Help
Options
Didn't know it?
click below
click below
Knew it?
click below
click below
Don't Know
Remaining cards (0)
Know
retry
shuffle
restart
0:00
Embed Code - If you would like this activity on your web page, copy the script below and paste it into your web page.
Normal Size Small Size show me how
Normal Size Small Size show me how
APK3110C Ch13
| Question | Answer |
|---|---|
| What are the three principles of training? | Overload, specificity, reversibility |
| What is the overload principle? | muscles must be challenged by an unaccustomed FID for adaptations to occur |
| What is the overload principle dependent on? | FID, frequency, intensity, duration |
| What is the specificity principle? | adaptations occur specifically in the muscle fibers used and system involved (aerobic v. anaerobic) |
| What is the reversibility principle? | no overload or use of muscles |
| What are 3 other ways to refer to VO2 max? | max oxygen uptake, maximal aerobic power, aerobic fitness |
| What does VO2 max describe? | The max capacity of the body to move and use oxygen during exercise via large muscle groups |
| How can you measure VO2 max? | incremental exercise tests with a treadmill incline |
| What is the FID needed in order for endurance training to improve VO2 max? | 3+ times a week, 50%+ VO2 max, 20-60 minutes |
| T/F You can improve VO2 max via isometric and dynamic training | False |
| When does VO2 max increase? | After 2-3 months of training |
| How does VO2 max relate to mortality? | Indirect predictor of mortality, higher VO2 max means lower mortality |
| What is the average increase in VO2 max? | 15-20% |
| What causes initial increase in maxes? | neural adaptations |
| How large can VO2 maxes be in untrained individuals? | Up to 50% |
| How large can VO2 maxes be in trained individuals? | 2-3% |
| Why do trained individuals have smaller increases? | genetics have high initial maxes and require greater intensities to improve |
| T/F People with lower initial VO2 maxes require lower intensitys for improvement | True |
| What percent of adaptations are effected by heritability and ? | 47-50% |
| T/F There is no genetic variability for VO2 max | False |
| What is volitional exhaustion? | exhausing |
| What is the Fick equation? | maximal cardiac output x a-vO2 difference |
| What causes short term increases in VO2 max? | Primarily the stroke volume max increases |
| What causes long term increases in VO2 max? | Primarily improved a-vO2 difference, but also SV |
| What role does max HR play in increasing VO2 max? | It has no role |
| Why does a-vO2 difference increase over time? | Mitochondria become better at utilizing O2 |
| What causes variability amongst VO2 max improvements? | Differences in stroke volume max differences |
| What 3 factors affect stroke volume? | increased EDV/preload, decreased afterload, increased contractility |
| How does afterload decrease affect stroke volume? | decreased SNS activity causes a decreased amount of vasoconstriction, which increases the amount of blood flow into the heart as blood vessels dilate |
| How does contractility affect stroke volume? | the heart's contraction force increases and ejects more blood per pump |
| What 3 factors contribute to an increased EDV/preload? | increased plasma volume, increased fill time, increased venous return, increased ventricular volume |
| How does diastole correlate to an increase in SV? | The heart spends more time in diastole, so there is more time to fill atria with blood |
| Which factor is rest specific? | Fill time, as diastole decreases during maximal HR |
| Why does a-vO2 max increase? | more oxygen is extracted and used in the blood |
| What three factors cause a-vO2 increase? | increased capillary density, increase # of mitochondria, and increased muscle blood flow |
| How does capillary density affect a-vO2? | Icreased number means more widespread flow, and a slowed down rate to allow more time for exchange |
| What effect does SNS activity have on a-vO2 and SV? | More SNS activity means more vasoconstriction, so a decrease in SNS activity causes increase in a-vO2 and SV |
| What does our ability to continue prolonged submaximal work depend on? | maintenance of homeostasis |
| What are the three ways we maintain/reach steady state? | rapid transition in (faster stabilization = easier to maintain), reduced reliance on glycogen stores, and cardo/terhmoregulatory (body temp) adaptations |
| What are the two causes of adaptations? | structural and biochemical changes |
| What causes initial adaptations? | Neural/hormonal changes |
| what does endurance training affect? | fiber types and capillarity |
| what happens to fibers with endurance training? | they shift from fast to slow |
| what affects the extent of the changes? | intensity, duration, and previous training experience |
| Why do fibers shift from fast to slow? | they become more efficient as slow myosin increases, which is different type of ATPase that is more efficient and less fatigueable i.e. more work given for less ATP cost |
| what is angiogenesis | the generation of new capillaries |
| why is an increase in the number of capillaries good? | increases amount of bloow flow, waste removal, and O2 diffusion |
| what does a mitochondria increase do? | increases amount of fat utilization, increases oxidative capacity, improves mitochondrial turnover |
| what is mitochondrial turnover | removal of "bad" mitochondria and replacing them with functioning ones |
| when is the largest increase in mitochondria | first 5 days of training, numbers increase 50-100% |
| what effect does endurance training have on the O2 deficit | reduces the O2 deficit, steady state achieved sooner via oxidative production so requires less energy |
| what is the pH mechanism behind faster steady state | more oxidative production of ATP means less lactate buildup, less H+ ions, less PC depeltion, which reduces acidity, which then causes less homestatic disruption |
| what is the primary fuel of the NS | blood glucose |
| how does endurance training affect blood glucose | maintain b. glucose, rely more on fats |
| what are the 3 ways endurance training increases fat metabolism | increased FFA transport in blood, increased FFA across cell to mitochondria, increased mitochondrial oxidation of FFA |
| why are FFAs transported more | increased capillaries allow more time for them to be bind and be brought in |
| why are FFAs transported more across cytoplasm to mitochondria | increased number of mitochondria increases the surface area for FFA enzymes to come in |
| what are the two enzymes involved in FFA transportation | carnitine palmitoyltransferasel, fatty acid translocase |
| why do mitochondria increase amount of FFA oxidation | increased beta oxidation enzymes results in more acetyl coA, which can be used in the Krebs and decrease amount of glycolysis/glucose use |
| what is a free radical | highly reactive molecules with unpaired electrons that damage proteins, enzymes, and DNA |
| how are they produced | they are produced by contracting muscles and are what cause us to become fatigued |
| how does exercise training protect against free radicals | creates more endogenous (inherit) antioxidants, which protect us against them |
| what does it mean that muscle biochemical adaptions are local | they are confined to the specifically trained system, and will not apply to the system as a whole. |
| how is the sns affected by endurance training | activity begins to decrease, resulting in less E/NE as well as decreased HR and ventiliation |
| why is the SNS less activated | less feedback from chemoreceptors as adaptations increase |
| what happens to motor units as endurance training increase | less motor units are recruited and less energy is expended |
| how does training affect the chain of feedback, specifically motor unit recruitment from higher centers | reduces "feed forward" input from cardio center and brainstem, requiring less signals for muscles and making the lungs/muscles/etc more efficient |
| what causes inital decrease in vo2 max following detraining | decreased SV max |
| what causes long term decreases in vo2 max following detraining | decreased max avO2 differece because of decreased number ot mitochondria |
| how are muscle fibers affected by detraining | they shift from slow to fast |
| what happens to mitochondria with detraining | mitochondria rapidly die and decrease oxidative capacity, decreasing our max possible HR due to decreased bflow |
| what happens to capillary density with detraining | remains the same |
| what happens to mitochondria within one week of traning | 50% are lost |
| what happens to mitochondria within 2 weeks of training | almost all of the gained mitochondria are lost |
| how long does it take to gain back adaptations following retraining | 3-4 weeks |
| how does anaerobic exercise improve performance | increases buffering capacity (availibility to resist pH changes) |
| what portion of exercise relies on ATP-PC | first 10 seconds |
| what portion of exercise relies on both anaerobic and aerobic systems | 10-30 seconds |
| what portion of exercise relies primarily on aerobic systems | 30+ seconds |
| what types of fiber hypertrophy in anaerobic training | type II fibers |
| the _______ principle reveals that for a training effect to occur, a system or tissue must be challenged with an FID of exercise to which it is unaccustomed. over time, the tissue/system adapts to this increased load | overload |
| the _____ principle refers to the fatc that fitness gains are lost when training is stopped | reversiblity |
| the principle of _____ relates to the fact that the training effect is limited to the muscle fibers involved in the activity. in addition, the muscle fiber adaptation is driven by the type of activity | specificity |
| In healthy, sedentary subjects, the training-induced improvements in V̇O2 max that occur following short-term training (i.e., ~4 months) are due to increases in ____________________________. | max cardiac output |
| However, the training-induced improvements in V̇O2 max that occur following long duration training (i.e., ~32 months) are the result of both increases in __________(but not heart rate) and an increase in the _______________. | stroke volume; avO2 difference |
| The training-induced increase in maximal stroke volume is due to both an increase in ____________ and a decrease in ____________. | preload; afterload |
| The increased preload is primarily due to an increase in _____________________________ and an increase in plasma ____________ | EDV; plasma volume |
| The decreased afterload is due to a ____________ in the arteriolar constriction in the trained muscles, _______________ maximal muscle blood flow with no change in the mean arterial blood pressure. | decrease; increasing |
| The training–induced increase in the a-v̄ O2 difference is due to an increase in the ____________ of the trained muscles, which is needed to accept the increase in maximal muscle blood flow | capillary density |
| The greater capillary density allows for a slow red blood cell transit time through the muscle, providing enough time for _________ diffusion from the capillary into the muscle fiber. | oxygen |
| Endurance training improves the ability of muscle fibers to maintain ___________ during prolonged exercise. | homeostasis |
| Regular bouts of endurance training result in a ___________________ in muscle fiber types and ↑ the number of _________ surrounding the trained muscle fibers | shift from fast to slow; capillaries |
| Endurance exercise also ↑ _______________ volume in the exercised muscles | mitochondria |
| The combination of the ↑ in the density of capillaries and mitochondrial volume in the muscle fiber ↑ the capacity to transport ____________________________ from the plasma → cytoplasm → mitochondria | free fatty acids |
| The ↑ in the enzymes of beta oxidation ↑ the rate of formation of ____________ from FFA for oxidation in the Krebs cycle. This ↑ in fat oxidation in endurance- trained muscle spares liver and muscle ____________ and plasma __________ | acetyl CoA; glycogen; glucose |
| The ↑ in the enzymes of beta oxidation ↑ the rate of formation of ____________ from FFA for oxidation in the Krebs cycle. This ↑ in fat oxidation in endurance- trained muscle spares liver and muscle ____________ and plasma __________ | antioxidants; free radical/oxidative |
| Endurance training results in less disruption of the blood pH during submaximal work because endurance-trained muscles produce less _____________ and _____________ | lactate; H+ ions |
| The _______________ changes in muscle due to endurance training influence the heart rate and ventilatory responses to exercise | biochemical |
| The reduction in “feedback” from ________________ in the trained muscle and a decreased need to recruit __________to accomplish an exercise task result in reduced sympathetic nervous system, heart rate, and ventilation responses to submaximal exercise | chemoreceptors; motor units |
| Endurance exercise training also reduces ___________________ during submaximal exercise that results in a lower heart rate and ventilatory response during exercise. | central command outflow |
| After exercise ________________, V̇O2 max begins to decline quickly and can decrease by ~8% within 12 days after cessation of training, and declines by almost 20% following 84 days of detraining. | detraining |
| The decrease in V̇O2 max with cessation of training is due to a decrease in both _______________________ and _______________________, the reverse of what happens with training. | max SV; avO2 max |
| Exercise performance during submaximal exercise tasks also declines rapidly in response to detraining, due primarily to a decrease in the ___________________ in muscle fibers. | mitochondria |
| Muscle adaptations that occur in response to sprint training vary depending upon the ___________ of exercise. | duration |
| Short-duration (10–30 seconds) sprint exercise training results in increased _____________________, increases in the _____________________, and an improved ability to generate ________ via anaerobic energy systems | ??; buffering capacity; power |
Created by:
isabellamulet