lecture 21 Flashcards
(23 cards)
effects of chronic endurance training
training: 10 weeks; 6 times per week
- 3 x cycling: 3 x 5 @VO2max / 3 x 5 @ 55%VO2max
- 3 x running: As hard as possible for 30-40 min
“when we found that VO2max and endurance were still increasing as the study aproached its conclusion, we asked the subjects lif they would continue to train. unfortunately, they almost unanimously refused for the reason that they found exercie of this frequency and intensity too tiring an time-consuming. a number said they had wanted to drop out of the study but had continued out of a sense of responsibility and because they knew the study was scheduled to last only 10 wk. only one subject trained for an additional 3 wk.”
how did VO2max and exercise endurance improve?
what are the determinants of VO2max?
VO2 = Q x a-VO2diff (fick’s principle)
O2 uptake = flow of O2 rich blood x O2 extraction
central adaptation — pulmonary circulation
VO2max depends on Cardiac Output (Q)
if you want a high VO2max, you must increase cardiac output
Q = HR x SV
- HRmax does not change much with training
- therefore, changes in SV drive increases in Qmax
how does training improve SV?
total volume of blood pumped by the ventricle each beat/min (mL of blood per beat)
SV is preload, contractility, and afterload
Preload —> volume of blood received by the heart during diastole (EDV)
cardiac muscle
- physiological growth
afterload —> pressure heart must generate to open aortic valve
- decrease load, increases SV
- increase load, decreases SV
blood volume
blood volume - in 5 days BV goes up 10%
- increasing BV will improve VO2max after 11 days, which mean the SV is improving cardiac output
- BV is very important
Qpeak - increases 1.5 post exercise
BV - increases by 300 which allowed for an increase in SV, increase max cardiac output
after a phlebotomy — max cardiac output is reduced, and blood is removed
NOT NEEDED
total volume of blood pumped by the ventricle each beat (mL of blod per beat)
cardiac muscle
- physiological growth
ventricular dimensions
endurance athlete
- myocardium increase (thicker/stronger)
- LV larger, can accept more blood (same with RV)
- increase SV, cause pump out more blood
- vasodilation
athletes vs. non-athletes (diff between LV and RV)
- functional differences
- no functional differences between LV and RV - structural differences and aerobic capacity
- nice linar relationship with athletes, as they have stronger hearts. greater VO2max for both LV and RV
exercise makes… heart stronger, more blood in diastole, increase SV, increase cardiac output max
adaptations to endurance training
VO2 = SV x HR (doesn’t change with endurance training) x a-vO2diff
SV possibilities
- decrease peripheral resistance and decrease afterload
- increase RBC volume, increase plasma volume, increase blood volume, increase venous return, increase EDV
- increase ventricular compliance, increase ventricular dimensions (bigger chamber, bigger/stronger walls), increase contractile force (increase SV)
what are the determinants of VO2max?
VO2 = Q x a-vO2diff
“peripheral” adaptations related to O2 transport/delivery — peripheral circulation
red blood cell volume
- Erythrocyte (red blood cells) volume increases after 21 days, by 10%
arterial O2 content (CaO2)
the “a” in a-vO2 difference
CaO2 = (SaO2 x [Hb] x 1.34) + (0.003 x PaO2); therefore increase [Hb] = increase CaO2
where: SaO2 is Hb saturaton (%); [Hb] is Hb content (grams/100mL) 1.34 is the mL of O2 per g of Hb; PaO2 is partial pressure of O2 in blood
higher VO2max due to increase Hb content (increase CaO2)
musce blood flow (Q)
from hemodynamic perspective
total volume of blood flowing to exercising muscle (L of blood per minute)
Q = MAP (driving pressure) divided by TPR
total peripheral resistance to flow
- resistance = n x L divided by r^4
n = viscosity of blood
L = length of vessel
r = vessel radius
most of the increase in local blood flow to any tissue is determined by the calibre of resistance vessels (i.e. extent to wich they are constricted or dilated)
tissue BF = P (pie) r^4 divided by 8 n L
training reduces peripheral resistance
this facilitates greater muscle blood flow
Q = MAP divided by TPR
TPR can be reduced by:
1. arterial remodeling
2. improved arterial function
arterial remodeling
exercise training reduces vesse wal thickness and increases diameter
trained athletes have narrow walls, and bigger diameter
tennis player, can use both hands, and the non-dominant hand also makes the vessels have a bigger diameter, and narrow walls
femoral artery diameter increases with endurance athletes, and decreases with spinal cord injury, not using using spinal muscles at all
femoral wall thickness decreases with endurance athletes, and is very high in SCI patients
flow-mediated dilation
exercise training improves endothelial responsiveness to shear stress
4 weeks handgrip training for 20 min/day, 5x weekly @ 60% maximal voluntary contraction
peak dilation improves impressively from V1 base to V8
greater re-activity
peripheral resistance during exercise
vasoconstrictive signals during exercise are reduced in trained individuals
Q = BP / TPR — less total peripheral resistance = decrease afterload = increase stroke volume and increase muscle blood flow
capillarization
where gas exchange happens
exercise training increase suface area for tissue gas exchange
muscle fiber
capillary
4th order arteriole
3rd order arteriole
more capillary to fiber ratio = VO2max
0 weeks to 7 weeks — improvement of surface area
adaptations to endurance training
a-vO2diff — possibilities
- increase RBC volume, increase O2 extraction (gas exchaneg)
- increase capillarity, increase blood flow distribution to active muscle
- increase arterial function, decrease arterial wall thickness, decrease peripheral resistance
- increase sympatolysis, increase blood flow distribution to active muscle
**increase in mitochondria volume and oxidative capacity
what are the determinants of VO2max?
VO2 = Q x a-vO2diff
“muscle” adaptation
mitochondria
- citrate synthase
- succinate dehydrogenase
mitochondrial volume density
space within skeletal muscle occupied by mitochondria
VO2max related to mitochondrial volume
training —> cellular “stress” (increase Ca2+ metabolites) —> increase signaling molecules (AMPK, CaMK2) —> increase gene transcription factor (PGC - 1a) —> mitochondrial “biogenesis” —> then to two different options, increase number (i.e. proliferation) and increase size (i.e. hypertrophy)
increase number x size = increase mitochondril volume density
increase mitochondrial volume density in athletes
oblique section of vastus lateralis from untrained man and athlete wih high aerobic capacity
athlete — has more mitochondria
effects of increase mitochondria volume density
increases quantity and activation of enzymes in the TCA cycle and electron transport chain
max rate of products (succinate dehydrogease)
- untrained
- moderately trained
- highly trained — increase in activation, increase in volume density, increase in capability of oxidative phosphorylation
