Today, We’ll continue our discussion of:

• Central CV adaptations
• Peripheral CV adaptation
• Clinical case study: anemia

Rest or submax exercise…NO CHANGE

Max…INCREASE

Common Values of Q

14-16 L•min-1 untrained

20-25 L•min-1 trained

30-40 L•min-1 elite

Close “Association” Between Cardiac Output and VO2… (6:1 ratio) On Friday we’ll find out whether they “dissociate”!

Blood Pressure

Resting BP…DECREASES

systolic, diastolic, mean arterial pressure

Submax BP…decreases for given submax workrate

Max…no change

Do you remember… BP = Q x TPR

If Q max increases dramatically and BP stays the same, what must be happening to TPR?

Blood Flow

Three factors

• Increased capillarization
• Effective blood redistribution
• Greater total blood volume!

The Blood

INCREASE total blood volume

Increased plasma volume

Within days… ADH and aldosterone secretion

Long-term… increase plasma proteins

INCREASE in RBC

And yet…often a decrease in hematocrit

Blood Volume

Increases in BV, PV, RBV with training

Change in ratio of plasma to cells

This benefits endurance capacity?

Low blood viscosity enhances O2 delivery

Enhanced thermoregulation

a-vO2difference

Remember this equation? VO2 (ml/min) = Q (L/min) x a-vO2dif (ml/L)

If autologous transfusion, or EPO, or darbepoetin, increased his [Hb] 2 g/dl, what would be his calculated VO2 max?…all else being equal!

Theoretic initial data…

• Initial [Hb]=13.5 g/dl , w/ 100% saturated, Mixed Venous O2 content = 4 ml/dl; SVmax=180 ml/beat; HRmax= 200 bm
• What’s the Q?
  • 200 bpm x 180 ml/beat = 36,000 ml/min = 36 L/min
• What’s the a-vO2 dif?
  • arterial O2 = 13.5 gHb/dl x 1.34 mlO2/g = 18.1 ml/dl
  • a-vO2 dif = 18.1 ml/dl – 4 ml/dl = 14.1 ml/dl
  • Convert to ml/L…14.1 ml/dl x 10 dl/L = 141 ml/L
• VO2 (ml/min) = 36 L/min x 141 ml/L = 5076 ml/min
• VO2 (ml/kg/min) = 5076 ml/min / 75 kg = 67.7 ml/kg/min

Theoretical 'after' data... If doping increased Hb by 2 g/dl...

• [Hb] 15.5 g/dl , 100% saturated
• Mixed Venous O2 content = 4 ml/dl; SVmax=180 ml/beat; HRmax= 200 bm
• What’s the Q?
  • 200 bpm x 180 ml/beat = 36,000 ml/min = 36 L/min
• What’s the a-vO2 dif?
  • arterial O2 = 15.5 gHb/dl x 1.34 mlO2/g = 20.8 ml/dl
  • a-vO2 dif = 20.8 ml/dl – 4 ml/dl = 16.8 ml/dl
  • Convert to ml/L…16.8 ml/dl x 10 dl/L = 168 ml/L
• VO2 (ml/min) = 36 L/min x 168 ml/L = 6048 ml/min
• VO2 (ml/kg/min) = 6048 ml/min / 75 kg = 80.6 ml/kg/min
• Change from intial...(80.6-67.7)/67.7 8 100 = 19% increase!!!

The19% increase calculated in our hypothetical example is more than is observed in most existing research. Perhaps changes in viscosity affect flow rate and diffusion. Perhaps venous oxygen content is somewhat higher. Perhaps max Q is reduced slightly so SV is lower (we know max HR is stable). Below are data from an actual study in which autologous transfusions were performed on male subjects. A mean 12.8 % increase in VO2 was observed. Treadmill time to exhaustion was increased by 15.8% as well.

Let's stop talking about cheating and get back to talking about training.

a-vO@ dif INCREASE slightly at max with training

Why?

More effective redistribution of BF.

Tissue better able to extract oxygen from blood

Increase capillary density

Increase muscle oxidative capacity

Endurance performance continues to improve even when VO2 max fails to increase. An ongoing discussion persists in the physiology world about the factors contributing to this. Below is a model proposed by Bassett and Howley. Read more about it in MSSE May 1997.

Participation Points!

Refer to case study distributed Monday…

What was the cause of anemia in this athlete?

List two other typical causes of anemia in athletes.

If an athlete presents with a lower than desired Hb and Hct, should we immediately assume iron deficiency and recommend iron supplementation? Why, why not?