Exercise Physiology Final

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Exercise physiology final
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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


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


Protein hormone; kidneys stimulate new RBC

EPO injections raise both hematocrit and hemoglobin

  • increase aerobic capacity and time to exhaustion

Lots of health risks



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



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)


Age-associated decline in muscle mass

Etiology related to changes in:

Age related

  • Hormone status
  • Neural factors
  • Inflammation


  • 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


  • Abnormality occurring in specific organ or organ system
  • Osteoarthritis, diabetes, muscle fiber atrophy


  • 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


  • 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


  • 2/3 of VO2max increase due to SV
  • 1/3 due to a-vO2 difference


  • 100% of VO2max increase due to a-vO2 difference

The Disability Pathway Model


  • Abnormality occurring at the level of cell or tissue
  • Osteoarthritis, diabetes, muscle fiber atrophy


  • 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


  • 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




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


  • intake glucose and fat

Current model of cars and mcdonalds


  • 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



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

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Sequence of Rhabdomyolysis to compartment syndrome

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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


  • 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








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