Unit 4 Flashcards
1
Q
overload
A
Training effect occurs when a physiological system is exercised at a level beyond which it is not normally accustomed
- can be done by changing intensity, frequency and duration
2
Q
What is training specific to?
A
fiber type recruitment
energy system involved
type of contraction
3
Q
What is reversibility?
A
gains are not when overload is removed
4
Q
What is muscular strength?
A
maximal force that a muscle group can generate
- 1 repetition maximum
5
Q
What is muscular endurance?
A
ability to make repeated contractions against a SUBMAXIMAL load
6
Q
What is strength training?
A
high-resistance training (6-19 reps)
- results in strength increases
Low-resistance training (35-40 reps till fatigue)
- results in increases in endurance
7
Q
What is hypertrophy?
A
increase in muscle size which leads to an increase in muscle strength
- increase in size of existing muscle fibers (cross-sectional areas (contractile proteins) increase)
- occurs with resistance training
8
Q
What is atrophy?
A
decrease in muscle size that causes a decrease in muscle strength
Sarcopenia: loss of muscle mass
occurs with aging (greatest > 50)
9
Q
Muscle hierarchy review
A
muscle
fascicles
myocytes
contractile proteins: myosin and actin
arranged in functional units: sarcomeres
muscle cell membrane is called: sarcolemma
10
Q
excitation-contraction
A
Action potential from CNS travels down alpha motor neuron
Depolarization of sarcolemma leads to calcium ion release from sarcoplasmic reticulum
Ca++ release triggers cross-bridge formation and muscle contraction
11
Q
what is responsible for early gains in strength
A
strength gains during first 8 weeks of training are largely due to nervous system adaptations
12
Q
evidence that neural adaptations occur:
A
muscular strength increases in first 2 weeks of training without increase in muscle fiber size
phenomenon of “cross education” training of one limb results in increase of strength in untrained limb
13
Q
Neurological change adaptations
A
increased neural drive (in CNS):
- increased number of motor unit recruited
- increased firing rate of motor units
increased motor unit synchronization
improved transmission across neuromuscular junction
14
Q
resistance training and motor unit recruitment
A
increase is resistance training results in more synchronous recruitment of motor units
15
Q
synchronization of motor units
A
simultaneous “firing” of MUs
- MUs may be in same or different muscles
may produce more forceful contraction
improves rate of force development for brief periods
16
Q
Disinhibition
A
reduction in neurologic inhibitory signals
- less “autogenic inhibition” by Golgi tendon organ (GTO) system, which normally inhibits contraction
- no direct evidence (that resistance training alters GTO structure and functions in humans)
17
Q
increased strength preceds increase in muscle size
A
this suggests: intrinsic mechanism to increase force generating capacity
resistance training increases specific force of type 1 fibers but not type IIa/IIx
not due to actin/myosin per cross-sectional area
mechanism responsible for training-induced increase in specific tension in type 1 fibers appears to be linked to increased calcium sensitivity, resulting in greater number of cross-bridges bound to actin
18
Q
increase in muscle mass: hyperplasia
A
resistance training results in increased muscle mass
- hyperplasia is increased number of fibers
– evidence for relationship present in animals
unclear if hyperplasia occurs in humans
19
Q
increase in muscle mass: hypertrophy
A
resistance training results in increased muscle mass
hypertrophy: increased cross-sectional area of fibers
- hypertrophy likely the dominant factor in increased muscle mass
hypertrophy due to increased muscle proteins
increased fiber size in type 1 and type 2 fibers
- greater cross-sectional area = more actin and myosin
stop
20
Q
training for muscle hypertrophy
A
maximized by high-velocity eccentric training - causes disruption of sarcomere Z-lines
concentric training (only) could limit increases in muscle hypertrophy and strength gains
stimulated across a range of intensities
- 30-90% of 1 RM
- perform to volitional fatigue
stop
21
Q
Role of Satellite cells
A
stem cells superficial to the sarcolemma
resistance training activates satellite cells to divide and fuse with adjacent muscle fibers to increase myonuclei
resistance training-induced increases in myonuclei results in a constant ration between number of myonuclei and size of muscle fibers
support increased protein synthesis in larger muscle
stop
22
Q
resistance training results in…
A
parallel increases in muscle fiber size and number of myonuclei
23
Q
Resistance training adaptations in muscle
A
shift in muscle fiber type
transition from type IIx to type IIa
no increase in type I fibers
limited research to show prolonged effects
inconsistent findings on improving oxidative capacity
NOTE: endurance training increases mitochondrial volume and formation of new capillary
improves muscle antioxidant capacity
proportional increase in tendons/ligaments with muscle
provides greatest improvement in bone strength
24
Q
prolonged resistance training results in
A
increased protein synthesis
- muscle protein content is constantly changing
-after exercise: increase synthesis, decrease degradation
- synthesis must exceed degradation for 3+ weeks
25
muscle protein synthesis following a single bout of resistance exercise
protein synthesis increases 50-150% within 1-4 hours
duration of elevation varies by training status
- synthesis remains elevated for longer period of time in untrained individuals
26
Trained vs. untrained protein synthesis
trained reaches protein synesis sooner but percent increase in synthesis doesn't last as long
27
signaling events leading to protein synthesis
Key factors that contribute to resistance training-indueced increases in muscle protein synthesis
- mRNA increases resuling in protein synthesis at the ribosome
- ribosomes increase in number and elevate muscle's protein synthesis capacity (prior to hypertrophy)
- activation of the protein kinase "mechanistic target of rapamycin" (mTOR) is the key factor accelerating protein synthesis following a bout of resistance training.
-- historically, mTOR activation linked with insulin-like growth factor (IGF-1), but focus has shifted
28
mTOR activation
mechanoreceptors
Pa and rheb
Leucine increases leads to PA
ALL leads to mTOR activation and protein synthesis and muscle hypertrophy
29
supplemental information on mTOR
- Muscle contractions activate a sarcolemma mechanoreceptor stimulating synthesis of phosphatidic acid (PA)
- Contraction-induced activation of sarcolemma mechanoreceptors also activates extracellular signal-regulated kinase (Erk)-active Erk inhibits TSC2 which is an inhibitor of ras homolog enriched in brain (Rheb)
- Supplementation with the branched chain amino leucine, independent of resistance training, activates mTOR and promotes a small increase in muscle protein synthesis
- However, long-term supplementation with leucine does not result in muscle hypertrophy in sedentary individuals
30
molecular response seconds after resistance training
increase rheb and PA
31
molecular response minutes after resistance training
increase mTOR activation
32
molecular response hours after resistance training
increase protein synthesis
33
Hormones and hypertrophy
Testosterone, IGF-1, growth hormone are all linked to activation of mTOR pathway, but...
elevated post-exercise levels are not required for anabolism adn strength gains
- women have 45x lower postexercise testosterone
-even when accounting for baseline levels
- yet women still see robust increases in myofibrillar protein
- research indicated high vs. low circulating levels not necessary to stimulate muscle anabolism
34
Genetic influences on muscle mass
about 8-% of differences in muscle mass can be explained by genetic variation
many genes directly linked to mTOR signaling pathway
3 groups of responders to resistance training, depending on variable activation of specific skeletal muscle genes
- high responders
- moderate responders
- nonresponders (limited/no hypertrophy)
35
How many genes play a role on muscle mass
47 genes play a key role
36
detraining effect
muscle can atrophy when training stops, but decline is slower in comparison to endurance training
20 week rigorous training program results: 60% increase in strength and hypertrophy of all 3 fiber types
- 30 weeks of detraining: 31% decrease in strength, small amount of atrophy
- 6 weeks of retraining: rapid regain of strength and restoration of fiber size
most strength loss associated with nervous system changes rather than atrophy
37
Atrophy from prolonged inactivity
immobilization after injury, zero gravity, bed rest
7 days: 7-10% loss in muscle mass
20-30 days: 15-20% loss in muscle mass
results from imbalance between muscle protein synthesis and breakdown/degradation
prolonged disuse leads to increased free radicals, oxidative damage to muscle fibers, proteolysis and inhibition of mTOR pathway
38
Endurance training and VO2 max
training programs involve: large muscular engaged in continuous dynamic exercise
(>20 min, >3 times/week, >50% vo2 max)
high intensity interval training effective alternative
increase in VO2 max with training:
- high variability (2-50% increase) due to genetics: 50% of individuals VO2 max determined by genetics
shaking
39
concentric hypertrophy cause
resistance training caused by pressure overload
pathological: hypertension, aortic constriction
40
concentric hypertrophy result
heart have thick walls and small cavities to resist pressure
sarcomeres added in parallel increase myocyte cell width
41
Eccentric hypertrophy causes
endurance training
pathological: valve disease
42
Eccentric hypertrophy results
hearts have think walls and large cavities to make room for more blood
sarcomeres added in series increases myocyte cell length
43
Factors influencing stroke volume: cardiac contractility
strength of contraction when EDV, afterload, & HR constant
animal studies reveal greater force of ventricular contraction
improved "twist mechanisms" in endurance athletes
44
Factors influencing stroke volume: afterload
less resistance to blood flow during maximal exercise: because you are engaging more muscles
reduction in sympathetic vasoconstriction in trained muscle: higher stroke volume
45
Factors influencing a-vO2 diff
Results from increased extraction of O2 from blood
primary mechanism - increased capillary density
- accommodates increased muscle blood flow
- decreases diffusion distance to mitochondria
- slow rate of blood flow (more time for diffusion)
increase in mitochondrial volume
- contributes, but capacity of mitochondria to use O2 exceeds capability of heart to delivery O2 - not the key factor for VO2 max
46
endurance training changes in fiber types
shift from fast-to-slow muscle fiber type
- reduction in fast fibers and increase in slow fibers
- increases mechanical efficiency (due to greater slow myosin isoforms which have lower ATPase activity)
- Does NOT result in COMPLETE SHIFT
-- magnitude depends on duration of training and genetics
47
endurance training changes in capillarity
increased muscle capillarity
- enhanced diffusion of oxygen
- improved removal of wastes
48
Mitochondrial volume and turnover
two subtypes of mitochondria:
- subsarcolemmal and intermyofibrillar (80% located around contractile proteins)
endurance training increases volume of both subtypes
due to increase in size and number of mitochondria
mitochondrial biogenesis results in improved:
- oxidative capacity
- ability to utilize fat as fuel
promotes removal of damaged mitochondria (mitophagy)
49
Significance of incrased mitochondrial volume
Recall - study-state VO2 consumed during a moderate intensity exercise bout is not affected by training
- however, steady-state achieved more rapidly
This means mitochondria consuming the same number of O2 molecules per minute before and after endurance training
- but ATP-production is not different (improved)
50
influence of mitochondrial volume
with endurance training, ADP doesn't have to go back through glycolysis as they can be converted in ATP in mitochondria and so glycolysis slows
51
Influence of mitochondrial volume pt. 2
Increased volume = decreased cytosolic (ADP)
rate of ADP transport into mitochondria increases
- less phosphocreatine deletion
- reduced stimulation of glycolysis (PFK)
-- less production of lactate and H
52
Biochemical adaptations in muscle
exercise training induces mitochondrial biogenesis ( production)
reflected by nearly doubled levels of mitochondrial enzymes
53
Effect on Fuel Utilization: incr. transport of free fatty acids into muscle
- increase capillary density (enhanced delivery)
- incr. transporter capacity
-* fatty acid binding protein
-* fatty acid translocase (FAT)
54
effect on fuel utilization: increase transport of FFA from cytoplasm to mitochondria
- incr. FAT and carnitine transferase (CPT - 1)
55
effect on fuel utilization: increase mitochondrial enzymes associated with B-oxidation
increase acetyl-coA formation & high citrate levels (inhibits PFK
- starts creb cycle, more citrate say oxidative phosphoration it working and provides more rate limiting enzyme
56
HITT effect on mitochondria
HIIT adapts mitochondria and experiences mitochondrial fusion
- build more mitochondria to burn more fat
- combined training: increases mitochondrial number
-resistance training: no influence on mitochondrial volume, number, or perimeter
57
Effect of training on fuel utilization
incr. capillary density -> slower blood flow in muslce and increased FFA transporters -> increased uptake of FFA -> incr. FFA utilization -> spares plasma glucose (slows down fatigue
or
incr. Mitochondria number -> increased beta oxidation enzymes and carnitine transferase
58
additional adaptations of endurance traning
inproves muslce antioxidant capacity
- free radicals: molecules that contain an unpaired electron in their outer orbital; highly reactive and promote damage
-- produced during muscular contraction
- endurance training incr. endogenous antioxidant production
improves acid-base balance during exercise
- related to increase mitochondrial volume
- increased NADH shuttles (less lactic acid production)
- change in lactate dehydrogenase (LDH) isoforms: different affinity for substrate v. product ET means shift to more pyruvate than lactate
59
Effect of training on acid-base balance (ET improves)
incr. mitochondria leads to increased FFA oxidation and decreased PFK activity that decreases pyruvate formation with lower production of lactate leads to decreased lactate and H formation that maintains blood pH
or
increased mitochondria leads to increased mitochondrial uptake of pyruvate and NADH leads to decreased lactate and H formation that maintained blood pH
60
Time course of training adaptation
muscle contraction activates primary and secondary messengers
- transient incr. in MRNA levels and synthesis of new proteins
- mRNA levels typically peak in 4-8 hours, but return to baseline: increase w/ weeks of exercise
61
Enudrance-induced singnaling pathways for endurance training
primary signals for adaptations
-increased ca levels
-- released from sarcoplasmic reticulum
--sustained incr. levels of cytosolic ca
production of free radicals (oxidants)
- increase with exercise
increased AMP/ATP ratio
-accelerated due to ATP consumption
62
secondary messengers in skeletal muscle -1 endurance training: calmoduline-dependend Kinase (CaMK)
- activated by increase in cytosolic calcium
- promotes activation of PGC-1a
63
secondary messengers in skeletal muscle -1 endurance training: calcineurin
- activated by increase in cytosolic ca
- participates in adaptive shift from fast-to-slow transition
64
secondary messengers in skeletal muscle -1 endurance training: Nuclear factor Kappa B (NFkB)
- activated by increases in free radicals
- promotes synthesis of antioxidant enzymes
65
secondary messengers in skeletal muscle -2 endurance training: Mitogen-activated Kinase (p38)
activated by increases in free radicals
promotes activation of PGC -1a
66
secondary messengers in skeletal muscle -2 endurance training: PGC-1a
activated by increases in CaMK, p38, and AMPK
Master regulator of mitochondrial biogenesis
67
secondary messengers in skeletal muscle -2 endurance training: AMPK
improves metabolism
activated by shift in AMP/ATP ratio
stimulates glucose uptake & FFA oxidation during exercise
promotes activation of PGC-1a
68
endurance training primary signals
ca, amp/atp, free radicals
69
endurance training secondary signals
calcineurin, CaMK, AMPK, p38, NFkB, PGC-1a
70
response in seconds to endurance training
increase calcium, free radicals, amp/atp
71
response in minutes to endurance training
increase calcinurin. caMK, ampk, p38 and NFkB
72
response in hours to endurance training
increase PGC-1a
73
increase in days to endurance training
mitochondrial biogenesis
74
training-induced reduction in freedback for endurance training
Lower HR and ventilation increase
lower lactate and hydrogen production
less activation of chemoreceptors
larger and more mitochondrea
75
impact of detraining
no change to max HR
max of a-vO2 diff. decreases
cardiac output max decreases
max stroke volume decreases due to rapid loss of plasma volume
decrease in Vo2 max
76
time-course of training/detraining adaptations in mitochondrial content of skeletal muscle
training increases muscle fiber mitochondria till reaches Plato
- quickly returns w/retraining
- in 1-2 weeks adaptations are lost
77
Body composition
refers to body's chemical composition
various models divide the body into different compoenents
78
two compartment model
divides the body into two different components
- Fat mass: often described as relative body fat
- Fat free mass: all body tissue that is not fat (bone, muscle, connective tissue, organs)
79
Measuring body composition
*gold standard: underwater (hydrostatic) weighing
- subject is weighed on land and underwater
-amount of water displaced by subject is measured
- fat and fat-free tissue have different densities therefore body density can be used to calculate proportion of fat and fat-free mass
density = mass* volume
80
More on underwater weighing
technique also requires correcting for volume of air in lungs and GI tract
density of fat-free mass may differ slightly across individuals and population
however expensive and takes up a lot of space
estimated error: 2.7%
81
Air displacement
"bod pod" determines body volume based on amount of air displacement
need to control for variation in temperature, gas composition, subject's breathing during measurement
estimated error 2.2-3.7%
82
DEXA
Dual X-ray absorptiometry
estimates for whole body and different regions
- lean tissue, bone density and body fat
bone density measurements help to diagnose osteopenia and osteoporosis
more detailed
83
BIA
bioelectrical impedance analysis
electrodes built into hand grips/ footplate
device measure impedance of a mild electrical current through the body
technique proves an estimate of total body water, fat-free mass, and body fat
available for home use
estimated error 3.5-5%
84
Sum of skinfolds
subcutaneous fat represents a fraction of overall body fat
skinfold measurements are taken at 3 sites around the body
validated equations estimate total body fat based on measurements, age and sex
estimate error for proficient: 3.5%
85
healthy body fat
essential for hormone regulation, organ function, thermoregulation, health of nervous system, fertility etc.
higher body fat in women due to sex-specific deposits such as breast tissue, hips, buttocks, and thighs
healthy with range based on age and sex
there is such a thing as to low, women higher then mens
86
Overweight and obesity
both terms used to describe the medical condition related to excess adipose tissue
newer definitions
clinical obesity: signs/symptoms of disease, organ dysfunction due to excess body fat
pre-clinical obesity: elevated risk but no current sign/symptoms of disease
however, these imply that absolute or relative percentage of body fat has been measured
- difficult to measure, expense and requires Equpment and time
measurements that compare weight to height (BMI) are commonly used as a surrogate
87
Body Mass Index (BMI)
weight in kg divided by height in meters squared
BMI=kg/m^2
easy to assess: simple measurements, minimal equipment
most commonly-used way to estimate body fat and classify individuals into weight categories
NOT A DIRECT MEASURE OF BODY COMPOSITION
NOT INTENDED TO BE A MEASURE OF INDIVIDUAL HEALTH
stop
88
weight and BMI
are not direct measurements of individual health and should not be used as a proxy for health
89
Relationship between BMI and all-cause mortality
overweight and obesity are associated with increased mortality
risk increases with higher BMI
90
Understanding the J curve of BMI
lower risk of diseases and death with DMI category of overweight (25-30) so not a straight line where lower is better
91
Additional health associations with obesity and being overweight
cardiovascular disease and dyslipidemia
type 2 diabetes
some cancers
liver and gallbladder disease
osteoarthritis
sleep apnea
depression, anxiety
SOME OF THESE RELATIONSHIPS MAY BE BI-DIRECTIONAL
92
Metabolic syndrome
one way to describe a cluster of risk factors associated w/diseases
93
Distribution of body fat matters
upper body (android: in abdominal) obesity: more common in men
- android obesity - higher risk for cardiovascular disease, elevated blood lipids and diabetes
lower body (in thighs/butt etc.) obesity: more common in women
-visceral fat poses a greater risk compared to subcutaneous fat
nooooo
94
Central Vs. Peripheral fat
central/visceral adiposity
- fat in abdomen and round organs
more pathogenic (harmful)
peripheral/subcutaneous adiposity
- fat in lower body and below skin
-less pathogenic
95
Waist circumference
often a better predictor of disease risk than BMI
- not as affected by fat-free mass as BMI
-caveat: it's harder to measure well and consistently
correlates with abdominal (visceral) fat, which is more important in disease risk
- may also be reported as waist-to-hip ratio
cutoffs for "high risk": men> 40 in, women > 35 in
nooo
96
Types of fat cells: white adipocytes
most abudant fat cells in the body
found subcutaneously, around the heart, and near the GI tract
allow for fuel storage as triglycerides
high amount of lipid, low amount of mitochondria
harmful because release hormones that can promote inflammation
97
Types of fat cells: brown adipocytes
smaller quantities
exist in fat pads on shoulders, upper back, and near kidneys
high amount of mitochondria
do not synthesized ATP
oxidize fat to produce heat
more brown fat = higher resting energy expenditure, decreased size of white fat cells
98
Types of fat cells: beige adipocytes
sometimes 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
99
Decoupling weight and health
weight stigma and bias is harmful
negative attitudes from healthcare providers about patient in larger bodies do affect patient outcomes
physical symptoms should not be attributed to patient weight unless/until other potential causes are addressed
100
More on weight/health
about 1/2 of individuals classified as overweight are metabolically healthy
over 30% of "normal weight" individuals are metabolically unhealthy
rate of eating disorders and disordered eating are increasing
WEIGHT CYCLING (repeated loss and regain of weight) IS ASSOCIATED WITH INCREASED MORTALITY
why?
101
Etiology of obesity
etiology (cause) of obesity is extremely complex and multifactoral
physiological factors
- heredity (genetics)
- hormonal impabalnces
- altered basic homeostatic mechanisms
lifestyle factors: not just individual choices/behaviors
-environment, diet, physical activity
102
impact of heredity on weight
evidence of genetic/hereditary link
weight gain varied across individuals. but weight gain between twins was similar
103
interaction between genes and environment: monogenic obesity
early-onset, severe obesity
- high genetic contribution
-single mutation in one gene
- large genetic effect
-rare
- high penetrance
- no environmental influence
104
interaction between genes and environment: polygenic obesity
common obesity
-low genetic contribution
-hundreds of variants in/near many genes
- each variant has a small effect
- common
-low penetrance
-environment is a key determinant
105
Genes and environment
during the time when obesity became more prevalent, our environment changes significantly
- decreased physical activity
- increased abundance of food
- concurrent improvements in long-term health due to improved sanitation and eradication of many infectious diseases
-stop
106
genetic variation and propensity to become obese
even with high abundance low genetic susceptibility don't gain that much weight but the average and high will
107
Trends in energy intake vs. expenditure
greater energy intake per day over past several decades
less physical activity at work/home, transportation, more sedentary time and slightly increased leisure time PA
108
influence of environment
cannot address someone at an individual level w/o looking at the influence of community/what they have access too as well as beliefs + relationships and the environment they are a part of
109
our built environment
behaviors do play a role in body weight but there are also a set of individual factors and environmental factors that also influence body weight
110
Weight management may include
prevention
intervention
maintenance
111
approaches to weight management
target the social ecosystem (environment) or target the individual
112
Primary weight management prevention
prevent the development of a condition
- difficult with obesity because much of population is affected
-risk of targeting children in prevention programs
113
secondary weight management prevention
manage health and prevent adverse health effects
- assess and treat hypertension. dyslipidemia, diabetes
- treatment of health conditions may overlap with weight management interventions
114
Lifestyle interventions
approaches that target systems/environment
- change the environment to support individual behavior changes (public health agencies, school and social groups)
approaches that target individuals:
- reduced calorie diet
- increased physical activity
-behavioral therapy
115
energy balance
energy intake: eating food that contains macronutrients
energy expenditure: *resting metabolism, PLUS physical activity/exercise, PLUS thermic effect on food
116
problems with simple solution
not all weight loss = 3500 kcal
during moderate weight loss, there is a loss of fat-free mass
- quarter FFM rule (25% loss is FFM)
the body adapts to major increase or decrease in energy intake
- resting metabolic rate (RMR) decreases by 20-30% within several weeks of a fast or very low-calorie diet
- all 3 components of total energy expenditure increase somewhat when eating increased calories so physical activity less effective
117
changes to metabolism with weight loss
alterations in total energy expenditure during weight loss slow the rate of weight loss over time
-decreased food consumption = decreased thermogenic effect of food
-decreased body weight = less FFM = decreased resting metabolic rate
- decreased body weight = decreased energy cost of physical activity
COMBINED, THESE EFFECTS SLOW THE RATE OF WEIGHT LOSS DESPIDE MAINTENANCE OF A REDUCED CALORIE DIET
118
effectiveness of popular diet plans
negative caloric balance is more influential than emphasis on specific macronutrients
119
Exercise considerations for weight management
exercise can maintain or increase fat-free mass
remember extra metabolic oxygen consumption happens after stopping exercise
exercise reduces visceral adipose tissue
EXERCISE ALONE DOES NOT LEAD TO SIGNIFICANT WEIGHT LOSS OVER TIME
120
Diet and exercise on weight loss
none of these loose enough weight loss to loose a big amount" loose about 8lb in 6 months
121
Weight loss from lifestyle changes
be approprietly skeptical of those who say it will absolutly take weight off and keep it off
- 1/7 probability of loosing 5% of body weight, even lower with diet and exercise to reach normal weight
122
Maintenance of weight loss
Majority of subjects who lose weight and move to a lower BMI category have subsequent re-gain and increase in body weight
About 80% of people who intentionally lost >10% of body weight regained within 1 year
Up to 2/3 of individuals who lose weight during diet and exercise interventions regain more weight than was originally lost
noooooo
123
harms associated with weight cycling
INDEPENDENT OF BMI
Mortality
Cardiovascular disease
Loss of fat-free/muscle mass
Some types of cancer
High blood pressure
Diabetes
Osteoporosis and fractures
Gallstones
124
Benefits of exercise
Regardless of weight loss, exercise (endurance and resistance training) provides benefits:
Reduced all-cause mortality
Protection against cardiovascular disease
Improvement in cardiac risk factors (blood pressure, cholesterol, diabetes)
Reduced risk of cancer
Reduced risk of stroke
Protection against severe illness or death from Covid-19
125
physical activity guidelines for health
150-300 minutes/week of moderate-intensity activity
Or 75-150 minutes of vigorous activity
And muscle strengthening activities
At least moderate intensity
Involving all major muscle groups
At least 2 days per week
PROGRESSING TOWARDS TARGETS MEANS SUBSTANTIAL BENEFITS FROM PHYSICAL ACTIVITY, EVEN IF NOT MEETING GOALS
126
weight loss medications
New class of medications: glucagon-like peptide 1 (GLP-1) receptor agonists
-Examples: semaglutide (Ozempic, Wegovy), tirzepatide (Mounjaro)
Treat type 2 diabetes and stimulate weight loss (5-15% BW)
-Slow digestion and increase feeling of satiety
-Enhance insulin secretion and suppress secretion of glucagon
Limited studies on long-term effects
-Concerns: nausea, stomach pain, pancreatitis, gallstones
-Likely to regain weight after stopping medication
127
Atmospheric pressure
weight of a column of air
highest pressure/air density at sea level, decreases at higher altitude
same relative air composition
decreased absolute quantity of gas molecules
- fewer O2 molecules = lower po2
128
partial pressure of oxygen
increase in altitude results in reduced partial pressure of O2
129
Altitude- change in pressure
low pressure & hypoxia caused by the fall in atmospheric pressure with increasing altitude
130
arterial oxygen saturation
decrease in PO2 with increasing altitude has a direct effect on Hb saturation
- low PO2 in inspired air reduces the pressure gradient between alveoli and pulmonary capillaries which impairs the rate of oxygen diffusion into blood
131
altitude Effects on short-term anaerobic performance
events lasting <2 min: performance is not limited by oxygen delivery to muscle (anaerobic pathways)
- anaerobic performance should not be affected by lower barometric pressure
lower air resistance may improve performance in jumping, sprinting events
132
altitude Effects on longer aerobic performance
VO2 max decreases linearly with increase in altitude
- impaired performance in longer Olympic races
133
altitude effects on cardiovascular function: VO2 max = HRmax X SVmax x (a-vO2 diff)max
HRmax does not change significantly but may be decreased
SVmax does not change significantly (but prolonged altitude exposure can lower plasma volume and SV)
- biggest variable that changes: arterial side of a-VO2 difference
134
altitude effects on cardiovascular function: HR response will be higher at a fixed submaximal workload
Each liter of blood is saturated with less oxygen so heart rate must increase to compensate
135
Altitude effects on respiratory function
Ventilatory response will be higher at a fixed submaximal workload
each liter of oxygen contains fewer oxygen molecules, therefore... ventilation must increase to compensate
136
Acclimatization to high altitude
chronic hypoxia (low PO2) leads to increase in cellular stress proteins: hypoxial-inducible factor-1 (HIF-1)
increased HIF-1 in kidneys triggers cell signaling to produce erythropoietin (EPO)
EPO leads to increase in red blood cell production, therefore increased hemoglobin and oxygen carrying capacity
137
Population-level high altitude adaptations
acclimatization cannot fully match the adaptations seen in permanent high-altitude residents
high altitude during childhood/developmental years produces most significant adaptations
different population adapt differently
138
Altitude training
significant variation in individual VO2max at altitude
significant variation in individual ability to improve VO2 max with altitude training
training at altitude may be less effective
- workout quality suffers at higher altitudes
- effect of exercise stimulus and exercise adaptations may be blunted
BEST ADVICE FOR PERFORMANCE: LIVE HIGH, TRAIN LOW
139
altitude death zone
above 8,000 m amount of O2 is insufficient to sustain life as we cannot acclimatize
extended stay in the zone without supplemental O2 will result in deterioration of bodily functions, loss of consciousness, and ultimately, death
non-essential bodily functions are suppressed
140
Extreme high altitude
climbing over 8,000m is near the limit of human capability
physiological stressors with mountain climbing: altitude, cold, solar radiation, strenuous exercise
minimal exertion requires extreme ventilatory response and can lead to respiratory distress
141
increased likelihood of success in extreme high altitude
higher baseline VO2max
primarily type 1 muscle fibers
strong hypoxic drive: hyperventilation
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other effects of hypoxia
decreased appetite
weight loss
- significant loss of lean mass
-decreased cross-sectional area of type 1 and w fibers
other complications:
-pulmonary edema
-cerebral edema
-acute altitude sickness, confusion and impaired cognition
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Temperature regulation: core
Humans maintain constant core body temp of 37 C
- above 45C can damage proteins
-below 34C can impair metabolism and cardiac function
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Temperature regulation: core and skin
Ideal gradient is 4C
exposure to cold temperatures can drastically increase gradient
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Body heat balance
contracting skeletal muscle produces heat
Exercise presents a challenge to maintenance of steady body temperature
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measuring core temperature
-rectal temperature
-tympanic (eardrum) temperature
-esophageal temperature
-ingestible sensors
-skin temperature typically an average over several locations
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Physiological thermostat
located in Preoptic anterior hypothalamus (POAH) and maintains relatively constant core temperature around a "set point"
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response to increase in core temperature
POAH responds to increase in core temperature by stimulating sweat glands (evaporation) and cutaneous vasodilation (withdrawal of vasoconstrictor tone)
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response to decrease in core temperature
POAH decreases skin blood flow via vasoconstriction
involuntary shivering occurs with significant drops
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Thermostat changes with fever
Pyrogens: proteins and signaling molecules from bacteria or virus change set point of body's thermostat to a higher level
- body increases heat production to bring core temperature up to new set point
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Thermal events during exercise
submaximal exercise in a cool/moderate environment:
- heat production increases, proportional to exercise intensity
-venous blood leaving working muscle distributes heat throughout body's core
-thermoreceptors in POAH direct response to increase heat loss
-internal temperature reaches a new, elevated, steady-state level (different from fever)
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Heat balance during exercise
regulated by adjustments in heat loss
-circulatory system is central to regulation
--blood flow is closer to skin to lose heat
any heat not lost must be stored in body tissues and causes damage
core temperature increases above 37C during many/most exercise bouts
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types of heat loss: radiation
transfer of heat via infrared rays to objects not in direct contact with body
60% of heat loss at rest
can also result in heat gain
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types of heat loss: conduction
heat loss due to contact with another surface
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types of heat loss: convection
heat transferred from body to air or water molecules
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type of heat loss: evaporation
point when water (sweat) gains sufficient heat, and is converted to gas (water Vapor)
-requires vapor pressure gradient between skin & air
* most important during exercise
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heat loss during steady state exercise
heat production happens immediately but it takes a little amount of time for heat loss to occur
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Heat loss during maximal exercise
evaporation is the thing you need to happen to manage heat but it doesn't happen immediately
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impact of hot environment
reduced ability to lose body heat
- increase core temperature and heart rate: risk of hyperthermia and heat injury
higher sweat rate
- risk of dehydration: loose up to 4-5L/hour
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Rate of sweating during exercise
eccrine sweat glands are distributed across skin surface
increase in body temperature leads to sympathetic stimulation of eccrine glands
-SNS also responsible for anticipatory sweating
increased sweat with hot environment, higher body temperature, larger body mass
genetic variations present in sweating but no significant difference in men V. women
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What impacts the effect of heat?
combination of heat and humidity are what poses risk for people during exercise
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impaired performance in heat: central nervous system dysfunction
decreased motivation
reduced voluntary activation of motor units
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impaired performance in heat: Cardiovascular dysfunction
reduced stroke volume
decreased cardiac output during high-intensity exercise
decreased muscle blood flow
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impaired exercise performance: accelerated muscle fatigue
increased radical production
decreased muscle pH
muscle glycogen depletion
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what kind of performance does heat impair?
prolonged submaximal performance (marathon, triathlon) and high-intensity sports (soccer, rugby)
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Accelerated muscle fatigue due to heat
Depletion of muscle glycogen
- increased rate of glycolytic enzymes & muscle glycogen breakdown
-dehydration may reduce muscle blood flow and oxygen availability
increased H production and lactate
increased free radical production
-cause fatigue and damage contractile proteins
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Cardiovascular dysfunction from heat
increased cardiovascular strain due to reduced SV, Q and muscle blood flow leading also to a higher HR
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
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central nervous system dysfunction from heat
reduced central motor drive
type II/IV afferent metaboreceptors are stimulated from hyperthermic muscle
results in inhibitory effects on the central motor drive decreasing recruitment of motor units
hyperthermia also reduces mental drive
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Heat injury/hyperthermia
*series of stages - progression can be interrupted if caught and treated early
- exercise-induced muscle cramps
-heat syncope: fainting/dizziness, low BP
-heat exhaustion: fatigue, confusion, dehydration
-heat stroke: rectal temperature >40.5C; disorientation and hot skin
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Acclimatization to heat
exercise in heat for 10-14 days for low or moderate intensity
-increases plasma volume and capacity to sweat (3X)
increases VO2 max, maximal cardiac output, and power output at lactate threshold, lower body temperature and HR response, reduces sodium loss in sweat
BEST PROTECTION AGAINST HEAT STROKE AND EXHAUSTION
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Factors related to heat injury
fitness: higher fitness lower risk of heat injury
hydration: no difference between water, electrolytes etc.
environmental temperature: convection/radiation dependent on gradient between skin and air temperature, high temperature may result in heat gain
clothing: expose as much skin as possible
humidity: evaporation is dependent on gradient between skin & air
wind: increase heat loss
metabolic rate: core temp. proportional to work rate, decreased pace/workload lowers physiological strain
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Exercise in cold environment
response to cold stress: cutaneous vasoconstriction, shivering, non-shivering thermogenesis
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Heat production when cold
small amount of metabolic heat produced at rest
voluntary heat production: exercise (70-80% of energy released)
involuntary heat production
- shivering, hormones (thyroxine, catecholamines)
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peripheral vasoconstriction
reduced convective heat loss as a result of decreased blood flow to skin
constriction of blood flow to all areas other than the head
-increases tissue insulation
-controlled by SNS
-shunts blood to deep vessels/core
-protects core body temperature at the expense of skin temperature
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Thermogenesis (involuntary)
shivering increases energy expenditure by 3-5X
skin temperature is primary signal for shivering
- POAH activates when senses afferent cold in skin and spinal cord, increases in HR, VO2 and oxygen delivery
non-shivering thermogenesis
- brown adipose tissue, norepinephrine and thyroid hormones
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Other physiologic responses to cold
increase in urine formation by ADH (vasopressin) as vasoconstriction increases fluid load to heart, so body believes it needs to get rid of excess fluid
cold air can trigger asthma
increase workload on the heart
- vasoconstriction increases total peripheral resistance and afterload which is why risk of shoveling for those who heart issues
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Hypothermia
heat loss exceeds heat production: core temp less than 35C
- risk of death if core less than 25C
-higher risk in cold water immersion
-severe hypothermia could result in cardiac arrhythmias or cardiac arrest
-loss of judgement
-frostbite
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wing chill chart
cold and wind are conducive to heat loss
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wind chill chart: age
older then 60 less tolerant to cold
children experience faster falls in body temp
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Cold acclimation
when acclimated individuals experience:
- later onset of shivering
-maintain heat production with less shivering, more Non shivering thermogenesis
-maintain higher average hand/foot temperature during cold exposure
--due to intermittent peripheral vasodilation
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Ergogenic aids
*be skeptical of things that say they improve athletic performance
- look at where the information came from
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Dietary supplements
Not regulated by FDA
may not contain correct amount of active ingredients and may also contain contaminants
- Creatine is the only exception with proof that it works as it improve anaerobic power, strength, sprint performance, increases body mass through water retention
- precursors to testosterone are banned in competition and carry risks of impaired cholesterol
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Blood doping
goal: infuse extra red blood cells to increase hemoglobin and oxygen-carrying capacity
autologous (subjects own blood removed, stored, and reinfused) vs. Homologous (transfusion)
performance improvement observed with 2-3 units, more volume comes with increased risk
increased red blood cells can also be stimulated naturally by living at high altitude or through use of synthetic EPO
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Mechanical Aids
carbon-fiber plated shoes, running prostheses
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Warmup to improve performance
indirect: general tasks to increase body temperature or arousal
direct: scaled-back version of task
identical: practicing exact task
goal: slightly increase in body temperature and VO2 compared to baseline; reduce physiological strain
skilled performance is enhanced w/direct and identical practice, possibly facilitated by indirect
* Passive stretching impairs muscle strength/power
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Endurance training adaptations: energy system/fuel source
aerobic metabolism
uses glucose, glycogen or free fatty acids
requires oxygen
takes place in mitochondria
relies on cardiac output oxygen extraction at capillaries
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endurance trailing adaptations: stimulus for adaption
primary signal: repeated submaximal muscle contractions
result: increased ca, AMP/ATP ratio, free radicals
cell signaling involves primary and secondary messengers
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endurance training adaptations: where do adaptations occur?
increased plasma volume, capillary density
changes in mitochondrial volume and oxidative enzymes
changes in muscle fiber type
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Endurance training adaptations: how are adaptations beneficial?
greater CO and a-Vo2 difference
greater VO2max
better muscle efficiency
better and faster aerobic metabolism (+ inhibition of glycolysis)
better use of FFA
better acid-based balance
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Endurance training adaptations: time course for adaptations and de-training
fast: changes in plasma volume
slower: changes in muscle cells, capillary density, cardiac contractility
faster: adaptations more susceptible to change w/detraining
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Resistance training adaptations: energy system/fuel source
anaerobic metabolism
ATP-PC or anaerobic glycolysis
Fuel: glucose or glycogen
takes place in cytosol
does not require oxygen
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resistance training adaptations: stimulus for adaptations
primary signal: strong muscular contraction
triggers mechanoreceptors on muscle cell membranes
activates secondary messengers and mTOR pathway
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Resistance training adaptations: where do adaptations occur?
satellite cells on muscle fibers
increased muscle cell nuclei, ribosomes
increased ca sensitivity in muscle fibers
tendon, bone
nervous system
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resistance training adaptations: how are adaptations beneficial?
better recruitment and synchronization of motor units
increased protein synthesis, muscle cross-sectional area (hypertrophy)
stronger contraction of type 1 fibers
stronger bones, tendons
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resistance training adaptations: time course for adaptations and de-training
Fast: neural adaptations
slower: hypertrophy, changes to muscle fibers
faster adaptations more susceptible to change with detraining
