Metabolic Demand Dictates Muscle Blood Flow and the Hyperemic Response to Low Intensity Exercise
This study aimed to 1) quantitatively resolve in vivo muscle blood flow dynamics in response to contractile activity and 2) characterize the relationship between contraction‐induced hyperemia and metabolic demand in O 2 over the physiological range of muscle function in the rat hindlimb. Anesthetize...
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| Published in: | The FASEB journal Vol. 31; no. S1 |
|---|---|
| Main Authors: | , , , , |
| Format: | Journal Article |
| Language: | English |
| Published: |
01-04-2017
|
| Online Access: | Get full text |
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| Summary: | This study aimed to 1) quantitatively resolve
in vivo
muscle blood flow dynamics in response to contractile activity and 2) characterize the relationship between contraction‐induced hyperemia and metabolic demand in O
2
over the physiological range of muscle function in the rat hindlimb. Anesthetized Wistar rats (males, n=9) were placed supine in a homemade MR‐compatible apparatus designed to measure lower leg muscle contractile activity via a force transducer attached to the Achilles tendon. Contractions were electrically induced by direct sciatic nerve stimulation for 3min at 0.5 Hz, 0.75 Hz, 1 Hz, 2Hz, 3 Hz, 4 Hz, and 5 Hz. Stimulations were applied in random order for each rat and a recovery period of 20 min was observed between two consecutive stimulations. Contraction‐induced blood flow changes were quantified in the femoral vein using a surface array
1
H coil positioned over the thigh from phase contrast velocity map images on a 7T scanner (Bruker, Germany). Measurements immediately followed each contraction and were recorded continuously over the 20 minutes of recovery (time resolution = 15s). In a subset of 4 rats, muscle blood flow was also assessed every 30 seconds during stimulation. The corresponding O
2
delivery rate in μmol·min
−1
·g muscle
−1
was determined assuming an arterial content in O
2
of 7.60 μmol [1]. Contraction‐induced hyperemia significantly increased with stimulation intensity from 19.6 ± 5.7 ml·min
−1
·100g muscle
−1
to 89.4 ± 17.1 ml·min
−1
·100g muscle
−1
following 0.5Hz and 5Hz stimulations, respectively. However, the relative increase in blood flow per gram force was significantly reduced following stimulations performed above 2Hz. Assuming a constant ATP cost per twitch of 0.26 μmol ATP·g muscle
−1
and a Phosphate to O
2
ratio of 6 [2], the results showed that O
2
delivery matches the calculated demand in O
2
for intensity up to 2Hz. More specifically, the rate of O
2
delivery increased from 1.81 ± 0.52 μmol ·min
−1
·g muscle
−1
to 6.34 ± 0.9 μmol ·min
−1
·g muscle
−1
in response to 0.5 Hz and 2 Hz stimulations respectively while the metabolic demand in O
2
ranged from 1.55 ± 0.18 μmol ·min
−1
·g muscle
−1
at 0.5Hz to 6.37 ± 0.46 μmol ·min
−1
·g muscle
−1
at 2Hz. However at intensities above 2 Hz O
2
delivery was insufficient to meet the calculated metabolic demand. Measurements performed during stimulation suggest that muscle perfusion was compromised presumably due to intramuscular pressure during the contractile phase for these frequencies. At all intensities blood flow returned to baseline within 20 min following an exponential decay but above 2 Hz the kinetics were more complex with an early delay that increased with increasing frequencies. These results suggest that within muscle aerobic range (i.e. ≤ 2Hz [2]) metabolic demand for O
2
is the primary controller of contraction‐induced hyperemia. However, above this threshold, the systematic delay in recovery blood flow suggests that factors other than those sensing O
2
demand may be contributing to post‐exercise hyperemia, potentially metabolic acidosis or elevated temperature.
Support or Funding Information
NIH/NIDDK R01‐ DK095210 |
|---|---|
| ISSN: | 0892-6638 1530-6860 |
| DOI: | 10.1096/fasebj.31.1_supplement.710.10 |