Genetics (most important)

Physical activity

Endocrine influences

Environmental factors

Nervous system activation

Nutritional status

Adaptations w/in the nervous system

Account for the rapid and significant strength increases occurring w/ out increase in muscle size 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)

individual muscle fiber enlargement (hypertrophy)

FT fibers can be 45% larger in weight trained indiv.

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

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

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

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

Hormones

Dietary supplements

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

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

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

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

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

Decreased muscle fiber size (atrophy)

Decreased number of muscle fibers

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

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

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

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 increases up to age 30

Plateaus from age 30-50

Declines 1% per decade between 50-70

30% loss per decade after 70

Maximum rate of work performance

Power = Force x Velocity

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

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

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 VO_2max 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

Behavioral

• Protein/energy intake
• Disuse atrophy

Changes in force producing capability of muscle tissue

Changes in neural activation of muscles

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

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

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

Emphasis on strength development

Moderate to high intensity (>60% 1RM)

Slow velocity (concentric phase 2-4s)

Age 18-82

Elite olympic or power lifters

Type lla fiber area decreased with age, but still higher than that of control

Above functional threshold, increases in strength do not increase function

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 power training: +15%

Strength training: +3%

Control: -3%

HSPT can lead to stop 5 feet sooner

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

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)

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

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

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

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

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

Genetics

Gender

Race

Hormonal factors (estrogen)

Nutrition (calcium/phosphorus)

Weight bearing exercise

Lifestyle factors

Life expectancy increased steadily from weekly energy expenditure of 500-3500 kcals

Active men lived 1-2 years longer than sedentary

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

*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

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

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

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

Increased strain on myofibrils

• Overstretched Sarcomere Theory
• Individual sarcomeres within myofibrils are damaged from weakest to strongest

Disruption of the cytoskeleton

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

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

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

Increased hydroxyproline at 48 hours post-ex

Pain reported at distal 1/3 of muscle

Muscle more compliant than CT

Type lV nerve endings sensitive to 38-48 C

Higher local temperatures generated during eccentric exercise

Rhabdomyolysis exacerbated by hyperthermia

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

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

Primary factors

• Trauma (crush injury)
• Burns
• Exercise

Secondary factors

• A lot

The presence of secondary factors may exacerbate the damage due to exercise

Rhabdo -> myoglobinuria -> acute renal failure (ARF)

Rhabdo -> compartment syndrome -> loss of function

Rhabdo -> hyperkalemia -> life threatening dysrhythmias

Surgical intervention

• Fasciotomy

At risk muscle groups:

• Non compliant compartment
• --Lower leg muscles
• ----Tibialis Anterior
• ----Soleus

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

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%)

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

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

caused by excess sweating/dehydration

fatigue and weakness

headache and myalgia

nausea and vomiting

dizziness

cramps

irritability

sweating

chills

100-104.9F

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

causes by thermoregulatory failure (10% mortality rate)

CNS dysfunction: sudden onset

• Confusion
• Hallucination
• Bizarre behavior
• Disorientation

Extreme core temperature (104-106F)

Rapid cooling (.2 C/min)

• Evaporative cooling
• Ice packs to neck, axillae, groin
• Cool IV fluid infusion (no oral fluids)

Use caution when exercising

Start exercise gradually, increase gradually

Remain hydrated

Watch out for combinations