Exercise Physiology Flashcards
Index of oxygen consumption, VO2
mL/min/kg At rest:L 3.5ml/min/kg = 1.5 MET
The types of fuel being utilized can be determined by Respiratory Quotient (RQ)
RQ= VCO/VO2 (volume of carbon dioxide to the rate of oxygen consumption)
RQ for carb is
1.0
RQ for fat is variable but averages to
0.7
RQ for protein is
0.8 (it is not used as a fuel because we save these for proteins)
If we were to measure an RQ of 0.7, that would tell us what?
the person is deriving 100% of energy from fat metabolism not from carbohydrates
If we were to measure an RQ of 1.0, what would that tell us?
it would tell us that the person is deriving their energy from carb
RQ cannot be measure in vivo - it is measure of what’s going on at the cellular level but the best to do is to measure it
at the mouth- called respiratory exhcnge ratio. We can adjust CO2 by adjusting our breathing rate. If you hyperventilate you increase co2 given off so RER WOULD NOT EQUAL RQ Here. Same for if you hypoventilate
So RER (respiratory exchange ratio) = RQ when
the body’s total CO2 content stays constant
1 MET = 1 Kcal/kg/hour
e.g. a 70 kg person performing a 3 MET activity for 1 hour would consume approximately 210 Kcal/hr (3x 70)
Machine that measures O2 consumption: rate of O2 inspired times the fractional O2 minus rate of O2 expired times the fractional O2 gives you the volume of O2 consumed
ViO2 x FiO2 – ViO2 x FeO2
When you start with a person at rest their O2 consumption is miniscule. As you start to increase the intensity of exercise this raises O2 consumption initially then it comes to a steady state
O2 demand = supply. As you continue to increase the intensity, O2 comsumption increases and levels off. But this doesn’t stay like this forever. At some point you intensity will be increased so much and you will see no further increase in O2 consumption. They have reached their max VO2. Their maximal ability to consume oxygen
Linear relationship between O2 consumption and exercise intensity. As you increase this for a long time you will reach max VO2
but some people can go to supramax. But this is not supported by aerobic metabolism at this point. VO2 max is the best measure of aerobic fitness
What limits maximal O2 consumption?
lungs, heart, vasculature and muscle itself can limit it
Linear phase of ventilatory response is when you are doing mild to moderate exercise. You would expect that arterial stuff is stimulating ventilation but you do not see any change in arterial PO2 though mild to moderate. Neither do Arterial PCO2 and pH. Therefore there are other things (joint receptors, muscle receptors, catecholamines)
But then there is a breakpoint where ventilation increases out of proportion to exercise intensity. Here anerobic mechanisms take over as a result lactic acid is made, and pH is decreases (acidosis)==» hyperventilation (helps to resolve the acidosis.
In heavy exercise, alveolar O2 will increase because of the hyperventilation. Arterial CO2 decreases (cuz you are breathing it out.
Venous O2 will be decreased and CO will be increased. Does the lung limit O2 consumption? NOOOOOOOO
Hb sat is the same as when you are at rest.
Does the heart limit O2 consumption?
CO response to increasing exercise intensity is linear.
CO = HR x SV
HR response is linear increasing - because of increased sympathetic drive to the SA node
SV increases linearly with mild to moderate exercise then it levels off.
SV = EDV - ESV (as exercsise intensity increases, ESV decreases). So the problem is with EDV that causes the leveling…EDV = filling volume time x heart rate. Filling time is reduced…so there are two competing factors: increasing ESV and decreasing EDV so you get a leveling off).
So in mild to moderate exercise heart rate and SV are both contributing to the increase in CO
In intense exercise
we rely more on HR to contribute to the increased cardiac output as compared to SV
CO distribution in muscle during exercise
Blood flow to skeletal muscel increases 5 fold more than CO becausse we start diverting more O2 to muscles when blood vessels are vasodilating.
There is also vasoconstriction in the gut, spleen and inactive muscles.
Muscles are better at extracting O2 from blood vessels (so venous content progressively decreases). Arterial stays constant
Does the CO limit maximal O2 consumption?
If that were true, then if we could deliver more O2 to working skeletal muscle, max oxygen consumption would increase. We can increase O2 delivery to skeletal muscle by blood doping.—adding back RBC to increase Hb and increasing oxygen carrying capacity. if you increase HCT by 10% then the O2 consumption would increase by 10%
Does the ability of the skeletal muscle to consume O2 ever limit VO2 max?
not usual in normal people but pts. with COPD, dialysis or pts. on bed rest
Answer: it is the maximal ability of the LV to pump blood to the skeletal muscle that
will limit your maximal O2 consumption
BP Response depends on
- muscle mass being used.
Using large muscles you would expect no increase in Diastolic BP. You would expect Systolic BP to increase. MAP should increase but not greatly…modestly.
BP and small muscle groups
you get a greater increase in systolic pressure and greater increase in MAP. It is the amount muscle, the more muscle, the lower the BP
BP and large muscle
vasodilation and vasoconstriction in inactive muscle so groups SO TPR will decrease. Using large muscle groups you will get more vasodilation and you BP will not be high
BP Response depends on
- static v. dynamic contraction
Blood flow substantially increases when performing static contractions up to 30% but as you increase the intensity beyond 30%, the blood flow starts to decline. By 70% MCV- vessels to that muscle occlude so BP increases when performing static (isometric) contractions. Advice: use them rhythmically
Anerobic ATP production are fast to turn on in response to need but are not long term
are limited in the capacity to sustain repeated contractions. Myokinase catalyzes ATP to keep the levels up. Creatine phosphate rephosphorylates ADP to make ATP. Glycolysis
Aerobic methods include
oxidation of carbs and fatty acids
Anerobically provided ATP is important
a. during the transition period from one level of activity to a higher level of activity
b. whenever exercise demands the anerobic threshold of the individual - you don’t use anerobic until you hit the lactate threshold and you increase lactic acid production at high intensity exercises. Ventilatory threshold correlates with the lactic threshold
Four factors that influence RER; 1. exercise intensity
At rest 0.85: fat = carb.
At higher intensity, muscles are switching over to use more carbs and less fat
At very high or max intensity: RER increases - muscles are using more carbs than fat. RER also indicates hyperventilation
Four factors that influence RER; TIME
With prolonged work, muscle move towards fat > carb. non-depletable fat stores while carbs are depletabl
Four factors that influence RER; Prior dietary history
previous carb diet, RER will be higher. low carb = low RER
Sources of carbs:
- blood glucose, 2. liver glycogenolysis and 3. liver gluconeogenesis. As exercise intensifies, muscles take up more and more glucose from blood despite the fact that exercise inhibits insulin release.
So with exercise insulin production goes down
but despite this muscle uptake increase and glucose can provide 40% of the energy
Arterial blood glucose is well maintained during exercise unless the exercise is performed for a long period of time without
carbohydrate intake. Under these conditions, hypoglycemia can occur and result in fatigue or an inability to continue the exercise after very prolonged exercise
Glycogen source in muscle
they use their glycogen stores the greater the intensity of the exercise. Glycogen depletion is sever when exercise is performed to fatigue ~75% VOmax and is the major cause of fatigue at the work rate. Fatigue is likely due to other factors at different exercise intensities
Fat source for muscle:
FFA: stress stimulates lipolysis: FFA delivery to skeletal muscle and they get taken up. muscles will oxidize the fat.
What about their lactic acid production between the trained v. untrained dogs? lower in the trained animals because they are not exercising at their VO2 max.
Since the untrained animals will have more lactic acid around and lactic acid is an inhibitor of lipolysis, they must rely more on carbs than on fats for energy.
So the choice of substrates for skeletal muscle is fitness level
fit person will use more fats and less carbs than an unfir person and their RER is will be lower. It is a carb-sparing effect: they will spare their glycogen stores and won’t develop hypoglycemia
Training: VO2max should change with training
the decline in VO2 with bed rest is much more pronounced than with simple cessation of training or a decrease in habitual activity level
increases in activity increases VO2 max. But it reaches some genetically limited peak.
VO2 max is a product of maximal cardiac output x maximal O2 difference (how much O2 is extracted from this blood).
What effect does training have on these two. Maximal ability to extract O2 is highest in the very well trained people, because O2 extraction is diffusion. When they are trained their is an increase in capillary density–>increased surface area. Aeroobic training stimulates mitochondrial synthesis… which will consume more oxygen
Training increases maximal cardiac output
because CO: HR x SV. HR does NOT change with training. Training affects maxSV….more blood is ejected. Due to increase in LVVolume. 2. Heart muscle strengthened and can eject more muscle per beat.
At sub-maximal work-rate a trained person can perform
any O2 consumption with a lower HR and an higher SV
RPP: rate-pressure product = HR x SBP
tells you myocardial oxygen need. Fit individual RPP is lower, heart requires less oxygen, less blood, operating more efficiently and can work in skeletal muscle instead
Any given work rate is less stressful after training. As you become more fit, epinephrine
the trained body perceives any given work rate as less stressful as evidenced by lower circulating levels of catecholamines at any given VO2
RPE number (Rating of Perceived Exertion) - very, very light—> very, very hard
The number reported on the chart multiplied by 10 will reflect the heart rate at that exercise level.
Endurance performance continues to increased with prolonged training despite a leveling off of VO2max
The increase in mitochondrial content is assoc with a marked improvement in endurance capacity and greater resilience on fat as a metabolic fuel at any given work rate.
With long term training (months to years), VO2max may not further increase but the ability to sustain a progressively higher % of VO2 max does, resulting in improved endurance performance. Due to the continued changes in skeletal muscle mitochondria as training occurs
How do you increase cardiovascular fitness
- use large muscle groups
- train 3x-5x/week
- 20 - 60 mins of exercise
- intensity must be suffiencient
- apply the RPE scale
- apply the overload principle - in order to improve you have to stop doing the same things over, increase the intensity
Stronger muscles
maximally can generate more force, do more work, have more - but normally we don’t ask muscles to work at their maximal effort. A stronger muscle can do the same work at a lesser recruitment level– they will be less fatigued and therefore will be able to do this work longer with more repeats
Stronger muscles favorable impact ADLs, prevent falls, performance in athletics and can impact bone density
Also affected by neural properties: recruitment level and firing frequency
Strength Training increases by 2 phenomena in the early and the late:
Neural happens early - you learn how to strength train better
Within a couple of weeks, muscles hypertrophy - because the growth stimulus stimulates actin and myosin filaments (contractile units- crossbridges).
Opposite happens (atrophy) when you don’t use it
Is hyperplasia responsible for the hypertrophy?
No, muscle tissue does not undergo mitosis.
How to increase muscle strength?
- exercises for the upper extremities, lower extremities and trunk (8 - 10 exercises).
- choose weight that can be lifted 8-12 times TO FATIGUE (if you don’t use exercise it to fatigue you will not recruit new motor units - they are the hardest to recruit but they have the greatest capacity to hypertrophy
- do 1 to 3 sets (do it once, take a break then do it again)
- exercise 2 - 3x a week (leave 24-36 hrs to let the rate of synthesis exceed the rate of degradation)
- 1x a week may be sufficient to maintainance
- apply overload principles - keep upping the ante by increasing the weight
Health Implications of exercise
- enhanced sense of well-being
- retards loss of work capacity and strength that occur with age
- better able to accommodate STRESS
- helps prevent and/or reverse risk factors associated with many chronic dz prevalent in the general population, especially CHD
regular physical activity is inversely associated with
- cardiovascular dz (stroke, PVD)
- CV dz risk factors (HTN, high TG and low cholesterol, platelet adhesiveness and aggregation, insulin needs and glucose tolerance
- Colon cancer and reproductive cancers
- obersity
- osteoporosis
- anxiety and depression
- dementia generally and Alzheimer’s
People who exercise regularly even though they have so many ailments etc, have
postpone sickness and death for a long time
Exercise and cardiovascular disease have four risk factors
- smoking
- hyperlipidemia
- hypertension
- sedentary behavior - independent factor
Exercise and lipids
regular physical exercise decreases total serum triglycerides (especially those who started with high TG).
- It increases the HDL profile
- It doesn’t decrease total cholesterol but it increases the level of good cholesterol (HDL)
Exercise and HTN
regular exercise decreases both systolic and diastolic BP….good for borderline HTN
Severe HTN needs drugs, but should be recommended
The higher the physical fitness or physical activity level, the greater reduction in relative risk for both coronary artery disease specifically
and all cardiovascular disease in general. this is a dose responsive curve that the higher the dose, the better the response - dose response effect …the more you exercise, the less is your risk of heart dz
-being moderately exercise is good enough
Exercise and Obesity - role of exercise
- expends calories during and after exercise
- better match of calorie intake and expenditure
- maintains Lean Body Mass (good to keep this high because you are always expending energy, even at rest) and so prevents decrease in BMR with weight loss
Excess mortality increases with increasing BMI
Combining exercise with caloric exercise is best
and you might gain muscle
Recommendations
- aim for 500kCal/day deficit (250 kcal decreases intake, 250 kcal increased activity)
- obese will need greater caloric restriction and greater calorie expenditure
- avoid sudden, large decreases in caloric intake
- include resistance exercises to maintain lean body mass
- expect pattern of fat loss to mirror pattern of fat gain (so don’t do spot exercises)
- remember small things add up overtime
The biggest effect is seen between those who
are completely sedentary and those who perform even minimal amounts of physical activity
Current exercise recommendations for health and quality of life
- a minimum of 30 mins of moderate physical activity, 5 days per week, or a minimum of 20 minutes of vigorous activity, 3 days/week
- combinations of moderate and vigorous activity can be performed to meet this recommendation
- alternatively accumulate 150 mins of exercise/week
- may be broken down into 3 ten minute sessions/day
- moderate intensity can be 50% VO2 max for healthy adults or as low as 40% VO2 max in patients with low fitness
- include moderately intense resistance training for major muscle groups
- recognize the does-response relationship between physical activity and health
