Exam 2 Flashcards
Why is blood glucose control important?
short term problems of uncontrolled blood sugar levels: hypoglycemia, hyperglycemia, diabetic ketoacidosis
longterm problems: damage to the vessels of heart, kidneys, eyes, and nerves
What is the negative effect of too little blood glucose?
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
What is the negative effect of too much blood glucose
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)
WHen blood glucose increases does insulin increase or decrease?
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.
What happens to fat uptake in adipose tissue when insulin increases?
there is an increase in fat uptake because the insulin brings sugar out of the bloodstream and into the cells for storage
What happens to fat uptake in adipose tissue when insulin decreases?
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
What happens to fat release when insulin decreases?
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
What happens to fat release when insulin increases?
fat is stored when insulin increases because there’s enough glucose to fulfill the body’s energy requirement
What happens to protein synthesis when blood insulin is high?
High Insulin = High Protein Synthesis
because energy is readily available through glucose, we dont’t need to resort to FFA release
What happens to protein synthesis when blood insulin is low?
Low insulin = High Protein Breakdown
because FFA help with created ATP through glucagon and epinephrine
When does gluconeogenesis occur?
Low blood glucose = gluconeogenesis
occcurs in the liver: synthesized from pyruvate, lactacte, glycerol (non-carb substrates)
Where is glycogen stored?
liver and muscle celss
glycogen is the storage form of glucose
When does glycogenolysis occur?
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
What is the effect of epinephrine on blood glucose? on adipose tissue fat release/uptake?
- 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
Type I vs Type II diabetes
Type of Disorder
Type I: autoimmune disorder
Type II: Metabolic disorder
Type I vs Type II diabetes
Insulin level
Type I: Hypoinsulinemia
Type II: Hyperinsulinemia
Type I vs Type II diabetes
Age of Onset
Type I: predominantly in youth
Type II: predominantly after age 40
Type I vs Type II diabetes
Genetic Component
Type I: weak
Type II: strong
Type I vs Type II diabetes
Proportion of diabetes patients
Type I: 5-10%
Type II: 90-95%
Type I vs Type II diabetes
Insulin depndence
Type I: permanent
Type II: permanent only in subset of patients
Type I vs Type II diabetes
Insulin Resistance
Type I: low
Type II: High
Type I vs Type II diabetes
Onset
Type I: acute and potentially severe
Type II: Mostly mild, insidious
Type I vs Type II diabetes
Other
Type I: Often normal body weight (or thin/wasted)
Type II: frequently linked to obesity
What happens to the cells responsible for releasing insulin in type I diabetics?
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
What happens to insulin levels in type II diabetics?
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
Why are type II diabetics obese while type I are normal or wasted?
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
How does diet and exercise effect Type I diabetes?
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
How do diet and exercise effect Type II diabetes?
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
IDDM
insulin dependent diabetes mellitus: Type I Diabetes
NIDDM
non-insulin dependent diabetes mellitus: Type II Diabetes
Gestational Diabetes
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%)
Mechanisms/Process of Insulin resistance
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
How is glucose transported?
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
What does glut4 do?
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
What does insulin do?
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
What does glucagon do?
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
Primary Prevention of Diabetes
Moderate exercise intensity and a good diet
Secondary Treatment of Diabetes
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
Tertiary Care of diabetes
knowing that you are a diabetic; delay onset of more symptoms in terms of well balanced diets and increasing circulation
Common treatments on diabetes
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
Exercise recommendations for diabetics
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)
Contraindications to Exercise in Diabetics
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
Fasting blood glucose levels
Normal: 70-100 mg/dl
Diabetic: >180 mg/dl
OGTT: Oral glucose load, blood glucose, and urine sample every 15-30 mins
Normal will recover within 2 hours
Diabetics/glucose intolerance: high levels
Glycosylated hemoglobin
%glycosylated (glucose attached) = 4-6%
Diabetics can be 11-15%
Urine tests
not as accurate
influences by fluid intake/urine concentration
Non Specific Response of the Immune System
- 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
Immune Responses to Exercise: Leukocytes
- rapid increase WBC
- increase neutrophils, monocytes
- direct relation to ex intensity/duration
- duration most important factor
Immune Responses to Exercise:
Window of Opportunity
after exercise certain cell types rapidly decrease which could supress the immune system
Innate Immunity
Nonspecific
Recognize non-self without prior exposure
- Neutrophils
- monocytes
- Natural Killer cells
- Complement System: a way that innate and acquired systems work together
Acquired Immunity
Specificity to infectous agent Memory of Prior Exposure -T Cells -B Cells -Complement System: innate and acquired work together
T Cells
arrive to help “learn”
create T memory cells
T killer cells act on pathogen
What do T helper cells do
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
Roles of granular leukocytes and their function in the immune system
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
Roles of nongranular leukocytes and their function in the immune response
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
Where do B and T cells mature and then marticulate and concentrate?
- 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
Complement System
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.
How does the immune system attack a foreign pathogen?
- 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
Antibody formation
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.
3 classes of antibodies
3 classes of antibodies:
• IgG: main antibody in blood stream
• IgA: found in external secretions
• IgE: create allergic symptoms (lactose intolerance)
Cell mediated immunity
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
Intensity of Exercise and Immune Response
- 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.
Window of Susceptibility after prolonged intense exercise
- 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.
Mechanisms for development of cancer
-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
Malignant Cells
capable of spreading beyond the site of origin. They divide much more rapidly than they should; produce tumors
why are tumors dangerous
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
Metastasis
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
Causes of Cancer
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
Arsenic, asbestos, and nickel lead to
Lung cancer
asbestos embeds itself in the tissue and permanently stays there
Formaldehyde can cause
nasal and nasopharyngeal cancer
Alcohol can cause
oral, esophageal, and opharyngeal cancer
Tobacco can cause
lung cancer, head/neck cancer, esophageal cancer, and bladder cancer
Sunlight (UV radiation) can cause
skin cancer
Most common cancer in males
prostate cancer
most common cancer in females
breast cancer
What cancer is the most deadly?
Lung Cancer
also 2nd most prevalent
What are preventative measures/early detection recommendations for cancer?
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
How does exercise provide protective mechanisms to cancer?
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
How does exercise provide protective mechanisms against against colon cancer?
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%
Survival Rate of Colon Cancer
5 yr: 90%
After Metastasis: 5 yr: 65%
8% of time it spreads to lungs/liver
survival rate of breast cancer
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
When is the incidence rate of breast cancer increasing
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
Estradiol and Breast Cancer
Estradiol is an endogenous hormone
Imbalance between estrogen and progesterone stimulates cell proliferation
What increases the risk of breast cancer?
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%
Risk factors associated with breast cancer
- 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
PA and breast cancer
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
Exercise recommendations for those individuals in cancer treatment or post treatment
-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
Motives and barriers for exercise during cacner treatment
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
Motives and barriers for exercise during cancer survivorship
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
Primary Amenorrhea
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
Secondary amenorrhea
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
Oligomenorrhea
less than 10 menstrual cycles per year
cycles are more than 35 days apart
Prevalence of amenorrhea in Atheletes Vs Nonathletes
Nonathletes: 1-5%
Athlletes: 20-25% greater
prevalence of amenorrhea in weight bearing vs non weight bearing activity
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
Follicular phase of the menstrual cycle
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
Ovulation phase of menstrual cycle
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
Luteal phase of menstrual cycle
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
What could possibly happen when luteal phase is shortened?
Higher risk or chance of amenorrhea (decreased risk in gonadotropins)
Menstruation
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
How long is a normal menstrual cycle?
usually 28 days (SD=7)
Low energy availability leads to menstrual dysfunction…How
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
Exercise stress hypothesis of amenorrhea
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)
Body composition hypothesis of menstrual dysfunction
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
Energy availability hypothesis of menstrual dysfunction
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
