Exercise Science Ch 1-6 Flashcards

1
Q

Muscle Fiber type that relaxes slowly

A

Type 1

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2
Q

Muscle Fiber type that relaxes rapidly

A

type 2 a and 2b

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3
Q

3 types of joints

A

Fibrous ( sutures, skull)
synovial ( elbow knee)
cartilaginous ( IV discs)

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4
Q

outer layer of muscle

A

epimysium

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5
Q

surrounding each fasciculus, or group of fibers

A

perimysium

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6
Q

surrounds individual muscle fibers

A

endomysium

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7
Q

sarcomere

A

smallest contractile unit of muscle

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8
Q

calcium binds with what protein during muscle contractions and leads to what

A

troponin, tropomyocin moving to allow actin and myosin cross-bridging

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9
Q

hydrolysis or power stroke

A

shortening of muscle ATP -> ADP +P

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10
Q

recharge phase of muscle contraction

A

ATP is
available to assist in uncoupling the myosin from the actin, and
sufficient active myosin ATPase is available for catalyzing the
breakdown of ATP.

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11
Q

Which bands elongate

A

I and H

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12
Q

Steps of Muscle Contraction

A

Initiation of ATP splitting (by myosin ATPase) causes myosin head to be in an
―energized‖ state that allows it to move into a position to be able to form a bond with
actin.
2. The release of phosphate from the ATP splitting process then causes the myosin head
to change shape and shift.
3. This pulls the actin filament in toward the center of the sarcomere and is referred to as
the power stroke; ADP is then released.
4. Once the power stroke has occurred, the myosin head detaches from the actin but
only after another ATP binds to the myosin head because the binding process
facilitates detachment.
5. The myosin head is now ready to bind to another actin (as described in step 1), and
the cycle continues as long as ATP and ATPase are present and calcium is bound to
the troponin.

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13
Q

the maximal amount of force the motor unit can develop.

A

tetanus

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14
Q

Type I muscle fiber

A

(slow-twitch)
efficient and fatigue resistant have a high capacity for aerobic energy
supply, but they have limited potential for rapid force development, as
characterized by low myosin ATPase activity and low anaerobic power

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15
Q

Type 2a muscle fier

A

(fast-twitch)
inefficient and fatigable and as having low aerobic power, rapid force
development, high myosin ATPase activity, and high anaerobic power

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16
Q

Type 2b muscle fiber

A

IIx (fast-twitch)

show less resistance to fatigue then Type IIa

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17
Q

How Can Athletes improve Force Production?

A

Incorporate phases of training that use heavier loads in order to
optimize neural recruitment.
x Increase the cross-sectional area of muscles involved in the desired
activity.
x Perform multimuscle, multijoint exercises that can be done with
more explosive actions to optimize fast-twitch muscle recruitment.

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18
Q

Muscle spindle

A

When a muscle is stretched, deformation of the muscle spindle
activates the sensory neuron, which sends an impulse to the spinal cord, where it synapses with a motor neuron, causing the muscle
to contract.

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19
Q

Golgi Tendon Organs (GTO)

A

Golgi tendon organs are proprioceptors located in tendons near the
myotendinous junction.
x They occur in series (i.e., attached end to end) with extrafusal
muscle fibers.
x When an extremely heavy load is placed on the muscle, discharge
of the GTO occurs.
x The sensory neuron of the GTO activates an inhibitory interneuron
in the spinal cord, which in turn synapses with and inhibits a motor
neuron serving the same muscle.

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20
Q

Hemoglobin and RBC

A

Hemoglobin transports oxygen and serves as an acid–base buffer.
• Red blood cells facilitate carbon dioxide removal.

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21
Q

What type of lever is triceps extension

A

first class, ( I know stupid)

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22
Q

Power

A

work x Time (s)

Power (W)

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23
Q

Work

A

Force x displacement(m)

Work ( J)

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24
Q

negative work

A

work performed on a muscle rather than by a muscle

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25
Q

Rotation work

A

Torque ( Nm) x angular displacement

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26
Q

force and speed of contraction relationship

A

force capability of muscle declines as the

velocity of contraction increases.

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27
Q

strength to mass ration small and large athletes

A

Given constant body proportions, the smaller athlete has a higher strength-
to-mass ratio than does the larger athlete.

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28
Q

Catabolism:

A

the breakdown of large molecules into smaller molecules, associated with
the release of energy.

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29
Q

Anabolism:

A

the synthesis of larger molecules from smaller molecules; can be
accomplished using the energy released from catabolic reactions.

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30
Q

Metabolism:

A

the total of all the catabolic or exergonic and anabolic or endergonic
reactions in a biological system.

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31
Q

Three basic energy systems exist in muscle cells to replenish ATP:

A

The phosphagen system
• Glycolysis
• The oxidative system

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32
Q

Phosphagen System

A

Provides ATP primarily for short-term, high-intensity activities
active at the start of all exercise regardless of
intensity
The phosphagen system uses the creatine kinase reaction to maintain the
concentration of ATP.
• The phosphagen system replenishes ATP rapidly.

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33
Q

Glycolysis

A

The breakdown of carbohydrates, either glycogen stored in the muscle or glucose
delivered in the blood, to resynthesize ATP

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34
Q

The end result of glycolysis (pyruvate) may proceed in one of two directions:

A

1) Pyruvate can be converted to lactate.
• ATP resynthesis occurs at a faster rate but is limited in duration.
• This process is sometimes called anaerobic glycolysis (or fast
glycolysis).

• 2) Pyruvate can be shuttled into the mitochondria.
• When pyruvate is shuttled into the mitochondria to undergo the Krebs
cycle, the ATP resynthesis rate is slower, but it can occur for a longer
duration if the exercise intensity is low enough.
• This process is often referred to as aerobic glycolysis (or slow
glycolysis).

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35
Q

Glycolysis and the Formation of Lactate

A

The formation of lactate from pyruvate is catalyzed by the enzyme lactate
dehydrogenase.
• The end result is not lactic acid.
• Lactate is not the cause of fatigue.
• Glucose + 2Pi + 2ADP → 2Lactate + 2ATP + H2O
• Lactate can be transported in the blood to the liver, where it is converted
to glucose.
• This process is referred to as the Cori cycle.

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36
Q

Glycolysis Leading to the Krebs Cycle

A

Pyruvate that enters the mitochondria is converted to acetyl-CoA.
• Acetyl-CoA can then enter the Krebs cycle.
• The NADH molecules enter the electron transport system, where they can
also be used to resynthesize ATP.
• Glucose + 2Pi + 2ADP + 2NAD+ → 2Pyruvate + 2ATP + 2NADH +
2H2O

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37
Q

Energy Yield of Glycolysis

A

Glycolysis from one molecule of blood glucose yields a net of two ATP
molecules.
• Glycolysis from muscle glycogen yields a net of three ATP molecules.

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38
Q

Control of Glycolysis

A

Stimulated by high concentrations of ADP, Pi, and ammonia and by a
slight decrease in pH and AMP
• Inhibited by markedly lower pH, ATP, CP, citrate, and free fatty acids
• Also affected by hexokinase, phosphofructokinase, and pyruvate kinase

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39
Q

Lactate Threshold and Onset of Blood Lactate

A

Lactate threshold (LT) represents an increasing reliance on anaerobic
mechanisms.
• LT is often used as a marker of the anaerobic threshold.
• Lactate threshold (LT): the exercise intensity or relative intensity at which
blood lactate begins an abrupt increase above the baseline concentration.
• LT begins at 50% to 60% of maximal oxygen uptake in untrained
individuals.
• It begins at 70% to 80% in trained athletes.
• OBLA is a second increase in the rate of lactate accumulation.
• It occurs at higher relative intensities of exercise.
• It occurs when the concentration of blood lactate reaches 4 mmol/L.

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40
Q

The Oxidative (Aerobic) System

A

Primary source of ATP at rest and during low-intensity activities
• Uses primarily carbohydrates and fats as substrates
• Glucose and Glycogen Oxidation
• Metabolism of blood glucose and muscle glycogen begins with glycolysis
and leads to the Krebs cycle. (Recall: If oxygen is present in sufficient
quantities, the end product
of glycolysis, pyruvate, is not converted to lactate but is transported to the
mitochondria, where it is taken up and enters the Krebs cycle.)
• NADH and FADH2 molecules transport hydrogen atoms to the electron
transport chain, where ATP is produced from ADP.

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41
Q

Fat Oxidation

A

Triglycerides stored in fat cells can be broken down by hormone-sensitive
lipase. This releases free fatty acids from the fat cells into the blood,
where they can circulate and enter muscle fibers.
• Some free fatty acids come from intramuscular sources.

• Free fatty acids enter the mitochondria, are broken down, and form acetyl-
CoA and hydrogen protons.

• The acetyl-CoA enters the Krebs cycle.
• The hydrogen atoms are carried by NADH and FADH2 to the
electron transport chain.

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42
Q

Protein Oxidation

A

Protein is not a significant source of energy for most activities.
• Protein is broken down into amino acids, and the amino acids are
converted into glucose, pyruvate, or various Krebs cycle inter-mediates to
produce ATP.

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43
Q

Control of the Oxidative (Aerobic) System

A

Isocitrate dehydrogenase is stimulated by ADP and inhibited by ATP.
• The rate of the Krebs cycle is reduced if NAD+ and FAD2+ are not
available in sufficient quantities to accept hydrogen.
• The ETC is stimulated by ADP and inhibited by ATP

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44
Q
Effect of event duration and intensity on primary energy system used
0-6
6-30
30-2min
2-3min
> 3min
A
  • 0-6 seconds, extremely high intensity, phosphagen
  • 6-30 seconds, very high intensity, phosphagen and fast glycolysis
  • 30 sec – 2 minutes, high intensity, fast glycolysis
  • 2-3 minutes, moderate intensity, fast glycolysis and oxidative system
  • > 3 minutes, low intensity, oxidative system
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45
Q

Ranking of rate and capacity of ATP production

• 1 = fastest/greatest, 5 = slowest/least

A

Phosphagen: Rate of ATP production: 1, Capacity: 5
• Fast Glycolysis: Rate of ATP production: 2, Capacity: 4
• Slow Glycolysis: Rate of ATP production: 3, Capacity: 3
• Oxidation of Carbohydrates: Rate of ATP production: 4, Capacity: 2
• Oxidation of Fats/Proteins: Rate of ATP production: 5, Capacity: 1

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46
Q

Substrate Depletion and Repletion

• Phosphagens

A

Creatine phosphate can decrease markedly (50-70%) during the first stage (5-30
seconds) of high-intensity exercise and can be almost eliminated as a result of
very intense exercise to exhaustion.
• Postexercise phosphagen repletion can occur in a relatively short period; complete
resynthesis of ATP appears to occur within 3 to 5 minutes, and complete creatine
phosphate resynthesis can occur within 8 minutes.

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47
Q

Substrate Depletion and Repletion

Glycogen

A

The rate of glycogen depletion is related to exercise intensity.
• At relative intensities of exercise above 60% of maximal oxygen uptake,
muscle glycogen becomes an increasingly important energy substrate; the
entire glycogen content of some muscle cells can become depleted during
exercise.

• Repletion of muscle glycogen during recovery is related to postexercise
carbohydrate ingestion.
• Repletion appears to be optimal if 0.7 to 3.0 g of carbohydrate per kg of
body weight is ingested every 2 hours following exercise.

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48
Q

Bioenergetic Limiting Factors in Exercise Performance

Light Marathon

A
Most limiting to least limiting
Muscle Glycogen: 5
• Liver Glycogen: 4-5
• Fat Stores: 2-3
ATP and Creating Phosphate: 1
Lower pH: 1
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49
Q

Bioenergetic Limiting Factors in Exercise

Moderate (1500 m run)

A
Most limiting to least
Muscle Glycogen: 3
Lower pH: 2-3
Liver Glycogen: 2
ATP and Creating Phosphate: 1-2
Fat Stores: 1-2
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50
Q

Bioenergetic Limiting Factors in Exercise Performance

Heavy (400 m run)

A
Most limiting to least
Lower pH: 4-5
ATP and Creating Phosphate: 3
• Muscle Glycogen: 3
• Liver Glycogen: 1
• Fat Stores: 1
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51
Q
Bioenergetic Limiting Factors in Exercise Performance
Very Intense (Discus)
A
Most limiting to least
ATP and Creating Phosphate: 2-3
• Muscle Glycogen: 1
• Liver Glycogen: 1
• Fat Stores: 1
• Lower pH: 1
52
Q

Bioenergetic Limiting Factors in Exercise Performance

Very Intense Repeated (Sets of 10 reps in Snatch exercise at 60% 1 RM)

A
Most limiting to least
ATP and Creating Phosphate: 4-5
• Muscle Glycogen: 4-5
Lower pH: 4-5
• Liver Glycogen: 1-2
• Fat Stores: 1-2
53
Q

Excess postexercise oxygen consumption (EPOC): Factors Responsible

A

oxygen uptake above resting values
used to restore the body to the preexercise condition; also called postexercise oxygen
uptake, oxygen debt, or recovery O2.
Replenishment of oxygen in blood and muscle
• ATP/CP resynthesis
• Increased body temperature, circulation, and ventilation
• Increased rate of triglyceride–fatty acid cycling
• Increased protein turnover
• Changes in energy efficiency during recovery

54
Q

Phosphagen: Work to Rest Period Ratios,

A

1:12 – 1:20

55
Q

Fast Glycolysis: Work to Rest Period Ratios,

A

1:3 – 1:5

56
Q

Fast Glycolysis and Oxidative: Work to Rest Period Ratios,

A

1:3- 1:4

57
Q

• Oxidative: Work to Rest Period Ratios,

A

1:1 – 1:3

58
Q

variables to manipulate with HIIT

A

intensity of the active portion of each duty cycle
• duration of the active portion of each duty cycle
• intensity of the recovery portion of each duty cycle
• duration of the recovery portion of each duty cycle
• number of duty cycles performed in each set
• rest time between sets, number of sets
• recovery intensity between set
• mode of exercise for HIIT

59
Q

Interval Training

A

Interval training is a method that emphasizes bioenergetic adaptations for a more
efficient energy transfer within the metabolic pathways by using predetermined
intervals of exercise and rest periods.
• Much more training can be accomplished at higher intensities

• Difficult to establish definitive guidelines for choosing specific work-to-
rest ratios

60
Q

Combination Training

A

Combination training adds aerobic endurance training to the training of anaerobic
athletes in order to enhance recovery (because recovery relies primarily on
aerobic mechanisms).
May reduce anaerobic performance capabilities, particularly high-strength,
high-power performance
• Can reduce the gain in muscle girth, maximum strength, and speed- and
power-related performance
• May be counterproductive in most strength and power sport

61
Q

General Adaptation Syndrome

A

refers to how the adrenal gland responds to a noxious

stimulus (stressor)

62
Q

Anabolic hormones

A
(hormones that promote tissue building) such as insulin, insulin-like
growth factors (IGFs), testosterone, and growth hormone
63
Q

Catabolic hormones

A

(can degrade cell proteins) such as cortisol and progesterone.

64
Q

Steroid Hormone Interactions

A

A steroid hormone passively diffuses across the sarcolemma of a muscle fiber.
• It binds with its receptor to form a hormone-receptor complex (H-RC).
• H-RC arrives at the genetic material in the cell’s nucleus and ―opens‖ it in order
to expose transcriptional units that code for the synthesis of specific proteins.
• RNA polymerase II binds to the promoter that is associated with the specific
upstream regulatory elements for the H-RC.
• RNA polymerase II transcribes the gene by coding for the protein dictated by the
steroid hormone.
• Messenger RNA (mRNA) is processed and moves into the sarcoplasm of the cell,
where it is translated into protein.

65
Q

Polypeptide Hormone Interactions

A

Made up of chains of amino acids; examples are growth hormone and insulin
• They are not fat soluble and thus cannot cross the cell membrane
• Cyclic adenosine monophosphate-dependent (cyclic AMP-dependent) signaling
pathway
• Cytokine-activated JAK/STAT signaling pathway
• Prototypical growth factor, mitogen-activated signaling pathway

66
Q

Amine Hormone Interactions

A

synthesized from the amino acid tyrosine (e.g., epinephrine, norepinephrine, and
dopamine) or tryptophan (e.g., serotonin)

67
Q

Mechanisms contributing to changes in peripheral blood concentrations of hormones:

A
Fluid volume shifts
• Tissue clearance rates
• Hormonal degradation
• Venous pooling of blood
• Interactions with binding proteins in the blood
68
Q

There are three primary hormones involved in muscle tissue growth and remodeling:

A
  • Testosterone
  • Growth hormone (GH)
  • Insulin-like growth factors (IGFs)
69
Q

Testosterone

A

The primary androgen hormone that interacts with skeletal muscle tissue
• Effects on muscle tissue: GH responses that lead to protein synthesis, increased
strength and size of skeletal muscle, increased force production potential and
muscle mass
• Diurnal variations
• Men: exercise later in the day is more effective for increasing overall
testosterone concentrations over an entire day.
• Women: there are lower concentrations and little variation during the day.
• Large muscle group exercises result in acute increased serum total testosterone
concentrations in men.

70
Q

Free Testosterone and Sex Hormone–Binding Globulin

A

A higher total (bound) testosterone level allows for the potential of more
free testosterone.
• The free hormone hypothesis states that only the free hormone interacts
with target tissues.

71
Q

Testosterone Responses in Women

A

Women have 15- to 20-fold lower concentrations of testosterone than men
do, and if acute increases occur after a resistance training workout, they
are small.

72
Q

Training Adaptations of Testosterone

A

It appears that training time and experience may be very important factors
in altering the resting and exercise induced concentrations

73
Q

Growth Hormone

A

Secreted by the pituitary gland
• Interacts directly with target tissues, which include bone, immune cells, skeletal
muscle, fat cells, and liver tissue
• Regulated by neuroendocrine feedback mechanisms and mediated by secondary
hormones
• GH release patterns altered by age, gender, sleep, nutrition, alcohol consumption,
and exercise
• Efficacy of Pharmacological Growth Hormone
• Pharmacological use of GH has unknown and unpredictable results.

74
Q

Growth Hormone Responses to Stress

A

GH responds to exercise stressors, including resistance exercise.
• GH response depends on load, rest, and volume of exercise.
• Less rest: higher GH
• 10RM: higher GH
• 3 sets: higher GH
• Growth hormone release is affected by the type of resistance training
protocol used including the duration of rest period. Short rest period types
of workouts result in greater serum concentrations compared to long rest
protocols of similar total work;

75
Q

Growth Hormone Responses in Women

A

GH concentrations and responses to exercise vary with menstrual phase.
• Women have higher blood levels of GH than do men.

76
Q

Training Adaptations of Growth Hormone

A

There is little change in single measurements of resting GH concentrations
in resistance-trained individuals.
• Training-related changes in GH include a reduction in GH response to an
absolute exercise stress and alterations in GH pulsatility characteristics.

77
Q

Insulin-Like Growth Factors

A

Exercise Responses of Insulin-Like Growth Factors
• Insulin-like growth factor I (IGF-I) is most studied because of its role in
protein anabolism.
• Exercise results in acute increases in blood levels of IGF-I.
• Training Adaptations of Insulin-Like Growth Factors

• Changes in IGF-I appear to be based on the starting concentrations before
training.
• If basal concentrations are low, IGF-I increases.
• If basal concentrations are high, there is no change or it decreases.

78
Q

Cortisol
-effects
resistance exercise
- training

A

Role of Cortisol
• Catabolic effects
• Converts amino acids to carbohydrates, increases the level
of enzymes that break down proteins, and inhibits protein synthesis

• Resistance Exercise Responses of Cortisol
• Cortisol increases with resistance exercise.
• Training may reduce the negative effects of this increase.
• Vast differences are observed in the physiological role of cortisol in acute
versus chronic responses.
• Resistance exercise protocols that use high volume, large muscle groups,
and short rest periods result in increased serum cortisol values. Though
chronic high levels of cortisol may have adverse catabolic effects, acute
increases may contribute to the remodeling of muscle tissue.

79
Q

Catecholamines

A

Primarily epinephrine but also norepinephrine and dopamine
• Role of Catecholamines
• Increase force production via central mechanisms and increased metabolic
enzyme activity
• Increase muscle contraction rate
• Increase blood pressure
• Increase energy availability
• Increase blood flow
• Augment secretion rates of other hormones, such as testosterone
• Training Adaptations of Catecholamines
• Heavy resistance training has been shown to increase the ability of an
athlete to secrete greater amounts of epinephrine during maximal exercise
• Training protocols must be varied to allow the adrenal gland to engage in
recovery processes and to prevent the secondary responses of cortisol,
which can have negative effects on the immune system and protein
structures.

80
Q

To increase testosterone

A

Large muscle exercises (deadlifts, squats, power clean)
• Heavy resistance (85 to 95% of 1 RM)
• Moderate to high volume of exercise achieved with multiple sets or exercises
• Short rest intervals (30 seconds to 1 minute)
• Two years or more of resistance training experience

81
Q

To increase growth hormone

A

Use high intensity (10 RM or heavy resistance) with
• 3 sets of each exercise (high total work) and
• Short (1 min) rest periods.
• Supplement diet with carbohydrate and protein before and after workouts.

82
Q

adrenal hormones and exercise for promoting recovery

A

High volume
• Large muscle groups
• Short rest periods
• Vary all these factors to allow adrenal gland to engage in recovery process

83
Q

hormones that affect growth, repair, and exercise stress

mechanisms.

A

Insulin, thyroid hormones, and beta-endorphins

84
Q

Comparing performance of weight lifters with different body weight:

A

load lifted/ body weight ^(⅔)

85
Q

Law of mass action

A

The concentrations of reactants or products (or both)

in solution will drive the direction of the reactions.

86
Q

energy system with heat biproduct

A

phosphogen

87
Q

what leads to fatigue in glycogen system

A

H- build up leading to fatigue due to inhibiting glycolytic reactions and muscle excitation
As pH decreases could lead to metabolic acidosis
Pyruvic acid removal 30-60 min

88
Q

rate limiting step in glycolysis ( most imp. regulator)

A

Phosphofructokinase

ATP is an allosteric inhibitor of PFK ( decreases turn over rate)
AMP is an allosteric activator of PFK ( increases turn over rate)

89
Q

Biproduct of krebs cycle

A

CO2

90
Q

Allosteric regulation

A

end product of a reaction or series of reactions feeds back to regulate the turnover rate of key enzymes in the metabolic pathways.

91
Q

Net production of oxidative energy system

A

NET production of 38 ATP since Krebs uses 2

92
Q

Fats vs carbs oxidative system

A

Fats primarily used at rest, Carbs primarily used with activity
With High intensity aerobic activity almost all carbs are used
With prolonged high intensity activity shift back to use of fats and carb

93
Q

Allosteric binding sites

A

substances other than hormones can enhance or reduce the cellular response to the primary hormone.

94
Q
Physiological Adaptations to Resistance Training
   Muscular Strength: 
• Muscular Endurance: 
• Aerobic Power: 
• Maximal Rate of Force Production: 
• Vertical Jump:
A

Muscular Strength: Increases
• Muscular Endurance: Increases for high power output
• Aerobic Power: No change or increase slightly
• Maximal Rate of Force Production: Increases
• Vertical Jump: Ability increases

95
Q
Physiological Adaptations to Resistance Training
Anaerobic Power: 
• Sprint Speed: 
• Fiber Size: 
• Capillary Density: 
• Mitochondrial Density:
A
Anaerobic Power: Increases
• Sprint Speed: Improves
• Fiber Size: Increases
• Capillary Density: No change or decreases
• Mitochondrial Density: Decreases
96
Q
Physiological Adaptations to Resistance Training
• Stored ATP: 
• Stored Creatine Phosphate: 
• Stored Glycogen: 
• % Body Fat: 
• % Fat Free Mass:
A
  • Stored ATP: Increases
  • Stored Creatine Phosphate: Increases
  • Stored Glycogen: Increases
  • % Body Fat: Decreases
  • % Fat Free Mass: Increases
97
Q

Size Principle

A

• Low-threshold motor units are recruited first and have lower force capabilities
than higher-threshold motor units.
• Typically, to get to the high-threshold motor units, the body must first recruit the
lower-threshold motor units.
• Exceptions exist, especially with respect to explosive, ballistic contractions that
can selectively recruit high-threshold units to rapidly achieve more force and
power.

98
Q

Neuromuscular Junction adaptations to resistance training

A

Possible changes with anaerobic training include
• increased area of the neuromuscular junction (NMJ);
• more dispersed, irregularly shaped synapses and a greater total length of
nerve terminal branching; and
• increased end-plate perimeter length and area, as well as greater dispersion
of acetylcholine receptors within the end-plate region.

99
Q

Bilateral deficit in untrained individuals

Bilateral facilitation in trained or stronger individuals

A

Bilateral deficit in untrained individuals - the force produced when both limbs
contract together is lower than the sum of the forces they produce when
contracting unilaterally
• Bilateral facilitation in trained or stronger individuals - an increase in
voluntary activation of the agonist muscle groups occurs
• Changes in muscle activity of the antagonists during agonist movements

100
Q

Hyperplasia

A

an increase in the number of muscle fibers via longitudinal

fiber splitting.

101
Q

Muscle hypertrophy

A

The process of hypertrophy involves both an increase in the synthesis of the
contractile proteins actin and myosin within the myofibril and an increase in the
number of myofibrils within a muscle fiber. The new myofilaments are added to
the external layers of the myofibril, resulting in an increase in its diameter.

102
Q

In response to resistance training

type 1 &2

A

Resistance training results in increases in both
Type I and Type II muscle fiber area.
• Type II fibers have greater increases in size than Type I fibers.

103
Q

Fiber Type Transitions

A

There is a continuum of fiber types: I, Ic, IIc, IIac, IIa, IIax, IIx.
• Muscle fiber transitions occur during training.
• This means that a shift of the type of myosin adenosine triphosphatase (ATPase)
and heavy chains takes place during training.
• Transformations from IIx to IIax to IIa can be seen, and then small percentages
change to IIac and IIc.
• Exercise activities that recruit motor units with Type IIx muscle fibers initiate a
shift toward IIa fibers.

104
Q

Other Muscular Adaptations in response to resistance training

A

Structural and Architectural Changes
• Resistance training increases myofibrillar volume, cytoplasmic density,
sarcoplasmic reticulum and T-tubule density, and sodium-potassium ATPase
activity.
• Sprint training enhances calcium release.
• Resistance training increases angle of pennation.
• Other Muscular Adaptations
• Reduced mitochondrial density
• Decreased capillary density
• Increased buffering capacity (acid-base balance)
• Changes in muscle substrate content and enzyme activity

105
Q

Minimal essential strain (MES)

A

Trabecular bone responds more rapidly to stimuli than does cortical bone.
• Minimal essential strain (MES) is the threshold stimulus that initiates new bone
formation.
• The MES is approximately 1/10 of the force required to fracture bone.
• Forces that reach or exceed a threshold stimulus initiate new bone formation in
the area experiencing the mechanical strain.

106
Q

overreaching

A

Excessive training on a short-term basis

107
Q
Acute Responses to Aerobic Exercise
• Cardiovascular Responses
 CO
SV
HR
A

Cardiac Output
• From rest to steady-state aerobic exercise, cardiac output initially
increases rapidly, then more gradually, and subsequently reaches a
plateau.
• With maximal exercise, cardiac output may increase to four times the
resting level.
• End-diastolic volume is significantly increased.
• At onset of exercise, sympathetic stimulation increases stroke volume.
• Heart rate increases linearly with increases in intensity.

108
Q

CO2 delivered to the lungs

A

Most carbon dioxide removal is from its combination with water and delivery to
the lungs in the form of bicarbonate.

109
Q
Physiological Adaptations to Aerobic Endurance Training
Muscle strength: 
• Muscle endurance:
• Aerobic Power: 
• Maximal rate of force production: 
• Vertical Jump: 
• Anaerobic Power: 
• Spring Speed:
A
  • Muscle strength: No change
  • Muscle endurance: Increase for low power output
  • Aerobic Power: Increases
  • Maximal rate of force production: No change or decreases
  • Vertical Jump: Ability unchanged
  • Anaerobic Power: No change
  • Spring Speed: No change or improves slightly
110
Q

Physiological Adaptations to Aerobic Endurance Training

Muscle Fibers

A

Fiber Size: No change or increases slightly
• Capillary density: Increases
• Mitochondrial density: Increases

111
Q

Physiological Adaptations to Aerobic Endurance Training

Metabolic Energy stores

A

ATP: Increases
• Creatine Phosphate: Increases
• Glycogen: Increases
• Triglycerides: Increases

112
Q

Physiological Adaptations to Aerobic Endurance Training
Connective Tissue
—-Ligament, tendon, bone density

A

Ligament strength: Increases
• Tendon strength: Increases
• Bone density: No change of increases

113
Q

Physiological Adaptations to Aerobic Endurance Training

  • -%Body Fat:
  • -Fat free mass
A
  • % Body Fat: Decreases

* Fat-Free Mass: No Change

114
Q

Altitude changes

  • –Pulmonary changes
  • –Hematologic changes
A

Changes begin to occur at elevations greater than 3,900 feet (1,200 m):
• Increased pulmonary ventilation
• Increased cardiac output at rest and during submaximal exercise due to
increases in heart rate

• Values begin to return toward normal within two weeks.
• Several chronic physiological and metabolic adjustments occur during prolonged
altitude exposure.
• Pulmonary: Hyperventilation
• Acid-Base: Body fluids become more alkaline
• Cardiovascular
• Cardiac output increases
• Submaximal heart rate increases
• Stroke volume remains the same or is slightly lowered
• Hematologic
• Increased red blood cell production
• Increased hematocrit
• Increased viscosity
• Decreased plasma volume

115
Q

Overtraining:

  • -Cardiovascular response
  • -Biochemical
  • -Endocrine
A

• Cardiovascular Responses
affect heart rate.
• Biochemical Responses
• increased levels of creatine kinase,
indicating muscle damage.
• Muscle glycogen decreases with prolonged periods of overtraining.
• Endocrine Responses
• Overtraining may result in a decreased testosterone-to-cortisol ratio,
decreased secretion of GH, and changes in catecholamine levels.

116
Q

Markers of Aerobic Overtraining

17

A

• Decreased performance
• Decreased percentage of body fat
• Decreased maximal oxygen uptake
• Altered blood pressure
• Increased muscle soreness
• Decreased muscle glycogen
• Altered resting heart rate
• Increased submaximal exercise heart rate
• Decreased lactate
• Increased creatine kinase
• Altered cortisol concentration
• Decreased total testosterone concentration
• Decreased ratio of total testosterone to cortisol
• Decreased ratio of free testosterone to cortisol
• Decreased ratio of total testosterone to sex hormone–binding
globulin
• Decreased sympathetic tone (decreased nocturnal and resting
catecholamines)
• Increased sympathetic stress response

117
Q

Selective Recruitment-

A

inhibiting lower threshold motor units and in their place activate higher threshold motor units. Used when force is needed at high speeds. This is for instance in used a vertical jump. Quicker to recruit some and not all motor units.

118
Q

Cardiac Output change with exercise

A

can increase 4x with exercise ~ 5L/min to ~20 L/min

119
Q

Stroke volume during exercise

A

Stroke volume increases at the onset of exercise until it reaches about 40-50% of maximal oxygen uptake. This is when SV plateau begins

120
Q

Diastolic blood pressure with aerobic activity

A

Diastolic decreases with aerobic activity due to dilation. Normal at rest muscles receive about 15% of blood supply with exercise increases to about 90%.

121
Q

Mean arterial pressure

A

average blood pressure throughout the cardiac cycle.

122
Q

Early neurologic gains in aerobic training

A

Early gains in endurance and fatigability are often due to neurological changes. Muscle activation will be rotation meaning that synergistic muscles will alternate between activation in rest to allow for lower energy expenditure.

123
Q

Glycogen sparing

A

raining can lead to glycogen sparing ( less use of of glycogen during exercise) and increase in fat utilization within the muscle leading to prolonged performance. A person may be exercising under the same maximal oxygen uptake, but with greater ease.

124
Q

Myoglobin

A

Myoglobin transports oxygen into cell. Increases in response to aerobic training

125
Q

Maximal oxygen consumption

A

Most adaptations in maximal oxygen consumption occur in the first 6-12 month period of training. Continued improvements can be attributed to the following adaptations to training: increases in running efficiency and increase lactate threshold. Metabolic changes included increased respiratory capacity , lower blood lactate concentrations at any given submaximal exercise intensity, increased mitochondrial and capillary densities, and improved enzyme activity.

126
Q

Blood doping

A

These athletes will tolerate changes in altitude and temperature better
People will have lower HR, lower pH values in response to exercise
Increasing RBC will lead to inc in blood volume allowing for improved circulation to all areas
Increase risk for stroke, MI, PE

127
Q

Overtraining

A

Functional overreaching
Overtraining followed by a period of rest before a game
Non Functional overreaching
Loss of sport performance due to overtraining. Athlete requires weeks to months of rest to recover
Increased training intensity can lead to increase in resting diastolic BP
Higher levels of CK can be found in body indicating muscle damage
Muscle glycogen decreases with prolonged periods of aerobic overtraining ( potentially diet related?)