α-Stimulation protects exercise increment in skeletal muscle oxygen consumption

S. H. Nellis, S. F. Flaim, K. M. McCauley, Robert Zelis

Research output: Contribution to journalArticle

3 Citations (Scopus)

Abstract

Oxygen consumption (VO2) in an isolated, autoperfused, statically exercising canine gracilis muscle (2.5% P0) was studied in low blood flow (Q) states induced by constant norepinephrine (NE) infusion and by mechanical occlusion (MO). Q and VO2 were evaluated at rest [Q(c) and VO(2c)], after 5 min of exercise [Q(e) and VO(2e)] and after 5 more min of exercise with either NE or MO [Q(t) and VO(2t)]. Data were normalized and plotted as the [VO(2e) - VO(2t)]/[VO(2c) - VO(2e)] vs. [Q(e) - Q(t)]/[Q(c) - Q(e)] and equations of the lines for NE (y = 0.090x + 0.048) and for MO (y = 0.488x + 0.070) were determined. The slopes of the lines, tested by analysis of covariance, were significantly different (P < 0.005). These data indicate that when NE reduced Q during exercise, the exercise induced increment in VO2 was protected to a greater degree than when MO reduced Q under similar conditions. To determine if the effect of NE on VO2 was secondary to a β-adrenergic-receptor-mediated stimulation of skeletal muscle metabolic processes, the experiments were repeated in the presence of β-blockade with propranolol. In the presence of β-blockade, the effects of NE on skeletal muscle VO2 were unchanged. It is therefore hypothesized that the mechanism of this effect of NE may be an increase in the efficiency of oxygen extraction resulting from a redistribution of blood flow to more active muscle fiber regions.

Original languageEnglish (US)
JournalAmerican Journal of Physiology - Heart and Circulatory Physiology
Volume7
Issue number3
StatePublished - Jan 1 1980

Fingerprint

Oxygen Consumption
Norepinephrine
Skeletal Muscle
Propranolol
Adrenergic Receptors
Canidae
Oxygen
Muscles

All Science Journal Classification (ASJC) codes

  • Physiology
  • Cardiology and Cardiovascular Medicine
  • Physiology (medical)

Cite this

@article{9bf0d402713740ed90969812568e80ad,
title = "α-Stimulation protects exercise increment in skeletal muscle oxygen consumption",
abstract = "Oxygen consumption (VO2) in an isolated, autoperfused, statically exercising canine gracilis muscle (2.5{\%} P0) was studied in low blood flow (Q) states induced by constant norepinephrine (NE) infusion and by mechanical occlusion (MO). Q and VO2 were evaluated at rest [Q(c) and VO(2c)], after 5 min of exercise [Q(e) and VO(2e)] and after 5 more min of exercise with either NE or MO [Q(t) and VO(2t)]. Data were normalized and plotted as the [VO(2e) - VO(2t)]/[VO(2c) - VO(2e)] vs. [Q(e) - Q(t)]/[Q(c) - Q(e)] and equations of the lines for NE (y = 0.090x + 0.048) and for MO (y = 0.488x + 0.070) were determined. The slopes of the lines, tested by analysis of covariance, were significantly different (P < 0.005). These data indicate that when NE reduced Q during exercise, the exercise induced increment in VO2 was protected to a greater degree than when MO reduced Q under similar conditions. To determine if the effect of NE on VO2 was secondary to a β-adrenergic-receptor-mediated stimulation of skeletal muscle metabolic processes, the experiments were repeated in the presence of β-blockade with propranolol. In the presence of β-blockade, the effects of NE on skeletal muscle VO2 were unchanged. It is therefore hypothesized that the mechanism of this effect of NE may be an increase in the efficiency of oxygen extraction resulting from a redistribution of blood flow to more active muscle fiber regions.",
author = "Nellis, {S. H.} and Flaim, {S. F.} and McCauley, {K. M.} and Robert Zelis",
year = "1980",
month = "1",
day = "1",
language = "English (US)",
volume = "7",
journal = "American Journal of Physiology",
issn = "0363-6135",
publisher = "American Physiological Society",
number = "3",

}

α-Stimulation protects exercise increment in skeletal muscle oxygen consumption. / Nellis, S. H.; Flaim, S. F.; McCauley, K. M.; Zelis, Robert.

In: American Journal of Physiology - Heart and Circulatory Physiology, Vol. 7, No. 3, 01.01.1980.

Research output: Contribution to journalArticle

TY - JOUR

T1 - α-Stimulation protects exercise increment in skeletal muscle oxygen consumption

AU - Nellis, S. H.

AU - Flaim, S. F.

AU - McCauley, K. M.

AU - Zelis, Robert

PY - 1980/1/1

Y1 - 1980/1/1

N2 - Oxygen consumption (VO2) in an isolated, autoperfused, statically exercising canine gracilis muscle (2.5% P0) was studied in low blood flow (Q) states induced by constant norepinephrine (NE) infusion and by mechanical occlusion (MO). Q and VO2 were evaluated at rest [Q(c) and VO(2c)], after 5 min of exercise [Q(e) and VO(2e)] and after 5 more min of exercise with either NE or MO [Q(t) and VO(2t)]. Data were normalized and plotted as the [VO(2e) - VO(2t)]/[VO(2c) - VO(2e)] vs. [Q(e) - Q(t)]/[Q(c) - Q(e)] and equations of the lines for NE (y = 0.090x + 0.048) and for MO (y = 0.488x + 0.070) were determined. The slopes of the lines, tested by analysis of covariance, were significantly different (P < 0.005). These data indicate that when NE reduced Q during exercise, the exercise induced increment in VO2 was protected to a greater degree than when MO reduced Q under similar conditions. To determine if the effect of NE on VO2 was secondary to a β-adrenergic-receptor-mediated stimulation of skeletal muscle metabolic processes, the experiments were repeated in the presence of β-blockade with propranolol. In the presence of β-blockade, the effects of NE on skeletal muscle VO2 were unchanged. It is therefore hypothesized that the mechanism of this effect of NE may be an increase in the efficiency of oxygen extraction resulting from a redistribution of blood flow to more active muscle fiber regions.

AB - Oxygen consumption (VO2) in an isolated, autoperfused, statically exercising canine gracilis muscle (2.5% P0) was studied in low blood flow (Q) states induced by constant norepinephrine (NE) infusion and by mechanical occlusion (MO). Q and VO2 were evaluated at rest [Q(c) and VO(2c)], after 5 min of exercise [Q(e) and VO(2e)] and after 5 more min of exercise with either NE or MO [Q(t) and VO(2t)]. Data were normalized and plotted as the [VO(2e) - VO(2t)]/[VO(2c) - VO(2e)] vs. [Q(e) - Q(t)]/[Q(c) - Q(e)] and equations of the lines for NE (y = 0.090x + 0.048) and for MO (y = 0.488x + 0.070) were determined. The slopes of the lines, tested by analysis of covariance, were significantly different (P < 0.005). These data indicate that when NE reduced Q during exercise, the exercise induced increment in VO2 was protected to a greater degree than when MO reduced Q under similar conditions. To determine if the effect of NE on VO2 was secondary to a β-adrenergic-receptor-mediated stimulation of skeletal muscle metabolic processes, the experiments were repeated in the presence of β-blockade with propranolol. In the presence of β-blockade, the effects of NE on skeletal muscle VO2 were unchanged. It is therefore hypothesized that the mechanism of this effect of NE may be an increase in the efficiency of oxygen extraction resulting from a redistribution of blood flow to more active muscle fiber regions.

UR - http://www.scopus.com/inward/record.url?scp=0018819114&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0018819114&partnerID=8YFLogxK

M3 - Article

AN - SCOPUS:0018819114

VL - 7

JO - American Journal of Physiology

JF - American Journal of Physiology

SN - 0363-6135

IS - 3

ER -