due to hardening of arteries, excessive peripheral resistance (enhanced nervous tone or kidney malfunction)
pressures of 250-300 for systole and >90 mm Hg for diastole
aerobic exercise can modestly lower BP
extent is unclear, but beneficial for normotensive and hypertensive individuals
resting BP also lowers significantly, possibly due to higher circulating catecholamines after training
decreased peripheral resistance to blood flow, decreasing BP
exercise may enhance sodium elimination by kidneys
static and dynamic resistance exercise will increase peripheral resistance to BF
even at light loads, e.g., 25% 1RM
potential for harm for those with heart and vascular disease
chronic resistance training does not appear to increase resting BP, and can blunt the response to a single bout
dilation of blood vessels in working muscles will decrease TPR, increase BF to working muscle
may see a small rise in systole, 140-160 mm Hg, then levels off
diastole may increase or decrease 10 mm
Hg, or remain unchanged
Increase in systole, mean, and diastole with increase in Q
greatest changes are in systole, diastole may change only ~12%
systole and diastole significantly higher than with leg exercise, even at same intensity
may be due to smaller vasculature, increased resistance to flow
heart will have to work harder
after submax exercise, systolic pressure can be temporarily (2-3 hrs) depressed below pre-exercise levels
B/c TPR remains low after exercise
has its own blood supply
has dense capillary network
@ rest, normal BF to myocardium is ~200-
250 ml, 5% of Q
@ rest, 70-80% of oxygen is extracted from the blood in coronary vessels
in other tissues, @rest, ~25% of the oxygen is extracted
coronary BF will increase during exercise to meet myocardial oxygen requirements, can increase 4-6X above resting levels
1. Increased myocardial metabolism causes dilation of coronary vessels
2. Increased aortic pressure forces a larger amount of blood into coronary circulation
coronary BF is 2.5X greater during diastole than during systole
heart has limited ability to generate energy anaerobically
has a 3X higher oxidative capacity than skeletal muscle
have the greatest mitochondrial density, well adapted for fat catabolism as primary source of ATP resynthesis
Figure 15-9 this is the substrate use of the heart at rest, during exercise, and during recovery
glucose, fatty acids, and lactate provide energy for the heart
during heavy exercise, with a large concentration of lactic acid in the blood, the heart can use lactate for 50% of its total energy
during prolonged submax activity, 70% of energy comes from fatty acids
metabolic patterns are similar for TR and
UNTR, but TR have a greater contribution of fats to the total energy requirement
increase in myocardial contractility and heart rate will increase the demand for oxygen
estimate myocardial workload and oxygen consumption, use product of peak systole and heart rate
index of relative cardiac work
called the double product, or rate-pressure product highly related to myocardial oxygen consumption and coronary BF
RPP = SBP X HR with training in cardiac patients, a higher RPP can be achieved before ischemic symptoms appear this measure is used in coronary heart disease patients
rapid adjustments are necessary during exercise, possible by constriction and dilation of smooth muscular bands of arterioles
additionally, venous capacitance vessels stiffen
can rapidly redistribute blood to meet metabolic demand of exercise, while preserving adequate flow and pressure throughout the system
changing diameter of blood vessels is most important factor regulating regional flow
resistance to flow changes with vessel diameter (to the fourth power)
reducing diameter by 1/2, causes flow to decrease 16X
1 in 30-40 capillaries is open at rest opening capillaries during exercise will
1. Increase muscle blood flow
2. Due to the increase in channels, increased blood volume can be delivered with only small increases in velocity of flow
3. Enhanced vascularization will increased the effective surface for exchange between blood and muscle cells
local factors can increase the dilation of arterioles and precapillary sphinchters
1. Decrease in oxygen supply
2. Increase in temperature
3. increase in carbon dioxide
4. increase in acidity
5. increase in adenosine
6. increase in ions of magnesium and potassium
these are autoregulatory mechanisms
sympathetic and to small extent, parasympathetic portions of autonomic
NS provide a central vascular control
muscles contain sensory nerve fibers which are sensitive to substances released in local tissue during exercise: causes vascular responses
central regulation ensures that the area with the most need for oxygen gets the most blood flow
norepinephrine is the general vasoconstrictor, and is released at certain sympathetic nerve fibers
(adrenergic fibers)
other sympathetic fibers can release
ACH, causing vasodilation (cholinergic fibers)
dilation of blood vessels is due more to a reduction in vasomotor tone than to an increase in action of either sympathetic or parasympathetic dilator fibers
sympathetic nerves terminate in the medullary portion of the adrenal gland
with activation, epi is released in large quantities, norepi in small quantities
epi and norepi cause a constrictor response, except in blood vessels of the heart an skeletal muscle
during exercise, hormonal control is minor in the control of regional BF
BF is decreased to the skin, gut, spleen, liver, and kidneys as a general response
Nerve centers above the medullary region are active both before and at the onset of exercise to cause increases in the rate and contractility of the heart, as well as to change regional blood flow
sympathetic cholinergic outflow plus local metabolic factors acting on chemosensitive nerves and on blood vessels cause dilation in active muscles
this reduces peripheral resistance, allowing for greater blood flow
constriction adjustments will then occur in less active tissues as exercise continues, so that perfusion pressure can be eliminated factors influencing venous return:
1. action of muscle and ventilatory pumps
2. stiffening of the veins
3. increase in venous tone with an increase in Q
Q = HR X SV
primary indicator of the functional capacity of the circulation to meet the demands of
PA
Direct Fick
Q = O
2 consumed/ (a-v)O
2
Indicator
Dilution: examine an indicator dilution curve
CO
2 rebreathing, indirect Fick
Q = CO
2 production/ (v-a)CO
2
X 100
Impedance
SV
Preload
Afterload
Contractility
BP
Systemic Vascular Resistance (SVR)
Can index the values to body size