phys of activity exam 2

fatigability/muscle fatigue

an activity-induced decline in maximal force or power of a muscle (related to disruption in cross bridge cycling and is reversible with rest)

what is fatigability influenced by?

sex, age, demands of task, stress, disease processes

after a fatiguing exercise...

-reduction in force

-takes longer to get to peak force and back to baseline

-less ATP (won't be able to break cross bridgees)

-changes with Ca2+ (main reason for increased relaxation time)

central fatigue

spinal and supraspinal mechanisms (not driving the muscle correctly)

peripheral fatigue

mechanisms that occur at or distal to the neuromuscular junction (within the muscle itself)

mechanisms for central fatigue

inhibition of motor cortex and alhpa motor neuron, alterations in motor neurons (resting membrane potential or amount of NT), physiological factors, pain

mechanisms of peripheral fatigue

muscle itself is the issue, failure of neuromuscular transmission (decreased amount of NT or NT not binding), action potential propagation, increased Ca2+ release, depletion of SR, buildup of metabolic biproducts

why does impaired binding of Ca2+ impact peripheral fatigue

less exposure of actin active sites, H+ decreases binding affinity, decreased Ca2+ sensitivity

why does depletion ofo ATP impact peripheral fatigue

creatine splits from P during forceful contractions, accumulation of Pi, decreased O2 availability

muscle afferents

group 3-thin myelinated free nerve endings in CT, skeletal and cardiac muscle; primarily mechanical receptors

group 4-unmyelinated free nerve endings in CT of skeletal and cardiac muscle within small vessels fo muscle; primarily responsive to metabolic stimuli

influence of sex on neuromuscular performance

males have more muscle mass, females are less fatigable than males, females have greater deficits in time-to-task failure with stress

influence of aging on neuromuscular performance

-sarcopenia

-loss of cortical gray matter

-loss of cortical inhibition

-slower cross bridge mechanics and slower rates of Ca2+ uptake into SR

with age what decreases...

strength, power, contraction speed, time it takes to get to peak force, increased variability of contraction, more fatigable

how does muscle mass influence muscle strength, fatigability and steadiness?

number of cross bridges available to bind, fiber type distribution, occlusion of feed arteries

how does cross bridge cycling influence muscle strength, fatigability and steadiness?

Ca2+ kinematics, enzyme activity, fiber type distribution

how do neural factors influence muscle strength, fatigability and steadiness?

integrity of neuromuscular junction, voluntary activation, MU recruitment and discharge rate

how does muscle pain/soreness influence muscle strength, fatigability and steadiness?

ROM issues, decreased strength/power/performance, neural impairments

recovery necessary for adaptation

48 hours=optimal (>96 hours=loss of benefits and may have atrophy)

how long should rest breaks be in between sets?

1:1 ratio between time of exercise and rest time

what can EMG determine excitability of?

-skeletal muscle excitability (M-wave)

-spinal pathways (H-reflex)

-supraspinal pathways

-can assess fatigability of the NM system

look at the skeletal muscle excitability diagrams

bet (H-wave and M-wave)

most common complaint or cancer treatment

fatigue

how to treat cancer related fatigue

exercise! 150 mins/week of aerobic or strength training

what is the goal of successful cancer care?

full return to pre-diagnosis activity and comfort level

side effects of surgical cancer treatment

pain, limited ROM, scarring, soft tissue shortening and restrictions, muscle weakness, limited function

side effects of chemotherapy

fatigue, weakness, pain, cardiotoxicity, peripheral neuropathy, weight gain, weight loss, muscle wasting, osteopenia

side effects of radiation therapy

acute effects=fatigue, desquamation, pain

late effects=soft tissue restrictions, fibrosis, pain

long term effects

a symptom that starts during cancer treatment and continues after the conclusion of treatment (fatigue, pain, weakness)

late effects

a symptom that is a result of cancer treatment that develops months or years after treatment (cardiac issues, lymphedema, radiation fibrosis)

radiation fibrosis

can develop 18-36 months after treatment and they need to be on a stretching program immediately

surgical cancer treatment

surgical removal of a tumor, a clean margin of tissue around the tumor and often lymph nodes

medical oncology treatment

the use of chemotherapy, hormonal therapy, and biological drugs to kill or slow cancer cell growth

radiation oncology treatment

the use of high energy particles to kill or damage cancer cells

T/F you can do manual therapy in the radiation field once the skin starts to show redness

false

if the skin is ok...

superficial modalities (ice, heat, TENS, manual therapy) are ok if a person has active cancer

in areas that are cancer free...

US and ESTIM are ok

physical agents that are NOT ok...

US over cancer, ESTIM over cancer, soft tissue work over current radiation, US over a previously irradiated area

post surgical goals

elimiate pain, restore mobility, restore tissue flexibility, restore strength, restore ADLs, safe intro to activity, education and infection prevention

post surgical rehab

pts should be on a walking program immediately, pts with pending chemo and/or radiation should begin strength training for core, legs and arms

consequences of uncontrolled hyperglycemia

increased risk for vascular disease, neuropathies, and impaired wound healing

normal A1C and FPG

A1C

Prediabetic A1C and FPG

A1C 5.7-6.4%

FPG 100-125 mg/dL

Diabetic A1C and FPG

A1C >6.5%

FPG >126 mg/dL

if someone has had poor glucose control over time what will be elevated (A1C or FPG?)

A1C

diabetes will cause...

reduced strength and increased fatigability

primary goal with diabetes management

glycemic control

what two things offer the best outcome to control hyperglycemia?

diet and exercise

for people that have type 2 diabetes what is a special consideration with aerobic exercise?

no more than 2 consecutive days without aerobic exercise

HIIT training with individuals with diabetes

best way to moderate blood glucose levels post-exercise, helps with overall glucose control (**must include a warm up and a cool down)

what is a contraindication to exercise for people with diabetes?

blood sugar of

early morning exercise may result in...

elevations of blood glucose

for people with T1 DM if combo training...

do resistance before aerobic training to reduce risk of hypoglycemia

contraindication for resistance training with DM

uncontrolled HTN

what is a retinopathy?

microvascular damage to the retina (should not perform vigorous aerobic or resistance training)

impact of impaired sensation with DM

risk for diabetic foor ulcer

what is the critical triad for foot ulcers

neuropathy, minor foot trauma, foot deformity

what hormones affect plasma glucose levels?

glucagon, insulin, epinephrine, cortisol

glucagon at rest vs with exercise

at rest it regulates release of glucose from the liver, with exercise glucagon levels increase in proportion to intensity

glucagon and insulin with higher exercise intensity

insulin levels will decrease and glucagon levels will increase

peak risk for hypoglycemia

6-12 hours after strenuous exercise

hypoglycemia early signs and symptoms

pulse strong and rapid, skin is pale and sweaty, headache, hunger, agitated, nervous, anxious, tingling of mouth/fingers, fatigue, weakness

Hypoglycemia late signs and symptoms

headache, blurred or double vision, drowsiness, confusion, seizure, loss of consciousness/coma

what to do if someone is experiencing hypoglycemia

if conscious provide carbs! if unconscious call EMS

tips to avoid hypoglycemia

avoid injecting insulin into exercising limbs, increase carb consumption, have carbs ready and available, change insulin timing or dosing in relation to exercise

autonomic neuropathy s&s

blunted HR response, impaired BP response (no increase in SBP), silent ischemia, anhidrosis, decreased thirst sensation

hyperglycemia

elevated plasma glucagon levels

hyperglycemia s&s

increased thirst, polyuria, weakness, dry mouth, tachycardia, hypotension, fatigue/confusion

static stretching prescription

10-30 second hold, 2-4 reps, 2-3 days/week

pre-contraction stretch

contract muscle being stretched or its antagonist (75-100% of max) hold for 10 seconds (**greater acute increase in ROM than static stretching)

what are we changing with stretching?

viscoelastic deformation, increased sarcomeres in series, neuromuscular relaxation

why is sudden cardiac death risk lower in females?

estrogen

VO2 max

how much oxygen can the muscle (tissue) extract

SV

what volume of blood can the heart expel with each beat

what is in charge of cardiovascular regulation with exercise

central command and sensory modalities (GTO, muscle afferents)

why will HR increase before exercise begins>?

PS withdrawal

HR regulation with exercise

central command and increased symoathetic outflow

sympathetic affect on the heart

catecholemines will cause vasoconstriction in non-active tissues and dilation in active tissues (=increased bp), also increased contractility

what is a pressor response?

a neural mechanism that helps to regulate HR and BP during exercise (increases HR and BP)

what are group 3 afferents?

mechanoreceptors that sense contraction and respond to compression

what are group 4 afferents?

metaboreceptors that respond to metabolite buildup in the muscle

where do both group 3 and 4 afferents send info to?

medulla

why is there a HR max?

because the heart still needs time to fill up

with a heart transplant what happens?

removal of native heart severs neural connection, slower peak HR, smaller difference in resting and max HR (**need longer warmup to allow catecholemines to circulate)

SV response to exercise

linear with intensity until about 40% of max, then plateaus because we only have so much blood (blood volume is limiting factor)

afterload

resistance the heart is fighting against to pump blood (if we decrease afterload we can increase SV)

preload

volume of blood in ventricles at end of diastole

what assists with venous return?

skeletal muscle pump and respiratory pump (both increase venous return/preload which increases SV)

end diastolic volume can...

increase contractility (more stretch=harder contraction=increased SV)

what two factors increase stroke volume

SNS (epinephrine) and stretch (contractility)

what meds can increase SV

inotropes and peripheral dilators

if we want to increase CO with the least work of the heart, which do we want to increase?

stroke volume

what measures the work of the heart?

rate pressure product (HR x SBP)

implications with blockage in coronary blood flow

as HR (RPP) increases this also increases O2 demand and if there is a blockage they may not be meeting the demands

what do you expect to happen to systolic and diastolic blood pressure?

systolic should increase and diastolic decreases slightly or stays the same

why do we want DBP to stay the same

it measures pressure within the heart at rest and affects preload...if it increases we will not fill the heart as much

with isometric exercise how do we expect BP to respond?

increase in SBP and DBP (TPR does not decrease) **concerning with pts that have HTN and CAD

what is the goal of blood flow restriction training

mimic effects of high intensity exercise by creating a hypoxic environment with low loads

hypothesized physiological mechanisms with blood flow restriction training

satellite cell proliferation, blood pooling=cellular swelling=protein synthesis, endothelial cell function improves and NO is more available

what are contraindications to blood flow resistance training?

clotting disorders and uncontrolled HTN

UE vs LE exercise blood pressure response

UE=increased SBP and DBP

LE=increased SBP and DBP to a lesser degree

**smaller muscles doing the same work=greater sympathetic nervous system activation