Unit 4 try 2 Flashcards
1
Q
overload
A
physiological system is exercised at a level beyond what it’s normally accustomed through changing time, intensity, frequency, duration
2
Q
Specificity
A
training is specific to fiber type recruited, energy systems involved and type of contractions
3
Q
reversibility
A
gains are lost when overload is removed
4
Q
muscular strength
A
maximal force that a muscle group can generate
5
Q
muscular endurance
A
ability to make repeated contractions against a submaximal load
6
Q
strength training
A
high resistance training results in strength increase, low-resistance training results in endurance increase
7
Q
hypertrophy
A
increase muscle size & strength, occurs w/resistance training
8
Q
atrophy
A
decrease muscle size & strength, occurs w/aging
9
Q
Hierarchy of muscles
A
muscle -> fascicles -> myocyte -> contractile proteins -> arranged functional units (sarcomeres) -> muscle cell membrane (sarcolemma)
10
Q
Early gains in strength
A
nervous system adaptations: strength increase w/o size increase due to increase firing power and cross education training
11
Q
Neural adaptations to resistance training
A
increase motor unit recruited, firing rate of motor units, motor unit synchronization & improved transmission across neuromuscular junction
- Resistance training = synchronization of motor units
12
Q
Disinhibition
A
reduction of neurological inhibitory signals that allow for higher contraction of muscles
13
Q
mechanism responsible for training-induced increase in specific tension in type 1 fiber appears to be linked to…
A
increased Ca sensitivity, resulting in greater number of cross bridges bound to actin
14
Q
Hyperplasia
A
increase number of fibers, unclear if it occurs in humans
15
Q
hypertrophy
A
increased copss-sectional area of fibers due to increased muscle proteins and fiber size & actin/myosin
- maximized by high-velocity eccentric training that causes disruption of sarcomere z-line
16
Q
Satellite cells & resistance training
A
satellite cells divide and fuse w/adjacent muscle fibers to increase Myo nuclei through resistance training to support increased protein synthesis/larger muscles
17
Q
resistance training results in…
A
parallel increases in muscle fiber size & number of myonuclei
18
Q
shift in fiber type in endurance training
A
IIx -> IIa bc more resistant to fatigue improved muscle antioxidant capacity, proportional increase in tendons/ligaments w/muscle + Provides greater improvement in bone strength, & increased protein synthesis
19
Q
Factors leading to protein synthesis in resistance training
A
mRNA increases causing protein synthesis at ribosome, ribosome increase in number, elevated muscle protein synthesis capacity, activation of mTOR accelerates protein synthesis
20
Q
m Tor resistance training steps
A
muscle contractions leads to phosphatic acid (PA) which inhibits ras homolog enriched in brain (rheb) that with chain amino leucine, activates mTOR
21
Q
Testosterone, IGF-1 & growth hormone effect on mtor in resistance training
A
all linked to activation of mtor and elevated post-exercise levels are not required for strength gain
22
Q
Resistance training and genetics
A
80% of differences in muscle mass can be explained by genetics - high, moderate, & non responders
23
Q
Detraining and resistance training
A
can cause atrophy but declines slower compared to endurance training -> most strength loss associated w/nervous system changes rather than atrophy
24
Q
Atrophy and resistance training
A
increase free radicals, oxidative damage to muscle fibers, proteolysis/inhibition of mTOR pathway
25
endurance training adaptations
increases in VO2max w/training -> 50% determined by genetics
-> 45% increase in vo2max, 10% in cardiac output & 25% increase in max a-vo2 diff after 32 mo
26
endurance training and stroke volume factors
EDV is primary mechanism of incr. blood flow, increase in left ventricle volume, results in slower resting HR (Bradycardia)
- increase in blood volume due to increase plasma volume & red blood cell volume
27
concentric hypertrophy
due to pressure overload (resistance training) - when heart has thick walls w/small cavities
-> sarcomeres added in parallel to increase myocyte cell width
28
eccentric hypertrophy
due to volume overload (endurance training) - heart has thin walls w/large cavities
-> sarcomeres added in series to increase myocyte cell length
29
cardiac contractility and endurance training
strength of contraction when EDV, afterload & HR are constant, improved twist mechanics
30
after load and endurance training
less resistance to blood flow bc more muscles engaged, reduction in sympathetic vasoconstriction
31
influencing a-vo2 diff and endurance training
results from increased extraction of O2 primary increased by increased capillary density that accommodates from increased muscle blood flow, decreased diffusion distance to mitochondria and slow rates of blood flow
-> increase in mitochondrial volume contributes not is not a key factor
32
changes in fiber type and endurance training
increase in slow fibers, increased mechanical efficency (due to greater slow myosin isoforms that lower ATPase activity)
33
increased muscle capillary & endurance training
increased muscle capillary be enhanced diffusion of oxygen, and improved removal of waste
34
increases in sarcolemma and intermyofibrillar mitochondria and endurance training
increases in sarcolemma and intermyofibrillar mitochondria due to increase in size & number - all promotes removal of damaged mitochondrial
-> mitochondrial biogenesis improves oxidative capacity and ability to utilized fat as fuel and overall improves ATP production
35
effect of increased mitochondrial volume due to endurance training
increase in mitochondrial volume means ADP doesn't have to go back through glycolysis, they can be converted into ATP in mitochondria and so glycolysis slows
-> also means less phosphocreatine depletion and lactate/H production
36
exercise training induces mitochondrial biogenesis
reflected by nearly doubled levels of mitochondrial enzymes
37
endurance training effect on fuel utilization
increase transport of FFA into muscle
-increase capillary density
- increase transporter capacity
-fatty acid binding proteins
-fatty acid translocase
38
fatty acid binding protein
transport FFA to mitochondria
39
Fatty acid translocase
transmembrane protein in myocyte transfer FFA from blood stream to muscle cells for metabolism
40
increase transport of FFA from cytoplasm to mitochondria from endurance training is a result from
Fat and carnitine transferase (CPT-1)
41
Fat and Carnitine transferase (CPT-1)
transport of longtain FFA from cytosol to mitochondria for metabolism
42
increase of mitochondrial enzyme associated w/ b-oxidation during endurance training is a result from
increase acetyl-coa formation & high citrate levels that inhibits PFK
43
HITT adaptation and mitochondria
adapts mitochondria and experience mitochondria fusion, build more mitochondria to burn more fat
44
endurance training effects
improves muscle antioxidant capacity to counteract free radical and improve acid-base balance during exercise due to mitochondrial volume, NADH shuttles and change in lactate dehydrogenase isoforms to make less lactate
45
increase in mRNA levels from endurance training
transient increase in mRNA levels and synthesis of new proteins and mRNA levels typically peak in 4-8 hours, but returns to baseline
46
primary signaling pathway changes in endurance training
increased ca, production of free radicals, increased AMP/ATP ratio
47
secondary messengers & endurance training
calmoduline-dependint kinase (caMK) activated by increase cytosolic ca and promotes PGC-1a activation
calcineurin, nuclear factor kappa B, mitogen-activated kinase, and PGC-1a, AMPK
48
Calcineurin
activated by increase in cytosolic ca, participates in adaptive shift from fast-to-slow twitch fibers
49
Nuclear factor Kappa B (NFkB)
Activated by increase in free radicals, promotes synthesis of antioxidant enzymes
50
Mitogen-activated kinase (p38)
activated by increase in free radicals, promotes activation of PGC-1
51
PGC-1a
activated by increase in CaNK, P38, & AMPK, "master" regulator of biogenesis
52
AMPK
activated by shift in AMP/ATP ratio, stimulates glucose uptake & FFA oxidation during exercise, promotes activation of PGC-1a
53
Training-induced reduction in endurance training
lower HR and ventilation increase, less activation of chemo-recepotrs, lower lactate/H production, larger & more mitochondria
54
Impact of detraining endurance training
no change in HRmax, decrease in a-vo2 diff max, Qmax, SVmax and Vo2max
55
detraining a-vo2 diff max in endurance training
due to loss of oxidative enzymes
56
detraining SV max in endurance training
due to loss of plasma volume
57
time-course of training/detraining adaptations
increase muscle fiber mitochondria content, reaches Plato, quickly returns w/retraining, 1-2 weeks = adaptations are lost
58
Underwater weighing
Corrects for volume of air in body, expensive and takes up a lot of space
Error 2.7%
59
air displacement
determines body volume based on amount of air displaced
- control for variation in temperature, gas composition, subject's breathing during measurement
error 2.2-3.7%
60
Dexa
estimates for whole body and different regions: lean tissue, bone density, body fat
61
BIA: bioelectrical impedance analysis
electrodes built into hand grips or footplates measures impedance of a mild electrical current through the body
-provides an estimate of total body water, fat-free mass, and body fat
error 3.5-5%
62
sum of skinfolds
skinfold measurements taken at 3 sites around body
equation estimates total body fat based on measurements, age and sex
estimated error 3.5%
63
gold standard for weight measurement
underwater (hydrostatic) weighing
64
Dexa is also used for
bone density measurements to help diagnose osteopenia and osteoporosis
65
body fat: lower does not always equal better
essential for hormone regulation, organ function, thermoregulation, health of nervous system, fertility
- there is such a thing as too long
-women higher body fat then mens
66
upper body (android) fat
more common in men
- higher risk du to cardiovascular diesease, elevated blood lipids and diabetes
67
Lower body (gynoid) fat
more common in women
68
visceral fat/central adiposity
poses a greater risk
fat in abdomen and around organs
-more pathogenic
69
peripheral/subcutaneous adiposity
fat in lower body and below skin
less pathogenic
70
weight circumference
* Often a better predictor of disease risk than BMI as it’s not as affected by fat-free mass as BMI but it is harder to measure
* Correlates with abdominal (visceral) fat, which is more important in disease risk
71
White adipocytes
* Most abundant fat cells in the body, found subcutaneously, around the heart, and hear the GI tract
* Allows for fuel storage as triglycerides
* High amount of lipid, low amount of mitochondria
* Release hormone that can promote inflammation which is why it’s harmful to health
72
brown adipocytes
* Smaller quantities
* Exist in fat pads and on shoulders, upper back, and near kidneys
* High amount of mitochondria
* Do not synthesize ATP
* Oxidize fat to produce heat
* More brown fat = higher resting energy expenditure, decreased size of white fat cells
* Better for health
73
Beige adipocytes
* Called brite fat cells
* Similar to brown adipocytes
* Increase overall energy expenditure
* Endurance training may promote conversion of white fat cells to beige fat cells
74
BMI uses and limitations
* Not a direct measure of body composition
* Not intended to be a measure of individual health
* Most commonly-used way to estimate body fat and classify individuals into weight categories
75
Relationship between BMI and mortality
* Higher BMI means an individual has excess body fat but not true because aging effects and person with large muscle mas
* Lower BMI is better: not true bc weight loss due to cancer, chronic conditions etc.
* Smoking, weight loss due to disease, sarcopenia, malnutrition
* BMI cutoffs can be used to determine if an individual is overweight or obese: but differences in individual presentation differences in race and ethnicity
* Individuals in “overweight” BMI category have lowest all-cause mortality
* BMI cannot discriminate between body fat % and lean body mass
76
Metabolic syndrome
* One way to describe cluster of risk factors associated with disease
* Looks at many variables together
77
assumptions around weight and health
o Weight stigma/weight bias
* Weight stima and bias is harmful
78
aptitudes of Heathcare providers around weight
* Negative attitudes from healthcare providers about patients in larger bodies do affect patient outcomes
* Physical symptoms should not be attribute to patient weight unless/until other potential causes are addressed
79
weight cycling
weight cycling is associated with increased mortality
80
monogenic obesity
* Early-onset, severe obesity
* High genetic contribution
* Single mutation in one gene
* Large genetic effect
* Rare
* High penetrance
* No environmental influence
81
Polyenoic obesity
* Modest genetic contribution
* Hundreds of variants in or near many genes
* Each variant has a small effect
* Common
* Low penetrance
* Environment is a key determinant
82
interaction between genes and environment (biopsychosocial model)
* Obesity is extremely complex and multifactual, individual choices at an individual level can’t describe it all
* Weight gain varied across individuals, but weight gain between twins was similar: genetic/hereditary link
* Cannot address someone at an individual level w/o looking at the influence of community/what they have access to as well as beliefs and relationship and the environment they’re a part of
* Behaviors do play a role in body weight but there are also set of individual factors and environmental factors that influence body weight
83
changes in environment over time
* Decreased physical activity
* Increased abundance of food
* Concurrent improvement in long-term health due to improved sanitation and eradication of many infectious diseases
* Even w/high abundance, low genetics don’t gain that much weight but the average and high will
84
intake Vs. expenditure
* Greater energy intake per day due to less physical activity
* Less PA at work and at home, less PA for transportation, more sedentary time, unchanged or slightly increased leisure time PA
85
components that make-up daily expenditure
* Resting metabolism is the biggest part of energy expenditure
* Exercise causes an increase in energy expenditure for the exercise itself and nonthermal activity thermogenesis
* Resting metabolic rate plus physical activity/exercise plus thermic effect of food
86
how metabolism changes in response to weigh gain/loss
* Resting metabolic rate decreases by 20-30% within several weeks of a fast or very low calorie diet
* 25% of weight lost is fat-free mass (quarter FFM rule)
* Weight tapers off originally but then plateaus
* Alterations in total energy expenditure during weight loss low the rate of weight loss over time: decreased thermogenic effect of food, decreased resting metabolic rate, decreased energy cost of physical activity
* Combined, these effects slow the rate of weight loss despite maintenance of a reduced calorie diet
87
Primary prevention
prevent the development of a condition: hard to do and risk of targeting children
88
secondary prevention
manage health and prevent adverse health effects: assess and treat illness, treatment and health conditions may overlap with weight management interventions
89
lifestyle interventions
change the environment to support individual behavior changes or target individuals through reduced calorie diet, increased physical activity and/or behavioral therapy
90
effectiveness of various diets
* Negative caloric balance is more influential than emphasis on specific macronutrients
91
diet vs. exercise vs. diet + exercise
* Exercise can maintain/increase fat-free mass, extra metabolism happens after stopping exercise
* Exercise reduces visceral adipose tissue
* *exercise alone does not lead to significant weight loss over time
* Neither diet or diet and exercise loose enough weight to loose a big amount (D&E = 8kg, D=4, E=2)
92
maintenance of weight loss over time
* 80% who lost >10% o body weight regained it within 1 year
* Up t0 2/3 of individuals who lose weight during diet and exercise interventions regain more weight than was originally lost
93
Likelihood of significant and sustained weight loss
* Annual probability of losing 5% of body weight is 1/8 in men and 1/7 in women
* Much lower when looking at helping someone reach a “normal” weight
94
weight cycling on body
* Independent of BMI it leads to increased risk/rates of mortality, cardiovascular disease, loss of fat-free/muscle lass, some types of cancer, high blood pressure, diabetes, osteoporosis and fractures and gallstones
95
effectiveness of weight loss medication, surgery
* Medication: 5-15% wl of bw by slowing digestion and increase feeling of satiety, enhance insulin secretion and suppress secretion of glucagon
* Likely to regain weight after stopping medication
* Surgery: 30% exercise should still be prescribed, large amount of rapid weight loss = increased loss of fat free mass that exercise can help preserve
* Exercise may also help with long-term weight maintenance and glucose control
* Still gain some weight back
96
physical activity guidelines
* Adults: 150-300 minutes/week of moderate-intensity activity or 75-150 minutes of vigorous activity and muscle strengthening activities at moderate intensity involving al major muscle groups at least two days per week
* Progressing towards target means substantial benefits from physical activity, even if not meeting goal
97
benefits of exercise in adults and children
* Reduced all-cause mortality, protection against cardiovascular disease, improvement in cardiac risk factors, reduced risk of cancer, reduced risk of stroke, protection against severe illness or death from COVID
98
need for exercise in conjunction with weight loss medication or surgery
* large amount of rapid weight loss = increased loss of fat free mass that exercise can help preserve
* Exercise may also help with long-term weight maintenance and glucose control
99
changes in atmospheric pressure and partial pressure of gases
* Same relative air composition, decreased absolute quantity of gas molecules
* Increase in altitude results in reduced partial pressure of O2
* Low pressure and low oxygen caused by the fall in atmospheric pressure with increasing altitude
100
effect of altitude on hemoglobin saturation
* Low Po2 in inspired air reduces the pressure gradient between alveoli and pulmonary capillaries which impairs the rate of oxygen diffusion into blood
* Decrease in PO2 with increasing altitude has a direct effect on Hb saturation
101
effects on short-term (anaerobic) and longer (aerobic) exercise performance
* Anaerobic performance: performance not limited by oxygen delivery to muscles so not affected by low barometric pressure
* Lower air resistance may improve performance in jumping, sprinting events
* Aerobic performance: VO2 max decreases linearly with increase in altitude, impaired performance the higher the altitude gets
102
changes in cardiovascular functions with altitude
* HR max doesn’t change significantly but may decrease
* SV max does not change significantly (but prolonged altitude exposure can lower plasma volume and SV)
* Biggest variable that changes: arterial side of a-VO2 diff
* HR will increase since each liter of blood is saturated with less oxygen so heart rate must increase to compensate
103
changes in respiratory functions with altitude
* Ventilatory response will be higher at fixed submaximal workload, each liter of oxygen contains fewer oxygen molecules so ventilation must increase to compensate
104
acclimation to altitude
* Chronic low PO2 (hypoxia) leads to increase in cellular stress proteins: HIF-1 in kidneys which triggers cell signaling to produce erythropoietin which increases red blood cell production increasing hemoglobin and oxygen carrying capacity
105
live high, train low principle
* Training at altitude less effective since workout quality suffers as effect of exercise stimulus and exercise adaptations may be blunted however high altitude during childhood produces most significant adaptations
106
effects of extreme high altitude
* Above 8,000 m amount of O2 insufficient to sustain life and so you cannot acclimatize. Extended stay in the zone without supplemental O2 will result in deterioration of bodily functions, loss of consciousness, and death
* Non-essential bodily functions are suppressed
* Minimal exertion requires extreme ventilatory response and can lead to respiratory distress
107
increased likelihood of success at extreme altitude
* Higher baseline VO2max
* Primarily type 1 muscle fibers
* Stronger hypoxic drive: hyperventilation
* Hypoxia leads to decreased appetite, weight loss, etc.
108
nervous system control of body temperature
o Preoptic anterior hypothalamus
o Regulation of blood flow to increase/decrease body temperature
109
radiation
transfer of heat via infrared rays to objects not in direct contact with body
-60% of heat loss at rest (but can gain heat this way too)
110
conduction
heat loss due to contact with another surface
111
convection
heat transferred from body to air on water molecules
112
evaporation
point where water gains sufficient heat, and is converted to gas - most important during exercise
- requires vapor pressure gradient between skin and air
113
effects of heat/cold on cardiovascular function
decreased motivation, and reduced voluntary action of motor unit
* Type II/IV afferent metaboreceptors are stimulated from hyperthermic muscle, results in inhibitory effect on central motor drive decreasing recruitment of motor units
114
effects of heat/cold on cardiovascular dysfunction
reduced stroke volume, decreased cardiac output during high-intensity exercise, Decreased muscle blood flow
115
effects of heat/cold on muscle function
* Accelerated muscle fatigue: increased radical production, decreased muscle pH, muscle glycogen depletion, increased H and lactate production
116
effects of heat/cold on cardiovascular system
reduced SV, decreased Q during high-intensity exercise, decreased muscle blood flow
* Decreased proportion of blood flow to muscle as blood is partially diverted to skin to help cool the body – not a problem with submaximal exercise without dehydration
117
effects of cold on body
* Increase urine formation from increased fluid load to heard from vasoconstriction
* Increases workload of heart as vasoconstriction increases total peripheral resistance and aterload
118
heat acclimation
o Heat injury/hyperthermia: stages that if interrupted and treated early progress will stop
o Exercise in heat for 10-14 days for low or moderate intensity to increase plasma volume, capacity to sweat 3X more, increased VO2 max, maximal cardiac output and power output at lactate threshold, lower body temp and HR response, reduces sodium loss in sweat
* Higher fitness = lower risk of heat injury, inadequate hydration increases risk of heat injury, higher temperature may result in heat gain, skin exposure, humidity, wind, metabolic rate: decreased pace/workload lowers physical strain
119
cold acclimation
o Higher risk during cold immersion, result in cardiac arrhythmias and cardiac arrest, loss of judgement and frostbite
o Age a factor: older adults and young children
o Acclimation: ate onset of shivering, maintain heat production with less shivering, more nonshivering thermogenesis, maintain higher average hand/food temperature during cold exposure due to intermittent peripheral vasodilation
120
interaction of heat + humidity and cold + wind
o Heat with humidity and cold with wind are more damaging to body
121
shivering and non-shivering thermogenesis
o Non-shivering thermogenesis: brown adipose tissue, norepinephrine and thyroid hormones
* thyroxine and catecholamines
o Shivering: increases production by 5X
