because they arent usually obese, but they need to strictly contol blood glucose levels and monitor levels often and specific times

Meals should be consistent and insulin doese need to match food intake

Be careful with prolonged exercise: risk of hypoglycemia

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28
Q

How do diet and exercise effect Type II diabetes?

A

Dieting may help decrease and control weight, which may improve insulin insensitivity

Exercise increases insulin sensitivity (via Glut 4)

Should increase fiber (move stuff through faster) and increase water uptake

They should also avoid table sugar and salt

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29
Q

IDDM

A

insulin dependent diabetes mellitus: Type I Diabetes

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30
Q

NIDDM

A

non-insulin dependent diabetes mellitus: Type II Diabetes

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31
Q

Gestational Diabetes

A

develops during the 2nd or 3rd trimester and disappears after delivery

treatment focuses on diet, but sometimes in severe cases insulin injections are used

Can be problemattic for the baby (gestational diabetes can increase the baby’s chance for type I and mom’s chance for type II by 35-60%)

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32
Q

Mechanisms/Process of Insulin resistance

A

Environmental Factors (physical activity, diet, obesity, etc) and genetic factors (family history, ethnic backgrounds, various genes) lead to insulin resistance, which leads to hyperglycemia and hyperinsulemia which then results in impaired beta cell function, finally causing type 2 diabetes

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33
Q

How is glucose transported?

A

after you eat, insulin increases which stimulates various glucose transporters.

Insulin causes glut 4 to move fom inside the cell to the membrane to increase transport

Type 1: do not have insulin from pancreas to bring the glucose into the cell
Type 2: desensitized insulin; glucose won’t enter the cell

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34
Q

What does glut4 do?

A

Glut 4 moves from the central region of the cell out to the membrane during contraction and becomes a pathway for insulin reception

It’s stimulated by muscle contraction (post exercise to replenish CHO stores)

Glut 4 becomes active and bring sugar into the cell…may become hypoglycemis during exercise due to depleted CHO stores

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35
Q

What does insulin do?

A

only hormone to decrease blood glucose

when blood glucose increases insulin levels oncrease (beta-cells are directly sensitive to glucose)

This increases uptake, use and storage of glucose and increases glycogenesis in the liver, increases synthesis of FFA, decreases release of FFA from adipose tissue, and increases protein synthesis

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36
Q

What does glucagon do?

A

secreted by pancreas: works opposite to insulin

If we’re low on blood sugar, the body has a fight or flight response so we can burn glucagon and epinephrine to burn protein thus creating ATP for us

decrease in blood glucose decreases insulin release which increases glycogenolysis and increases gluconeogenesis

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37
Q

Primary Prevention of Diabetes

A

Moderate exercise intensity and a good diet

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38
Q

Secondary Treatment of Diabetes

A

oral glucose tolerance tests; trying to figure out if you are a diabetic; support hosin and circulation for lower limbs to turn over blood flow; trying to avoid insulin injections with diet and exercise

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39
Q

Tertiary Care of diabetes

A

knowing that you are a diabetic; delay onset of more symptoms in terms of well balanced diets and increasing circulation

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40
Q

Common treatments on diabetes

A

If insulin is destroyed in the GI tract it must be injected…3 types

  • Rapid, intermediate, and long lasting
  • depends on eating habits
  • continuous subcutaneous infusion which frequently checks blood glucose and avoids pump failure

Oral sulfonyluteas: stimulate release of inuslin from pancreas, increase insulin sensitibity, Only used in NIDDM (need active beta cells)

Type II can take supplements: orlastat

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41
Q

Exercise recommendations for diabetics

A

exercise can increase CV fitness, increase psychological well-being, decrease body fat (better weight control) and increase insulin sensitivity; always should wear something stating their diabetic
Type I: be careful with prolonged exercise, do not take insulin immediately before exercise (blood sugar levels can get too low)
Type II: will have a fair amount of fatigue at the beginning because the improvements of insulin sensitivity will not occur right away; exercise can help or prevent or delay the onset of type II (5-7 days/week at a moderate intensity is best)

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42
Q

Contraindications to Exercise in Diabetics

A

Type I: could become hypoglycemic (injected insulin doesn’t decrease, too much glucose uptake) could occur hours after exercise stopped. The liver/muscles are more sensitive during and immediately post exercise which means increased glucose uptake to replenish glycogen stores. Vigorous exercise could be harmful (eye hemmorrhage). 150 min/week of moderate intensity is most beneficial

Type II: risk factors associated with obesity

43
Q

Fasting blood glucose levels

A

Normal: 70-100 mg/dl
Diabetic: >180 mg/dl

44
Q

OGTT: Oral glucose load, blood glucose, and urine sample every 15-30 mins

A

Normal will recover within 2 hours

Diabetics/glucose intolerance: high levels

45
Q

Glycosylated hemoglobin

A

%glycosylated (glucose attached) = 4-6%

Diabetics can be 11-15%

46
Q

Urine tests

A

not as accurate

influences by fluid intake/urine concentration

47
Q

Non Specific Response of the Immune System

A
  • Inflammation
  • Redness, swelling, heat, and pain
  • Cells release chemical signals (histamine) that increase capillary blood flow (swelling) and draw WBCs to the scene
  • Neutrophils: first cells to arrive, destroy foreign cells by phagocytocis
  • Monocytes (macrophages): 2nd to arrive, phagocytosis and clean up cells and debris
  • Natural killer cells: lyse foreign cell membrane
48
Q

Immune Responses to Exercise: Leukocytes

A
  • rapid increase WBC
  • increase neutrophils, monocytes
  • direct relation to ex intensity/duration
  • duration most important factor
49
Q

Immune Responses to Exercise:

Window of Opportunity

A

after exercise certain cell types rapidly decrease which could supress the immune system

50
Q

Innate Immunity

A

Nonspecific
Recognize non-self without prior exposure

  • Neutrophils
  • monocytes
  • Natural Killer cells
  • Complement System: a way that innate and acquired systems work together
51
Q

Acquired Immunity

A 
Specificity to infectous agent
Memory of Prior Exposure
-T Cells
-B Cells
-Complement System: innate and acquired work together
52
Q

T Cells

A

arrive to help “learn”
create T memory cells
T killer cells act on pathogen

53
Q

What do T helper cells do

A

activate antibody response of B-cells which are dormant until activated

Bcells enlarge into lymphoblasts when contacted by Tcells: lymphoblasts form plasmablasts: plasmablasts divide rapidly into plasma cells: each plasma cell creates 2000 antibodies per second

54
Q

Roles of granular leukocytes and their function in the immune system

A

Granular leukocytes (Ben and Phyllis are GRANdparents)

  • neutrophils: 60-70% total WBC, enzymes which destroy.degrade bacteria, 1st cells to arrive at the site, phagocytic for microphages (bacterial infections) their life span is short, <10 hours after release
  • eosinophils: 1-3% total WBC, help with allergic reactions/parasitic infection
  • basophils: 0.3-0.5% of WBC; contain heparin/histamine, involved in allergic/stress responses
55
Q

Roles of nongranular leukocytes and their function in the immune response

A

Nongranular leukocytes: monocytes/macrophages and lymphocytes

  • Monocytes: 2nd cells to arrive at the scene; largest of the WBC, accounts for 3-8% of the total WBC; life span is three times larger than granulocytes. They are phagocytic for macrophages
  • Lymphocytes: consists of B cells, T cells, and Natural Killer Cells. Makes up 20-30% of total WBC
56
Q

Where do B and T cells mature and then marticulate and concentrate?

A
  • lymph organs: bone marrow (produces all WBC) and lymph nodes (concentrated lymphocytes and macrophages along the lymphatic venis)
  • B cells: made, mature, and are stored in the bone marrow and lymph tissue and wait for activation
  • T cells: made in bone marrow and mature in the thymus glanf. Then take residence in the lymphoid tissue waiting for activation
  • Helper T Cells: major regulator of immune function; secrete lymphokines (protein mediators)
  • Killer T Cells: rough and ouch that kill anything that gets in their way
  • Supressor T Cells: slow everything down
57
Q

Complement System

A

group of proteins which become active when antigen is present they bind to bacteria (they open pores in bacteria membrane, fluids and salt moves into the bacteria cell, bacteria cells burst and swell)/ The complement system tags (coats) the outer surface of invaders for attack by phagocytes. Same response for innate and acquired.

58
Q

How does the immune system attack a foreign pathogen?

A
  • Non-specific Response
  • Specific Defenses: have memory of prior attacks. Cell mediated response if from the T Cells….then b cells give the antibody-mediated response. T and B cells respond simultaneously
59
Q

Antibody formation

A

prior to activation, B cells are dormant. Contact with a specific antigen causes B cells to enlarge (they become lymphoblasts).

Some lymphoblasts become plasmablasts which divide rapidly (4 days = 500 plasma cells).

These plasma cells produce antibodies (2000 antibodies/second) the lymphoblasts that don’t become plasmablasts form new B-cells. These are memory cells which become dormant.

So when a second exposure to the pathogen occurs, the response is much faster.

60
Q

3 classes of antibodies

A

3 classes of antibodies:
• IgG: main antibody in blood stream
• IgA: found in external secretions
• IgE: create allergic symptoms (lactose intolerance)

61
Q

Cell mediated immunity

A

T cells respond to antigen, similar to Bcell response, only there are no antibodies…instead there are a lot of new T cells. T memory cells are also formed

  • Helper T Cells: major regulator of immune function
  • Killer T Cells: rough and touch that kill anything that get in their way
  • SUpressor T cells: slow everything down
62
Q

Intensity of Exercise and Immune Response

A
  • Leukocytosis: increases white blood cells rapidly, increases neutrophils and monocytes. Directly related to exercise intensity/duration. Indirect relation to fitness level. Duration is the most important factor (number stays increased for several hours after prolonged exercise). Brief exercise has a smaller increase than endurance exercise does. All T cell concentrations increase, but suppressor cells increase more than helper t cells. B cells increase dramatically, but decrease rapidly. Natural killers increase 50-300% (which could burn up the disease before you even feel it)
  • T response is suppressed by prolonged exercise. Returns to baseline 2 hours after exercise. Brief exercise (less than an hour) has no effect on T cells. Untrained vs trained have no response on T cells. This T cell response takes time; it’s just a cellular type of immunity.
  • B cells take training and development; T cells don’t.
  • Fatigue: more susceptible to disease
  • Athletes: more susceptible during intense training and major competition
  • Regular activity: less susceptibility to certain illness (common colds)
  • Dual effect: intense training increases susceptibility, moderate training decreases susceptibility
  • Natural killer cell activity increases (cytotoxic activity increases) with intense/prolonged endurance activities
  • Neutrophil function increases with moderate exercise and decreases with intense exercise
  • Lymphocyte response: no significant difference with exercise.
63
Q

Window of Susceptibility after prolonged intense exercise

A
  • Athletes are at higher rates of some illnesses (infectious mononucleosis, upper respiratory illnesses). Overtraining causes more illness/fatigue. Athletes are more likely to perceive illness and seek medical attention to improve performance.
  • With prolonged aerobic exercise (>2 hours), there’s a brief change in immunity. Lymphocyte, neutrophil and natural killer cell functions all decrease.
  • Study done said marathon participants are 5 times more likely to contract URI than similarly trained who didn’t compete….infectious illness increases with training volume and after major competition.
64
Q

Mechanisms for development of cancer

A

-cancer is caused when abnormal cells divide rapidly due to a mutation in the DNA of the cell that is caused by a number of different factors (illness/disease, genetic mutation, irregular immune response, radiation)

increased risk for developing cancer with physical inactivity

65
Q

Malignant Cells

A

capable of spreading beyond the site of origin. They divide much more rapidly than they should; produce tumors

66
Q

why are tumors dangerous

A

tumors put pressure on nearby tissues/organs

Sometimes they invade tissues and organs directly and make invaded tissues susceptible to infection

Tumors also release substances that destroy tissues in close proximity

67
Q

Metastasis

A

the spreading of cancer cells from one organ or tissue to another.

Usually spread through the bloodstream or lymph system

Most common metastic sites: brain, bone, liver, lungs

68
Q

Causes of Cancer

A

Genetic Contribution (5-10% of all causes) and is much lower than the obesity genetic connection

Carcinogens can usually be avoided:
-arsenic asbestos, nickel
-formaldehyde
-alcohol
0tobacco
-sunlight
-lead, PBA, bacon
69
Q

Arsenic, asbestos, and nickel lead to

A

Lung cancer

asbestos embeds itself in the tissue and permanently stays there

70
Q

Formaldehyde can cause

A

nasal and nasopharyngeal cancer

71
Q

Alcohol can cause

A

oral, esophageal, and opharyngeal cancer

72
Q

Tobacco can cause

A

lung cancer, head/neck cancer, esophageal cancer, and bladder cancer

73
Q

Sunlight (UV radiation) can cause

A

skin cancer

74
Q

Most common cancer in males

A

prostate cancer

75
Q

most common cancer in females

A

breast cancer

76
Q

What cancer is the most deadly?

A

Lung Cancer

also 2nd most prevalent

77
Q

What are preventative measures/early detection recommendations for cancer?

A

Colon and rectal cancer: PA increasing speed of digestion; high fiber diet;
colonoscopy after age 40

Breast Cancer: regular self-breast exam beginning after puberty and annual mammogram beginning @ 40; blood hormone profile and PA to help balance abnormalities

Prostate Cancer: Prostate exam each year after 40 years old; earlier if a family history

78
Q

How does exercise provide protective mechanisms to cancer?

A

PA enhances innate immune system so it is easier for our bodies to fight infections

Increases ventilation and perfusion of lung tissue

Obesity makes people resistant to insulin high levels of insulin are associated with cancer

79
Q

How does exercise provide protective mechanisms against against colon cancer?

A

Speeds up transit time in colon (gravitational pull)

Colon cancer develops over several decades (usually late 50s)

abnormal tissue in colon can cause polyps

Possible carcinogens are chemical preservatives, substances found in our food

Occupational PA can decrease the risk of colon cancer by 25-50%

80
Q

Survival Rate of Colon Cancer

A

5 yr: 90%
After Metastasis: 5 yr: 65%

8% of time it spreads to lungs/liver

81
Q

survival rate of breast cancer

A

1 in 8 women will have breast cancer…1 in 28 will die

5 year survival rate: 97% (catching it early yields a high percentage rate because it is a slow spreading cancer)

After Metastasis: 5 year survival rate is 21-77%

10% is hereditary

50-60% of women with inherited mutations will develop breast cancer by 70

82
Q

When is the incidence rate of breast cancer increasing

A

from childbearing age to menopause

  • estrogen levels (estradiol) are higher in concentration so breast tissue is greatly affected during these years
  • birth control possibly increases risk as well
  • breast cell division begins at menarch and ends at meopause; altered by physical activity
83
Q

Estradiol and Breast Cancer

A

Estradiol is an endogenous hormone

Imbalance between estrogen and progesterone stimulates cell proliferation

84
Q

What increases the risk of breast cancer?

A

Excessive Exposure associated with breast cancer:

  • menarche before age 12
  • Nulliparity (no kids)
  • Menopause after 55 (<45 half the risk)
  • Oral contraceptives increases risk slightly
  • Long term hormone replacement therapy (10+ years)
  • irregular menstrual cycles deceases risk by 50%
85
Q

Risk factors associated with breast cancer

A
  • leading cause of death in women between 15-54 yrs of age
  • family history (1st degree relative doubles risk)
  • high socioeconomic status: children at a later age, fewer childern or hormone replacement therapy increases risk
  • obesity as a child or high fat diets increase risk
86
Q

PA and breast cancer

A

Like Prostate cancer: breast cancer has a strong connection with PA

  • Occupational active jobs decrease risk by 30-40%
  • leisure activity decrease risk 12-60%
  • physical activity can modulate the production, metabolism, and excreting of sex hormones

Exercise increases immunity, decreases lifetime ovulatory cycles, exercise decreases obesity

Decreased ovarian production of estrogen, reduced in fat produced estrogen and increase in sex hormone binding glouline that render estrogen inactivity

87
Q

Exercise recommendations for those individuals in cancer treatment or post treatment

A

-exercise during cancer will increase physical function, psychological function and could decrease risk of reoccurance

once cancer is in remission exercise needs to be long term

88
Q

Motives and barriers for exercise during cacner treatment

A

Motives: maintain a normal lifestyle, cope with treatments, gain control over cancer and life, cope with stress, get mind off of treatment, feel better/improce well being, imporve immune function, improve energy level

Barriers: feeling sick, fatigue/tiredness, nausea/vomiting, lack of time, pain/soreness, chemotherapy, diarrhea

89
Q

Motives and barriers for exercise during cancer survivorship

A

Motives: Recover from treatments, reduce risk of recurrence, improve strength and fitness, increase energy, relieve stress, control/lose weight, improve self-esteem, improve cardiovascular health,, feel better/improve well being

Barriers: lack of time, lack of energy, deconditioned, poor health, poor weather, lack of motivation, arthritis, lack of facilites, cancer reoccurence

90
Q

Primary Amenorrhea

A

When menarche has not occured by age 16 or absence of sexual development by age 15 (anorexia nervosa or extreme training)

Primary age of menarche is 12.4

91
Q

Secondary amenorrhea

A

occurs in females who previously had regular menstrual cycles, but not have absence of 3 to 6 consecutive cycles

Leaner individuals have a greater risk for amenorrhea; if they;re not lean, they have a decreased risk. If they’re not having formalized intense training, they have an even smaller chance of amenorrhea

92
Q

Oligomenorrhea

A

less than 10 menstrual cycles per year

cycles are more than 35 days apart

93
Q

Prevalence of amenorrhea in Atheletes Vs Nonathletes

A

Nonathletes: 1-5%
Athlletes: 20-25% greater

94
Q

prevalence of amenorrhea in weight bearing vs non weight bearing activity

A

Weight Bearing: 60%
Non weight bearing: 18%

Higher in weight bearing sports because the athletes need to be lighter on their feet, so leaner, lighter body mass is ideal

part of the issue is nutrient availability is generally compromised in all athletes due to training and attempting to maintain caloric balance; however this is even more pronounced in weight bearing athletes due to trying to maintain optimal performance body mass

95
Q

Follicular phase of the menstrual cycle

A

begins to develop in ovary at the cessation of menstrual flow (restarts system)

FSHO and LH help with follicle maturation and Follicles secrete estrogen

Estrogen stimulates gonadotropin releasing hormone (GnRH) which later stimulates LH (regeneration of estrogen).

Estrogen causes build up of endometrial tissue in uterus

Days 1-13

Body temp 36C

96
Q

Ovulation phase of menstrual cycle

A

Midpoint of cycle: Days 13-15

mature follicle ruptures and releases ovum.

Ovum then travels from ovary to fallopian tube to uterus. There’s a rush in LH.

Time when pregnancy is most likely to occur

Body temp increases to 37C

97
Q

Luteal phase of menstrual cycle

A

remaining follicle becomes corpus luteum

LH causes corpus luteum to grow

estrogen and progesterone are secreted

Progesterone stimulates glands (negative feedback)

Decreased gonadotropin

Days 15-28

98
Q

What could possibly happen when luteal phase is shortened?

A

Higher risk or chance of amenorrhea (decreased risk in gonadotropins)

99
Q

Menstruation

A

begins with day one of menses (egg/ovum is not fertilized)

Corpus luteum atrophies (cell dies)

Estrogen and progesterone decrease (feeding something that doesn’t need nourishment)

Endometrium is shed along with blood (No more negative feedback)

Starts 12 days after luteal phase

Days 1-7

100
Q

How long is a normal menstrual cycle?

A

usually 28 days (SD=7)

101
Q

Low energy availability leads to menstrual dysfunction…How

A

low energy availability means physiological and neuroendocrine response (changes in leptin, cortisol, insulin, growth hormone, IGF-I, T3, glucose, fatty acids, ketones, etc)

Produces a negative or inhibitory input to the hypothalamus

Hypothalamus does not release GnRH to the pituitary gland which doesn;t produce the surge in LH or FSH to the ovaries.

Due to these abnormal responses, the ovaries do not produce progesterone or estrogen, so the end result is abnormal menses

102
Q

Exercise stress hypothesis of amenorrhea

A

Stress activates hypothalamic-pituitary-adernal axis which causes the adrenal gland to release cortisol

Chronically elevated cortisol levels may suppress the release of GnRH from the hypothalamus

GnRH is the same as LHRH and is responsible for FSH and LH release from the anterior pituitary. Suppression of GnRH suppresses LH and FSH which decreases the release of estrogen and progesterone. The only effect of exercise is on energy availability.

Disproven because exercise has no effect of LH Pulsality (LH is normally released in discrete pulses normally)

103
Q

Body composition hypothesis of menstrual dysfunction

A

Menarche occurs with more than 22% body fat and is lost with 17% body fat. Disproven because obese women can be amenorrheic.

Leptin is a hormone that is secreted by adipose tissue and regulates the size of the adipose tissue stores with normal levels which suppresses the HPA axis decreasing cortisol secretion

Leptin signals info about dietary energy intake, decreases with exercise removes inhibition of HPA axis

104
Q

Energy availability hypothesis of menstrual dysfunction

A

Not enough fuel for brain

Brain needs energy and dietary intake is inadequate for both locomotion and reproduction so reproduction is stopped

restricted energy intake disrupts LH pulse frequency and amplitude (LH is released in discrete pulses which are necessary for ovaries to detect LH signal)

Exercise has no suppressive effect on the reproductive system beyond the impact of its energy cost on energy availability.

Regulation of the reproductive system in women can withstand up to 33% decrease in energy availability

Exercise Science and Health (1 decks)

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