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Exercise Physiology > Test2 Exphys I > Flashcards

Test2 Exphys I Flashcards

1
Q

5 gen f(c) of NS

A

control of internal environment along with the endocrine sys
voluntary ctrl of movement
involuntary ctrl of movement over vital life functions
programming spinal cord reflexes
assimilation of experiences necessary for memory and learning

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2
Q

CNS

A

brain and spinal cord

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3
Q

PNS

A

consists of neurons located outside CNS

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4
Q

What does the archeitecture of the bones in the body tell us about the CNS?

A

Body will work to preserve NS since it has most protection

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5
Q

Afferent divison of PNS consists of what 3 components?

A

somatic sensory
visceral sensory
special sensory

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6
Q

Efferent division PNS consist of what?

A

somatic motor and automatic motor

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7
Q

3 division of automotic motor

A

sympathetic, parasympathetic, and enteric

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8
Q

SNS controls

A

skel muscle

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9
Q

ANS controls

A

smooth, cardiac muscles and glands

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10
Q

cell body

A

center of operation also called soma or perikaryon

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11
Q

cell contains blank that does is the site of

A

cell body contains the nucleus, site of protein synthesis that produces neurotransmitters

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12
Q

Nerves have more blank so these use this substrate and why?

A

nerves have more mitochondria but uses more glucose and heart uses fats so the two main systems are not in competition for fuel

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13
Q

dendrites conduct

A

impulses toward cell body from the receptor

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14
Q

axon carries

A

electrical impulse away from cell body

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15
Q

axon may be coverd by

A

Schwann cells and forms discontinouous myelin sheath along length of axon

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16
Q

gaps of mylein sheath

A

Nodes of Ranvier

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17
Q

biggest nerve

A

sciatic nerve

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18
Q

synapse

A

contact points btwn axon of one neuron an dendrtite of another neuron, goes from electrical to chemical

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19
Q

The mitochondria in the neuron go through what energy system?

A

aerobic glycolysis

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20
Q

Multiple Sclerosis

A

neurological disease that destroys myelin sheaths of axons that has a genetic component and is due to an immune attack on the CNS myelin (autoimmune)

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21
Q

MS results in

A

progressive loss of NS f(x) causing fatigue, muscle weakness, poor motor ctrl, loss of balance, and mental depression

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22
Q

Exs can improve f(c)nal capacity of what disease?

A

MS

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23
Q

exercise for MS leads to

A

improved QOL

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24
Q

exercise can do what kind of harm if not controlled

A

can overheat nerves resulting in necrosis

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25
Q

neurons are what kind of tissue

A

excitable tissue (conducts stimulus)

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26
Q

Irritability in neurons

A

ability to respond to a stimulus and convert it to a neural impulse (dendrites and cell body) Once threshold reached,, impulse is processed throughout body

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27
Q

conductivity

A

transmission of the impulse along the axon

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28
Q

why is resting membrane potential negative?

A

because of protein anions that are stationary in the cell

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29
Q

synapse

A

small btwn presynaptic neuron and postsynaptic neuron

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30
Q

Neurotransmitter

A

chemical jumps synapse

chemical messenger released from presynaptic membrane for communication

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31
Q

Where does neurotransmitter bind to?

A

binds to receptor on postsynaptic membrane

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32
Q

neurotransmitter can cause

A

depolarization (EPSP) or hyperpolarization (IPSP) of the postsynaptic membrane

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33
Q

EPSP causes

A

depolarization

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34
Q

depolarization

A

Na+ influx into the cell, making the cell more positive and less negative, once threshold is reached

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35
Q

temporal summation

A

summing several EPSPs from presynaptic neuron

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36
Q

spatial summation

A

summing from several different presynaptic neurons

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37
Q

two types of EPSP

A

temporal and spatial

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38
Q

IPSP

A

cause hyperpolarization

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39
Q

hyperpolarization

A

make cell more negative

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40
Q

proprioceptors

A

receptors that provide CNS with information about body position in space ortientation

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41
Q

where are proprioceptors located?

A

located in joint and muscles

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42
Q

proprioceptors prevent

A

falls by forming a plan that tuned by the spine

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43
Q

kinesthesia

A

kinestic awareness

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44
Q

kinesthesia is

A

consciuous recognition of position of body parts and limb movement rates

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45
Q

free nerve endings are sensitive to

A

touch and pressure

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46
Q

free nerve endings are initially strongly

A

stimulated, then they adapt

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47
Q

Golgi-type receptors are found in

A

ligments and around joints and are diff from gto’s

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48
Q

golgi-type receptors are similar to what

A

free nerve endings in that they are pressure and touch sensitive

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49
Q

Pacinian corpuscles location

A

in tissues around joints

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50
Q

pacinian corpuscles detect what

A

rate of joint rotation

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51
Q

Muscle proprioceptors provide

A

sensory feedback to nervous system

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52
Q

muscle proprioceptors sensory feedback is from what 2 things

A

tension development by muscle and account of muscle length

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53
Q

2 types of muscle proprioceptors

A

muscle spindle

Golgi tendon organ

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54
Q

muscle spindle responds to

A

changes in muscle length

how long muscle is and joint location

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55
Q

muscle spindle consists of what 2 things

A

intrafusal fibers and gamma motor neurons

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56
Q

intrafusal fibers of muscle spindles are what

A

run parallel to normal muscle fibers (extrafusal fibers) to avoid injury

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57
Q

gamma motor neurons stimulate

A

intrafusal fibers to contract with extrafusal fibers by alpha motor neurons to contract

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58
Q

Stretch reflex

A

stretch on muscle causes reflex contraction such as knee-jerk and protective mech

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59
Q

How do muscle spindles work (4 steps)?

A

1) Muscle spindles (intrafusal) detect stretch of the muscle
2) Sensory neurons conduct AP to the spinal cord, exciting muscle and shortening (concentric)
3) Sensory neurons synapse with alpha motor neurons
4) Stimulation of the alpha motor neuron causes the muscle to contract and resist being stretched

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60
Q

GTO

A

inhibit muscle contraction, receives pull of muscle, so elongation

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61
Q

GTO monitor and this prevents what?

A

tension developed in the muscle, this prevents muscle damage during excessive force generation (inhibits the contracting muscle)

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62
Q

GTO stimulation results in

A

reflex relaxation of muscle

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63
Q

GTO have what kind of neurons that do what?

A

Inhibitory neurons send IPSPs to muscle fibers, thus, inhbiting max force of muscle

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64
Q

Ability to voluntarily oppose GTO

A

inhibition may be related to gains in strength

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65
Q

GTO MOA

A

1) GTO detect tension applied to a tendon
2) Sensory neurons conduct AP to the spinal cord, inhibiting the muscle and lengthening (eccentric)
3) Sensory neurons synaspe with inhibitory interneurons that synapse with alpha motor neurons
4) Inhibition of alpha motor neurons causes muscle relaxation, relieving the tension to the tendon, this is the only differnce from muscle spindle MOA

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66
Q

Muscle chemoreceptors are sensitive to

A

changes in the chemical environment surronding a muscle

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67
Q

3 major chemicals detected by muscle chemoreceptors

A

H+ ions, co2, and K+

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68
Q

Muscle chemoreceptors provide and why?

A

CNS with info about metabolic rate of muscular actvitiy, and it is vital for regulation of cardiovascular and pulmonary responses

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69
Q

Withdrawal Reflex

A

touch hot stuff

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70
Q

Withdrawal reflex contraction of

A

skel muscle occurs in response to sensory input, and not dependent on higher brain centers

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71
Q

Withdrawal reflex pathways of neural reflex include 3

A

sensory nerve sends impulse to spinal column, interneurons activate motor neurons, and motor neurons control movement of muscles

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72
Q

Reciprocal Inhibition

A

When EPSPs to agonist muscles to withdraw from stimulus, and IPSPs to antagonistic muscles

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73
Q

Example of reciprocal inhibition (flexors and extensors of elbow)

A

biceps brachii flexion receives EPSPs, and triceps extension is inhibited

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74
Q

Cross-extensor reflex

A

Opposite limb supports body during withdrawal of injured contralateral limb via extension reflex

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75
Q

example cross extensor reflex in elbow flexion and exten

A

The finger of the right arm touches a nail, this causes the flexor (biceps brachii) to be stimulated by pulling away and the extensor tricep is inhibited to allow the movement. The left arm, contralateral arm, does the opposite since the extensor in the left arm will stimulated (tricep) and the flexor (biceps) will be inhibited allow the left arm to hold down, thus, supporting the body.

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76
Q

Somatic Motor neurons of PNS are responsible for

somatic motor f(x)

A

carrying neural messages from spinal cord to the skeletal muscles, typically alpha nerves that are myleinated, rapid speed

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77
Q

Motor unit (somatic motor function)

A

motor neuron and all the muscle fibers it innervates

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78
Q

Innervation ratio (somatic motor function)

A

number of muscle fibers per motor neuron (extrafusal)

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79
Q

What does a low innervation ratio denote in muscles?

A

Low ratio in muscles that require fine motor control such as the eye muscles

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80
Q

what does a higher innervation ratio mean?

A

large muscles such as the quads and multipennate muscle

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81
Q

Motor unit recruitment

A

recruitment of more muscle fibers through motor unit activation

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82
Q

Size principle

A

smallest motor units recruited first, and produce larger EPSP and result in action potential sooner because it can achieve threshold since it is smaller

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83
Q

Types of motor units

A

Type S

Type FR or FF

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84
Q

Type S motor units

A

Type S is the smallest motor unit, slow, type I fibers and turn on first, utilize FFA and are oxidative, aerobic (red= gets lots of blood supply).

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85
Q

Type FR motor units

A

Fast, fatigue resistant, Very trainable, type IIa fibers, intermediate fibers, pink= have decent blood supply, oxidative but more glycolytic, turn on second

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86
Q

Type FF

A

Fast, fatigable, type IIx fibers, largest, and are powerful white fibers not big blood supply, like white meat on a chicken breast, turns on last

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87
Q

Recruitment pattern during incremental exercise turning on

A

type S –> type FR –> FF

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88
Q

Recruitment pattern during incremental exercise turning iff

A

FF–> FR – > S

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89
Q

Where is vestibular apparatus located?

A

in the inner ear

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90
Q

what is the vestibular apparatus similar to in construction?

A

a level’s bubble bar

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91
Q

Vestibular apparatus is responsible for what?

A

maintaining general equilibrium and balance such as maintaining head position

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92
Q

Vestibular apparatus is sensitive to

A

changes in linear and angular acceleration, that is stimulated by head movement (static and dynamic movement)

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93
Q

Vestibular apparatus controls

A

head and eye movement during physical activity/motion

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94
Q

Brain stem responsible for what?

A

Many metabolic f(c)
cardiorespiratory cntrl
complex reflexes

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95
Q

Major structures in brain stem

A

Medulla oblongatta
Pons
Midbrain
reticular formation

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96
Q

2 parts of brain that make up cerebrum

A

Cerebral cortex

motor cortex

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97
Q

Cerebral cortex three functions

A

organizations of complex movement
storage of learned experiences (memory)
reception of sensory information

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98
Q

2 fnctions of motor cortex

A

motor control and voluntary movement

recieves info from other brain regions (cerebellum) in order to formulate, initiate, and perpetuate movement

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99
Q

Cerebellum main f(x)

A

coordinates and monitors complex movement by incorporating feedback from proprioceptors

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100
Q

Cerebellum has connection to what 4 areas?

A

Motor cortex
mid brain
brain stem
spinal cord

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101
Q

What may cerebellum initiate ?

A

fast, ballistic movements

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102
Q

concussion

A

brain injury resulting from traumatic force

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103
Q

What four things may result from concussions?

A

Permanent brain damage or death from delayed brain swelling
Second-impact syndrome
same season repeat concssion
late-life consequences of repeated concussions such as AD

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104
Q

Central Fatigue by brain role during exercise induced fatique what are involed

A

Higher brain centers and/or motor neurons

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105
Q

Central fatigue what gets depleted?

A

excitatory neurotransmitters in the motor cortex

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106
Q

cental fatigue results in what

A

reduced motor output to muscle

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107
Q

Central govenor theory regulates

A

central control center regulates exercise performance by reducing motor output to exercising muscle

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108
Q

central governor theory protects

A

against catastrophic disruptions of homeostasis

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109
Q

3 motor functions of the spinal cord

A

Withdrawal reflex, others, and spinal tuning

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110
Q

other reflexes vital for

A

control of voluntary movement

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111
Q

spinal tuning is

A

voluntary movement translated into an appropriate muscle action.

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112
Q

higher brain centers do what in spinal tuning

A

high brain centers concerned w/ general parameters of movement

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113
Q

spinal tuning does what w/ movement

A

details of movement refined in spinal cord

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114
Q

subcortical and cortical movement areas send

A

a “rough draft” of the movement to association cortex

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115
Q

Cerebellum and basal ganglia convert

A

“rough draft” into movement plan

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116
Q

cerebellum is responsible for what movement of rough draft?

A

fast movements

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117
Q

Basal ganglia is responsible for what kind of movements?

A

slow, deliberate movements in rough draft

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118
Q

Rough draft from thalamus to motor cortex (motor cortex through thalamus)

A

Fowards message sent down spinal neurons for “spinal tuning” and onto the muscles

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119
Q

motor cortex through thalamus feedback from

A

muscle receptors and proprioceptors allows fine tuning of motor program

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120
Q

First structure in process of voluntary movement and what it does

A

Subcortical and cortical areas, is the intial drive to move sending rough draft

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121
Q

Second structure of voluntary movement is blank and what it does as well

A

Association cortex Move design of “rough draft”

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122
Q

Third structures’ involved in voluntary movement and action

A

Basal ganglia and cerebellum (fast) refine movement design

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123
Q

Four structure in voluntary movemnt and action

A

Thalamus = relay station for spinal tuning

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124
Q

5th structure in voluntary movement and action

A

motor cortex final executor of motor plan

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125
Q

last structure in voluntary movement and what it does

A

motor units execution of desired movement

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126
Q

What motivates voluntary movement?

A

limbic and reticualr formation

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127
Q

ANS responsibility

A

for maintaining internal environ by effector organs not under voluntary control such as smooth and cardiac muscle, and glands

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128
Q

Sympatheic division of ANS releases and this causes

A

NE that primarily excites an effector organ, and after stimulation, NE is removed from synapse or inactivated

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129
Q

Parasym division releases and this causes

A

ACh, primarily inhibits effector organ, and after stimulation, ACh is degraded by acetylcholinesterase

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130
Q

5 ways exs enhances brain health

A

Enhances learning and memory
Stimulates formation of new neurons
Improves brain vascular function and blood flow
Attenuates mechanisms driving depression
Reduces peripheral factors for cognitive decline such as inflamation, HTN, and insulin resistnace

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131
Q

regular exs can protect brain against

A

disease and certain types of brain injury (stroke)

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132
Q

exercise improves

A

brain function and reduces the risk of cognitive impairment associated with aging

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133
Q

Regular exercise increases

A

brain growth factors

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134
Q

increased brain growth factors cause brain health to get better in three meaans

A

cognition
neurogenesis
vascular function

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135
Q

Human body contains over how many skel muscles?

A

600

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136
Q

what percentage of total body weight is skel muscles?

A

40-50%

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137
Q

4 functions of skel muscle

A

force production for locomotion and breathing
force production for postural support
protection
heat production during cold stress

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138
Q

Flexor muscle actions

A

decreases jt angle

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139
Q

extensors muscle actions

A

increases joint angle

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140
Q

epimysium

A

surrounds entire muscle, outside layer

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141
Q

perimysium surronds

A

bundles of muscle fibers, fascicles

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142
Q

Endomysium surrounds

A

individual muscle fibers

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143
Q

basement membrane of muscle

A

just below endomysium, is eplithelial tissue

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144
Q

sarcolemma

A

muscle cell plasma membrane

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145
Q

Satellite cells

A

undifferentiated cells

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146
Q

undifferentiated cells

A

immature

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147
Q

satellite cells reside in

A

basement membrane between sarcolemma and endomysium

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148
Q

satellite cells play a role in

A

muscle growth and repair when stimulated by physical stress such as exercise, and they increase the number of nuclei so they are multinucleated

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149
Q

Myonuclear domain

A

cytoplasm surrounding each nucleus, and each nucleus can support a limited myonuclear domainq

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150
Q

More nuclei potentially allow for what?

A

greater protein synthesis of actin and myosin via DNA in nucleus

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151
Q

what adaptations are satellite cells vital for?

A

strength training adapts

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152
Q

Myofibrils contain

A

contractile proteins; actin and myosin

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153
Q

actin

A

thin

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154
Q

myosin

A

thick filament, heads bind to actin

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155
Q

Sarcomere includes

A

Z line, M line, H zone, A band, and I band

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156
Q

SR

A

storage sites for Ca2+

Terminal cisternae

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157
Q

NMJ

A

Junction btwn motor neuron and muscle fiber

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158
Q

motor unit

A

motor neuron and all fibers it innervates

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159
Q

Motor End Plate

A

Pocket formed around motor neuron by sarcolemma

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160
Q

Neuromuscular celft

A

short gap between neuron and muscle fiber

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161
Q

ACh is released from

A

the motor neuron

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162
Q

When ACh is released from motor neuron, it causes an

A

EPP (end plate potential)

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163
Q

EPP

A

depolarization of muscle fiber as sarcolemma becomes permeable to a Na+ if threshold value achieved

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164
Q

Sliding filament model aka

A

swinging lever-arm model

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165
Q

Muscle shortening occurs due to the movement of the actin filament over the

A

myosin filament

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166
Q

Formation of

A

cross-bridges btween actin and myosin filaments

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167
Q

power stroke

A

cross bridging

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168
Q

Reduction in dist btw Z lines of the sarcomere

A

contraction

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169
Q

Actin Has 2 vital proteins called

A

tropmyosin and troponin

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170
Q

Myosin filaments have tiny what

A

protein projections on each end that extend towards the actin filaments; crossbridges

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171
Q

5 steps in sliding filament theory

A 
Rest
Excitation-coupling
contraction
recharging
relaxation
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172
Q

Write out how muscle contracts

A

do it guy

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173
Q

In the center of the sarcomere, the thick filaments lack what?

A

myosin heads

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174
Q

WHere are myosin heads present?

A

They are only present in areas of myosin-actin overlap.

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175
Q

Myosin thick filament

A

Each thick filament consists of many myesin molecules whose heads protrude at opposite ends of the filament

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176
Q

Actin thin filament consists of

A

2 strands of actin subunits twisted into a helix plus 2 types of regulatory proteins (troponin and tropomyosin)

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177
Q

What happens at resting step of sliding filament theory?

A

Troponin and tropomyosin prevent actin/myosin crossbridging

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178
Q

What is required for a muscle contraction ?

A

ATP

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179
Q

What breaks down ATP for muscle contraction?

A

myosin ATPase

ATP–> ADP + Pi

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180
Q

3 sources of ATP

A

PC
Glycolysis
Oxidative phosphorylation

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181
Q

During excitiation-contraction coupling phase what is being depolarized?

A

Depolarization of motor end plate (excitation) is coupled to muscular contraction

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182
Q

excitation-contraction coupling AP travels down

A

Transverse Tubules and causes release of Ca++ from SR

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183
Q

Once AP travels down T tubules to cause Ca++ release from SR what does Ca2+ bind to? To do what/why is this necessary?

A

troponin and causes position change in tropomyosin, and exposing active sites on actin

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184
Q

What kind of state is formed between actin and myosin and what does this cause?

A

a strong binding state and this causes a contraction to occur if ATP is present

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185
Q

First step in excitation of contraction

A

AP in motor neuron causes release of ACh into synaptic cleft

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186
Q

Second Step in excitation phase of contraction

A

ACh binds to receptors on motor end plate, leads to depolarization that is conducted down T tubules, which causes release of Ca2+ from the SR

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187
Q

First step in contraction phase of excitation-contraction coupling

A

At rest, myosin crossbridges in weak binding state

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188
Q

2nd step in contraction phase of excitation-contraction coupling

A

Ca++ binds to troponin, causes shift in tropomyosin to uncover active sites, and cross bridges forms strong binding state

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189
Q

3rd step in contraction phase of excitation-contraction coupling

A

Pi released from myosin, crossbridge movement occurs as per a pivoting action of the myosin heads referred to as a power stroke

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190
Q

4th step in contraction phase of excitation-contraction coupling

A

ADP released from myosin

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191
Q

5th step in contraction phase of excitation-contraction coupling

A

ATP attaches to myosin, breaking the crossbridge and forming weak binding state. Then ATP binds to myosin, broken down to ADP+Pi, which energizes myosin and continues as long as Ca++ and ATP are present

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192
Q

pivoting action of the myosin heads referred to as a

A

power stroke

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193
Q

Muscle Fatigue definition

A

decline in muscle power output due to decrease in force generation and in shortening velocity

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194
Q

Muscle fatigue two characteriscs

A

force generation and shortening velocity

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195
Q

During muscle fatigue in high intenisty exs what acculmates and what does that cause?

A

Acculmuation of lactate, H+, ADP, Pi, and free radicals. This causes/ diminishes cross bridges bound to actin

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196
Q

Long duration of high intensity exercise is due to?

A

Muscle factors that include acculmation of free radicals, electrolyte imbalance, and glycogen depletion

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197
Q

Muscle cramp def

A

spasmodic, involuntary muscle contractions

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198
Q

Muscle cramp cause theories (2)

A

Electrolyte depletion and dehydration theory

Altered Neuromuscular control theory

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199
Q

Electrolyte depletion and dehydration theory for muscle cramps

A

Water and Na+ loss via sweating causes spontaneous muscle contractions

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200
Q

Altered Neuromuscular control theory

A

Muscle fatigue causes abnormal activity in muscle spindle and GTOs, which leads to increased firing off of motor neurons resulting in a muscle cramp

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201
Q

Biochem props of muscle fibers

A

Oxidative capacity and type of myosin ATPase

202
Q

oxidative capacity

A

of capillaries, mitochondria, and amount of myoglobin

203
Q

type of myosin ATPase

A

speed of ATP degradtion

204
Q

Contractile properties of muscle fiber types

A

maximal force production, speed of contraction (Vmax), and muscle fiber efficiency

205
Q

Maximal force production

A

force per unit of cross-sectional area

206
Q

speed of contraction (Vmax)

A

myosin ATPase activtiy

207
Q

Type I fibers appear

A

darkest stains of myosin ATPase

208
Q

Type IIa fibers appear

A

lightest staining of myosin ATPase

209
Q

Type IIx fibers appear

A

inbtwn light and dark stains of myosin ATPase

210
Q

Immunohistochemical stainining

A

selective antibody binds to unique myosin proteins, and fiber types differentiated by color diff

211
Q

Gel Elctrophoresis

A

ID myosin isoforms specific to different fiber types

212
Q

Nonathletes have how much of percent of each fiber?

A

50% slow and 50% fast

213
Q

Power athletes such as sprinters have higher percentage of what fibers?

A

fast fibers

214
Q

Endurance athletes have higher percentage of

A

slow fibers

215
Q

Isometric muscle action

A

muscle exerts force without changing length

216
Q

pulling against moving object is what kind of muscle action?

A

isometric

217
Q

Postural muscles are what kind of muscle action?

A

isometric

218
Q

dynamic muscle action is also known as

A

isotonic

219
Q

2 types of isotonic/dynamic muscle actions

A

concentric/shortening-contraction

eccentric

220
Q

concentric muscle contraction

A

muscle shortens during force production

221
Q

Eccenctric

A

muscle produces force but length increases

222
Q

What muscle contraction is assoicated with fiber injury and soreness? why?

A

eccentric

Myosin heads are ripped out of actin binding site, causes pain and the inflamation

223
Q

Muscle twitch

A

contraction as the result of a single stimulus

224
Q

Latent period of muscle contraction

A

5 ms

225
Q

Contraction aspect of muscle twitch is when what is developed?

A

tension for 40 ms

226
Q

relaxation in muscle twitch

A

50 ms

227
Q

Speed of shortening is greater in .. . ? Why?

A

fast fibers

SR releases Ca++ @ faster rate and higher ATPase activity

228
Q

Force regulation of muscle 3 factors

A

Types and numbers of motor units recruited
Initial muscle length
Nature of the neural stimulation of motor units

229
Q

Types and number of motor units recruited depends on 2 thing for greater force production

A

more motor units= greater force

Fast motor units = greater force

230
Q

Initial muscle length

A

“Ideal” length for force generation (perpendicular jt angle)

Increased cross-bridge formation

231
Q

Nature of neural stimulation of motor units depends on

A

frequency of stimulation

232
Q

3 aspects of frequency of stimulation

A

Simple twitch
Summation
Tetanus

233
Q

Less than optimal length for length tension relationship in skel muscles

A

fewer cross-bridge interactions = reduced tension development

234
Q

optimal length for length-tension relationship in skel muscle

A

Maximal cross-bridge interaction = maximal tension dvp

235
Q

Greater than optimal length for length-tension relationship

A

No cross-bridge interxn = no tension dvpment

236
Q

Force-velocity relationship

A

At any absolute force, the speed of movement is greater in muscle with higher percent of fast-twitch muscle fibers. (faster contraction with fast fibers)

237
Q

According to the force-velocity relationship, the maxima velocity of shortening is

A

greatest at the lowest force and is true for both fibers

238
Q

Force-power relationship

A

At any given velocity of movement, the power generated is greater in a muscle with a higher percent of fast twitch fibers, and peak power increases with velocity up to movement speed of 200-300 degrees/sec. Power decreases beyond this velocity cuz force decreases with increasing movement speed.

239
Q

Sarcopenia

A

loss of muscle mass with aging

240
Q

With aging there is loss of ______ fibers and a gain of _____

A

fast fibers and gain in slow fibers

241
Q

What can delay age-related muscle mass?

A

resistance training

242
Q

Diabetes associated with

A

progressive loss of muscle mass

243
Q

Diabetes combined with

A

age-related loss

244
Q

What can protect people with diabetes

A

aerobic and resistive training

245
Q

Cancer causes

A

cachexia

246
Q

cachexia

A

rapid loss of muscle mass

247
Q

Cachexia from cancer results in

A

weakness, accounts for 20% deaths in cancer patients

248
Q

Regular exercise and nutrition therapy may counteract what

A

cachexia

249
Q

regular exercise stimulates

A

protein synthesis

250
Q

Muscular dystrophy

A

hereditary defects in muscle protein

251
Q

MD results in

A

loss of muscle fibers and weakness

252
Q

Duchene muscular dystrophy is most common in

A

childhood

253
Q

DMD progression

A

varies based on specific disease type

254
Q

The circulatory works with the

A

pulmonary/ respiratory sys

255
Q

Purposes of the cardiorespiratory sys

A

Transport O2 and nutrients to tissues
Removal of CO2 wastes from tissues
Regulation of body temperature

256
Q

2 major adjustments of blood flow during exercise

A

Increased CO/Q

Redistribution of blood flow

257
Q

Heart creates (its job)

A

pressure to pump blood

258
Q

Arteries and arterioles carry blood

A

away from the heart

259
Q

capillaries job

A

exchange of o2, co2, wastes, and nutrients with tissues

260
Q

Veins and venules carry blood

A

toward the heart

______

261
Q

Pulmonary circuit is what side of the heart?

A

right side of the heart

262
Q

Pulmonary circuit pumps what kind of blood to where via what?

A

Pulmonary pumps deoxygenated blood to the lungs via the pulmonary arteries*

263
Q

Pulm circuit returns

A

oxygenated blood to the left side of the heart via pulmonary veins*

264
Q

Pulmonary veins and pulm arteries

A

go in same direction just carry different carries different blood
Veins usually carry deoxygenated, but pulm veins oxygenated, while arteries usually carry oxygenated blood, but pulm arteries carry deoxygenated blood

265
Q

systemic circuit is what side of heart

A

left side of heart

266
Q

systemic circuit pumps

A

oxygenated blood to the whole body via arteries

267
Q

systemic circuit returns

A

deoxygenated blood to the right side of the heart via veins

268
Q

Heart wall consists of these 3 layers

A

epicardium
myocardium
endocardium

269
Q

Wall of heart receives blood supply via ____ and has high demand for _____ and ______

A

coronary arteries

high demand for o2 and nurtrients

270
Q

Myocardial infarction is what?

A

MI is a blockage in coronary blood flow results in cell damage

271
Q

Exercise training does what for MI?

A

EXs training protects against heart damage during MI

272
Q

How does exercise training protect heart during MI?

A

Angiogenesis

273
Q

Epicardium is what anatomical landmark as well

A

visceral pericardium

274
Q

Epicardium characteristics

A

serous membrane including blood capillaries, lymph capillaires, and nerve fibers

275
Q

Function of Epicardium

A

serve as lubricative outer covering

276
Q

Myocardium characteristics

A

cardiac muscle tissue seperated by connective tissues and including blood capillaires, lymph capillaries, and nerve fibers

277
Q

Myocardium F(x)

A

provides muscular contractions that eject blood from the heart chambers

278
Q

endocardium characteristics

A

endothelial tissue and a thick subendothelial layer of elastic and collagenous fibers

279
Q

endocardium f(c)

A

serves as protective inner lining of the chambers and valves

280
Q

Are contractile proteins: actin and myosin found in both the heart and skeletal muscles? Yes or no, eh

A

Yes

281
Q

How is the shape of skel and heart muscle differ?

A

The heart muscle is shorter than skeletal muscle fibers and branching, while skel muscle is elongated with no branching

282
Q

What is the difference between skel and heart muscle amount of nuclei?

A

Heart muscle : single nuclei

Skel muscle: multinucleated

283
Q

Do both heart and skel muscles have Z discs? yes

A

yes

284
Q

are both heart and skel muscle striated?

A

yes

285
Q

Do heart and skel muscle both have cellular junctions? What is the differnce if there is one?

A

Only heart does. The heart mucle has intercalated discs while the skel muscle has no junctional complexes.

286
Q

Do both heart and skel muscle have connective tissue? Any differences?

A

Both have connective tissue.
Heart muscle has endomysium for conenctive tissue.
Skel muscle has epimysium, perimysium, and endomysium with connective tissue.

287
Q

HEART muscle energy production

A

aerobic primarily

288
Q

skel muscle energy production both

A

aerobic and anerobic

289
Q

Ca2+ source for contraction for both muscles and any diff?

A

both have SR, but heart also gets extracellular Ca++

290
Q

Neural control of the heart muscle is

A

nonvoluntary

291
Q

Neural control of the skel muscle is

A

voluntary

292
Q

Regeneration potential in heart muscle?

A

None- no satellite cells present

293
Q

Regeneration potential in skel muscle?

A

Some possibiliteis via satellite cells

294
Q

Why is regular exercise cardio protective?

A

reduce incidence of MI

Improves survival from MI

295
Q

Exercise reduces amount of what?

A

myocardial damage from MI

296
Q

Exercise reduces amount of myocardial damage from MI causes 2 improvements:

A

Improvements in heart’s antioxidant capacity

Improved function of ATP-sensitive K+ channels

297
Q

Cardiac cycle

A

systole and diastole

298
Q

systole is what phase and what happens

A

contraction phase

Ejection of blood, 2/3 blood is ejected from ventricles per beat

299
Q

diastole what phase and what happens?

A

relaxation phase

filling w/ blood

300
Q

At rest, what happens in cardiac cycle?

A

At rest, diastole is longer than systole

301
Q

During exs, cardiac cycle

A

During Exercise, both systole and diastole are shorter

302
Q

Diastole pressure changes in ventricles

A

During diastole, pressure in ventricles is low

303
Q

Diastole and atria

A

During diastole, the atria are filling with blood

304
Q

diastole and valves

A

AV valves open when ventricular P is less than atrial pressure

305
Q

systole pressure in ventricles does what

A

pressure increases/rises

306
Q

systole blood is

A

ejected in pulmonary and systemic circulation

307
Q

systole and valves

A

semilunar valves open when ventricular pressure is greater aortic presure

308
Q

Heart first sound lub is what?

A

closing of AV valves

309
Q

heart second sound dub is what?

A

closing of aortic and pulmonary valves (semilunar)

310
Q

Arterial blood pressure is expressed as

A

systolic over diastolic

311
Q

systolic pressure

A

pressure generatered during ventricular contraction/ systole

312
Q

Diastolic presure in the

A

arteries during cardiac relaxation

313
Q

Pulse pressure is the

A

difference btween systolic and diastolic

314
Q

MAP

A

average pressure n the arteries during cardiac cycle

315
Q

MAP = eqn

A

DBP + .33x (SBP-DBP)

316
Q

Korotkoff sounds first phase

A

a clear tapping sound, onset of the sound for 2 consecutive beats is considered systolic

317
Q

Korotkoff sounds second phase

A

the tapping sound followed by a murmur

318
Q

Korotkoff sounds 3rd phase

A

a loud crisp tapping sound

319
Q

Korotkoff sounds 4th phase

A

abrupt, distinct muffling sound, gradually decreasing intensity (pre diastolic)

320
Q

Korotkoff sounds 5th phase

A

The disapperance of sound, is considere diastolic BP- 2 points below last sound heard

321
Q

Normal BP

A

<80

322
Q

Pre HTN

A

120-139/80-89

323
Q

Stage 1 HTN

A

140-159/90-99

324
Q

Stage 2 HTN

A

> /= 160/ >/= 100

325
Q

Stage 3 HTN

A

180/110 to 215/125

326
Q

hypotension

A

</= 90/60

327
Q

HTN bp = to or above

A

140/90 mm Hg

328
Q

Primary/essential HTN cuase

A

etiology unkown

329
Q

primary/essential HTN % of HTN

A

90% of HTN

330
Q

Secondary HTN result of some other

A

disease process

331
Q

HTN is risk factor for:

A

LVH
Atherosclerosis and MI
Kideny Damage
stroke

332
Q

Factors that influence ABP

A

MAP determinatns, short and long term regulation

333
Q

Determinants of MAP

A

Q

TVR

334
Q

MAP = formula

A

Q x TVR

335
Q

Short term regulation is what NS

A

SNS

336
Q

Short term regulation happens with what

A

baroreceptors in aorta and carotid arteries

337
Q

Increase BP causes baroreceptors to do what?

A

decrease SNS activity

338
Q

Decrease BP causes baroreceptors to ?

A

increase SNS activity

339
Q

Long term regualtion of BP is by what organ

A

kidney and either direct or indirect mech

340
Q

How down kidney regulate long term bp?

A

via control of blood volume (renin-angiotensin-aldosterone/ diuretics)

341
Q

Renin-angiotensin-aldoseterone is what mechanims?

A

longterm indirect mechanism

342
Q

Decreased arterial bp causes release of

A

renin

343
Q

Renin does what

A

catalyzes conversion of angiotensinogen from Liver to angiotensin I

344
Q

ACE from lungs and endothelial converts

A

angiotensin I to angiotensin II

345
Q

angiotensin II increases

A

blood volume

346
Q

How does angiotensin II increase blood volume?

A

stimulates aldosterone secretion from renal cortex
promotes ADH release
triggers hypothalamic thirst center

347
Q

Angiotensin II directly increases BP how , and most potent one of these

A

vasoconstriction

348
Q

5 factors increasing BP

A 
blood volume increases
HR increases
SV increases (Q increases)
Blood viscosity increases
Peripheral resistance increase (TVR )
349
Q

Contraction of heart depends on

A

electrical stimulation of the myocardium

350
Q

Components of conduction system

A 
SA node 
AV node
AV bundle
bundle branches
purkinje fibers
351
Q

SA node is located over what and does what?

A

right atrium

pacemaker, initiates depolarization

352
Q

AV node is located where and does what

A

floor of atria

pass depolarization to ventricles

353
Q

why brief delay at AV node?

A

Breif delay at AV node allows for ventricular filling

354
Q

Bundle branches where located

A

to left and right ventricle

355
Q

purkinje fibers located

A

throughout ventricles

356
Q

First step in conduction system of heart

A

AP originates in SA node and travel across the wall of the atrium from SA node to the AV node

357
Q

2nd step in conduction system of heart

A

AP pass through AV node and along AV bundle, which extends from the AV node, through the fibrous skeleton, into the interventricular septum

358
Q

3rd step in conduction system of heart

A

The AV bundle divides into right and left bundle branches, and AP descend to the apex of each ventricle along the bundle branches

359
Q

4th step in conduction system of heart

A

AP are carrried by the Purkinje fibers from the bundle branches to the ventricular walls

360
Q

EKG

A

records the electrical activity of the heart

361
Q

P wave

A

artrial depolarization

362
Q

QRS complex time afer the P wave

A

0.10 second after P

363
Q

QRS complex whats really happening hot stuff

A

Ventricular depolarixation and atrial repolarization

364
Q

T wave is what

A

ventricular repolarization

365
Q

ECG abnormalities may indicate

A

coronary heart disease

366
Q

ST-segment depression can indicate what

A

myocardial ischemia

367
Q

ECG during GXT used to eval

A

cardiac function

368
Q

GXT and EKG allows person to

A

observe EKG during exs and changes in BP

369
Q

Atherosclerosis

A

fatty plaque that narrows coronary arteries

370
Q

atherosclerosis reduces

A

blood flow to myocardium resulting in myocardial ischemia

371
Q

S-T segment depression suggests

A

myocardial ischemia

372
Q

1) Growth hormone supports/decreases the action of cortisol during exercise. GH will increase/decrease with exercise intensity, and well-trained athletes will have a greater/lesser GH response than untrained individuals.

A

supports

increase

373
Q

2) Epinephrine/norepinephrine are ___________- acting hormones and will provide glucose in the liver through ____________________ breakdown, instead of gluconeogenesis.

A

fast-acting

glycogen breakdown

374
Q

3) Epinephrine and norepinephrine will increase/during as exercise duration increases. As a person becomes more trained, he will secrete more/less hormone during exercise compared to a lesser-trained individual.

A

increase

less

375
Q

4) Epi/norepi will bind to a _________________________ receptor on a pancreatic _________________ cell to cause glucagon release.

A

Beta-adrenergic

Alpha pancreatic cell

376
Q

5) Epi/norepi will bind to a _________________________ receptor on a pancreatic _________________ cell to cause insulin suppression.

A

alpha-adrenergic

beta

377
Q

6) The result of both of the above actions will be an increase in plasma __________________, a decrease in plasma ___________________, and the breakdown of liver ___________________.

A

glucagon
insulin
glycogen

378
Q

7) For most exercise intensities, plasma insulin will increase/decrease compared to rest. However, at very high intensity, plasma insulin may slightly increase/decrease in order to allow _____________________ into the cell as an energy source.

A

decrease
increase
glucose

379
Q

8) Because trained individuals are more/less sensitive to hormones levels, glucagon levels will change little/greatly in trained people during exercise.

A

more

little

380
Q

9) What are the two primary results of epi/norepi (and therefore insulin and glucagon) response during exercise ?

A

TG breakdown in FFA, thus increasing plasma FFA

GLycogen breakdown into glucose to maintain blood glucose levels

381
Q

10) Fatigue can be defined as the inability to maintain _____________________ or ________________________ during repeated muscular contractions.

A

power output or force

382
Q

Fitness is what ? 2 parts

A

General health promotion

stresses moderation of activity

383
Q

Performance is what sports?

A

competitive sports

384
Q

Does performance or fitness require higher dose needed for success?

A

Performance

385
Q

Fitness is what to performance

A

Fitness is a secondary benefit of activity

386
Q

performance has many factors affected by what?

A

fatigue

387
Q

6 sites of fatigue

A 
CNS Function
Diet
Strength and Skill
Environment
Energy Production Anaerobic
Aerobic Energy Production
388
Q

Fatigue

A

Inability to maintain power output or force during repeated muscle contractions

389
Q

Central fatigue

A

Central nervous system

390
Q

Peripheral fatigue

A

Neural factors
Mechanical factors
Energetics of contraction

391
Q

Reduction in motor units activated is what kind of fatigue?

A

central fatigue

392
Q

Reduction in motor unit firing frequency is what kind of fatigue?

A

central fatigue

393
Q

Central nervous system arousal can alter the state of fatigue what kind of fatigue By facilitating motor unit recruitment
Increasing motivation
Physical or mental diversion is this?

A

central fatigue

394
Q

Serotonin linked to what 3 things?

A

relaxation, euphoria, arousal suppression

395
Q

Amino acid tryptophan (Trp) is precursor to

A

serotonin

396
Q

Free (unbound) Trp (f-Trp) shares carrier across

A

BBB into brain with BCAA

397
Q

Prolonged exercise:

A

↑ lipolysis; FFAs compete with Trp in binding to albumin; more f-Trp available for transport to brain

398
Q

Hypothesis for prolonged exercise : more BCAA will compete with

A

f-Trp for transport across BBB; less serotonin synth; less fatigue

399
Q

Peripheral Fatigue: Neural Factors site

A

Sarcolemma and transverse tubules

400
Q

Sarcolemma and transverse tubules is the ability of muscle

A

membrane to conduct an action potential

401
Q

Peripheral Fatigue neural factor inability of what pump to do what

A

Inability of Na+/K+ pump to maintain action potential amplitude and frequency

402
Q

Neural factor for peripheral fatique can be improved by

A

Can be improved by training

403
Q

An action potential block in the T-tubules

Reduction in Ca+2 release from sarcoplasmic reticulum

A

neural factor

404
Q

Peripheral Fatigue: Mechanical Factors (3)

A

Cross-bridge cycling and tension development
High H+ concentration may contribute to fatigu e
Longer “relaxation time” is a sign of fatigue

405
Q

Cross-bridge cycling and tension development depends on:

A

Arrangement of actin and myosin
Ca+2 binding to troponin
ATP availability

406
Q

High H+ concentration may contribute to fatigue due to:

A

Reduce the force per cross-bridge
Reduce the force generated at a given Ca+2 conc.
Inhibit Ca+2 release from SR

407
Q

Longer “relaxation time” is a sign of fatigue Due to

A

slower cross-bridge cycling

408
Q

Peripheral Fatigue: Energetics of Contraction

A

Imbalance in ATP requirements and ATP generating capacity

409
Q

Imbalance in ATP requirements and ATP generating capacity due to

A

Accumulation of Pi
Inhibits maximal force
Reduces cross-bridge binding to actin
Inhibits Ca+2 release from SR

410
Q

Rate of ATP utilization is slowed faster than rate of ATP generation due to

A

Maintains ATP conc. – protective effect – minimize change in homeostasis!

411
Q

Muscle fiber recruitment in increasing intensities of exercise

A

Type I  Type IIa  Type IIx
Slow oxidative  fast oxidative glycolytic  fast glycolytic
Up to 40% VO2 max: type I fibers recruited
40–75% VO2 max: Type IIa fibers recruited
Exercise >75% VO2 max: requires IIx fibers
Results in increased lactate, H+ production

412
Q

The Energy Continuum

A

Energy systems do not “turn on/turn off”

413
Q

Ultra Short-Term Performances duration

A

Events lasting <10 seconds

414
Q

Ultra Short-Term Performances Dependent on recruitment of Type II muscle fibers why?

A

Generate great forces that are needed

415
Q

Ultra Short-Term Performances what is important?

A

Motivation, skill, and arousal are important

416
Q

Ultra Short-Term Performances what is energy source?

A

Primary energy source is anaerobic
ATP-PC system and glycolysis
Creatine supplementation may improve performance

417
Q

Short-Term Performances duration

A

Events lasting 10–180 seconds

418
Q

Short-Term Performances shift from type of metabolism

A

Shift from anaerobic to aerobic metabolism
70% energy supplied anaerobically at 10s
60% supplied aerobically at 180s

419
Q

Primary energy source for short term performances and resultins in and intereferes with?

A

Anaerobic glycolysis is primary energy source
Results in elevated lactate and H+ levels
Interferes with Ca+2 binding with troponin

420
Q

Intermediate-Length Performances duration

A

Events lasting 21–60 minutes

421
Q

Intermediate-Length Performances energy system

A

Predominantly aerobic
Usually conducted at <90% VO2 max
High VO2 max is important

422
Q

Intermediate-Length Performances Other important factors

A 
Running economy
High percentage of type I muscle fibers
Environmental factors 
Heat
Humidity
State of hydration
423
Q

Long-Term Performances duration

A

Events lasting 1–4 hours

424
Q

Long-Term Performances energy system

A

Clearly aerobic

425
Q

Long-Term Performances and VO2max

A

High VO2max not as important

426
Q

what is is vital for long-term performances?

A

Environmental factors more important

427
Q

Influences on long term performances?

A

Maintaining rate of carbohydrate utilization
Muscle and liver glycogen stores decline
Ingestion of carbohydrate
Maintain carbohydrate oxidation by the muscle
Consumption of fluids and electrolytes
Diet also influences performance

428
Q

Is VO2max Important in Distance Running Performance?

A

VO2 max sets the upper limit for ATP production in endurance events
Even though race is not run at 100% VO2 max

429
Q

long term Performance also determined by:

A

%VO2 max at which runner can perform
Estimated by the lactate threshold
Running economy

430
Q

Training program should match the

A

anaerobic and aerobic demands of the sport

431
Q

Overload

A

Increased capacity of a system in response to training above the level to which it is accustomed

432
Q

Specificity

A

Specific muscles involved

Specific energy systems that are utilized

433
Q

Reversibility

A

When training is stopped, the training effect is quickly lost

434
Q

Men and women respond

A

similarly to training programs

435
Q

Exercise prescriptions should be

A

individualized

436
Q

Training improvement is always greater in individuals

A

with lower initial fitness

437
Q

50% increase in VO2 max in

A

sedentary adults

438
Q

10–15% improvement in

A

normal, active subjects

439
Q

3–5% improvement in

A

trained athletes

440
Q

1-2% improvement in

A

elite athletes

441
Q

Genetics plays an important role in

A

how an individual responds to training

442
Q

Åstrand and Rodahl: quote

A

“If you want to become a world-class athlete, you must choose your parents wisely.”

443
Q

Anaerobic capacity is more genetically determined

A

than aerobic capacity

444
Q

Training can only improve anaerobic performance to

A

a small degree

445
Q

Training can only improve anaerobic performance to a small degree dependent on and determined in

A

Dependent largely on fast (IIx) fibers

Determined early in development

446
Q

Warm-up

A

Increases cardiac output and blood flow to muscles
Increases muscle temperature and enzyme activity
Opportunity for stretching exercises
Believed to reduce risk of muscle injury

447
Q

Workout

A

Training session

448
Q

Cool-down

A

Return blood “pooled” in muscles to central circulation

Reduce hypotensive response

449
Q

Aerobic power: measure determined by

A

VO2max

Determined by max cardiac output, a-v O2 diff

450
Q

Training to Improve Aerobic Power

A

Long, slow distance
High-intensity, continuous exercise
High-intensity interval training (HIIT, which includes supramaximal sprint interval training (SIT)

451
Q

Aerobic power should be geared toward improving:

A

VO2 max
Lactate threshold
Running economy

452
Q

Long, Slow Distance benefits

A

economy, VO2max

453
Q

Long, Slow Distance intensity

A

Low-intensity exercise

50-60% VO2 max or 70% HRmax

454
Q

Long, Slow Distance duration

A

Duration greater than would be expected in competition

455
Q

Long, Slow Distance is Based on the idea that , but?

A

training improvements are based on volume of training
However, more is not always better
1.5 hours/day training may result in better performance than 3 hours/day

456
Q

High-Intensity, Continuous Exercise appears to be what?

A

Appears to be the best method of increasing VO2 max and lactate threshold

457
Q

High-intensity exercise

A

At or slightly above lactate threshold
80–90% HRmax
≥90% HRmax or 95% HRR also suggested

458
Q

High-Intensity, Continuous Exercise duration

A

Duration of 25–50 min

Depending on individual fitness level

459
Q

High-Intensity Interval Training Benefits

A

Benefit: lactate and H+ clearance

460
Q

High-Intensity Interval Training are

A

Repeated exercise bouts

Separated by brief recovery periods

461
Q

High-Intensity Interval Training Work effort

A

(repetition)
Distance to be covered
Intensity: 85–100% HRmax
Duration: >60 seconds to improve VO2 max

462
Q

High-Intensity Interval Training Rest interval

A

Light activity such as walking

1:1 ratio of work to rest; can be up to 1:3

463
Q

High-Intensity Interval Training Number of interval sets and repetitions depends on

A

Depends on purpose of training and fitness level

464
Q

Supramaximal Sprint Repeats are % vo2max

A

100-150% VO2max

465
Q

Supramaximal Sprint Repeats is performed on and how

A

Performed on cycle ergometer
Sprint as hard as possible against high resistance
Brief work effort: 20-30 s

466
Q

Supramaximal Sprint Repeats Benefits:

A

Increased oxidative/endurance capacity
PFK, LDH, PDH, citrate synthase, cytochrome oxidase, MCT, ↑ lipid oxidation, ↓ glycogenolysis, ↓ lactate accumulation
But, no increase in VO2max
Benefits come in form of increased lactate threshold

467
Q

Altitude Training Improves Exercise Performance at Sea Level

A

Altitude training may not always improve performance at sea level
Lower training intensity at altitude may result in de-training
Live-High, Train-Low
Spend sleeping and resting time at altitude
Increases red blood cell volume and oxygen transport capacity of blood
Train at lower altitude
Better performance gains compared to living and training at sea level

468
Q

Historically, training to improve maximal aerobic power has used three methods: and one new method

A

(1) interval training, (2) long, slow-distance, and (3) high-intensity, continuous exercise. Supramaximal sprint training enhances endurance capacity via lactate threshold, but not VO2max

469
Q

Although controversy exists as to which of the training methods results in the greatest improvement in VO2 max, there is growing evidence that it is

A

intensity and not duration that is the most important factor in improving VO2 max.

470
Q

The “Live-High, Train-Low” altitude training program provides significant

A

endurance performance gains compared to training and living at sea level.

471
Q

Most injuries are a result

A

of overtraining
Short-term, high-intensity exercise
Prolonged, low-intensity exercise

472
Q

The “ten percent rule” for increasing training load

A

Increase intensity or duration ≤10% per week

473
Q

Other injury risk factors

A 
Strength and flexibility imbalance
Footwear problems
Malalignment
Poor running surface
Disease (arthritis)
474
Q

ATP-PC system

A

Short (5–10 seconds), high-intensity work repeats
30-yard dashes for football players
30- to 60-second rest intervals
Little lactate + H+ is produced, so recovery is rapid

475
Q

Glycolytic system

A

Short (20–60 seconds), high-intensity work repeats
Very demanding training
May alternate hard and light training days
Remember supramaximal sprint training? Good for all energy systems

476
Q

Strength Training Adaptations

A

Increased muscle mass

477
Q

Hypertrophy

A

Increased muscle fiber diameter

Responsible for most of the increase in muscle size

478
Q

Hyperplasia

A

Increased number of muscle fibers

479
Q

Central nervous system changes for strength training adaptations

A 
Increased motor unit recruitment
Altered motor neuron firing rates
Enhanced motor unit synchronization
Removal of neural inhibition
“motor morons become motor geniuses”
480
Q

Delayed onset muscle soreness (DOMS) occurs

A

Appears 24–48 hours after strenuous exercise

481
Q

How does DOMS occur?

A

Due to microscopic tears in muscle fibers or connective tissue
Results in cellular degradation and inflammatory response
Not due to lactic acid

482
Q

What type of exercise/ contraction causes DOMS?

A

Eccentric exercise causes more damage than concentric exercise

483
Q

How to avoid DOMS?

A

Slowly begin a specific exercise over 5–10 training sessions to avoid DOMS

484
Q

Why more damage with eccentric exercise?

A

More force production
Due to LESS cross bridge detachment throughout the contraction
More attachment = more force production

485
Q

Steps Leading to DOMS

A

Strenuous muscle contraction results in muscle damage
Membrane damage occurs
Including sarcoplasmic reticulum
Calcium leaks out of SR and collects in mitochondria
Inhibits ATP production
Activates proteases which degrade contractile proteins
Results in inflammatory process
Increase in prostaglandins/histamines
Edema and histamines stimulate pain receptors

486
Q

A bout of unfamiliar exercise results

A

in DOMS

487
Q

Following recovery, another bout of same exercise results

A

in minimal injury

488
Q

Theories for the repeated bout effect

A

Neural theory

489
Q

Neural Theory

A

Recruitment of larger number of muscle fibers

490
Q

Connective tissue theory

A

Increased connective tissue to protect muscle

491
Q

Cellular theory

A

Synthesis of protective proteins within muscle fiber

492
Q

Overtraining not overload

A

Workouts that are too long or too strenuous

Greater problem than undertraining

493
Q

Performing non-specific exercises do not

A

enhance energy capacities used in competition

494
Q

Failure to schedule a long-term training plan results in

A

Misuse of training time

495
Q

Failure to taper before a performance results in

A

Inadequate rest; compromises performance

496
Q

Common Training Mistakes

A 
Overtraining 
Undertraining
Performing non-specific exercises 
 Failure to schedule a long-term training plan
Failure to taper before a performance
497
Q

Overtraining SX

A 
Decrease in performance
loss of BW
Chronic fatigue
increased number of infections
psychological staleness
Elevated HR and blood lactate levels during EXS
498
Q

Tapering

A

Short-term reduction in training load prior to competition

499
Q

Tapering allows what?

A

Allows muscles to resynthesizes glycogen and heal from training-induced damage

500
Q

Tapering Improves performance in both

A

strength and endurance events

Athletes can reduce training load by 60% without a reduction in performance

Exercise Physiology (5 decks)

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