Blood flow and pressure relationships which determine V̇O(2max)

W. F. Brechue, Bill Ameredes, J. K. Barclay, W. N. Stainsby

Research output: Contribution to journalArticle

19 Citations (Scopus)

Abstract

The role of O2 delivery in regulating V̇O(2max) has been studied in an isolated gastrocnemius-plantaris muscle preparation contracting in situ; recent data addressing this issue are presented. V̇O2 increases nonlinearly with stimulation frequency reaching a peak at 5 twitches·s-1 or 1 tet·s- 1 (200 ms trains, 50 imp·s-1). Further increases in stimulation frequency result in a lower V̇O2. Measured V̇O2 maxima are less than predicted V̇O2 capacity, and peak V̇O2 during tetanic contractions is greater than that during twitches. Above 150 imp·min1, V̇O2 is directly related to the level of blood flow attained as VȮ2/Q (arterial-venous O2 difference) is fixed by some unknown mechanism. Increasing blood flow, with a pump, during l·s-1 tetanic contractions increases O2 diffusive conductance and peak V̇O2. When O2 delivery is reduced, ischemic hypoxia appears to result in more rapid reductions in muscle performance than hypoxic hypoxia because of decreases in perfusion pressure and Q. 31 P-NMR studies reveal that reductions in creatine phosphate and energy charge are similar between ischemia and hypoxia suggesting a common regulator, O2. We conclude that V̇O(2max) is limited by O2 delivery as a result of a limited and uneven distribution of muscle blood flow. These limitations appear secondary to mechanical restraints imposed by contraction duty cycle and vascular compression.

Original languageEnglish (US)
Pages (from-to)37-42
Number of pages6
JournalMedicine and Science in Sports and Exercise
Volume27
Issue number1
StatePublished - 1995
Externally publishedYes

Fingerprint

Blood Pressure
Skeletal Muscle
Muscles
Phosphocreatine
Blood Vessels
Ischemia
Perfusion
Pressure
Hypoxia

ASJC Scopus subject areas

  • Orthopedics and Sports Medicine
  • Public Health, Environmental and Occupational Health
  • Physical Therapy, Sports Therapy and Rehabilitation

Cite this

Blood flow and pressure relationships which determine V̇O(2max). / Brechue, W. F.; Ameredes, Bill; Barclay, J. K.; Stainsby, W. N.

In: Medicine and Science in Sports and Exercise, Vol. 27, No. 1, 1995, p. 37-42.

Research output: Contribution to journalArticle

Brechue, W. F. ; Ameredes, Bill ; Barclay, J. K. ; Stainsby, W. N. / Blood flow and pressure relationships which determine V̇O(2max). In: Medicine and Science in Sports and Exercise. 1995 ; Vol. 27, No. 1. pp. 37-42.
@article{686481bc2cc2468b9f31e705a8895f05,
title = "Blood flow and pressure relationships which determine V̇O(2max)",
abstract = "The role of O2 delivery in regulating V̇O(2max) has been studied in an isolated gastrocnemius-plantaris muscle preparation contracting in situ; recent data addressing this issue are presented. V̇O2 increases nonlinearly with stimulation frequency reaching a peak at 5 twitches·s-1 or 1 tet·s- 1 (200 ms trains, 50 imp·s-1). Further increases in stimulation frequency result in a lower V̇O2. Measured V̇O2 maxima are less than predicted V̇O2 capacity, and peak V̇O2 during tetanic contractions is greater than that during twitches. Above 150 imp·min1, V̇O2 is directly related to the level of blood flow attained as VȮ2/Q (arterial-venous O2 difference) is fixed by some unknown mechanism. Increasing blood flow, with a pump, during l·s-1 tetanic contractions increases O2 diffusive conductance and peak V̇O2. When O2 delivery is reduced, ischemic hypoxia appears to result in more rapid reductions in muscle performance than hypoxic hypoxia because of decreases in perfusion pressure and Q. 31 P-NMR studies reveal that reductions in creatine phosphate and energy charge are similar between ischemia and hypoxia suggesting a common regulator, O2. We conclude that V̇O(2max) is limited by O2 delivery as a result of a limited and uneven distribution of muscle blood flow. These limitations appear secondary to mechanical restraints imposed by contraction duty cycle and vascular compression.",
author = "Brechue, {W. F.} and Bill Ameredes and Barclay, {J. K.} and Stainsby, {W. N.}",
year = "1995",
language = "English (US)",
volume = "27",
pages = "37--42",
journal = "Medicine and Science in Sports and Exercise",
issn = "0195-9131",
publisher = "Lippincott Williams and Wilkins",
number = "1",

}

TY - JOUR

T1 - Blood flow and pressure relationships which determine V̇O(2max)

AU - Brechue, W. F.

AU - Ameredes, Bill

AU - Barclay, J. K.

AU - Stainsby, W. N.

PY - 1995

Y1 - 1995

N2 - The role of O2 delivery in regulating V̇O(2max) has been studied in an isolated gastrocnemius-plantaris muscle preparation contracting in situ; recent data addressing this issue are presented. V̇O2 increases nonlinearly with stimulation frequency reaching a peak at 5 twitches·s-1 or 1 tet·s- 1 (200 ms trains, 50 imp·s-1). Further increases in stimulation frequency result in a lower V̇O2. Measured V̇O2 maxima are less than predicted V̇O2 capacity, and peak V̇O2 during tetanic contractions is greater than that during twitches. Above 150 imp·min1, V̇O2 is directly related to the level of blood flow attained as VȮ2/Q (arterial-venous O2 difference) is fixed by some unknown mechanism. Increasing blood flow, with a pump, during l·s-1 tetanic contractions increases O2 diffusive conductance and peak V̇O2. When O2 delivery is reduced, ischemic hypoxia appears to result in more rapid reductions in muscle performance than hypoxic hypoxia because of decreases in perfusion pressure and Q. 31 P-NMR studies reveal that reductions in creatine phosphate and energy charge are similar between ischemia and hypoxia suggesting a common regulator, O2. We conclude that V̇O(2max) is limited by O2 delivery as a result of a limited and uneven distribution of muscle blood flow. These limitations appear secondary to mechanical restraints imposed by contraction duty cycle and vascular compression.

AB - The role of O2 delivery in regulating V̇O(2max) has been studied in an isolated gastrocnemius-plantaris muscle preparation contracting in situ; recent data addressing this issue are presented. V̇O2 increases nonlinearly with stimulation frequency reaching a peak at 5 twitches·s-1 or 1 tet·s- 1 (200 ms trains, 50 imp·s-1). Further increases in stimulation frequency result in a lower V̇O2. Measured V̇O2 maxima are less than predicted V̇O2 capacity, and peak V̇O2 during tetanic contractions is greater than that during twitches. Above 150 imp·min1, V̇O2 is directly related to the level of blood flow attained as VȮ2/Q (arterial-venous O2 difference) is fixed by some unknown mechanism. Increasing blood flow, with a pump, during l·s-1 tetanic contractions increases O2 diffusive conductance and peak V̇O2. When O2 delivery is reduced, ischemic hypoxia appears to result in more rapid reductions in muscle performance than hypoxic hypoxia because of decreases in perfusion pressure and Q. 31 P-NMR studies reveal that reductions in creatine phosphate and energy charge are similar between ischemia and hypoxia suggesting a common regulator, O2. We conclude that V̇O(2max) is limited by O2 delivery as a result of a limited and uneven distribution of muscle blood flow. These limitations appear secondary to mechanical restraints imposed by contraction duty cycle and vascular compression.

UR - http://www.scopus.com/inward/record.url?scp=0028837345&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0028837345&partnerID=8YFLogxK

M3 - Article

VL - 27

SP - 37

EP - 42

JO - Medicine and Science in Sports and Exercise

JF - Medicine and Science in Sports and Exercise

SN - 0195-9131

IS - 1

ER -