phys of activity exam 1

fascia

thick layer of CT tha covers muscle belly

epimysium

just below fascia, more delicate layer around muscle belly

fascicle

bundle of muscle fibers

perimysium

CT that surrounds each fascicle

endomysium

CT that surrounds each individual muscle fiber

thin vs thick filament

thin = actin

thick = myosin

H zone

only myosin

A band

both actin and myosin

I band

only actin

Myosin heavy chain (MHC)

contractile form

myosin light chain (MLC)

regulate rate of contraction

thin filaments structure

actin contains binding sites for myosin. troponin is a regulatory protein that controls position of tropomyosin, contains ca binding sites. tropomyosin is a regulatory protein that wraps around actin and covers binding sites.

sarcomere contraction changes in zones

A band doesn't change length, I band and H zone shorten

at rest membrane potential

K passive leak out. Na/K pump active (2 K in, 3 NA out). net loss of positive ions from inside cell

T tubules

spread AP through and into sarcolema

benefits of more myosin ATPase

cross bridge cycling can happen faster

all-or-none principle

when a motor unit is activated the fibers contract maximally or not at all

3 factors of muscle force

# of motor units recruited, type of motor unit recruited, firing rate

Type 1 muscle fiber

slow oxidative, slow twitch, low fatigability, low force

type IIa muscle fiber

fast oxidative glycolytic, fast twitch, medium fatigability and medium force

type IIx muscle fiber

fast glycolytic, fast twitch, high fatigability and high force

functional capacity

involvement of multiple systems (lungs, heart, blood, muscle) to deliver nutrients in order to make ATP

is the volume of O2 consumed (VO2) proportional to energy cost of exercise?

yes

general ex perscription (warm up, conditioning, cool down, strethching)

5-10 min light to mod warm up. 20-60 min conditioning. 5-10 min light to mod cool down. 10 min minimum stretching

hypothalamus is both...

neural and hormonal

3 primary functions of nervous system

monitor internal and external environment. integrate info. initiate and coordinate a response by activating muscles and glands

why might total blood flow to forearm increase when biking

while total bf inc most of that was to the skin to relive heat. there was actually a dec in forearm muscle bf

how does heat help muscle performance

enzymes work better, inc nerve conduction, inc bf and thus inc O2 delivery

exercise effects on blood

dec pH, inc temp, inc CO2

FITT reccomendations for resistance training

F= 2d/w for each major muscle group

I= 60-70% 1RM / 40-50% 1RM for older adults /

trainees self select loads...

often too low (53% of 1RM)

therabands replaced how often?

1-2 months

SAID principle

specific, adaptation, imposed, demand. (practice like you play)

isometric advantages

target weak muscles, work in pain free range, improve strength without overstressing, analgesic effect

isometric disadvantages

strength gain limited, not functional, boring

isometric intensity for strength

66-100% of max

isometric holds time

holding more than 10 seconds is not very productive. muscle force dips from 100% to around 50% after 8-9 sec

isotonic activation advantage

strengthen through full ROM, equipment accessible

isotonic disadvantage

resistance varies throughout ROM, eccentric phase causes muscle damage

DOMS

due to muscle damage not lactate

closed chain advantage and disadvantage

functional and stable but can also compensate

open chain advantage and disadvantage

specific but less stable

2 for 2 rule

2 sessions in a row, on last set, you can do 2 more reps, you can inc weight

protein intake

1.7 g/kg bw optimal (post workout good time), normal rec is 1.2-1.6 g/kg bw

satellite cell fusion

training muscle adds nuclei to muscle. more nuclei = more protein synthesis

mTOR

increases protein synthesis

recovery time

48 hours required for adaptation, over 96 hours is too long

preferred fuel source of the body

carbs. less O2 required than fat, only substrate that can be used in anaerobic metabolism

too much glucose bad why?

glucose is cytotoxic. brain hemorrhage results in glucose from the blood killing brain cells.

glycogenolysis

breakdown of glycogen to glucose, glycogen phosphorylase plays major role

glycogenesis

formation of glycogen from glucose

role of carbs in body

energy source, protein sparer, primer for fat catabolism

Tryglycerides

glycerol and 3 fatty acids

lipolysis

seperation of glycerol and FA in a triglyceride

beta oxidation

fat metabolism, end product is acetyl coA

role of lipids in body

energy source and reserve, protects organs, thermal insulation, vitamin carrier

ketosis

liver converts acetyl CoA into ketones, ketones can be used as fuel, accumulation of ketones can put body in state of ketosis which can significantly disrupt physiological function

role of proteins in body

structural components, cellular transport, enzymes, blood clotting, form contractile apparatus, energy

PCR system

short term high energy. 10s

anaerobic glycolysis inhibit by and stim by

inhibited by a dec in pH and citrate. stimulated by epinephrine, insulin, presence of ADP/AMP

anaerobic glycolysis end products

2 pyruvate, 2 NADH, 2 ATP

fate of pyruvate

if O2 = becomes acetyl CoA and goes through aerobic

if no O2 = lactate

can lactate be converted back to pyruvate in the presence of O2?

yes

lactate clearance

transamination = forms keto acids and amino acids (go throguh gluconeogenesis in liver), sweat, oxidation (primary method during and post ex)

lactic acid production

muscle contraction, enzyme activity (lactate dehydrogenase or pyruvate dehydrogenase), fast glycolytic muscle fibers rely on glycolysis, SNS activation, insufficient O2 levels.

causes of lactate accumulation

decreased redox potential, inc activation of fast twitch muscle fibers, rate of lactate production exceeds removal

how is lactate used as energy

sent to liver, converted back to pyruvate, sent through gluconeogenesis, back to muscle as glucose (presense of O2)

clinical relevance of lactic acidosis

problem for pt's with pulmonary problems. can be a predictor of mortality in hospital.

normal vs hyperlactemia vs severe lactic acidosis

normal =

anaerobic ex characteristics of children

delayed accumulation of lactate but dec power. larger RELATIVE lactate threshold, neurohormonal regulation theory (dec activation of SNS and endocrine), liver better at gluconeogenesis due to inc BF

anaerobic ex characteristics in older adults

dec ATP-PC stores at rest, inc ADP and creatine in muscles, dec power, dec capacity, lower maximal lactate levels, lower mechanical power and capacity

EPOC

O2 consumption during recovery is above normal resting value

during transition from rest to ex energy supplied from...

O2 transport, utalization of O2 stores in capillary blood and myoglobin, splitting of stored ATP-PC, anaerobic glycolysis

causes of EPOC

restoratino of ATP-PC and O2 stores, inc cardiovascular-respiratory function, inc hormonal levels, inc body temp (main contributer), lactate removal, energy substrate shift

pyruvate oxidation to acetyl CoA yields?

1 NADH and 1 CO2

citric acid cycle yields?

3 NADH, 1 FADH, 1 ATP, 2 CO2

ETC input and output

input = 10 NADH, 2 FADH

output = H2O and ~32 ATP

ATP counts in matabolism phases

glycolysis =2

TCA = 2

ETC = 32

Beta oxidation

each 18 carb FA yeilds ~129 ATP (triglyceride has 3), glycerol metabolism yields 19 ATP. roughly 406 ATP from one triglyceride

protein as fuel source?

deamination required of an AA in the AA pool. leaves carbon compound (energy use) plus nitrogen. nitrogen used to create urea and eliminated in urea excretion

RQ

ratio of amount of CO2 produced over the amount of O2 consumed at cellular level at rest.

RER

Ratio of volume of CO2 produced over volume of O2 consumed on a total body level

CHO RQ, Fat RQ, RQ>1?

fat RQ = 0.7

CHO RQ = 1

RQ over 1 = high CHO metabolism and addition of anaerobic metabolism. sign of extreme work

energy metabolism at rest (fat vs CHO)

30% CHO / 70% Fat

energy metabolism, short term (

mostly anaerobic, PCR + glycolysis

energy metabolism prolonged ex

mostly aerobic, switch from carbs to fats and carbs store deplete

MET

unit that represents metabolic equivalent in multiples of resting rate O2 consumption of any given activity. resting generally 3.5 MET's

1 MET =

1 MET = 1 kcal/kg/hr

factors affecting lower economy in children

high BMR, large SA/mass ratio (loss of heat), immature running mechanics, less efficient ventilation, dec anaerobic capacity

factors affecting lower economy in older adults

recruitment of additional MU's, gait instability, antagonist cocontraction

economy

total metabolic cost

major limiting factor of VO2 max

rate of diffusion (O2 from blood to cell)

(aerobic) trained muscle

more myoglobin = more intramuscular O2

(aerobic) angiogenesis

one of most important parts of trained muscle (diffusion distance dec)

inc in mitochondrial size and number decreases what?

dec lactic acid accumulation

can muscle fiber shift type?

maybe slightly / a little bit

oxidative stress in ex

acute ex does increase acute oxidative stress but a training adaptation occurs overtime and levels out with inc antioxidants

endurance training and muscle energy usage

inc fat mobilization and utilization. inc glycogen and triglyceride stores

(aerobic) metabolic adaptations to regulatory hormones

rise in glucagon is less, supression of insulin is less, rise in epi/NE, GH, and cortisol all less (allows for utalization of less energy, for longer time)

(aerobic) metabolic adaptations to carbs

inc muscle and liver glycogen, slower rate of glycogen depletion, less CHO in fuel mixture, inc rate of glycogenolysis (sprint training)