Ex. Phys. Acute Exercise Responses Flashcards
effect of onset of exercise (30 SECONDS OR LESS) on neuromuscular system
intensity and mode of exercise will dictate which fibers and how many are recruited
effect of onset of exercise on metabolism
all modes and intensities of exercise will elicit a spike in immediate system use at the beginning
muscular contraction also will ramp up glycogenolysis and glycolysis to provide adequate ATP replenishment
O2 stored on myoglobin is utilized for aerobic ATP production because an adequate O2 supply has yet to be established
effect of onset of exercise on cardiovascular system
due to increased metabolic demands
- PSNS activity inhibited
- SNS releases Norepi to
- -increase HR and SV
- -restrict blood flow from gut, kidneys, etc. via vasoconstriction to help shunt blood to active muscles and skin
- this happens because of feed forward hypothalamus activity and feedback from the exercise pressor reflex
effects of onset of exercise on respiratory system
due to increased metabolic demands of exercise
- PSNS activity inhibited
- SNS releases Epi and Norepi to dilate bronchioles
- blood flow is redistributed to ventilatory and skeletal muscle via vasoconstriction
why do these respiratory changes occur
because of feed forward medulla and pons activity and feedback from the exercise pressor reflex
what happens to VE during acute exercise
will increase to accommodate exercise intensity
- increases are proportional to effort at low to moderate intensities
- increases are disproportionately large at high intensitis
initial VE increases are due to
enlarged VT
neuromuscular system during exercise
intensity and mode of exercise will dictate which fibers and how many are recruited
if working muscle fibers fatigue, additional fibers are recruited to maintain force output
-replacement fibers may be of the same type or a different type (usually higher order fibers, if available)
metabolism during exercise
- intensity
- upregulation of aerobic metabolism
- glycogen
- higher intensity exercise
intensity of exercise will dictate which energy system predominates to replenish ATP utilized for muscular contraction
regardless of intensity, aerobic metabolism will be upregulated to some extent
-once O2 stored in myoglobin is used up, more is needed
new glycogen constantly will be formed from glucose via glycogenesis to provide a steady supply of glucose for glycolysis
at higher exercise intensities, all of the pyruvate generated from glycolysis cannot be converted to Acetyl-CoA and shuttled into the mitochondria, so it’s converted to lactate
GLYCOGENOLYSIS? occurs here
exercise intensity and O2 use
prolonged low-intensity exercise will demand a lot of O2
short-duration and/or high intensity exercise will demand less O2
glucose and glycogen levels during extended exercise (hours)
may be depleted so much that exercise intensity is compromised
in such cases, new glucose is created from fatty acids and amino acids via gluconeogenesis
H+ and lactate relationship
up to lactate threshold, lactate will act as a buffer for H+ buildup
passed lactate threshold, H+ will begin to accumulate within the muscles
what happens to the H+ ions after lactate threshold
while some of the H+ stays in the muscles, much of it diffuses into the muscle capillaries and is transported in blood to
-liver to be turned into glucose or reconverted to pyruvate and oxidized to CO2 and H2O to produce ATP, or
-other muscles/tissues to be utilized as a fuel source
H+ travels with lactate
cardiovascular system during exercise
- SNS and PSNS
- myocardial O2 consumption
SNS and PSNS activity dynamically balance one another during exercise to maintain Q
-due to baro/chemoreceptor feedback, metabolite buildup, and stress on vessel walls
myocardial O2 consumption increases up to 4x the amount associated with rest due to increased cardiac function associated with a higher Q
-main determinant of this is HR
CV drift
during prolonged, steady state exercise, SV and MAP pregressively decrease, and HR progressively increases
-fluid loss due to sweating will probably result in a sizeable drop in blood volume, so SV will decrease and HR will increase to compensate
blood shunting
during prolonged, steady state exercise, EDRFs (particularly nitric oxide) are released from working tissues to induce vasodilation despite systemic SNS vasoconstriction
this effectively shunts blood toward tissues in need and away from tissues that are in less need of O2 and nutrients
aerobic effects on CV
big metabolic demands to get O2 and nutrients to working muscles, so there is an
-increase in Q, HR, SV, EF, and SBP
-no change in DBP
“volume load” exercise - the CV responses are attributed to increased preload
overall result - big decrease in TPR to facilitate peripheral blood flow
resistance effects on CV
artificial vaso/venoconstriction from muscle contraction and/or Valsalva maneuver significantly increase SBP, DBP, and MAP
however, little to no change in Q, SV, and HR due to lower metabolic demand
“pressure load” exercise - the CV responses are attributed to huge afterload
overall result… big increase in TPR
TRADITIONAL RESISTANCE TRAINING NOT CIRCUIT TRAINING
supine vs. upright exercise
with supine exercise, greater preload/venous return increases SV and decreases HR
any given exercise intensity requires a certain cardiac output
arm vs. leg exercise
- at all absolute workloads
- explanation
- difference is attributed to
at all ABSOLUTE (specific) workloads, arms elicit greater CV responses than legs
-increased HR, SBP, DBP, VO2, VE, RER, and LA
-decreased SV
-lactate threshold reached sooner
increased vasoconstriction in legs during arm workouts may contribute to the parameters above
difference is probably attributed to amount of muscle mass activated and work capacity of each muscle group
respiratory system
- VE
- after initial VE increase
- steady state VE
- incremental exercise
VE will increase to accommodate exercise intensity
-increases are proportional to effort at low to moderate intensities
-increases are disproportionately large at high intensities
after initial VE increases at exercise onset, subsequent VE increases are due typically to increased f
steady state VE takes awhile to achieve
during incremental exercise, VE will begin to increase disproportionately at intensities greater than 50-60% of VO2max
purpose of VE disproportionate increase
provide more O2 to muscles in need and the other is to help regulate blood pH, which drops at higher intensities due to increased pCO2 and H+ concentrations
ventilatory threshold
point where a disproportional increase in VE and VCO2 occurs
ventilatory threshold vs. lactate threshold
not the same thing, but typically occur around the same time
VT can be used to approximate LT
Hb affinity change
-due to
will decrease at the tissue level to provide enough O2 to working muscles
-due to increases in PCO2, 2,3 BPG, H+, etc. that are produces by the working muscles
ventilation as a limiting factor for exercise
VE cost may require up to 15% of VO2 and Q during intense, prolonged exercise
-the O2 consumed by respiratory muscles is, therefore, not available for other working skeletal muscles
lung effect at or near maximal intensity aerobic exercise
normally not a limiting factor
- VE has been shown to rise despite plateaus in VO2 & Q
- maximal expansion of pulmonary capillaries limits %SO2 at maximal exercise
- when these capillaries can no longer expand, blood flow in this area speeds up, which reduces RBC transit time
- -consequently PaO2 decreases (arterial hypoxemia), which limits exercise performance
neuromuscular post-exercise
the muscles stop working, so there’s not much to say
metabolism post-exercise
- mitochondrial exercise
- what’s this called
- they extent of this depends on
mitochondrial respiration will ramp up to replenish ATP depleted from muscular contraction
- called Excess Post-exercise Oxygen Consumption (EPOC)
- extent of EPOC depends on the mode and intensity of the exercise
glucose and glycogen synthesis post-exercise (metabolism)
increase to replenish glucose depleted during exercise
-20-30 minute window following exercise where this is particularly active, hence the reason it is very important to eat shortly after a workout
lactate and waste products post-exercise (metabolism)
shuttled out of the muscles into the blood circulation or surrounding tissues
cardiovascular system post-exercise
when exercise is over, a period of increased Q delivers the O2 necessary for mitochondrial respiration (EPOC) and shuttles lactate and waste products away from the muscles
-as equilibrium is restored, Q drops via reductions in HR and SV
respiratory system post-exercise
when exercise is over, a period of increased VE supplies the O2 necessary for mitochondrial respiration (EPOC) and rids the body of excess CO2
-as energy stores are replenished, VE decreases to resting levels
hormones, metabolism, and exercise
- what affects it
- these hormonal responses have a significant effect on
the intensity and duration of exercise both influence the hormonal responses observed during and following exercise
these hormonal responses have a significant effect on the training adaptations that occurs with various forms of exercise - their importance cannot be understated
exercise response on insulin
decreases during exercise, but increases in efficiency so that glucose can be effectively uptaken by the muscles
-even though it is decreasing, you are still getting more glucose into the cell
exercise response on glucagon
increases a little with exercise intensity, but more dramatically as exercise duration increases
epinephrine
immediate increase in response to exercise, with gradual increase over exercise duration and/or at higher exercise intensities (particularly >75% VO2max)
exercise response on norepinephrine
generally mimics response of epinephrine
exercise response on cortisol
immediate increase in response to exercise
continues to increase with short-duration high intensity exercise
during longer duration, lower intensity exercise (50-65% VO2max) cortisol will initially spike, then decrease gradually over time
note on cortisol
while cortisol can be helpful during exercise, high levels following exercise, in some ways, are not
mode and intensity of exercise, nutrition, and rest, should all be considered to mitigate the residual effects of cortisol
exercise response on growth hormone
dramatically increases with exercise intensity (>75% VO2max), but also gradually increases with longer duration exercise
high-intensity exercise effect on GH will counter cortisol effect
exercise response on insulin-like growth factor-1
generally mimics response of growth hormone
IGF-1 note
while GH and IGF-1 can be helpful during exercise, they also have important post-exercise responses that largely influence recovery and exercise adaptations
the goal, almost always, is to try and maximize GH and IGF-1 levels during and post-exercise
what is fatigue
a decline in maximal force generating capacity
NM recruitment strategy may change to maintain muscle contraction or preform work
it can have detrimental effects on daily activities and exercise performance alike
site of fatigue
may be dependent upon type of activity
type II fibers fatigue faster than type 1, and type IIx fibers faster than IIa
mechanisms of fatigue
central fatigue
peripheral fatigue
metabolic fatigue
central fatigue
failure of CNS to initiate signals to muscles
- could be a feedback mechanism - muscle stress or damage may send afferent information to the CNS, which detects problems and inhibits signals to muscles to decrease motor unit recruitment
- could be a neurotransmitter thing - elevation of FFA in blood, concomitant increase of free tryptophan uptake in brain (travels on albumen), which promotes serotonin synthesis, and fatigue is induced (more likely during endurance training)
peripheral fatigue
failure of a-motor neuron to transmit signals
failure of neuromuscular junction to relay signal
failure of excitation-contraction coupling process
failure of a-motor neuron to transmit signals
- AP conductance may be reduced, but
- typically, the a-motor neuron isn’t fatiguing - the signals that it receives are reduced by CNS
failure of neuromuscular junction to relay signal
-limited data suggests that Ach depletion may occur in type II fibers, but not well-studied in humans as of yet
failure of excitation-contraction coupling process
MOST LIKELY
substantial K+ efflux from muscle occurs during exercise, which may impair muscle AP (restored by NA+K+ ATPase pump)
disruption of AP transmission through DHP, EDFP and ryanodine receptors results in less Ca2+ release
metabolic fatigue
exhaustion hypothesis
accumulation hypothesis
exhaustion hypothesis
you deplete or significantly reduce something (ATP, CrP, glycogen)
accumulation hypothesis
LA increases, spurring H+ release, which might inhibit
- Ca2+-troponin binding
- Ca2+ release and reuptake
- sarcolemma excitability
- various enzyme activity (HK, PFK, etc.)
- ATP hydrolysis and synthesis
duration of fatigue
-different lengths
could be a few seconds up to a few minutes (high frequency fatigue, HFF)
could be a few minutes up to hours
could be several hours to days (low frequency fatigue, LFF)
few seconds to minutes (HFF)
often associated with short-duration high intensity exercise
due to overstimulation of muscle fiber, K+ efflux temporarily impairs ability of muscle fiber to depolarize
once Na+-K+-ATPase pump can restore ion gradients, muscle fiber can respond normally again
few minutes to hours
often associated with extended duration high intensity exercise
sometimes ion gradients and ATP-CrP restoration are not enough
-both of these are typically restored quickly during recovery periods, but sometimes there is not a resultant increase in the ability to exert force
when muscle glycogen stores are depleted there still exists other fuel sources (lipids, amino acids), yet the muscle cannot use these to perform extended high-intensity work; therefore, glucose/glycogen levels must increase to restore muscle function
several hours to days (LFF)
often associated with endurance exercise, but also can be associated with high intensity exercise that elicits DOMS
initial decline in force production is due to excessive Ca2+ exposure or free radical during excitation-contraction coupling process (usually this is related to endurance exercise)
extended decline in force production likely due to myofilament damage within the muscle (seen in both endurance and high intensity exercise)
contractile failure sends feedback to the CNS, which then inhibits a-motor neurons to reduce/prevent muscular work and further damage
