Lecture Exam #1 Flashcards
1
Q
6 senses
A
hearing seeing smell taste touch Kinesthetic awareness
2
Q
responsibility of kinesthetic awareness
A
joint receptors
3
Q
system responsible for motivational drives and needs
A
Limbic system
4
Q
functional unit of muscle cell
A
Sarcomer
5
Q
two roles of calcium during muscle contraction
A
Ca+ in axon termianl causes release of acetycholing
Ca+ binds to regulatory site on troponin removes inhibition between actin and myosin
6
Q
three roles of ATP during muscle contraction
A
release of energy -> myosin head pulls actin over myosin (powerstroke)
new ATP attaches to myosin head -> seperation of actin and myosin
when nerve impulse stops ATP used to pump Ca+ back to sarcoplasmic reticulum
7
Q
process that breaks ATP down and moves myosin head
A
myosin ATPase
8
Q
muscle fiber types
A
Fast twitch Glycholiytic (anaerobic)
Fast twitch Oxidative Glycholytic (intermediate - between aerobic and anerobic capilities)
Slow twitch oxidative (aerobic)
9
Q
size principle
A
larger cell bodies require greater neural stimulation in order to depolarize (FT muscle fiber)
motor units with smaller cell bodies get recuited first
10
Q
which muscle fibre type has the largest cell body
A
Fast twitch Glycholytic
11
Q
what does the max. tension depent on
A
actin-myosin binding
12
Q
muscle fibre type with highest max. tension
A
fast twitch glycholytic
13
Q
what does the speed of a contraction depend on
A
size of axon (myelinated)
myosin ATPase
14
Q
muscle type with lowest endurance
A
slow twitch oxidative
15
Q
what does the length of a msucle contraction depent on
A
ability to recycle or regnerate ATP (slower endurance)
16
Q
motor unit
A
one motor neuron and all by it contolled muscle fibres
17
Q
rest before muscle contraction
A
actin and myosin are seperated
tropomyosin blocks actin binding site
Ca+ stored in Sarcoplasmic Reticulum
18
Q
steps of muscle contraction
A
release of Ca+ through nerve impulse causes release of acetycholine
ACH attaches to receptors that causes opening of Na+ channels and depolarization
AP causes release of Ca+ from SR
Ca+ binds to troponin receptors and moves tropomyosin away from blocking position
myosin head attaches to actin and pulls it over myosin filament
ATP binds to myosin head and releases it from actin
ATPase causes new attachement and further contraction
19
Q
power stroke
A
tilting of myosin head and mpulling of actin filament
20
Q
what causes power stroke
A
stored energy
21
Q
relaxation after muscle contraction
A
nerve impulse stops
Ca+ released from troponin binding site and transported back to SR
tropomyosin moves into blocking position
myosin head moves back
22
Q
what system allows Ca+ to travel away and back to the SR
A
Longitudinal Tubules
23
Q
why does the right side of the brain controls the majority of our bodie´s left side movement
A
because 90% of pyramidal motor tracts cross
24
Q
brain area behind the central sulcus
A
sensory cortex
25
brain area prior to central sulcus
primary motor cortex
26
brain are prior to primary motor cortex
pre motor cortex
27
responsibility of pre motor cortex
unconcious, fine tuning, highly skilled
28
responsibility of primary motor cortex
concious, voluntary movement
29
responsibility of sensory cortex
interprets information
30
pituitary gland
controlled by hypothalamus
| master gland
31
basal ganglia
grey matter
32
disease if grey matter is damaged
parkinson - lose muscle control
33
responsibility of cerebellum
coordination
34
A band
myosin, overlapping actin
35
H zone
only myosin area
36
I Band
lighter area
| actin
37
z lines
attached to sarcolemma
| groove for t-tubules to go deep into sarcolemma
38
where is Acetycholin stored
in synaptic vesicles
39
where is Ca++ within the muscle fibre stored
sarcoplasmic reticulum
40
responsibility of the midbrain
visual acuaity
41
responsibility of the medulla
heart rate
blood flow
respiration rate
42
responsibility of pons
respiration rate
facial expression
general eye movement
43
muscle fiber distribution in untrained people (genetic)
almost 50 % FT
50 ST
exceptions exist (some are born with a higher distribtion of one fiber type then others)
44
difference in gender and fiber type distribution
gender does not affect the fiber type distribution
45
fiber types in location of body
each individual has different fiber types in different parts of the body
46
fiber types within a motor unit
only same fiber types within one motor unit
47
why do motor units operate at "all-or-none" principle
because all are the same muscle fiber types - they need the same stimuli to get depolarized
48
what determines the force production
Actin and Myosin Binding
# of fibers within a motor unit
# of motor units activated
size of fiber within an active motor unit
balance between stimulating and inhibitory neurotransmitter
49
stimulating neurotransmitter
Acetycholin (AcH)
50
inhibitory neurotransmitter
gamma amino butyric acis (GABA)
51
twitch
a single muscle fiber contraction
52
summation
new stimuli while muscle fiber is still contracted - next contraction starts at a higher level and is stronger
53
tetanus
max. contraction
muscle cramp
not desrable
54
what muscle fiber type has more actin and myosin?
fast twitch
55
when is max. tension of a muscle gnerated
when length reaches peak tension range
| 120% of resting muscle
56
how can max tension of a muscle be increased
prestretch before movement
57
what kind of training can improve prestretch
biometric training
58
what 3 factors additionally affect force production
initial length of muscle fiber
angle of pull
architecture of tendon and muscle fiber
59
angle of pull
different angles determine different force production
60
muscle types
Fusiform
| Penniform
61
Fusiform muscles
parallel fibers running length of muscle
fibers insert into tendon
greater range of motion
less strangth and resistance to pull - greater risk to insure
62
Penniform muscles
fibers arranged diagonal to the direction of pull
fibers attached to tendon in small spaces
short range of movement
great strength and great resistance to injury
63
subdivisions of fusiform muscle
fusiform
bicipital
triangular
64
subdivisions of penniform
unipennate
bipennate
multipennate
65
metabolic by-products of muscle fatigue
lactic acid
| ketone bodies
66
what causes muscle fatigue
metabolic by-products -> decrease of pH -> interference of Ca+ release Actin-Myosin binding & ATP breakdown
depletion (Abbau) of Neurotransmitter (neural fatigue)
depletion of phosphagen (PC & ATP)
67
what leads to an increase in force
```
hypertrophy (increase in muscle size)
hyperplasia (increase in muscle fiber #)
increase in motor unit recruitment
prestretch
change of fibertype
```
68
agonist
contracting muscle
69
antagonist
relaxing muscle
70
high intensity speed training forms what kind of muscle fiber
fast twitch, decreases % slow twitch muscle fibers
71
low intensity endurance training forms what kind of muscle fiber
slow twitch, decreases % fast twitch muscle fiber
72
what is the most documented muscle fiber conversion due to training
SO to FOG
73
what does a reduced neural inhibition lead to
increase in motor unit recruitment
74
addition of strength training within endurance training
increase time to exhaustion while performing submax workload
75
addition of endurance training to strength program
may reduce strength gains from strength training
76
ATP use per day
at rest 40 kg
| heavy exercise 720 kg
77
phosphagen metabolism
highest power
lowest capacity
breakdown of ATP into ADP + Pi + E
extremely low ATP earned
78
enzyme within phosphagen metabolism
Myosin ATPase to breakdown ATP
| CPK and AK
79
formation of ATP
CP + ADP -> ATP + C (use of CPK Enzyme)
| ADP +ADP -> ATP +AMP (use of AK Enzyme)
80
when is phosphagen metabolism used
0-30 sec
| high intensity
81
location of phosphagen metabolism
sarcoplasm
82
energy pathway of phosphagen metabolism
phosphogen breakdown
83
starting product of phosphagen metabolism
ATP and CP
84
location of anaerobic glycolysis
sarcoplasm
85
energy pathway of anaerobic glycolysis
glycolytic (breakdown of glucose or glycogen)
86
starting product of anaerobic glycolysis
carbohydrate (CHO)
87
enzymes of anaerobic glycolysis
```
H-LDH (phosphorylase)
M-LDH (Hexokinase HK)
PFK (phosphofructokinase)
PK (pyruvate kinase)
A.T. (alanine transaminase)
```
88
by-product of anaerobic glycolysis
pyruvate broken down into lactic acid and alanine to live
89
relationship between lactic acid and pH
increase in lactic acid -> decrease in pH
90
earned ATP from anaerobic glycolysis
first 2 ATP invested, later 4 earned
| Net +2 ATP
91
when is the anaerobic glycolysis used
30sec. - 3-4 min
| high intensity
92
starting product of aerobic glycolysis/oxydative metabolism
pyruvic acid transformed into acetyl CoA
93
location of aerobic glycolysis
starts in sarcoplasm, end in mitochondra
94
eneryg pathway of aerobic glycolysis/oxidative metabolism
Glycolytic (breakdown of glycogen and glucose) in sarcoplasm
| Krebs cycle and Electron Transport System in Mitochondria
95
enzymes of aerobic glycolysis/oxidative metabolism
CS (Citrate synthase)
SDH (succinate dehydrogenase)
IDH (isocitrate dehydrogenase)
96
earned ATP with the aerobic glycolysis/oxydative metab.
Net in skeletal muscle 36 ATP
| Net in cardiac muscle 38 ATP
97
when is oxydative metabilism used
3-4 min. - 2-3 h.
| moderate intensity
98
by products of oxydative metabolism
CO2 and H2O
99
what is beta fat oxidation based on
triglycerides = glycerol + 3 fatty acids
100
location of beta (fat) oxidation
TG starts in Sarcoplasm
| Beta oxidation in mitochondria
101
pathway of beta (fat) oxidation
beta oxidation, kreb´s cycle, Electron transport system all in mitochondria
102
starting product of beta (fat) oxidation
Acyl CoA
| Carnitine - transporter
103
enzymes within the beta (fat) oxidation
```
lipase (HSL)
thiokinase
thiolase
carnitine fatty acid
transferase
```
104
by-product of beta (fat) oxidation
ketone bodies (decrease in pH)
105
ATP earned by beta (fat) oxidation
1 Fatty acid = 100-150 ATP
106
when is the beta (fat) oxidation used
during continous low activity
107
factors that determine lactate production
oxidative metabolism´s ability to accept pyruvate into krebs cycle
ability of the ETS to accepts NADH+H+ and FADH+H+
ability to form alanine from the breakdown of carbohydrates
ratio of M-LDH (forms lactate) to H-LDH (clears lactate)
108
factors of phosphagen metabilism to increase capacity
increase in training
increase in muscle mass
increase in creatine ingestion
109
factors of anaerobic glycolysis to increase capacity
increase in muscle mass
increase in alanine transaminase
increase ratio of H-LDH and M-LDH
110
factors of aerobic glycolysis/oxidative metabolism to increase capacity
capacity is based on muscle and liver glycogen stores
increase in training
increase in CHO loading
increase in fluid ingestion
111
factors of beta (fat) metabolism to increase capacity
increase CHO
112
power
speed ATP can be produced and released at
113
what is power of phosphagen metabolism based on
enzyme activities
114
what is power of anaerobic glycolysis based on
enzyme activities
115
what is power of aerobic glycolysis(oxidative metabolism based on
O2 delivery rate
| enzyme activity
116
what is power of beta (fat) metabolism based on
fat mobilization
enzyme activity
O2 delivery rate
117
H+ and e- carrier within the ETS
cytochromes
118
when do NAD carrier take action
glycolysis of cardiac muscle, in krebs cylce, beta (fat) oxidation, and conversion of pyruvate to acetyl CoA
119
how many ATP can be earned when NAD dropps of H+
3 ATP
120
when do FAD carrier take action
in glycolysis of skeletal muscle, krebs cycle, and beta (fat) oxidation
121
molecule for carbohydrates and fat to enter krebs cycle
Acetyl CoA
122
how many ATP are in aerobic glycolysis already formed before entering the mitochondria
cardiac muscle 2 invested, 10 formed
Net of 8 ATP
skeletal muscle 2 invested, 8 formed
Net of 6 ATP
123
where do NAD and FAD carry H+ and e- to to form ATP
Electron Transport System (ETS)
124
Mitchell´s Chemiosmotic Hypothesis
electron transfer leads to pumping of protons out of matrix generating proton gradient which leads to phosphorylation of ATP
125
how many ATP are formed in pyruvate oxidation in the Krebs cycle and ETS
15 ATP x 2 rounds = 30 ATP
126
Fat metabolism energy yield
Fat 9 Kcal/gm
Carbohydrates 4 Kcal/gm
protein 4 Kcal/gm
alcohol 7 Kcal/gm
127
how many carbons are in each fatty acid
12-18
128
what does free fatty acid needs to get formed to, to enter the mitochondria in beta oxidation
acyl CoA
129
carrier of Acyl CoA into mitochondria
carnitine
130
why do energ systems respond in a certain order
by- or end-products of energy systems stimulat enzymes of other nergy systems
quick energy systems are often less complex
slower energy systems depend often on intramuscular metabolic factors and other systems likecardiorespiratory and circulatory systems
131
HSL stimulating hormones and fat mobilization
```
thyroxine
cortisol
glucagon
epinephrine
norepinephrine
```
132
hormones that inhibit HSL and fat mobilization
Insulin
133
what increases stimulating hormone release
exercise
134
role of caffein
stimulates HSL and fat mobilization
| stimulates phosphoralyse in glycolysing and glycogen mobilization
135
what does an increase in carbohydrate loading lead to
increases aerobic glycolysis and beta (fat) oxidation capacity due to an increase in muscle glycogen
136
best way for a carbohydrate loading program before a competition
1-2 days long hard exercise - exhaustion
2-3 days low carbohydrate diet
2-3 days high carbohydrate diet
competition
137
what can carbohydrate loading be used for
to improve endurance performance in events longer than 60-80 min at 65-85% of VO2max or 75-85% of max HR
138
what is understood as a low CHO diet
50 % of calories from CHO
| 4g of CHO per kg of BW
139
high CHO diet
70% of calories from CHO
| 10G of CHO per kg of body weight
140
CHO and fluid during exercise
event < 90 minutes -> 4-8 ounces of cold water every 10-15 minutes
event > 90 minutes -> 4-8 ounces of cold water containing 5-10% glucose solution every 10-16 minutes
141
what does the ingestion of caffeine prior to exercise lead to
5g/kg of BW 40 min prior to event
improves fat mobilization -> power of fat ocidation
enhance mobilization of muscle glycogen
142
critical aspect of caffeine ingestion prior to event
neg. diuretic effect -> dehydration
| critical to maintain fluid during exercise
143
how does creatine monohydrate ingestion help prior to an event
maintain higher muscle creatine levels
increase phosphocreatine resynthesis -> allows high intensity for longer time
allows to shorten resting time between high intensity exercise
increase phosphagen and anaerobic glycogen capacity
144
how does CHO loading benefits high intensity, short duration athletes
increasing work time to exhaustion
145
what needs to be considered as important with CHO loading for sprinters
important to not gain BW
146
poitive effects of sodium bicarbonate ingestion
buffering of H+ released from lactic acid
| increase lactic acid tolerance and capacity of anaerobic glycolysis
147
changes in phosphagen metabolism due to endurance training
increase in [ATP], CP, CPK, AK
| increase in reaction time -> increase in power
148
changes in oxydative metabolism due to endurance training
```
increase [myoglobin], O2 delivery
increase in krebs cycle enzyme, ETS cytochrome and beta oxidation enzyme activity
increase in Lipase (HSL) activity
mucle [glycogen]
Triglyceride in muscle
```
149
oxidative changes in fiber type specificity
greater in SO and FOG than in FG
150
glycolytic changes in fiber type specificity
greater in FT than in ST
151
phosphagen changes due to endurance training in children
increase in [ATP] and [CP], increase in capacity
152
glycolysis changes due to endurance training in children
increase in power
153
changes in phosphagen metabolism following strenth training
increase ATP and CP level
increased myosin ATPase CPK and AK levels
increased capacity
154
changes in anaerobic glycolysis due to strength training
increased enzyme levels
| increased power
155
changes in oxidative metabolism due to strength training
increase muscle glycogen decreased [mitochondria/fiber volume ratio
increased FT fiber area/ST fiber ratio
muscle hypertrophy
156
when does strength training in children show an effect
after puberty
157
peripheral sensory receptors
muscle spindles
golgi tendon organs
joint receptors - proprioreceptors
158
muscle spindles
operate functional spinal cord level
sense length of muscle fibres
reflex contraction
co-activation of extra- and intrafusal fibers
159
golgi tendon organs
reflex inhibition (inhibits muscle to overcome to high force
160
input into motor coretx
sensory cortex
| limbic system
161
proprioreceptors
feedback to sensory cortex = kinesthetic awareness
162
gamma efferent
nerves from from spinal cord coming
163
afferent from muscle spindle
nerves to spinal cord going
top one primary annulospinal ending
bottom secondary flower spray endind
