Exercise Physiology Final
6 factors that affect the development and maintenance of muscle
Genetics (most important)
Physical activity
Endocrine influences
Environmental factors
Nervous system activation
Nutritional status
Neural factors
Adaptations w/in the nervous system
Account for the rapid and significant strength increases occurring w/ out increase in muscle size early on
Neural factor adaptations for RT early on
1) Greater efficiency in neural recruitment patterns (learning)
- Increases activation of agonist
- Decreased co-activation
- Coordination of syngergists
2) Increased central nervous system activation
- Increased cortical drive
- Increased a-motor unit excitability (cortical and peripheral)
3) Increased motor unit recruitment and firing
4) Improved motor unit synchronization
5) Lowering of neural inhibition (disinhibition)
Muscle growth with overload training results primarily from...
individual muscle fiber enlargement (hypertrophy)
FT fibers can be 45% larger in weight trained indiv.
Hypertrophy contributes to increased forced production...
Muscle w/ more contractile proteins can generate greater force
RT also thickens and strengthens connective tissue (improves integrity of tendons and ligaments)
Increased tendon stiffness transmits muscle force more powerfully
Causes of strength and hypertrophy
Myofibrils thicken and increase in number through splitting
- Different than muscle fiber splitting
Oblique pull of actin on Z line creates stress that results in longitudinal splitting
In response to RT, an increase in FT fiber area
- Significant increase in ratio of FT/ST fiber area
- No increase in % distribution of fibers
Hyperplasia in animals
Increased satellite cell activation
- dormant myogenic stem cells that develop into new fibers
Increased longitudinal splitting of muscle fibers (not myofibrils)
Clear evidence of hyperplasia
Hyperplasia in animals
Disagreement in scientific community
Argument that we are born w/ a fixed number of muscle fibers
Accident victims had 10% more fibers (and larger) in dominant leg
Body builders fibers are no bigger than those of control subjects
- Argue that they have more fibers
Some evidence exists to support it
Majority of data support an enlargement of existing individual fibers from overload training
Types of performance enhancing substances
Hormones
Dietary supplements
1994 DSHEA Act
Dietary Supplement Health and Education Act (DSHEA)
- Supplement regulatory and governing body
- guidelines for manufacturing, labeling, health claims
Supplements are not held at the same standards as food and drugs and are not regulated by the FDA
Banned by various athletic organizations
Changes in neural activation of muscles (which leads to decreased strength in men and women)
Inability to maximally activate individual muscles
- Reduced cortical drive
- Altered a-motor neuron excitability
- NMJ degradation
- Impaired E-C coupling
Inability to coordinate groups of muscles
- Increased co-activation of agonist/antagonist
- Incrased antagonist activation
- Reduces net maximal joint torque; limits rate of force development
- Disrupted agonist/synergist activation
Erythropoietin
Protein hormone; kidneys stimulate new RBC
EPO injections raise both hematocrit and hemoglobin
- increase aerobic capacity and time to exhaustion
Lots of health risks
Creatine
Dietary supplement
Increase strength, reduce fatigue, enhance recovery
Body mass changes
- increases in body weight, especially fat-free mass
Side effects
- unwanted weight gain, GI distress, possible dehydration, kidney strain, gateway drug
- No significant side effects
Caffeine
Stimulant
Most widely used drug in world
Increases time to exhaustion; effects on sprint or power performance unclear
Increase fat use, spares glycogen
On banned list - limits amount in urine
"Graying of America"
In 2000, 13% of the population are 65 or older
Life expectancy at 65 is now 17 years
Fastest growing segment of the older population are the > 85 years
Changes in muscle mass with aging
1% loss in muscle mass per year after the age of 35
1.5-2.5% decline in muscle mass per year after age 60
Muscle fiber changes with aging
Decreased muscle fiber size (atrophy)
Decreased number of muscle fibers
Decreased muscle fiber size (atrophy) with aging
Men 20-29 and 60-65
- Type l - no change
- Type ll - 25% decrease
Men 19-84
- Type l - 6% decrease
- Type ll - 35% decrease
Decreased number of muscle fibers with aging
25% loss in men ages 19-37 to 70-73
Muscle of 20 yr old = 70% fibers
Muscle of 80 yr old = 50% fibers
Quality of muscle changes
Selective loss of type ll fibers
- Type l fiber % increased from 40% to 55% in men ages 20-30 and 60-65
Role of hormonal changes in sarcopenia
Muscle contains at least 5 different myosin heavy chain isoforms
- MHC controls rate of cross-bridge reactions (speed)
Older muscle may express multiple myosin heavy chain isoforms in the same fiber
- Blurs distinction btwn. type l and type ll fibers
Muscle strength
Maximum capacity to generate force or tension
Muscle CSA
Intrinsic factors
- fiber type, architecture, specific force
Neural factors
- Motor unit recruitment/firing rate, synchronization, co-contraction
Strength loss with aging
Strength increases up to age 30
Plateaus from age 30-50
Declines 1% per decade between 50-70
30% loss per decade after 70
Muscle power
Maximum rate of work performance
Power = Force x Velocity
Power vs strength over time
Power declines sooner and more rapidly than strength
Men and women compared in their 70s vs 20s
- force 50% lower
- power 70-75% lower
Strength loss 1-2% per year after 60
Power loss is around 3.5% per year
Why does power decline more rapidly than strength?
Decreased muscle force
- decreased fiber number and size
- Loss of motor units; asynchronous firing
- decreased specific force
- decreased cortical drive, a-MN excitability, and NMJ degeneration
Decreased muscle velocity
- Motor unit remodeling (type l)
- decreased nerve conduction velocity
- decreased shortening velocity (25%); SR impairment
- increased co-activation - agonist/antagonist
- increased antagonist activation
Aerobic capacity
Declines around 1% per year from age 25
Rate of decline may be half that in physically active people
A 0.5 L/min lower VO2max in older vs younger
Older muscle is unable to utilize oxygen the way younger muscle can
- Reduced oxygen extraction (a-VO2 diff)
- Reduced sympathetic activity (Q=HRxSV)
Sarcopenia
Age-associated decline in muscle mass
Etiology related to changes in:
Age related
- Hormone status
- Neural factors
- Inflammation
Behavioral
- Protein/energy intake
- Disuse atrophy
What factors are responsible for decreased strength in older men and women
Changes in force producing capability of muscle tissue
Changes in neural activation of muscles
Changes in force producing capabilities of muscle
Decrease in specific tension of indiv. fibers
Relative increase in type l fiber characteristics
- multiple MHC isoforms
- death of a-motor neurons (spinal cord) -> death of some fibers and re-innervation of some
Muscle atrophy
- From death of some muscle fibers
Changes in neural activation of muscles
Inability to maximally activate individual muscles
- Reduced cortical drive
- Altered a-motor neuron excitability
- NMJ degradation
- Impaired E-C coupling
Inability to coordinate groups of muscles
- Increased co-activation of agonist/antagonist
- Incrased antagonist activation
- Reduces net maximal joint torque; limits rate of force development
- Disrupted agonist/synergist activation
The Disability Pathway Model
Pathology
- Abnormality occurring in specific organ or organ system
- Osteoarthritis, diabetes, muscle fiber atrophy
Impairment
- Abnormality occurring in specific organ or organ system
- Loss of muscle strength, flexibility, and aerobic capacity
Functional limitation
- Limitation in performing fundamental tasks at whole body level
- Loss of mobility, inability to lift objects, climb stairs
Disability
- Limitation in performing socially defined roles within social or physical environment
- No longer visits relatives or walks in neighborhood
Traditional approach to RT in adults
Emphasis on strength development
Moderate to high intensity (>60% 1RM)
Slow velocity (concentric phase 2-4s)
Can resistant training maintain muscle mass throughout life?
Age 18-82
Elite olympic or power lifters
Type lla fiber area decreased with age, but still higher than that of control
Functional threshold
Above functional threshold, increases in strength do not increase function
Why would older adults need to improve muscular power?
Power is a stronger predictor of physical functioning in older adults than muscle strength
We lose power sooner and more rapidly than strength over the lifespan
Loss of power w/ age is due to greater decline in speed compared to force
- Older adults get "slower" faster, and "weaker" more slowly
High-speed function (braking speed) test
High speed power training: +15%
Strength training: +3%
Control: -3%
HSPT can lead to stop 5 feet sooner
High-speed power training in older adults
Achieve the same increases in strength as a program specifically designed to increase strength
Provides broader training effect on power and speed than strength training
Improves high-speed functional tasks related to safety
People perceive it as easier than strength training
Why does pulmonary function decline with aging
Decline in elasticity of bony thorax
- stiffening of chest wall due to changes in chest, ribs, articular cartilage
Decrease in elastic recoil of lungs (greater compliance)
- Decline in some static and dynamic lung volumes
- increase oxygen cost of breathing
Weakening (and loss) of muscles involved with respiration
- Less force generation (increased O2 cost)
Decrease in alveolar surface area
- increased alveolar size, decreased pulmonary vascularization
Decrease in CNS responsiveness
- respiratory center (Medulla) less responsive to peripheral stimulation (chemoreceptors, machanoreceptors)
How does aerobic exercise impact pulmonary function in older adults
Most changes are irreversible
- chest stiffness, lung compliance, loss of muscle, alveolar size, CNS change
Training can increase pulmonary vascularization and strengthen respiratory muscles
- increased gas exchange capability
- decreased oxygen cost
Cardiovascular function and aging
Cardiac output (HR x SV)
- decreases steadily w/ aging (due to decreased max HR and SV)
- Reduced sympathetic stimulation reduces both HR and ventricular contractile force (SV)
- Highly trained compensate for decreased HR with increased cardiac filling and increased SV through Frank-Starling mechanism
a-vO2 difference is smaller with aging because of reduced peripheral blood flow
- decreased capillary to fiber ratio
- reduced arterial cross-sectional area
- fewer mitochondria/oxidative enzymes
Are there gender differences in aerobic trainability in the elderly?
Men and women: 20% increase in VO2max
Men
- 2/3 of VO2max increase due to SV
- 1/3 due to a-vO2 difference
Women
- 100% of VO2max increase due to a-vO2 difference
The Disability Pathway Model
Pathology
- Abnormality occurring at the level of cell or tissue
- Osteoarthritis, diabetes, muscle fiber atrophy
Impairment
- Abnormality occurring in specific organ or organ system
- Loss of muscle strength, flexibility, and aerobic capacity
Functional limitation
- Limitation in performing fundamental tasks at whole body level
- Loss of mobility, inability to lift objects, climb stairs
Disability
- Limitation in performing socially defined roles within social or physical environment
- No longer visits relatives or walks in neighborhood
Bone mass and aging
90% of peak bone mass achieved by age 20 (peak by age 30)
Decreases about 1-2% per year after age 60 (30-50% decline)
Osteoporosis contributes to 90% of hip fractures
- 15-20% 1 year mortality rate from hip fractures
- 50% will not be able to live independently
Factors affecting bone mass
Genetics
Gender
Race
Hormonal factors (estrogen)
Nutrition (calcium/phosphorus)
Weight bearing exercise
Lifestyle factors
Life expectancy from exercise
Life expectancy increased steadily from weekly energy expenditure of 500-3500 kcals
Active men lived 1-2 years longer than sedentary
How do we measure inactivity
Lack of defined exercise
- less than 150 min/wk or 30 min/day
Lack of movement (steps)
- Less than 8-10,000 steps/day (4-5 miles/day)
Prolonged sitting
- If sitting, not moving
Can obtain defined exercise goals but be otherwise inactive
Prolonged periods with no muscular activity
When activity was necessary for survival
*continuous circle
Thrifty storage
- replenish skeletal muscle glucose and TG; more efficient storage of excess glucose and TG in adipose tissue
- More thrifty storage = more likely to survive through famine/activity phase until feast
Famine and activity
- Essentially simultaneous
- Decrease glycogen and TG stores
Feast
- intake glucose and fat
Current model of cars and mcdonalds
Feast
- intake glucose and fat
- unlimited food supply w/out exercise-induced reduction of glucose and TG in skeletal muscle
Thrifty storage
- High storage of excess glucose and TG in adipose tissue; little goes to skeletal muscle
Cycle stalls
- excess glucose/FFA gets shunted into an even greater and unhealthy storage
- precipitates the metabolic syndrome
Metabolic syndrome
- Elevated BP and plasma glucose, central obesity, high TG, low HDL
Physical inactivity and mortality
Low fitness category resulted in highest number of deaths per 10,000
Simply by moving out of low fitness category, you improve longevity
Being sedentary is the GREATEST risk for premature death
Activity that produces soreness
Unaccustomed, novel physical activity (weekend warriors)
Unaccustomed increases in activity (trained athletes)
Activities emphasizing eccentric contraction
- running downhill, jumping, weight training, hiking, walking down stairs
How is muscle damaged in eccentric contractions
Increased strain on myofibrils
- Overstretched Sarcomere Theory
- Individual sarcomeres within myofibrils are damaged from weakest to strongest
Disruption of the cytoskeleton
Calcium activated damage
Initially, mechanical (force, strain)
- 2-3 days after eccentric exercise ultrastructural damage becomes worse
- Protein degradation not elevated until 48 hours
Secondary damage
- Calcium Activated Neutral Proteases (CANP)
- Inflammation
- Cant keep up with Ca removal, Ca infiltrates sarcomere
Delayed onset muscle soreness (DOMS)
Appears 6 hours after exercise
Peak 24-48 hours after exercise
Resolved by 5-7 days
Dull aching pain; pain evident upon movement
Distal 1/3 of muscle, MT junction
Lactic acid theory of DOMS
Produced during high intensity exercise
Quickly carried away from the muscle (lactate shuttle, Cori Cycle, heart)
Downhill running produced less lactic acid than level running
Connective Tissue Theory of DOMS
Increased hydroxyproline at 48 hours post-ex
Pain reported at distal 1/3 of muscle
Muscle more compliant than CT
Elevated Temperature Theory of DOMS
Type lV nerve endings sensitive to 38-48 C
Higher local temperatures generated during eccentric exercise
Rhabdomyolysis exacerbated by hyperthermia
Soreness perception
Polymodal pain receptors in muscle
- Mechanical
- Chemical
- Thermal
*All three stimuli present during inflammation
Inflammation
Mechanical: swelling
Chemical: bradykinins, histamines, prostaglandins (PGE2)
Thermal: elevated temperature
*Strong evidence that inflammation plays a role in DOMS
*Cardinal signal is elevated temperature
Rhabdomyolysis characteristics
Severe breakdown of skeletal muscle tissue
Characterized by....
- Severe muscular pain
- Severe weakness, strength loss
- Swelling, stiffness
- Increased muscle protein levels in blood
- --Creatine kinase (CK) > 600 U/L
- --myoglobin
- Dark urine
Rhabdomyolysis factors
Primary factors
- Trauma (crush injury)
- Burns
- Exercise
Secondary factors
- A lot
The presence of secondary factors may exacerbate the damage due to exercise
Clinical sequence of Rhabdomyolysis
Rhabdo -> myoglobinuria -> acute renal failure (ARF)
Rhabdo -> compartment syndrome -> loss of function
Rhabdo -> hyperkalemia -> life threatening dysrhythmias
Sequence of Rhabdomyolysis to renal failure

Sequence of Rhabdomyolysis to compartment syndrome

Rhabdomyolysis Treatment
Surgical intervention
- Fasciotomy
At risk muscle groups:
- Non compliant compartment
- --Lower leg muscles
- ----Tibialis Anterior
- ----Soleus
Rhabdomyolysis Treatment (from result of hyperkalemia?)
Calcium chloride
Glucose and insulin
Prevalence
- Hyperkalemia occurs in 10-40% of rhabdomyolysis patients
- Exacerbated by ARF
- Life threatening condition, most severe 12-36 hours post-injury
What happens when we exercise?
Heat increases 20x more than at rest
Heat dissipation occurs 4 ways...
- conduction - via contact (2%)
- convection - to air surrounding body (10%)
- radiation - (60%)
- evaporation - (30%)
What happens when we exercise in HOT environments?
at 95F, radiation ceases
At 100% humidity, sweat loss to environment ceases
- 1ml sweat removes 0.6 kcal heat
- 1-2 L/hr not uncommon
Under these conditions, increase in body temperature can cause thermal injury in 15-20 min
How does the body respond to hot environment?
Peripheral vasodilation (heat dissipation)
Vasodilation decreases BP
Change in BP results in peripheral vasoconstriction, increases core temp, and reduces heat loss
Heat dissipation is compromised by thermoregulatory mechanisms and environment
Heat exhaustion - acute heat injury
caused by excess sweating/dehydration
fatigue and weakness
headache and myalgia
nausea and vomiting
dizziness
cramps
irritability
sweating
chills
100-104.9F
Heat exhaustion treatment
Remove from hot environment
Lie person flat, elevate feet 12 inches
Correct dehydration and electrolyte imbalance (sports drink, IV may be necessary)
Cool w/ ice packs to neck, axillae, groin
Encourage rest
Recovery complete in 2-3 hours
Heat stroke - extreme hyperthermia
causes by thermoregulatory failure (10% mortality rate)
CNS dysfunction: sudden onset
- Confusion
- Hallucination
- Bizarre behavior
- Disorientation
Extreme core temperature (104-106F)
Heat stroke treatment
Rapid cooling (.2 C/min)
- Evaporative cooling
- Ice packs to neck, axillae, groin
- Cool IV fluid infusion (no oral fluids)
To avoid Rhabdomyolysis
Use caution when exercising
Start exercise gradually, increase gradually
Remain hydrated
Watch out for combinations