α-Stimulation protects exercise increment in skeletal muscle oxygen consumption

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

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13 Scopus citations

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)
Pages (from-to)H331-H339
JournalAmerican Journal of Physiology - Heart and Circulatory Physiology
Volume7
Issue number3
DOIs
StatePublished - 1980

All Science Journal Classification (ASJC) codes

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

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