Electical Signal for communication between periphery and brain

Must Be generated by stimulus

-70 mV Difference in electrical charge outside and inside

High Na

Medium K

Inside more negative

Na wants to enter but cant

K leaves the cell

When outside of the cell becomes less negative

More Na channels open

Na enters

Requires nerve impulse

When inside becomes more negative

more K

Makes it more difficult for nerve impulse to arise

Stages of AP

Stage 1

Membrane depolarizes to threshold voltage

Na channels open, Na enters cell

K channels begin to open slowly

NA CHANNELS CLOSE

K CHANNELS OPEN

K CHANNELS REMAIN OPEN, ADDITIONAL K LEAVES CELL

HYPERPOLARIZING IT

VOLTAGE GATED K CHANNELS CLOSE

LESS K LEAKS OUT OF CELL

MOTOR DIVISIONS

AUTONOMIC

MOTOR DIVISIONS

SOMATIC

SENSORY RECEPTORS

MECHANORECEPTORS

SENSORY RECEPTORS

THERMORECEPTORS

SENSORY RECEPTORS

NOCICEPTORS

S R

PHOTORECPTORS

S R

CHEMORECEPTORS

^ HEART RATE BLOOD PRESSURE

^ BLOOD FLOW TO MUSCLES

^ AIRWAY DIAMETER

^ METABOLIC RATE

MENTAL ACTIVITY

^ DIGESTION URINATION

DECREASE HEART RATE AND DIAMETER

SENSORY MOTOR INTERGRATION

STEP 1

SMI

STEP 2

SMI

STEP 3

SMI

STEP 4

HOW DOES MUSCLE CONTRACTION WORK

Action potential (AP) starts in brain

Ca2+ binds to troponin which causes tropmyosin to move out of the way of the myosin binding site on actin.

Myosin ATPase breaks ATP down to a molecule of adenosine diphosphate (ADP) and phosphate (Pi) causing the myosin head to swing backwards and bind to the now-open site on actin.

The sarcomere, myofibrils, and muscle fibers shorten

LONG PERIODS

REQUIRES OXYGEN FOR ATP PRODUCTION

LOW INTENSITY AEROBIC EXERCISE 

DAILY ACTIVITIES

POOR AEROBIC ENDURANCE 

FATIGUE QUICKLY

PRODUCE ATP ANAEROBICALLY

MORE FORCE FASTER FATIGUE

SHORT HIGH INTENSITY 

SELDOM USED FOR EVERDAY

SHORT EXPLOSIVE SPRINTS

SMALLEST TO LARGEST

STRENGTH GAINS

MAY PRODUCE MORE FORCEFUL CONTRACTION

IMPROVES RATE OF FROCE DEVELOPMENT

INCREASE CAPABILITY TO EXERT STEADY FORCES

FREQUENCY OF NEURAL DISCHARGE

NEURAL DRIVE DURING MAXIMAL CONTRACTION

MOTOR UNIT SYNCHRONIZATIONA AND AND MOTOR RECRUITMENT DRIVES 

refelects actual structural change in muscle,

fiber hypertrophy and fiber hyperplasia

1-2 days after

z disk damage

not caused by blood lactate concentrations

White blood cells increase as soreness increases

muscle damage leads to inflammations as a results of pain

muscle damage equals glycongen resynthesis

slows/stops muscle repairs

limits fuel storage

minimize eccentric work early

start with low intensity and gradually increase

or start with high intensity exhaustive training to follow

inadequate energy delivery/metabolism

accumlation of metabiolic by products

failure of muscle contractile mechanism

altered neural control of muscle contraction

fraction of O^2 inspired x volume of inhaled air - volume of expired air x fraction of O^2

VO2 = (Vi x FixO2) - (Ve x FixO2)

FiO2 = .2093

FiO2 = ?

.2093

A function of energy derived from various fuel mixtures

The higher the RER the more carbs the lower the RER the more Fats

maximal O2 uptake

point at which o2 consumption doesnt increas with further intensity

coordinates intergration of physiologial system

controls substate metabolism

regulates fluid electrolyte balance

potent anabolic hormone 

builds tissues and organs

romotes mg hypertrophy

stimuates fat metabolism

Flight or fight

epinephrine 80% norepinephrine 20%

increase heart rate contractile force and blodd presure

increase glycogenolyisis ffa

blood flow to skeletal muscles

^ gluconeogenesis FFA mobilization prtotiend catabolism

Anti inflammatory anti immune

weakend immune system

weight gain 

weaken bones

hypertension

glucose release by liver

glucose uptake by muscles

glucagon

epinephrine

norepinephrine

cortisol