Exercise Physiology Exam Ii Part Ii

Front 1

Symptoms of Overtraining Syndrome

Back 1

- decline in physical performance
- decreased appetite and body weight loss
- muscle tenderness
- head, colds, allergic reactions, or both
- occasional nausea
- sleep disturbance
- elevated resting heart rate and blood pressure
- feeling of "heaviness" and loss of desire in training
- emotional instability

Front 2

Possible Causes of Overtraining

Back 2

- excessive training and emotional stress
- autonomic nervous system dysfunctions
- disturbances in endocrine function
- depressed immune function

Front 3

Sympathetic NS Overtraining Effects

Back 3

- increased resting heart rate and blood pressure
- loss of appetite and decreased body mass
- sleep disturbances
- elevated resting metabolic rate

Front 4

Parasympathetic NS Overtraining Effects

Back 4

- early onset of fatigue
- decreased HR and BP
- rapid HR recovery after exercise
- less common than sympathetic NS overtraining

Front 5

Training and Risks of Infection

Back 5

- very high activities = above average risk for infection
- moderate activities = below average risk for infection
- sedentary activities = average risk for infection

Front 6

Predicting Overtraining

Back 6

- increased in oxygen consumption for the same rate of work
- increased heart rate response to the same rate of work
- declines in performance

Front 7

Treatment of Overtraining

Back 7

- reduce training intensity for several days
- rest completely for 3-5 days
- seek counseling
- prevent overtraining by alternating easy, moderate, and hard training
- eat carbs
*rest and proper nutrition is best treatment

Front 8

Detraining: What is it?

Back 8

- cessation of regular training, may be due to inactivity or immobilization
- loss of muscle size, strength, power, endurance, speed, agility, and flexibility

Front 9

Loss of Muscle Strength

Back 9

- muscle atrophy accounts for main losses
- normal fiber recruitment by neurological means is disrupted
- muscle requires at least 10-14 days of training to retain original gains

Front 10

Loss of Endurance

Back 10

- decreased cardiorespiratory endurance
- oxidative enzyme activity decreases
- glycolytic enzymes remain unchanged for up to 84 days
- muscle glycogen content decreases
- acid-base balance disturbed
- muscle capillary supply/fiber type may change

Front 11

Detraining and Muscle Glycogen: Trained Swimmers vs Untrained

Back 11

trained decreases by 40% with in 4 wk period when compared to untrained individuals (after 4 weeks, the trained=untrained muscle glycogen levels)

Front 12

Loss of Cardiorespiratory Endurance

Back 12

- losses greater in trained individuals
- plasma volume decreases
- stroke volume decreases
- VO2 max decreases
- endurance performance decreases

Front 13

Bed Rest Effects on Detaining Individuals: Effects on HR, VO2 max, SV after 3 weeks

Back 13

3 weeks - 25 % reduction in VO2 max capability, stroke volume
- Elevation in HR/cardio respiratory
- After 3 weeks - it took 3 months to return to original position
- It takes a long time to get to peak level but it doesn’t take a long time to loose it among trained individuals

Front 14

Cardiovascular Functions Among Children
- cardiac output
- A-VO2
- BP

Back 14

- decreased cardiac output when compared to adults
- higher A-VO2 difference then adults
- lower blood pressure then adults

Front 15

Training Children

Back 15

20-30 mins 3 x week

Front 16

Benefits of Training for Children

Back 16

- Decrease heart disease risk factors
- Self-esteem
- Skill development
- Enhanced bone formation.
- Weight management

Front 17

Cardiorespiratory and Aging
- cardiac output
- HR
- SV
- circulation
- aerobic capacity

Back 17

- decreased cardiac output
- decreased maximum HR
- decreased stroke volume
- decreased circulation
- decreased in aerobic capacity (1% a year)

Front 18

Aging does not necessarily decreases or increases VO2 max?

Back 18

decrease

Front 19

Training Effects for SV and VO2 Max in the Elderly

Back 19

- when you keep intensity and volume of training high, your rate of decrease in SV and VO2 max with aging slows, especially between ages 30 and 50 and less so after age 50

Front 20

How Much Does VO2 Decrease During the Aging Process

Back 20

- If body composition and physical activity are kept constant, VO2max decreases only 2% to 5% per decade, rather than the 10% per decade normally attributed to aging

Front 21

Training the Elderly

Back 21

- 3 times per week
- Accumulated 30 minutes
- Use peak heart rate to calculate intensity (start low intensity)
- Produces greater improvement in muscle oxidative enzyme activities than in younger endurance-trained athletes

Front 22

Kavonen Equation for Heart Rate Recovery

Back 22

HRR = ((HR max - HR rest) x %) + HR rest

Front 23

HRR for Fit and Unfit Individual

Back 23

Fit - 50-85% HRR
Unfit - 40-39% HRR

Front 24

Muscular Response to Varying Intensities:
- high-intensity vs low-intensity
- aerobic intervals
- continuous training

Back 24

- high-intensity produces larger muscle mass then low-intensity
- aerobic intervals are repeated, fast-paced, brief exercise bouts followed by short rests
- continuous training involves one continuous, high-intensity exercise bout

Front 25

Parameters Affected by Training

Back 25

- heart size
- stroke volume
- heart rate
- cardiac output
- blood flow
- blood pressure
- blood volume

Front 26

Effects of Left Ventricular Hypertrophy in Relation to Varying Exercises

Back 26

- endurance trained - have highest/thickest/largest mitral valve, higher ventricle contraction forces,
- sedentary person has thin/small mitral valves
- resistance trained have moderately sized/thick mitral valves

Front 27

Ventricular Hypertrophy causes an increase in _______ due to increased _________.

Back 27

stroke volume/filling capacity

Front 28

Differences in EDV, ESV, and EF with Endurance Training

Back 28

- EDV increases because more blood is able to enter/fill the ventricle due to plasma volume expansion
- ESV is decreased because the heart grows bigger as a muscle mass and is able to contract more blood out of the heart more efficiently; therefore, less blood is left in the ventricle after systole.
- EF?

Front 29

Stroke Volume Adaptations in Response to Filling Time and Force of Contraction

Back 29

EDV increases causing an increased filling time/increased SV that causes a stretching mechanism on the heart tissue that increases surface area = causing a greater contractile force = forcing more blood to be pumped out of the ventricle

Front 30

Effects of HR on Training

Back 30

HR decreases with training

Front 31

Adaptations of RHR due to Exercise

Back 31

Overall, it decreases due to more blood returning to the heart due to training
- sedentary individuals can decrease HR by 1 beat/min per week during interval training
- highly trained endurance athletes may have resting heart rates of 40 beats per min or less

Front 32

Heart Rate During Submaximal & Maximal Exercise

Back 32

- submaximal exercise - decreases proportionately with the amount of training, as much as 20-40 beats per min after 6 months of moderate training
- maximal - remains unchanged/may decrease slightly

Front 33

Heart Rate Recovery Period and its Effects Due to Exercise

Back 33

- decreases in trained people
- can be influenced by heat/high altitudes that could prolong the recovery period
- not an accurate measurement to be compared among individuals due to outside factors

Front 34

Cardiac Output Effects Due to Submaximal and Maximal Exercises

Back 34

Submaximal - doesn't change or may decrease slightly
- could be due to increase in a-vo2 difference due to greater oxygen consumption or reduced oxygen consumption
Maximal - increases output considerably

Front 35

Cardiac Output Max Values in Untrained and Trained Individuals

Back 35

untrained: 14-20 L/min
trained: 25-35 L/min
large endurance athletes: 40 L/min

Front 36

Mechanism of Increased Blood Flow to Muscle in Relation to Training

Back 36

- increased capillarization of trained muscles
- greater opening of existing capillaries in trained muscles
- more effective blood redistribution - blood goes where it is needed
- increased blood volume

Front 37

Effects of Exercise on Diastolic/Systolic

Back 37

- diastolic changes little
- systolic increases changes significantly in maximum exercise
- BP can decrease with endurance training in HTN pts
- weight training can cause increases in systolic and diastolic during activity

Front 38

Mechanism of Increased Blood Volume in Relation to Training

Back 38

- increased plasma volume: due to increase in aldesterone/ADH that causes H2O reabsorption
- RBC concentration increases but plasma volume increases at a faster rate, thus hematocrit decreases
- increase in plasma volume causes the blood viscosity to decrease thus improving oxygen delivery

Front 39

Effects of Exercise on Tidal Volume

Back 39

remains unchanged at rest and during submaximal exercise but increases during maximal exertion

Front 40

Effects of Exercise on Respiratory Rates

Back 40

remains unchanged at rest, decreases during submaximal exercise, and increases during maximal exercise

Front 41

Effects of Exercise on Pulmonary Ventilation

Back 41

remains unchanged at rest but increases during maximal exercise

Front 42

Effects of Exercise on Pulmonary Diffusion and A-VO2 Difference

Back 42

pulmonary diffusion increases at maximal exercise and A-VO2 increases at maximal due to increase oxygen demand

Front 43

Does the Respiratory System Limit Endurance Performance?

Back 43

No

Front 44

Effects of Exercise on Lactate Threshold, Respiratory Exchange Ratio, and Oxygen Consumption

Back 44

- lactate threshould increases
- RER decreases for submaximal efforts but increases at maximal
- oxygen consumption is unaltered during rest, decreases at submaximal efforts, and increases up to 93% VO2 max until limited by oxygen delivery

Front 45

Muscular Adaptations Due to Exercise

Back 45

- increased size of ST fibers, transformation of FTa to ST
- increase in # of capillaries
- increased myoglobin content by 75-80%
- increased number of oxidative enzyme activity of mitochondria

Front 46

Adaptations Affecting Energy Sources

Back 46

- store glycogen and triglycerides better
- FFA are mobilized easier and more accessible
- increased ability to oxidize fat

Front 47

Even if an individual reaches peak VO2 max, endurance performance can increase due to...

Back 47

increase in lactate threshold

Front 48

Factors Affecting VO2 Max:
1. level of conditioning
2. heredity
3. age
4. gender
5. specificity of training

Back 48

1. the higher the initial state of conditioning, the smaller the relative improvement for the same program of training
2. heredity affects VO2 max less then 50%
3. decreases with age due to decreases with activity level
4. untrained women have 20-25% lower then untrained men while trained women have only 10% lower then trained men
5. closer the training is to the sport, the greater the improvement in the sport

Front 49

What Actually Limits Performance?

Back 49

Fatigue

Front 50

Leading Causes of Death in the US

Back 50

1. Cardiovascular Disease
2. Cancers
3. Accidents

Front 51

Types of Cardiovascular Diseases

Back 51

- CAD
- Stroke
- Heart Failure
- PVD

Front 52

Leading Cause of Death From Cardiovascular Disease

Back 52

Coronary Artery Disease (CAD)

Front 53

Definition of Coronary Artery Disease, Atherosclerosis, and Ischemia

Back 53

CAD - involves atherosclerosis in the coronary arteries
Aterosclerosis - narrowing of the arteries due to plaque formation
Ischemia - deficiency of blood flow to the heart due to CAD

Front 54

Definition of Angina Pectoris & Myocardial Infarction

Back 54

Angina Pectoris - chest pain
Myocardial Infarction - heart attack due to ischemia leading to irreversible damage and necrosis

Front 55

When Does Atherosclerosis Begin?

Back 55

Not age specific but pathological changes are noted in the blood vessels in infancy and progress during childhood

Front 56

Classifications for BP for Adults: Normal, Prehypertension, Hypertension

Back 56

Normal: 120/80
Prehypertension: 120-139/80-89
Hypertension:
Stage 1: 140-159/90-99
Stage 2: >160/>100

Front 57

HTN Statistics

Back 57

about one in every three adult Americans have HTN

Front 58

HTN Affects the Heart How?

Back 58

- causes the heart two work harder
- strains arteries and arterioles
- causes pathological hypertrophy of the heart
- can lead to atherosclerosis, heart attacks, stroke, and renal failure

Front 59

Definition of Stroke

Back 59

cardiovascular disease that affects the cerebral arteries

Front 60

Ischemic Stroke

Back 60

I:
cerebral thrombosis - a blood clot forms in a cerebral vessel at the site of atherosclerotic damage
cerebral embolism: an undissolved mass of material breaks loose from another site in the body and lodges in a cerebral artery

Front 61

Hemorrhagic Stroke

Back 61

cerebral hemorrhage: rupture of one of the cerebral arteries
subarachnoid hemorrhage: surface vessel on the brain ruptures, bleeding into the space between the brain and the skull

Front 62

Definition of Congestive Heart Failure and the Damage Caused

Back 62

- heart muscle becomes to weak and cannot maintain adequate cardiac output
- damage to heart from HTN , atherosclerosis, viral infection, heart attack
- blood backs up in vains causing systemic and pulmonary edema = irreversible damage requiring heart transplant

Front 63

3 Layers of the Artery Wall (from outer to inner)

Back 63

- tunica adventitia
- tunia media
- tunica intima

Front 64

Theory of the Pathophysiology of CAD

Back 64

1. Local injury induces dysfunction of the endothelium
2. Blood platelets and monocytes adhere to the exposed connective tissue
3. Platelets release platelet-derived growth factor that promotes smooth muscle cell migration from the media to the intima
4. Plaque forms at the site of injury
5. Lipids are attracted to the plaque

Front 65

Proposed CAD Markers

Back 65

- C-reactive protein (CRP): produced in the liver and smooth muscle cells within coronary arteries in response to injury or infection
- Fibrinogen: blood protein integral in the process of blood clotting
- Homocysteine: amino acid used to make protein
- Lipoprotein(a): similar to LDL-C; may reduce the ability to dissolve blood clots

Front 66

Lipoproteins Levels for Increased Risks of Heart Attack

Back 66

>5 = bad news!
<3 = low risk
LDL are bad too!

Front 67

What Triggers Metabolic Syndrome?

Back 67

insulin-resistance

Front 68

What is the Biggest Risk Factor For CAD?

Back 68

physical inactivity

Front 69

What Can be Done For Preventing CAD?

Back 69

low intensity exercises - can do high intensity exercise if you want added health benefits but they are not required to reduce risks

Front 70

Cardiac Rehabilitation Process

Back 70

Phase I - inpatient
Phase II - outpatient for 12 weeks
Phase III - ECG
Phase IV - no ECG