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test Flashcards

1
Q

yaya

A

yaya

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2
Q

What is the Fick equation?

A

VO2 = HR x SV x a-VO2diff.

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3
Q

What is absolute VO2? What is it expressed as?

A

Absolute VO2: the total volume of oxygen consumed
- Expressed as L/min

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4
Q

How can VO2 be predicted?

A

Based on the WORKLOAD of cycle ergometer

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5
Q

What is relative VO2? What is it expressed as?

A

Relative VO2: the total volume of oxygen consumed relative to body weight as this allows for the comparison of aerobic fitness among individuals
- Expressed as mL/kg/min

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6
Q

If you are 70kg and have an absolute VO2 of 3.5 L/min what is your relative O2 consumption?

A

VO2(mL/min)=3.5L/min X 1000mL/1L = 3500
VO2(mL/kg/min)=3500 mL/min/70kg = 50

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7
Q

What is the range/normal value for relative VO2 for
the following group of individuals:
(a) UT college-aged females
(b) UT college-aged males
(c) Active college-aged females
(d) Active college-aged males
(e) TR college-aged females
(f) TR college-aged males
(g) Competitive college-aged males and females
(h) What is the normal value for relative VO2 for elite marathon runners?
(i) What is the highest measured VO2max

A

(a) 30 - 35 mL/kg/min
(b) 35 - 45 ml/kg/min
(c) 40-45 ml/kg/min
(d) 45-50 ml/kg/min
(e) 50-60 ml/kg/min
(f) 55-65 mL/kg/min
(g) 65 to ~70 - 85 mL/kg/min
(h) Low 90s
(i) ~95 mL/kg/min; From a male-cross country skier

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8
Q

What characteristic is necessary to excel in aerobic events?

A

A high VO2max

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9
Q

How much can an UT increase their VO2max from UT state to TR state? When do results occur? How does this occur?

A

The novice individual can increase their VO2max by 20% in only three months (~90 days) of training.
- Largely due to the increase in blood volume, also causing an increase in SV

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10
Q

(a) If you have a man whose VO2 is 47 mL/kg/min, what category would he fit in?
(b) If you have a man whose VO2 is currently 36 mL/kg/min and was put through 3 months of training. What would be his VO2 by the end of those 3 months?

A

(a) Active college-aged males
(b) ~ 43.2 mL/kg/min = (36 x .20) + 36mL/kg/min

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11
Q

What does the Fick equation define?

A

Whole body O2 consumption

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12
Q

What are the three factors to consider that can alter with training?

A
  • HR
  • SV
  • a-vO2 diff.
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13
Q

Between Q and a-VO2diff. in the Fick equation, which of the two is considered the “oxygen delivery” and which the considered the “oxygen extraction”?

A

Q = oxygen delivery
a-VO2 diff. = oxygen extraction

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14
Q

To increase your whole body oxygen consumption (VO2), explain what is the most important factor, oxygen delivery or oxygen extraction? Consider the variables of the Fick equation in your explanation.

A

Increase in oxygen delivery (Q) = increase whole body oxygen consumption
- HR: NOT a huge concern in changing Q; since HR is under neural control, an individual has the ability to activate the SNS fully to achieve maximal HR
- SV: HUGE component to see changes in Q; since ath. have a larger chamber size and blood volume, this enhances the delivery of oxygenated blood to the active tissues = increase in oxygen extraction
- a-vO2 diff.: It is standard for the skeletal muscles to always extract 16 mL of O2/100 mL at the active tissues. To see difference, SV component of Q will then increase the amount of oxygen extraction

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15
Q

(a) What is the relationship between VO2 and Q?
(b) What does 1 L/min VO2 equal to?

A

(a) Direct linear relationship; greater amt of Q = greater rate of VO2
(b) 1 L/min VO2 = 6 L/min Q

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16
Q

What is the relative VO2 for the ATH and NA if their body weight is 70kg and their VO2max is the following?
ATH: 6,250
NA: 3,500

A

ATH:
6,250/70 = 90 mL/kg/min
NA:
3,500/70 = 50 mL/kg/min

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17
Q

Memorize the Fick equation for the ATH and NA in the order of HR x SV x a-VO2diff. (don’t forget the units)

A

ATH:
6,250 ml/min = 190 bpm x 205 mL x 16 mL of O2/100 ml of blood
NA:
3,500 = 195 bpm x 112 mL x 16 mL of O2/100 mL of blood

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18
Q

(a) Does maximal HR change in a TR vs. UT? Explain.
(b) Which variable in the Fick equation is a huge predictor/impact of one’s whole body oxygen consumption?

A

(a) No; due to SNS full activation at maximal HR
(b) Q (largely SV)

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19
Q

What is the Q for a college athlete vs. an elite athlete (cyclists)?

A

College athlete = 25 L/min Q
Elite athletes (cyclists) = 45 L/min Q

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20
Q

When an increase in VO2max occurs in training, how does it effect running velocity/speed?

A

An increase in VO2max in training results in a HIGHER running velocity/speed for a LONGER period of time

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21
Q

What is the difference between stroke volume in UT vs TR? What’s similar?

A

Difference: SV for TR occurs at a much larger number due to the further expansion in difference between the ↑EDV and ↓ESV versus individual who is UT.
Similar: There is still a liner increase up to 60%VO2max, until a plateau occurs.

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22
Q

(a) Reconsider the factors that cause ↑EDV, ↓ESV, an plateau in SV.
(b) What is the most important physiological adaptation for endurance athletes and how does it affects their stroke volume.

A

(a)
*Increased EDV
- LVEDD
- Venous Return

*Decreased ESV
- Contractility
- Blood Pressure

*Plateau @ 60% VO2max
- Heart Size (LVEDD)
- Blood Volume

(b) Blood volume is the most important adaptation, despite the morphological changes in the heart, as the heart can only pump out what it receives, in which it has the BIGGEST IMPACT on SV
- Increase in BV = increase in SV

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23
Q

Regarding SV, what occurs physiologically when an UT has suboptimal blood volume?

A

UT has inadequate amt. of oxygenated blood being delivered to the skeletal muscle during exercise
- Reduction in skeletal m. blood flow = maintenance in venous return, filling and blood pressure

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24
Q

What occurs to chamber size and and the L ventricular mass (muscle around the heart) in an aerobic athlete vs. a strength athlete? Why do these adaptation occur in a strength athlete?

A

Aerobic athlete: ↑ in chamber size and ↑in LVM
Strength athlete: NO CHANGE in chamber size (since skeletal m. can accept more blood than the heart can deliver) and ↑ in LVM (to overcome the resistance of blood flow in skeletal m.)

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25
Q

How does plasma vol. and blood vol. increase in response to aerobic exercise training?

A
  1. Activation of RAA hormone due to reduction in kidney blood flow (due to exercise/redistribution from splanchnic region)
    - Effect: retains H2O at kidneys and increase plasma vol.
  2. Erythropoietin - stimulate production of RBC; hormone
    - Released by kidney in response to decrease in kidney blood flow
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26
Q

(a) Who has a larger blood vol., an UT or TR?
(b) Which components of blood are upregulated?
(c) What is the overall percentage increase in BV from chronic training and how much does it equate to?
(d) When does increase in BV occur?

A

(a) TR
(b) Both hematocrit and plasma are upregulated
(c) 10% (~400-500mL of blood)
(d) 14-21 days

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27
Q

What has a greater increase, plasma or RBC? What does this cause in the viscosity in blood?

A

↑ in plasma is GREATER than ↑ in RBC
- Since hematocrit is less in TR athletes, blood becomes less viscous, making it easier for blood through the circulatory system

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28
Q

Compare the following during pretraining vs. posttraining:
Total blood volume
Plasma volume
RBC
Hematocrit

A

Pretraining:
Total blood volume: 5 L
Plasma volume: 2.8 L
RBC: 2.2 L
Hematocrit: 44%

Posttraining:
Total blood volume: 5.4 - 5.5L
Plasma volume: 3.3 L
RBC: 2.4L
Hematocrit: 42%

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29
Q

(a) Explain why the increase in EDV is greater than the decrease in ESV?
(b) Explain how the expansion of difference between EDV and ESV affect SV?

A

(a) Due to increase in LVEDD and blood vol.
(b) The expansion of difference between EDV and ESV allow for more blood to fill in L ventircle prior to contraction, resulting in more blood to be pushed out w/ contraction = Large increase in SV

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30
Q

What is the only variable that will account for Q?

A

Increase in SV

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31
Q

What largely causes an increase in VO2max?

A

An increase in oxygenated blood going to the tissues / Q

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32
Q

What’s the amount of oxygen being consumed / VO2 (L/min) at REST for trained and untrained?

A

EVERYBODY’S Q AT REST:
.4 L of O2/min OR 400mL of O2/min

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33
Q

Calculate the Q for trained and untrained individuals at rest?

A

1 L of O2 per min / .4 VO2 = 6 L of Q per min / .4 VO2
x = 2.4 L of Q/min at REST for EVERYBODY

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34
Q

What causes TR to have a higher Q and VO2max at higher intensity exercise?

A

↑SV = ↑Q (more oxygenated blood to active tissues)

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35
Q

How does training affect maximal heart rate?

A

Training DOESN’T affect maximal HR since it’s set by full activation of sympathetic nervous system

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36
Q

Why do TR have a lower resting HR and submaximal HR compared to UT?

A

Due to trained individ. having large BV, a low HR allows for adequate/proper filling of blood for it to be ejected from L vent.
- TR at rest: have a greater PNS activation

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37
Q

What is the single most important change that accounts for the increase in SV, which causes the increase in VO2max?

A

Blood volume

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38
Q

Explain why are the two “16s” from a-VO2diff. from the Fick equation are the same, but different for the ATH and NA.

A

Same: Arteries DELIVER 20mL of O2/100mL of blood to the tissues. Active tissues will EXTRACT 16mL of O2/100mL of blood

Difference: Since TR has 10% increase in BV giving them ~500mL of blood more, this enhances their oxygen delivery, in which also enhances the oxygen extraction at the active muscle in terms of absolute oxygen delivery

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39
Q

What occurs to whole body oxygen consumption (VO2) when oxygenated blood delivery is increased?

A

↑ oxygenated blood delivery to active tissue → ↑oxygen extraction = ↑ whole body oxygen consumption

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40
Q

Does the ventilatory system limit VO2max?

A

No

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41
Q

What does training do for maximal pulmonary ventilation rates?

A

Training can increase maximal pulmonary ventilation rates.

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42
Q

How can a-VO2diff. increase with training? (2)

A

Due to:
1) Increased oxygen extraction by the tissues (O2 utilization)
2) More effective blood distribution (increase in BV)

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43
Q

(a) While training can improve skeletal muscle metabolism (i.e., lactate threshold, respiratory exchange ratio), what’s the major limiting factor to one’s maximal oxygen consumption (VO2max)?
(b) Explain why this factor is more important than the peripheral adaptations (the ability to to use oxygen at a cellular level). Consider/relate this to Qmax.

A

(a) Oxygen delivery to the active muscle
(b) While the peripheral adaptations are important, oxygen delivery to the active tissues is the most important to see an increase in VO2max. This relates to Q because if you can increase the amount of oxygen blood being delivered to the active tissues, more oxygen can be extracted, resulting in increase in whole body oxygen consumption

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44
Q

What are the four cardiovascular adaptions that occur from aerobic training? Be sure to explain each one.

A
  • ↑ Blood flow to active muscle
  • ↑ Capillarization, capillary recruitment (peripheral adpt.)
    – Able to get more oxygenated blood to active tissues
    – ↑ Capillary:fiber ratio (peripheral adpt.)
    – ↑ Total cross-sectional area for capillary exchange
  • ↓ Blood flow to inactive regions (splanchnic region)
  • ↑ Total blood volume (400-400mL increase)
    – Single most important adaptation: allows for more blood to get to the active tissue
    – Prevents any decrease in venous return as a result of more blood in capillaries
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45
Q

(a) Is VO2 at rest the same or diff. for every individual? What is the VO2 at rest? (include units)
(b) Is VO2max the same or diff. for every individual? About how much is the increase is the VO2 max for an UT individual going to a TR state and what causes it?
(c) Is the Q at rest the same for every individual? What does this mean for VO2?
(d) Is the Q during exercise greater in TR than UT? Why? What does this mean for VO2?
(e) What happens to blood volume with training?
(f) What happens to SV at rest for a trained individual? What does this mean for HR for a TR?
(g) Is the HR for a TR lower than the HR for an UT at rest and during submaximal intensities? What does this mean for VO2max during submaximal intensity?

A

(a) VO2 is the SAME wether TR or UT; VO2 = 4L of O2/min
(b) VO2max is DIFF; 20% increase in VO2 from UT to TR state due to increase in Q
(c) Q is the SAME at REST wether TR or UT; which VO2 the same for everybody
(d) Q is greater in TR than UT due to the increase in BV in the TR; from elevation in BV causing an increase in SV, this results in the increase in VO2
(e) There’s a 10% increase in BV (~400-500mL) with training
(f) There’s an increase in SV at rest (due to increase in BV); HR will be much lower for a TR
(g) Yes. TR will have a much higher VO2max than UT

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46
Q

What are the 5 variables to consider that control/sets the ceiling in VO2max? Distinguish which one have a huge impact on the ceiling.

A
  1. Training status and pretraining VO2max
  2. Hereditary!
  3. Sex
  4. Age
  5. High versus low responders
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47
Q

(a) Where does most improvement in VO2max depend on?
(b) Do we see more increase/improvement in VO2max from a sedentary individual or a trained individual?

A

(a) Relative improvement depends on fitness
(b) Sedentary; The more sedentary the individual, the greater the ↑ than a fit individual

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48
Q

(a) What determines the finite range for VO2max?
(b) What accounts for 20%-50% of variance in VO2max?

A

(a) Genetics
(b) Hereditary

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49
Q

(a) Compare the VO2 between an UT female and male
(b) Compare the VO2 between an TR female and male
(c) Explain the three factors to why we see a difference in VO2 between men and women

A

(a) Untrained female VO2max < untrained male VO2max
(b) Trained female VO2max closer to male VO2max
(c) The differences we see occurring here between females and males is largely due to stature. As a man, typically being a larger person, has both a larger heart (LV chamber size) and greater blood volume, thus having a much larger Q. Men also have a greater hematocrit/hemoglobin concentration (as per lack of menstruation).

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50
Q

(a) What relation does age have to do with VO2? (Consider the Fick equation)
(b) For master’s athlete, individuals that have high level training as they get older, what happens to their HR and why does this occur?

A

(a) Maximal HR decreases; there’s a decrease in 10bpm for every 10 years
(b) They see a decline in 5-7 bpm in every decade due to having an ability to FULLY activate SNS at high level training

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51
Q

What is the most important cardiovascular adaptation from chronic endurance exercise and how does this effect Fick equation?

A
  • Increase in blood volume
  • ↑ blood volume → ↑SV → ↑ Q → overall ↑ in VO2max
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52
Q

(a) What are the 5 morphological components that makes up an elite athlete?
(b) What are the 5 functional abilities that makes up an elite athlete?
(c) What are the 3 components that make up the performance abilities for an elite athlete, resulting in performance velocity?

A

(a) Muscle capillary density, stroke volume, aerobic enzyme activity, distribution of power output, and muscle fiber type composition or % Type I
(b) Maximal oxygen consumption, lactate threshold VO2, economy of movement, gross mechanical efficiency, and lactate threshold power or velocity
(c) Performance VO2, performance power, resistance to movement, and performance velocity

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53
Q

Is having a high VO2 all that matters when determining who will run the fastest and win the race? Explain.

A

VO2max is NOT the only thing that matters when determining who will run the fastest and win the race since it is one of the many variables that will make an impact on the result of the athlete. Furthermore, VO2 is contributed by other factors as well.

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54
Q

What is periodization? What does it allow?

A

Periodization: dividing the entire sport training season into smaller periods of time and training units
- allows for a VARIED training load OVER TIME that enables acute overload and overreaching without overtraining the athlete.

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55
Q

Considering the periodization…
(a) At what level would you want your athlete to be at? Define it
(b) What type of training would you want your athlete to do if plateau in performance occurs. What is happening to the vol. and int. in exercises and what does this do?
(c) What state will an athlete be at if they are training at a high int. and high vol. for a long period of time? Define it.

A

(a) Acute overload: Positive physiological adaptations and minor improvements in performance
(b) Overreaching: increase in vol. and intensity to reach optimal physiological adaptations and performance
(c) Overtraining: Physiological maladaptations, performance decrements, and overtraining syndrome

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56
Q

Give an example of an athlete’s training year that was similar to the one in class.

A

General preparation; 8-12 weeks
(Strength, CV training)
↓
Specific preparation
(↑int., ↑vol., sport specific power)
↓
17 weeks - COMP.
↓
Active recovery; 4-6 weeks
(non-sport related activities)

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57
Q

(a) Why must an athlete do different things throughout the training year?
(b) What do athletes have to change in throughout the training year?

A

(a) The athlete may be overtrained before the season even starts
(b) Athlete has to change the vol. and int. of their training throughout the training year, until ready into the season

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58
Q

(a) What is overreaching? What does this allow for the body to do?
(b) Why do you have to be cautious in your planning for overreaching? What should be done?

A

(a) Overreaching: systematic attempt to OVERSTRESS the body for a short period of training to overcome plateaus in performance.
- Allows body to adapt to a stronger stimulus
- Not the same as excessive training
- Short performance decrement followed by IMPROVED performance and function
(b) Overreaching can easily cross to overtraining
- After 1 week of overreaching, athlete should get back to their normal workload to get past their plateau performance = improvement

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59
Q

What is excessive training? How did this idea affect the “tradition” of training? What does this lead to?

A

Excessive training: Volume and/or intensity to an extreme
– For years, many athletes undertrained
– As intensity/volume ↑, so did performance
– But more is better is NOT TRUE after a point
– Can lead to ↓ strength, sprint performance (overtrained)

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60
Q

If one swimmer was to train 3-4hrs/day with multiple sessions compared to another swimmer who trained 1-1.5hrs/day with just one session, can more training lead to additional improvements than someone who has trained once a day.

A

No evidence that more is better
– Similar heart rate and blood lactate improvements
– No additional improvements from 2 times/day
*More is NOT necessarily better

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61
Q

(a) How is training volume determined?
(b) What happens if some sports reduce half of the volume of training?
(c) Is low intensity, high volume exercise appropriate for sprint type performance?

A

(a) Training volume should be sport specific; there should be a connection between training intensity and the actual competition
(b) Athletes can still maintain benefits and reduce risk, especially in weight-bearing exercises
(c) No

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62
Q

What are 4 things that can be seen in overtraining syndrome?

A
  1. More common with endurance athletes
  2. Early fatigue
  3. Increased resting and submaximal HR
  4. Increased resting BP
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63
Q

What are the 2 ways we can see detect overtraining in an athlete? Explain each one.

A
  1. Performance
    - Athlete may be much slower/fatigue earlier and may even work much harder
  2. HR and BP
    - OT ath has a an unusual slight increase in resting and submaximal HR that may look like UT
    - OT ath at submaximal HR have a bit more activation of SNS when doing exercises, thus cause slight increase
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64
Q

Explain why hormonal markers/measurements aren’t as effective in a real-life standpoint for detecting overtraining syndrome in athlete?

A

In real-life, sport team don’t typically collect blood from athletes post-season; in addition, the process is expensive (collecting blood, refrigerator)

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65
Q

Can overtraining syndrome be predicted? Elaborate why (5).

A

No, but can be avoided by creating a good training program
* Causes unknown, diagnostics/characteristics difficult
* Threshold different for each athlete
* Most coaches and trainers use (unreliable) intuition
* No preliminary warning symptoms
– Coaches do not realize until too late
– Recovery takes days/weeks/months of rest
* Biological markers (blood measurements) have limited effectiveness

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66
Q

How can overtraining syndrome be treated?

A

Treatment:
– Reduced intensity or rest (days to weeks)
~ Strength will not change for the athlete

67
Q

Are there preventative measures for avoiding overtraining syndrome?

A

Prevention:
– Periodization training - w/ rest days and low vol. and int.
– Adequate caloric (especially carbohydrate) intake

68
Q

What is tapering?

A

Tapering: reduction in training volume/intensity
– Prior to major competition (recovery, healing)
– 3 to 4 days
– Most appropriate for infrequent competition (competitions that occur once a week)

69
Q

What does tapering result in?

A

Results in increased muscular strength
– May be associated with contractile mechanisms
– Muscles repair, glycogen reserves replenished

70
Q

Does tapering result in deconditioning? Why?

A

Does NOT result in deconditioning
– Considerable training to reach VO2max
– Can reduce training by 60% and maintain VO2max

71
Q

How does tapering impact performance?

A

Leads to improved performance
– 3% improved race time
– 18 to 25% improved arm strength, power

72
Q

What is detraining?

A

Detraining: complete stop of formal aerobic training resulting in the losses of training-induced adaptations

73
Q

List and describe some of the losses that occur with detraining and when do they occur?

A

Significant CV losses within 12 d
– 27% ↓ VO2max: due to reductions in SV
– 25% ↓ submaximal stroke volume (due to ↓ PLASMA VOLUME): since no activation of RAA and release of EPO due to no reduction in kidney and splanchnic BF
– 25% ↓ maximal cardiac output: = rapid decline in VO2max

74
Q

With about 90 days of detraining…
(a) What are the 3 CV adaptations that decline?
(b) What are the 2 morphological CV adaptations that are still stable?

A

(a) BV, SV, and VO2max
(b) Chamber size (L ventricle) and muscle mass (LVM)

75
Q

(a) What happens to the capillary density and myoglobin concentration if TR starts to detrain?
(b) What happens to the oxidative capacity of the skeletal muscle if TR starts to detrain? How does this compare to an UT?

A

(a) Elevated levels of capillary density and myoglobin concentration are still stable/maintained after detraining
(b) A 20% decline in oxidative capacity occurs post 90 days of detraining
- But is still 50% higher compared to an individual who had not done any aerobic exercise

76
Q

What will happen to a TR ath. if they start training again after recently detraining?

A

When TR athlete starts training again after detraining, they START at a much HIGHER level than someone who never trained before
- They may also have the ability to get to their previously trained level at a FASTER rate
- However, the stability of these factors depend on the years of training
~ (EX: 6-12 months of training vs 10yrs of training)

77
Q

What happens to glycogen content of the skeletal muscle of an athlete if they start to detrain. When do results occur?

A

With 4 weeks of detraining, complete reversal of glycogen content deplete to the same amt. of a non-Tr skeletal m.

78
Q

What happens to the 1RM of a strength ath. if they start to detrain? Why does this occur? What happens to the # of 1RM?

A

1RM (strength) is maintained w/n 3-4 weeks of detraining, due to maintenance of muscle hypertrophy (and mobility) and protein expression
- The # of 1RM (muscular endurance) does decline

79
Q

How can detraining be prevented?

A
  • Losses occur when frequency and duration decrease by 2/3 of regular training load
    ~ A good portion of training adaptations can still be maintained
  • 70% VO2max training sufficient to maintain maximal aerobic capacity
    ~ Exercise intensity is important!
    ~ < 70%VO2max will result in reduction in VO2max and peripheral adaptations as the muscle needs to be activated and doing work
80
Q

What is ergogenic vs ergolytic?

A

Ergogenic: “work producing” substances
- Enhance/improve performance
Ergolytic: “work breaking” substances
- Inhibit work

81
Q

What are the four types of potential aid that is used in sport?

A
  1. Pharmacological agents
  2. Hormones
  3. Physiological agents
  4. Nutritional agents
82
Q

(a) What must be proven when researching ergogenic aids? Why?
(b) What is a pseudo-ergogenic response?

A

(a) Must be proven to enhance performance
– Claim alone insufficient
– True ergogenic versus pseudo-ergogenic responses
(b) Pseudo-ergogenic response: If a person claims that their substance or practice is enhancing their performance without it being backed by research

83
Q

What is a placebo and describe the placebo effect.

A
  • Placebo: inactive substance that looks like the real thing
  • Placebo effect: expectations affect physiological response
84
Q

What is a double-blind experimental design?

A
  • People running the experiment don’t know what they’re giving to subject, so that subject also does not know
  • Researchers also don’t have to influence the outcome of the study
85
Q

What do some scientific journals pertaining to ergogenic questions may or may not provide? What results do they often have?

A
  • Scientific journal MAY NOT provide clear answers to ergogenic questions (studies that contain negative findings is impossible to publish)
  • MAY be able to prove ergogenic response
  • Results often equivocal/questionable
86
Q

What are some factors that can limit research

A

– Technique, equipment inaccuracy
– Research methodology ; good study designs, but don’t get the outcome you want
– Testing situations (lab vs. field)

87
Q

(a) Can a person take a substance if there’s no negative side effects and doesn’t do anything?
(b) What if there’s a negative side effect?

A

(a) Fine for person to take it
(b) Don’t take it

88
Q

What is WADA and what does it do?

A

WADA / World Anti-doping Agency: establishes a level playing field, tests for PED

89
Q

(a) What is the criteria for prohibited substance of the World Antidoping Code?
(b) What should sport teams and athletes be aware of when it comes to ergogenic aids in their sports?

A

(a)
1. Substance or practice has the potential to ENHANCE sport performance
2. Substance or practice has the potential to HARM the athlete
3. Substance or practice VIOLATES THE SPIRIT OF THE SPORT
(b) Sport teams and athletes must be aware of what’s allowed or limited in their sport

90
Q

Name one type of pharmacological agent that was discussed in class. What does it do?

A

Pharmacological agent: Caffeine
- Central nervous sytem stimulant
- Sympathomimetic effects (increased activation of SNS); but weaker (to amphetamines)

91
Q

List the proposed benefits vs the proven effects of the following:
Caffeine

A

Proposed benefits:
– ↑ Mental alertness, feel more competitive
– More energy, reduced or delayed fatigue
– Enhanced mobilization of FFAs
– Glycogen sparing

Proven effects:
– ↑ Alertness, concentration, and mood
– ↓ Fatigue and reaction time (faster response)
– ↑ Blood FFA Concentration
– ↑ All aerobic performance

92
Q

Explain how caffeine affects/enhance prolong exercise. Consider what caffeine stimulates, the hormones and its effect.

A
  • Caffeine elevates SNS levels, causing an increase in secretion of Epi/NoE levles
  • If there’s an increase in catecholamine concentration in blood, that would also cause an increase in the activation of HSL, resulting in a greater breakdown of TG = ↑ FA circulation
93
Q

Explain how does caffeine affect glycerol and FFA levels during exercise?

A
  • Glycerol concentration is high due to TG being broken down from the elevated levels of catecholamines
  • There is an increase in FFA at the beginning of the exercise, but will deplete at the onset of exercise due to muscle contraction, but at later stages of exercise , FA levels will start to increase again
94
Q

Compare/explain the rate of fatigue of the skeletal muscle that had caffeine vs placebo (water). Why did this occur?

A

The subject who took the placebo (water) experienced fatigue set in, whereas the other subject who took caffeine was able to exercise ~15 mins longer due to their muscle glycogen levels still being high in the muscle
- When on caffeine, the rate of muscle glycogen use was slower…
- Since levels of FA was elevated in the blood, increasing the FA delivery to the skeletal m., it reduced reliance on muscle glycogen

95
Q

List the risks of caffeine

A

– Nervousness, tremors, insomnia
– Headache
– GI problems (known to be a diuretic, however… urine output was correlated to the vol. of fluid intake wether or not you had caffeine)

96
Q

What are the two types of hormonal agents discussed in class?

A
  1. Anabolic steroids
  2. Human growth hormone (hGH)
97
Q

(a) What are anabolic steroids and what are they used for?
(b) How have athletes become good at avoiding detecting for anabolic steroid use?

A

(a) Anabolic steroid: an ergogenic aid that has androgenic (similar to male sex hormones) effects, that can be used as a compound or an injectable
– Enhances anabolic function (builds bone, muscle)
(b) Athletes will cycle on and off the compunds when testing is announced
- Testing agencies only test for known anabolic steroid compounds

98
Q

List the proposed benefits for anabolic steroids

A

Proposed benefits on anabolic steroids:
– Increased fat-free mass (FFM), strength
– Reduced fat mass
– Facilitate recovery after exhaustive exercise

99
Q

Compare how athletes used anabolic steroids before vs. now.

A

Before - athlete CYCLE w/ anabolic steroids
Now - athletes dose w/ DIFFERENT FORMS of anabolic steroids to get an increase in effect

100
Q

What is the does threshold to achieve anabolic effect? What occurs with a small dose?

A

– Small doses ineffective
– Large, chronic doses very effective

101
Q

How does anabolic steroids achieve the effect of the larger muscle mass?

A

↑ of muscle mass on anabolic steroids due to ↑ rate of protein synthesis = ↑ # of nuclei = larger ↑CSA of muscle

102
Q

List the proven effects of anabolic steroids on the following:
(a) muscle mass, strength
(b) recovery from training.

A

(a) Proven effects on muscle mass, strength
– ↑ body mass, FFM
– ↓ Fat mass
– ↑ Total body potassium and nitrogen (FFM markers)
– ↑ Muscle size, strength ; makes it possible for women to achieve ↓FM, ↑MM (W only have 10% testosterone)

(b) Proven effects on recovery from training
– ↓ muscle fiber damage after exhaustive lifting ( due to more nuclei = ↑CSA)
~ Helps maintain performance and muscle mass throughout the season
– ↑ Rate of protein synthesis during recovery (rats)

103
Q

What type of players would typically use anabolic steroid?

A

Baseball pitchers
- Due to greater arm strength and faster recovery
- “Quadruple A” players (in hopes of getting into the major league)

104
Q

List the issues pertaining to anabolic steroid use.

A
  • Moral and ethical concerns ( lots of side effects = MAJOR REASON as to why it’s banned)
  • Fair competition (basis for World Anti-Doping Code): don’t want athlete to feel pressured into taking a compound to competitive when negative side effects occur
105
Q

What are the 5 risks and side effects associated with anabolic steroids?

A

1) Sexual risks
– Men: early growth stoppage (w/n prepubescent), suppression of normal hormones (testicular abnormalities - body causes atrophy of the gland to maintain circulation of hormone), excess estrogen (breast enlargement)
– Women: disrupted menstruation/ovulation, development of masculine sex characteristics (beard, deepening of voice)

2) Cancer risk: prostate, liver

3) Cardiovascular risk:
– Cardiac hypertrophy, cardiomyopathy, heart attack
– Thrombosis, arrhythmia, hypertension
– ↓HDL, ↑ LDL

4) Emotional and physiological risks
– ↑ Aggression (“roid rage”)
– ↑ Violence
– Potential drug dependence

5) Other risks
– Contracting hepatitis, HIV/AIDS
– ↓ Life span (mice)
– ↑ Incidence of birth defects
– Long-term effects of abuse unknown

106
Q

Explain what happens to HDL level when cycling anabolic steroids vs chronically using it

A

When cycling/off - HDL levels elevate again
However if chronically using anabolic steroid - might be chronic suppression of HDL levels

107
Q

If an athlete comes of the anabolic steroid, do they maintain the number of nuclei and elevated muscle mass?

A

Probably not

108
Q

(a) What type of agent is human growth hormone and what is the idea that it was used?
(b) What are the 6 proposed benefits of hGH use?

A

(a) Hormonal agent; for the idea it’s an anabolic hormone (to promote muscle mass and facilitate recovery)
(b) Six proposed benefits of hGH use
– Stimulates protein, nucleic acid synthesis
– Stimulates bone growth (young athletes)
– Stimulates IGF-1 synthesis (activates synthetic pathway for muscle hypertrophy)
– ↑ FFA mobilization, ↓ fat mass
– ↑ Blood glucose levels
– Enhances healing after injury

109
Q

(a) List the proven effects of hGH use
(b) List the risks of hGH use

A

(a) Proven effects of hGH use
– ↓Fat mass
– Young athletes: no anabolic effects (there’s already enough hGH circulating)
– Older men: ↑ FFM, ↑ bone density
(b) Risks of hGH use
– Acromegaly (bony eyebrows)
– Cardiomyopathy, hypertension (cardiovascular risks)
– Glucose intolerance/diabetes (via insulin injection - anabolic hormone stimulates protein synthesis)

110
Q

What are physiological agents and list the four aids that are discussed.

A

Physiological agents: Naturally occur in the body in which athletes will try to supplement the things that are present
- Blood doping
- EPO
- O2 supplementations
- Bicarbonate loading

111
Q

(a) What is blood doping?
(b) What does blood doping do to BV and what does that do to VO2max? (Consider Q)
(c) List the proposed benefits of blood doping
(d) List the proven effects of blood doping

A

(a) Blood doping: the means of which red blood cell count increases often through the transfusion of previously donated RBCs
(b) Artificial ↑BV → ↑SV →↑Q
- Due to ↑BV →↑Q setting a higher VO2max for higher level athlete doing aerobic performance
(c) Proposed benefits of blood doping (↑BV = ↑RBC)
– Enhanced oxygen-carrying capacity
– Improved aerobic endurance and performance
(d) Proven effects of blood doping
– ↑ VO2max (long term)
– ↑ Aerobic endurance (short term)

112
Q

(a) What is the lifespan for a RBC?
(b) When should you reinfuse blood when an event is coming up? Why?

A

(a) ~120 days ; not every RBC in body is same “age”
(b) 2-3 days before the event due to the lifespan of the RBC

113
Q

Explain how one can maximize the benefits of blood doping. In other words, what’s the process of blood doping?

A
  • Athlete draws out ~900+mL of their own blood
  • Must wait 5 to 6 weeks before reinfusion; in the meanwhile, athlete continue to train to reestablish their plasma vol. and [RBC]
  • Blood must be stored in freezer (not refrigerate), for long-term stability
  • Reinfuse the blood just a week or so (~2-3 days) before the event = ↑plasma vol and [RBC]
114
Q

Is blood doping effective in enhancing aerobic performance? How?

A

Blood doping is effective in enhancing aerobic performance
- Due to ↑ in Q, plasma volume, [RBC], and oxygen carrying capacity

115
Q

(a) List out the potential risks of blood doping (5)
(b) Despite the risks, should an athlete still continue blood doping? Why?

A

(a) Risks of blood doping
– Blood becomes too viscous = clotting
– Excessive clotting, heart failure
– Some sports set hematocrit LIMITS for competition
– Blood matching complications
– Exposure to bloodborne diseases
(b) No!
– Potential medical risks far outweigh benefits

116
Q

What is EPO and how is it different from blood doping?

A

EPO (erythropoietin): a naturally occurring (physiological agent) hormone that stimulates the increase of RBC production/concentration from a reduction in kidney BF ; initially for made chemotherapy patients
– Differs from blood doping simply is the mechanical filling to oxygen carrying elements in blood vs EPO which STIMULATE the production increase of oxygen carrying elements in blood

117
Q

List the proposed benefits vs the proven benefits of EPO

A
  • Proposed benefits of EPO
    – Increased hematocrit (RBC concent.)
    – Increased oxygen-carrying capacity (hemoglobin concent.)
  • Proven effects of EPO
    – ↑ Hemoglobin, hematocrit, and VO2max
    – ↑ Time to exhaustion
118
Q

(a) List the risk of EPO use
(b) Why is blood doping more dangerous than EPO?
(c) Can EPO be tested?

A

(a) Risks of EPO use
– Dangerous increase in blood viscosity (from over prod. of RBC/EPO)
– Blood clots, heart attack, heart failure, stroke
– Pulmonary embolism, hypertension
(b) Effects of EPO LESS PREDICTABLE than those of red blood cell reinfusion
(c) Difficult to test for since it is a physiological agent
- But can be testable via urine

119
Q

(a) List the proposed benefits of O2 supplementation
(b) List the proven effects of O2 supplementation

A

(a) Proposed benefits of O2 supplementation
– Increase dissolved oxygen in blood
– Delay fatigue, speed recovery
(b) Proven effects of O2 supplementation
– Preexercise treatment → little or no effect
– During exercise → ↑ work, work rate, metabolic efficiency, ↓ peak blood lactate levels (However, not practical in real-life setting)
– After exercise → no effect ; after exercise (at altitude) → may be some effect

120
Q

(a) Explain the idea as to why athletes use O2 supplementation
(b) Explain the problem behind their idea

A

(a) The idea that if you breath 100% oxygen, that will increase oxygen concentration in blood
(b) At sea level, an individual is breathing 20.93% O2, thus already have 100% saturation in hemoglobin, thus no effect, but may have some effect on an increase amt. of O2 dissolved in plasma (but blood doesn’t transport well in liquid)

121
Q

(a) List the risks of O2 supplementation
(b) Is O2 supplementation practical?
(c) Does training altitude have an effect in performance at sea level?
(d) How should athletes train if they have a competition in altitude.

A

(a) Risks of O2 supplementation
– No known risks
– Safety needs further research
– Oxygen equipment potentially dangerous
(b) Overall, simply not practical. Unless in laboratory setting
(c) It has little to no effect
(d) Athletes should train in altitude days before their competition to adjust

122
Q

(a) What is bicarbonate loading and what is it proposed to do?
(b) List the proven effects of bicarbonate loading.

A

(a) Bicarbonate loading: the intake of baking soda (+ water) with the hopes of seeing an increased blood pH (more basic) and buffering capacity to delay the onset of fatigue
(b) Proven effects of bicarbonate loading
– 300 mg/kg → ↑ all-out performance for 1 to 7 min
~ Glycolytic system turned on at a high rate = more lactate being able to be produced since a greater amt. of H+ can be buffered
– Enhanced H+ removal (↑ buffering capacity) from muscle fibers

123
Q

Explain what occurs to the physiologically if one was to do bicarbonate loading. Consider the following:
(a) Blood
(b) Amt. of H+ ions
(c) Fatigue - glycolysis and lactate

A

(a) There’s an increase in bicarbonate concentration in blood
(b) There’s less free H+ ions due to the bicarbonate buffer
(c) Thus allows for the athlete to turn on glycolysis to turn on at a high rate and to accumulate more lactate without the worry of fatigue occurring since the buffer is doing what it’s suppose to do

124
Q

(a) What are the risks of bicarbonate loading?
(b) Can bicarbonate be tested?

A

(a) Risks of bicarbonate loading
– GI discomfort (bloating, cramping)
– Sodium citrate → similar results without risks (bicarbonate is still stronger buffer)
(b) Bicarbonate is hard to test is this is naturally occuring

125
Q

What type of agent is creatine and where/what is the use of creatine known for?

A

Nutritional agent - Creatine
– Has a widespread use (from recreational to professional), and is mostly know in the weight room/resistance training in hopes of targeting the skeletal muscle as the idea to increase muscle mass

126
Q

(a) List the proposed benefits of creatine?
(b) Why do some people believe that creatine works?

A

(a) Proposed benefits of creatine
– Increased muscle PCr content (to do more reps)
~ HOWEVER… when mTOR all-or-none signaling pathway is on, additional reps won’t have much of an effect on muscle hypertrophy
– Enhanced peak power production
– Serves as buffer, helps regulate pH balance
– Enhanced oxidative metabolic pathways (won’t make sense for marathon runners)
(b) When someone takes PCr and since PCr is hydrophilic, the water will cause a hypertrophy in the muscle. But creatine does not do anything else other than enhance muscle PCr content

127
Q

(a) What does the ACSM conclude regarding creatine?
(b) At which type of activity does creatine appear to improve to?
(c) What is the typical recommendation of creatine intake?
(d) When should an athlete consume creatine to get the benefit of its effect in competition

A

(a) ACSM conclusions regarding creatine
– Enhances high-power-output activity
– Maximal strength or muscle mass not affected
– Results do not live up to expectations
(b) Appears to improve repeated high intensity sprint type activities
– Helps with PCr resynthesis if you have less than 3 mins. of recovery time between repeated bouts of sprint activity
(c) 20g/day (split into 4 5g doses throughout)
(d) 5-7 days before the event

128
Q

How can nutritional agent supplements get contaminated? (3)

A
  • Supplement marketing and labeling not overseen by FDA (as their not seen as food by FDA)
  • Purity of supplements and accuracy of supplement labels suspect
  • Contamination with banned substances can lead to disqualification, forfeit of medals
129
Q

(a) What is the recommended macronutrient balance for a normal mixed diet in percentage form?
(b) What is the optimal for?
(c) What is the problem with the recommended macronutrient balance being in percentage?

A

(a) Recommended macronutrient balance
– Carbohydrate: 50-55% of daily kilocalories
– Fat: <30% /(~25-30%) ; (<10% saturated) - makes up the balance of the diet once total cal. are figured)
– Protein: 15%
(b) Optimal for both performance and health
(c) People don’t know their caloric intake

130
Q

Despite weight gain and loss, does caloric intake matter if it’s in balance with activity?

A

No

131
Q

What is the preferred CHO intake that was discussed in class for the following: (Remember the units)
(a) Low-mod
(b) Mod-high
(c) High+

A

CHO g/kg
(a) Low-mod: 5-7
(b) Mod-high: 7-10
(c) High+: 10-12+

132
Q

(a) What is nitrogen balance and how is it measured?
(b) If an athlete plans on build muscle, which nitrogen balance should he/she be in?

A

(a) Nitrogen balance: the amt. of protein going in is the same amt. of protein going out
- Measured through the amt. of N from the amine group (NH2) of the amino acid
(b) Positive nitrogen balance (N in > N out)

133
Q

What is the preferred PRO intake that was discussed in class for the following. Specify the state of nitrogen balance for B, D, F : (Remember the units)
(a) RDA recc.
(b) Adults
(c) Active adults
(d) Training
(e) Heavy aerobic
(f) Max

A

PRO g/kg
(a) RDA recc.: 0.8
(b) Adults: 1.0 - 1.1 (LIKELY in nitrogen balance)
(c) Active adults: 1.2-1.3
(d) Training: 1.4-1.6 (PERFECT nitrogen balance)
(e) Heavy aerobic: 1.6-1.8 ( > than resistance ath.)
(f) Max: 2.0 (FULL nitrogen balance)

134
Q

(a) What is the typical glycogen content in the skeletal muscle after a overnight fast? Remember the units
(b) Compare the low-CHO diet (40%) vs the high-CHO diet (70%)
(c) What is essential in order to maintain adequate fuel source?
(d) Between a low-CHO diet vs a high-CHO diet, what should the athlete lean towards to have an adequate amt. of fuel for their training session?

A

(a) 120 mmol/kg muscle glycogen
(b) With the first 2hr training bout, both subjects have their muscle glycogen down, but with a High CHO diet, it was able to to have their muscle glycogen levels increase back to where it started in time for their next training bout.
- HOWEVER, with the subjects who had a Low CHO diet, there is a huge depletion in muscle glycogen compared to the the High CHO diet, that by the 3rd training bout, there was no use in muscle glycogen availability
(c) An adequate amt. off CHO is essential when trying to maintain adequate amt. of fuel so that muscle glycogen storage can be replenished for adequate fuel
(d) High-CHO diet!

135
Q

(a) How long does it take to see an alteration in muscle glycogen concentration if one was to change their CHO dietary intake?
(b) What will the alteration of muscle glycogen intake have an impact on?
(c) At 70%VO2 max, how is exercise performance impacted by the following diet:
- Low CHO diet (40%)
- Normal diet (50%)
- High CHO diet (70%)

A

(a) 1 week
(b) Exercise performance and the time to fatigue
(c) - Low CHO diet (40%): able to exercise just a bit after 50 mins.
- Normal diet (50%): just at 100 mins.
- High CHO diet (70%): just at 190 mins. (>200mins.)

136
Q

(a) Is there a limited capacity to how much glycogen can be stored in a skeletal m.?
(b) How much glycogen can muscle store?

A

(a) There’s a capacity to much glycogen can be stored in skeletal muscle
(b) Up to a little bit over 200mmol/kg

137
Q

Compare how CHO loading was done before vs. now

A
  • CHO loading before: 1 week leading up to the event, athlete MUST DEPLETE skeletal muscle glycogen (low CHO diet) prior to loading to see a substantial increase. After 3 days, athlete are put on a high CHO diet so that muscle glycogen content is relatively high
  • CHO loading now: Keep the athlete on a normal mixed diet (50% CHO) and continue to make them train and switch to a high CHO diet 3 days before the event. Muscle glycogen is still increased to the same level, but also makes it more tolerable for athletes during the first 3-4 days leading to event
138
Q

(a) What should athlete’s maximize the storage of to see an increase in performance?
(b) What should the athlete’s diet look like before an aerobic exercise/event? In other words what is carbohydrate loading?
(c) Along with CHO loading, what type of training should an athlete be in 3-4 days before the event?
(d) Where is the increase in glycogen content?
(e) Where is higher glycogen content available?
(f) What type of carbohydrates should the athlete intake?

A

(a) Maximal glycogen stores → ↑ performance
(b) Carbohydrate (glycogen) loading
– Tapering training week before event
– Days 6 to 4 before event: normal CHO diet (50%)
– Days 3 to 1 before event: high CHO diet (70%)
– Muscle glycogen stores increased = later fatigue
(c) Tapering (↓ vol + ↓ int.)
(d) In both muscle and liver
(e) In skeletal muscle
(f) Complex carbohydrates (glucose, dextrose): Starch, pasta, whole grain
* Simple/processed sugar is not ideal

139
Q

REVIEW: Describe the factors that causes fatigue during prolonged endurance exercise (in terms of not adding anymore fuel and only with the fuel you start with)

A

LOW LIVER + MUSCLE GLYCOGEN
LOW BLOOD GLUCOSE
= RUN OUT OF FUEL
Occurs within 70% VO2max with 2-3 hours of exercise (marathon)
a. Glycogen depletion
1. Muscle glycogen levels
- As exercise continues, muscle glycogen levels gets lower, so it will have to start relying on the glycogen in the liver and the blood glucose in order to maintain that glycolytic flux
2. Liver glycogen levels
- Liver glycogen converts to glucose via glycogenolysis to maintain the blood glucose
- However, due to limited supply of glycogen in the liver, the blood glucose level will also go down later in the exercise.
- Therefore, the rate of liver glycogenolysis is LESS/SLOWER than the rate of blood glucose uptake by the muscle, resulting in blood glucose to also go down
- Fatigue sets in due to the inability to provide an adequate supply of fuel to the muscle

140
Q

(a) If CHO is provided during prolonged exercise, what does that do to increase the time to fatigue?
(b) How does this also affect R value?

A

(a) The time to fatigue was improved by an hour, not due to the relation in the rate of muscle and liver glycogen utilization but rather maintenance of blood glucose concentration
- The intake of CHO vs. water was NO DIFFERENT on muscle GLYCOGEN UTILIZATION as well as liver glycogen
- HOWEVER, the subject who took CHO was able to exercise for an extra hour than the subject who drank water due to the intake of CHO MAINTAINING BLOOD GLUCOSE concentration to maintain glycolytic flux
(b) R value is higher at later stages of exercise = ↑ rate of CHO oxidation due to more CHO availabiltiy

141
Q

(a) What is the rate of assimilation for CHO to pass through the digestive tract and diffuse through blood?
(b) During aerobic exercise, what is the TIMING and AMOUNT of CHO that should be taken?
(c) How many grams per every minute was CHO taken in the study that was discussed?

A

(a) 1g CHO/min
(b) 60g/hour
(c) 20g CHO for every 20 mins in the exercise

142
Q

Discuss the mechanism of fatigue during prolonged exercise and the scenario if a subject was to consume 60g CHO/hr, how does that effect the athlete to exercise for a longer period of time.

A

MUST MENTION:
- low liver and muscle glycogen + low blood glucose = run out fuel
- 60g CHO/hr intake was able to maintain blood glucose concentration to increase the maintenance of glycolytic flux, however, it had no effect on muscle and liver glycogen utilization which is no different from the placebo

143
Q

(a) Is timing important in when you take CHO post-exercise in terms of optimizing rates of muscle glycogen storage?
(b) How much CHO should an athlete training at a high level consume?
(c) When should an athlete consume CHO following an exercise?
(d) How many hours total should an athlete consume CHO to maximize their storage of glycogen?

A

(a) Yes
(b) 1g of CHO/kg body mass (to ensure adequate amt. of CHO)
(c) Every 2 hours beginning immediately after exercise (0 h post exercise); or first 15 mins (worst case is delay of 45 mins)
(d) 6 hours total to maximize storage of glycogen

144
Q

(a) How much protein can an athlete add to their carbohydrate following exercise? What’s the ratio?
(b) What types of athlete can benefit from this and why?
(c) What type of protein can be used?

A

(a) 60g CHO + 15g PRO (4:1)
(b) Beneficial for endurance, and importantly resistance athletes. Since protein is an insulin enhancer, it helps transition the athlete from a catabolic state to an anabolic state post-exercise = better rates of protein synthesis (muscle hypertrophy)
(c) Whey protein (they contain essential A.A.)

145
Q

(a) Between hydration vs dehydration, which improves exercise performance?
(b) Compare how hydration vs dehydration effect HR

A

(a) Hydration is important for performance whereas dehydration can cause an individual to run slower
(b) Hydration - No change in HR (due to no change in plasma vol.)
Dehydration - HR increases (due to significant deduction in plasma vol. causing a decrease in SV = HR must increase to maintain Q)

146
Q

(a) What are sport drink composed of and what are it’s benefits?
(b) What does the CHO concentration in sport drinks do?

A

(a) Composed of water + energy (CHO) + electrolytes that has a widespread of performance benefits
(b) CHO concentration: energy delivery
– ↑ CHO content slows gastric emptying
– Most drinks have 6 to 8 g CHO per 100 ml fluid
~ Typically, it should be 10g/100mL = 10% sol.
– Mostly glucose (should be high quality), glucose polymers
~ Sometime high fructose corn syrup is used since it’s inexpensive and fructose is a disaccharide (glucose and sucrose); sucrose can’t be metabolize by the skeletal muscle, so it has to go to the liver to become glucose before it can be used by the muscle

147
Q

Define conduction and provide an example.

A

Conduction: The physical transfer of heat from one physical material to another physical material
- EX: seat

148
Q

Define convection and provide an example.

A

Convection: Transfer of heat to a liquid or a gas
- EX: sea and ambient air

149
Q

Define radiation.

A

Radiation: Radiate heat out into the environment

150
Q

Define evaporation and explain why it is not considered “sweat evaporation”?

A

Evaporation: Evaporation of water for heat transfer to occur
- Sweat dripping is NOT effective for heat transfer

151
Q

How does humidity play a role in sweat evaporation vs. a dry heat environment?

A
  • Humidity makes it HARDER for sweat to evaporate
  • Dry heat ALLOWS for sweat to be evaporated
152
Q

(a) What is the major mechanism of heat transfer at REST?
(b) What is the mechanism for majority of heat loss during EXERCISE?

A

(a) Radiation
(b) Sweating

153
Q

(a) What senses an increase in (internal) temperature?
(b) What becomes activated if core temp. increases and what are its 2 effectors?
(c) What are the purposes of these effectors?
(d) Where would blood mostly be distributed? Explain how this would effect venous return?
(e) Explain how the activation of sweat glands assist in regulating body temp.?

A

(a) Hypothalamus
(b) SNS - Of the skin: 1) blood vessels , 2) sweat glands
(c) For cooling purposes (heat transfer) by distributing blood closer to the surface of the skin
(d) To the periphery/skin = harder for venous return due to no muscle pump in the skin
(e) By increasing heat loss

154
Q

(a) Explain the 2 physiological cardiovascular response that occur when one is NOT accustomed to exercising in the heat?
(b) Explain the 2 physiological metabolic response that occur when one is NOT accustomed to exercising in the heat?
(c) Summarize three points as to why one is NOT accustomed to exercising in the heat, may fatigue sooner?

A

(a) Physiological cardiovascular response
- ↑VO2 (work much harder)
-↑HR (due to more blood going to the skin making it harder for venous return
(b) Physiological metabolic response
- Muscle glycogen is used at a faster rate (since individ. is working harder and fatigue may occur sooner)
- Blood lactate is much higher (since glycolysis is turned on at a higher rate)
(c) Working harder, using fuel sources at a faster rate (glycogen), producing more lactate = fatigue sooner

155
Q

(a) What is an early adaption with chronically exercising in the heat and how does this affect heat transfer?
(b) Explain why the core temperature doesn’t increase as quickly when an athlete is chronically exposed to heat? How does this affect body temp?
(c) Is HR affected for a heat-acclimated individual and why? What does this mean for venous return?
(d) Is VO2 affected for a heat-acclimated individual compared to a normal temp. exerciser?
(e) What accounts for energy expension and O2 conusmption to be lower in a heat-acclimated athlete?

A

(a) Athletes can sweat SOONER + MORE at the onset of exercise = Better and faster transfer of heat
(b) Blood has a better chance of going to the skeletal muscle and can dissipate/transfer heat out to the environment faster = maintained body temp.
(c) HR is unaffected/ much lower compared to a non-heat acclimated individual since not much blood is going to the periphery = venous return is maintained
(d) VO2 is NO different from exercising in heat vs. normal temp = not working as hard
(e) NOT much of a DRIFT in HR to maintain the same Q

156
Q

(a) Compare the the rate of muscle glycogen utilization between a heat-acclimated exerciser vs. neutral environment exerciser.
(b) Compare the the rate of lactate production between heat-acclimated exerciser vs. neutral environment exerciser.

A

(a) Rate of muscle glycogen use was the SAME in neutral vs heat environment
(b) Lactate production was also the SAME

157
Q

Compare the muscle glycogen between the two groups:
(a) Non-heat acclimated individ. vs heat acclimated individ.
(b) Heat acclimated individ. vs. room temp exerciser

A

(a) Non-heat acclimated individ. uses glycogen at a FASTER rate vs heat acclimated individ. which uses glycogen at a SLOWER rate
(b) Heat acclimated individ. uses glycogen at the SAME rate as someone who exercises at room temp

158
Q

(a) What changes occurs if someone exercises repeatedly in heat?
(b) How long does it take for one to see SHORT TERM acclimation to heat?
(c) How long does it take for one to see LONG TERM acclimatization to heat?
(d) What are the 4 effects of acclimation?

A

(a) Repeated exercise in heat → rapid changes for better performance in hot conditions
(b) 9-14 days (2 weeks)
(c) Months/years
(d) Effects of acclimation
– Cardiovascular function optimized
– Sweating rate, sweat distribution, and sweat content change
– Results in a lower core temperature during exercise
– Slower rate of muscle glycogen utilization

159
Q

(a) What happens to heart rate and cardiac output in a heat-acclimated individual? What does this effect?
(b) What is sweating like for a heat-acclimated individual and how does this benefit them?

A

(a) ↓ Heart rate, ↑ cardiac output
– Supports ↑ skin blood flow
– Greater heat loss, ↓ core temperature
(b) Widespread sweating EARLIER, MORE dilute
– Prevents dangerous Na+ loss
– Optimized heat loss

160
Q

List the health risks regarding exercising in the heart from least to most severe

A
  1. Heat cramps
  2. Heat exhaustion
  3. Heatstroke
161
Q

What is heat cramps? What causes it and who is most common to get it? What can prevent this?

A

Heat cramps:
* Severe, painful cramping of large muscles
* Triggered by Na+ losses, dehydration
* Most common in heavy sweaters
* Prevented by liberal Na+ (electrolytes), water intake (matched by sweat rate)

162
Q

How do you find sweat rate?

A

(Body weight before exercise – Body weight after exercise) / minutes of exercise = sweat per min (fluid intake)

163
Q

What is heat exhaustion? What causes it? How can this be prevented?

A

Heat exhaustion:
* Accompanied by fatigue; dizziness; nausea; vomiting; fainting; weak, rapid pulse
* Caused by severe dehydration from sweating
* Simultaneous blood flow needs of muscle and skin not met due to LOW blood volume
* Thermoregulatory mechanisms functional but overwhelmed
* Treatment: Stop exercise, move to a shade with air condition, and administer fluids containing electrolytes

164
Q

What is heatstroke? What causes it? What characterizes it?What occurs if untreated? How can this be treated?

A
  • Life threatening, most dangerous
  • Thermoregulatory mechanism FAILURE
  • Characterized by:
    – Core temp >40 °C
    – Confusion, disorientation, unconsciousness
  • If untreated, results in coma and death
  • Must cool whole body ASAP (e.g., ice bath)

Exercise Physiology (8 decks)

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