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the large majority of exercise physiology research has been performed exclusively in which populations?
18-22 year old college aged men
until the 1980s it was assumed that men and women would have the same physiological responses to exercise and nutrition
nutrition/exercise/recovery strategies have been generalized to women when they should not be
most studies dont involve women and if they do they are poorly designed
if women are included they are usually in follicular phase (hormones low)
small sample sizes so they group women + men together
researchers believe it is too difficult to study women with two phases
follicular phase
low hormone phase
luteal phase
high hormone phase
day 1
first day of bleeding
first day of follicular phase
key difference between men and women
menstrual cycle
women also sometimes take hormonal birth control
average woman’s cycle
28 day cycle dictated by cyclical changes in hormones regulated by the endocrine system
most abundant form of estrogen
estradiol (specifically 17β-estradiol)
estradiol at each point of cycle
low at beginning of follicular phase
gradual increase and peak at second half of follicular phase
sharp drop off at end of luteal phase (lowest at ovulation)
slight increase through first half of luteal phase
slight decrease (back to baseline) at end of luteal phase
luteinizing hormone (LH) at each point of cycle
very low at beginning of follicular phase, stays the same level
half way through follicular phase, small and quick bump up then back to same level
big, quick increase to peak at end of follicular phase right before ovulation
at ovulation goes back down to original level and stays there through entire luteal phase
follicle stimulating hormone (FSH) at each point of cycle
slight increase through first part of follicular phase
goes down (at same time that LH peak goes back down) in middle follicular phase
small peak right at ovulation (slightly before it)
back down at consistent low level through luteal phase
very slight increase at end of luteal
progesterone at each point of cycle
stays at same level through all of follicular phase (low)
after ovulation it goes up
through entire luteal phase goes steadily up to peak and steadily back down to baseline
prolactin-releasing hormone (PRH) in the hypothalamus (pathway after)
ACTIVATES → prolactin (PRL) in the anterior pituitary → breast (milk production in mammary glands)
prolactin inhibiting hormone (PIH/dopamine) in the hypothalamus (pathway after)
INHIBITS → prolactin (PRL) in anterior pituitary → milk production is inhibited
thyrotropin-releasing hormone (TRH) in the hypothalamus (pathway after)
ACTIVATES → prolactin (PRL) in anterior pituitary → breast (milk production stimulated)
OR
ACTIVATES → thyroid stimulating hormone (TSH) in the anterior pituitary → ACTIVATES thyroid gland → thyroid hormones (T3, T4) → many tissues
corticotropin releasing hormone (CRH) in the hypothalamus (pathway after)
ACTIVATES adrenocorticotropic hormone (ACTH) in anterior pituitary→ ACTIVATES adrenal cortex → cortisol → many tissues
growth hormone releasing hormone (GHRH/somatocrinin) in the hypothalamus (pathway after)
ACTIVATES growth hormone (GH)(somatotropin) in anterior pituitary → many tissues
OR
ACTIVATES growth hormone (GH)(somatotropin) in anterior pituitary → ACTIVATES liver → somatomedins (IGF) → many tissues
growth hormone inhibiting hormone (GHIH somatostatin) in hypothalamus (pathway after)
INHIBITS growth hormone (GH)(somatotropin) in anterior pituitary → inhibits effects in tissues/liver
gonadotropin releasing hormone (GnRH) in hypothalamus pathway on FSH
GnRH ACTIVATES → follicle stimulating hormone (FSH) in anterior pituitary → germ cells of gonads
OR
GnRH ACTIVATES → FSH in anterior pituitary → ACTIVATES endocrine cells in gonads → androgens/estrogens/progesterone → germ cells of gonads
gonadotropin releasing hormone (GnRH) in hypothalamus pathway on LH
GnRH ACTIVATES luteinizing hormone (LH) in anterior pituitary → germ cells of gonads
OR
GnRH ACTIVATES luteinizing hormone (LH) in anterior pituitary → ACTIVATES endocrine cells in gonads → androgens/estrogen/progesterone → germ cells of gonads
progesterone competes with the same receptor site for:
aldosterone (key for sodium balance) and
anti-diuretic hormone (ADH (arginine vasopressin) key for water balance)
key for water and thirst
2 weeks preceding the start of the woman’s period
high estrogen and progesterone
significant physiological changes
peak felt ~5 days before bleeding
significant changes in 2 weeks preceding start of period
drop in plasma volume by 8%
increase in core temperature by ~0.5 °C
change in metabolism to spare glycogen and increase reliance on fatty acids
increased amount of muscle catabolism from progesterone
increased amount of total body sodium losses
reset of plasma osmolarity
drop in plasma volume by ~8% WHEN?
in 2 weeks preceding start of period
PV is ~3L of the total ~5.5L of blood volume (intravascular compartment)
remaining ~2.5L consists of cellular elements of blood
less total blood for circulation and thermoregulation
increase in core temperature by ~0.5°C in 2 weeks preceding start of period does what
shortening the time to fatigue
decreasing heat tolerance
change in metabolism in 2 weeks preceding start of period
change to spare glycogen and increase reliance on fatty acids
reduce woman’s ability to use glucose as fuel
reduce woman’s ability to build lean muscle
increased muscle catabolism from progesterone in 2 weeks preceding start of period has what impact on exercise?
reduces ability to recover well
reduces ability to build lean muscle
increased amount of total body sodium losses in 2 weeks preceding start of period is from which hormone?
this is from progesterone
reset of plasma osmolarity in 2 weeks preceding start of period
lower plasma osmolarity
predisposes women to hyponatremia
estrogen and VO2 max in 2 weeks preceding start of period
estrogen blunts VO2 max from a metabolic and respiratory aspect
VO2 max is one of the best measures of aerobic fitness
cant access carbohydrate
increased respiratory rate
hard to hit the top end of VO2
CNS fatigue in 2 weeks preceding start of period
estrogen and progesterone affect CNS fatigue
lack of “mojo”: cant do exercises as well as they usually can
increase in blood osmolarity leads to:
osmoreceptor cells in hypothalamus detect increase in blood osmolarity →
release of ADH in pituitary gland →
collecting duct: increased permeability →
H2O reabsorption helps prevent further osmolarity increase →
back to homeostasis
*at the same time, osmoreceptors promote thirst → drinking reduces blood osmolarity back to set point → back to homeostasis
what can cause low blood volume/blood pressure?
dehydration
loss of blood
low blood volume/blood pressure leads to:
juxtaglomerular apparatus (JGA) → renin production → angiotensinogen → angiotensin II
AFTER angiotensin II, could be 2 pathways:
angiotensin II → arteriole constriction → homeostasis
OR
angiotensin II → adrenal gland → aldosterone → increased Na+ and H2O reabsorption in distal tubules → homeostasis
birth control pills
circulating amount of estrogen is 6-8x as high
“low hormone/placebo week”" is not actually low hormone
estrogen rebounds and results in high circulating amount of estrogen
IUD
better than pills
localized doses of progesterone
significantly reduces amount of hormones circulating
peri- and post-menopausal women: additional challenge
predisposition to store abdominal fat (leftover signals from estrogen)
much more difficult time maintaining muscle integrity
why do peri- and post-menopausal women struggle to maintain muscle integrity
increased catabolic drive: decreases muscle reparation and hypertrophy
difficult time gaining and maintaining lean mass
difficulty with neuromuscular drive to produce power
men dont have any of this (booo!)
during prolonged exercise, what happens to fluid and salt
fluid and salt losses through sweating
reduce plasma volume
leads to heart rate drift, hyperthermia, and reduction in performance
oral rehydration with water
reduces loss of plasma volume
lessens heart rate drift
lessens hyperthermia
inclusion of sodium in rehydration solution (~90mmol/l Na+)
double the sodium volume in sweat
restores plasma volume when ingested during exercise
expands plasma volume if ingested pre-exercise
hydration during exercise in real person speak
during exercise you lose water and salt through sweat
when you lose this water and salt, the watery part of blood also drops
less water in blood = blood more viscous
higher heart rate, lower power production, greater rise in core temp
leads to fatigue, reduced performance, and power decline at the end of a race
competition in the body during exercise
muscles and skin fight for blood
blood goes to muscles for metabolic function
blood goes to skin to get rid of heat produced by working muscles
when body water drops, competition becomes more fierce
skin blood flow wins: heat is a greater threat to body than keeping muscles working (which produces heat)
fatigue during exercise
due to drop in blood flow to muscle
less metabolism functioning
protein denaturing (contractile proteins denature in >~39°C)
most researchers recommend what amount to prevent fluid loss in exercise?
all athletes drink 10-12 ml of fluid per kg of bodyweight per hour (750-900 ml for 75 kg person) during exercise
new research on exercise/fluid loss
if you are exercising and maintaining your core body temp (not cold) you can drink according to thirst without performance decrements
difference between men and women for hydration
composition of the drink
NOT fluid needs per hour
two most influential female sex hormones
estrogen and progesterone
both change concentration across menstrual cycle and by oral contraceptive pill (OCP) usage
both influence sodium and water distribution (and thus fluid compartment volumes and dynamics)
estrogen and fluid
estrogens favor fluid retention
activating renin-angiotensin-aldosterone system
enhances vasodilation and capillary permeability
acts centrally to lower the operating set point of plasma osmolality (leftward shift in ADH sensitivity)
progesterone and fluid
antagonizes the renin-angiotensin-aldosterone system
does this through antagonism of the aldosterone receptor
competes directly with the same mineralcorticoid receptor as aldosterone
this could cause a transient natriuresis
progesterone makes you pee
natriuresis
increase in excretion of sodium through urine
estrogen/progesterone fluid impacts
concentrations of sex hormones have dramatic impacts on fluid
liver secretes WHAT?
liver secretes angiotensinogen → which turns into angiotensin I
decrease in renal perfusion (juxtaglomerular apparatus) does WHAT?
stimulates kidney to secrete renin → which stimulates angiotensinogen to change to angiotensin I
angiotensin I does what next?
the kidney and lungs secrete ACE, which stimulates the reaction: angiotensin I → angiotensin II
angiotensin II stimulates WHAT?
sympathetic activity
tubular Na+Cl- reabsorption and K+ excretion (H2O retention)
adrenal gland/cortex
arteriolar vasoconstriction (increase in BP)
pituitary gland posterior lobe
what is the effect of angiotensin II stimulating the adrenal gland/cortex?
secretes aldosterone → stimulates H2O retention
what is the effect of angiotensin II stimulating the posterior lobe of the pituitary gland?
secretes ADH, which stimulates → collecting duct (H2O absorption)
what is the overall impact of the renin-angiotensin-aldosterone system?
water and salt retention
effective circulating volume increases
perfusion of the juxtaglomerular apparatus increases
plasma volume is highest WHEN?
the preovulatory phase of the menstrual cycle
when estrogen levels are increasing
plasma volume at midluteal phase
drops as much as ~8%
due to fluid and protein movement into the interstitium
this is caused by the effects of estrogen on plasma albumin and plasma colloid osmotic pressure
how does estrogen effect plasma in midluteal phase
plasma proteins (such as albumin) are too large to penetrate the capillary wall freely
presence of greater concentration of plasma proteins in the intravascular compartment (in comparison to the interstitial fluid)
colloid osmotic (oncotic) pressure: the ratio (more in intravascular) sets up osmotic pressure that pulls fluid back into capillary
reduction in plasma proteins in luteal phase
results in reduction in plasma colloid osmotic pressure
less fluid pulled back into blood
more interstitial fluid
reduction in PV has important functional considerations
CBT and exercise
during exercise, core body temp (CBT) rises due to heat produced by working muscles
when CBT rises above 39°C (103°F), many body systems are compromised: drop in performance
how does body regulate CBT?
moving the blood to the skin and offloading heat through sweat
requires continual replenishment of body water required for perspiration and plasma volume
why do women face additional challenges in exercising?
perturbations of the female sex hormones
influences of hormones on fluid distribution, resting core temp, and resetting of thermoregulatory responses
high hormone phase of menstrual cycle- temperature
baseline core temp is reset to a higher internal temp
concomitant increase in the threshold for sweat onset
decreased sensitivity of cutaneous vasodilation
what does the reset of temp thresholds in the high hormone phase impact?
sweat onset, vasodilation, decreased baroreflex sensitivity
time to critical core temperature may be reduced
thermoregulatory control changes can compromise women’s exercise capacity (esp during heat)
plasma volume and heat
PV maintenance important for exercise performance (esp in heat)
maintained or increased PV:
reduces viscosity of blood
increases heat storage and transfer capacity
increases exercising cardiac output
increases maximal O2 uptake
maintained or increased PV does what to heat
ability to offload heat (by virtue of increased volume of circulating fluid) is increased
circulation to the periphery is enhanced
but fluid balance is usually not achieved (not even when fluid availability or gastric emptying rates prevent rates of ingestion and absorption from matching sweat rates)
overall changes ~1 week before period (luteal phase)
hormones high
bloating
holding more fluid between cells than in the blood
lose ~8% of plasma volume
no biggie if not exercising
if exercising, lose fluid available for sweat
progesterone makes women lose total body sodium
what happens if you cant sweat?
tough time regulating body temp during exercise
women need sodium in fluids to pull fluid into the blood
~1 week before period, progesterone makes women lose total body sodium, resulting in what risk?
leaves women more susceptible to hyponatremia than men
women salt consumption and workout
should consume ~1 teaspoon salt before long, hard, or hot workout (if weighs ~63.5 kg (140 lb))
if weighs ~54 kg (120 lbs) should have ¾ teaspoon
men and sodium
men do not have these sex hormone fluctuations
little sodium would help anyone hold onto fluid than no sodium at all, but:
men can get by with less sodium than women
overall: why do women need more sodium in fluids than men
during exercise: TBW loss and sodium loss
elevated sex hormones reduce resting PV by ~8% and increase sodium loss
reduced PV and increased sodium loss means loss of power (bc reduced blood circulation)
luteal phase affects thermoregulation more than follicular
less heat tolerance in high hormone phase
fatigue causes
depletion of carbs is one of the primary causes of fatigue during long sustained exercise
most critical cause of fatigue is drop of total body water and subsequent volume loss
average adult glycogen storage
~300-500 g of glycogen stored in muscles
~75-100 g of glycogen stored in liver
enough carb to run at moderate intensity for 20 miles
main objective of supplementing with carb during prolonged strenuous exercise
maintain blood glucose concentrations
estrogen and nutrition/exercise
estrogen is (at least partially) responsible for:
decreased reliance on hepatic glycogen stores
increased availability and oxidation of fatty acids
decreased amino acid breakdown during exercise
progesterone and nutrition/exercise
increases protein catabolism during exercise
decreases protein synthesis during recovery
17β estradiol in exercise
decrease hepatic glucose rate of appearance and disappearance
decrease total oxidation
results in relative sparing of hepatic glycogen storage during exercise
estrogen glycogen sparing in exercise
results in less glucose available for fluid co-transport mechanisms in intestines
less access to carbohydrates needed by muscles to perform at high intensities (thus decreased TBW and aerobic capacity)
how is water reabsorbed in the intestines?
through Na+/glucose cotransporters
it is believed that estrogen may influence estrogen metabolism how?
action on sympathetic nervous system
reduced catecholamine release at a given intensity and workload as compared to similarly trained men
studies performed on carb depleted women show what?
able to maintain blood glucose during follicular phase but not luteal phase
greater effect on glycogen sparing occurs during the high hormone phase of menstrual cycle
estrogen lipid utilization
estrogen promotes free fatty acid availability and lipid oxidation during exercise
possibly via an increased sensitivity to the lypolytic action of catecholamines
females and intramuscular triglyceride
intramuscular triglyceride content is dependent on dietary fat consumption
intramuscular stores generally much larger in females than males
utilized more in females at moderate intensity (90 min, 58% of VO2 max)
females: larger intramuscular triglyceride stores and rely more heavily on it during exercise
sex based differences in whole body substrate oxidation during exercise
lower respiratory exchange ratio (RER) of females compared to males for a given exercise intensity and duration of exercise
amino acids difference between male/female
greater amounts of amino acids are oxidized by males during exercise than females
progesterone and protein
progesterone increases protein catabolism with less protein synthesis
increased protein catabolism during exercise during luteal phase compared to follicular phase
increased protein catabolism = greater excretion of urinary urea nitrogen
higher circulating progesterone levels (or lower estrogen:progesterone ratio) promotes protein catabolism
estrogen does what to protein?
reduces protein oxidation
women and burning fat
women have a greater capacity for burning fat at a given intensity
sparing glycogen and using less amino acids
results in less glucose availability for fluid absorption and energy needs
progesterone effect on muscle
high levels of progesterone increase muscle breakdown
women carb consumption
can afford to ingest lower carb grams per hour during exercise during low hormone phase
need carb supplementation during high hormone phase
BCAAs (branched-chain amino acids)
women should ingest BCAAs (leucine, isoleucine, and valine) pre-exercise during the luteal phase to counteract progesterone’s effects, such as:
increased catabolic effects of exercise
blunting of protein synthesis
increased protein degradation at rest
increased glucose availability does what?
increase fluid balance
improve anaerobic ability
reducing dependence on fat as substrate → decreasing stimulus to store more fat
fat metabolism: exercise vs recovery
women metabolize more fat during exercise
opposite is true during recovery
women fat metabolism during exercise
use more fat during exercise
have greater fat stores
increased propensity to store glycogen while maintaining a steady energy flow during exercise
women fat metabolism during recovery
burn less fat than males during recovery
greater ability to maintain glycaemia during recovery period following prolonged exercise
could explain why lipolysis occurs to a lesser degree in females during this phase