Ammonia metabolism during intense dynamic exercise and recovery in humans

T Graham; Jens Bangsbo; PD Gollnick; Carsten Juel; Bengt Saltin

Ammonia metabolism during intense dynamic exercise and recovery in humans

T Graham, Jens Bangsbo, PD Gollnick, Carsten Juel, Bengt Saltin

Publikation: Bidrag til tidsskrift › Tidsskriftartikel › Forskning › peer review

61 Citationer (Scopus)

Abstract

Udgivelsesdato: August 1 1990

Originalsprog	Engelsk
Tidsskrift	American Journal of Physiology: Endocrinology and Metabolism
Vol/bind	259
Udgave nummer	2
Sider (fra-til)	E170-E176
ISSN	0193-1849
Status	Udgivet - 1990

Citationsformater

@article{cd926b3086e511dcbee902004c4f4f50,

title = "Ammonia metabolism during intense dynamic exercise and recovery in humans",

abstract = "This study examined the dynamics for ammonia (NH3) metabolism in human skeletal muscle during and after intense one-legged exercise. Subjects (n = 8) performed dynamic leg extensor exercise to exhaustion (3.2 min). MuscleNH3 release increased rapidly to a maximum of 314 +/- 42 mumol/min and declined immediately on cessation of exercise. Recovery was complete in approximately 20 min. Arterial [NH3] increased less rapidly and reached itsmaximum 2-3 min into recovery. These data demonstrate that NH3 clearance is more sensitive to the cessation of exercise than is NH3 release from skeletal muscle. Muscle [NH3] increased three to fourfold during exercise and represented 74 +/- 8% of the total net NH3 formation. Thus the change in muscle [NH3] alone underestimates the NH3 production. There was no evidence that the muscle-to-venous blood NH3 ratio shifts in accordance with the H+ data. Thus other factors must contribute to the NH3 release from active muscle. The total net NH3 formed corresponded with the intramuscular inosine 5'-monophosphate accumulation, suggesting that the NH3 was derived from AMP deamination. Changes in the known modulators of AMP deaminase (ATP, ADP, H+) were moderate, so the mechanisms initiating the deamination remain obscure.",

author = "T Graham and Jens Bangsbo and PD Gollnick and Carsten Juel and Bengt Saltin",

year = "1990",

language = "English",

volume = "259",

pages = "E170--E176",

journal = "American Journal of Physiology - Endocrinology and Metabolism",

issn = "0193-1849",

publisher = "American Physiological Society",

number = "2",

}

TY - JOUR

T1 - Ammonia metabolism during intense dynamic exercise and recovery in humans

AU - Graham, T

AU - Bangsbo, Jens

AU - Gollnick, PD

AU - Juel, Carsten

AU - Saltin, Bengt

PY - 1990

Y1 - 1990

N2 - This study examined the dynamics for ammonia (NH3) metabolism in human skeletal muscle during and after intense one-legged exercise. Subjects (n = 8) performed dynamic leg extensor exercise to exhaustion (3.2 min). MuscleNH3 release increased rapidly to a maximum of 314 +/- 42 mumol/min and declined immediately on cessation of exercise. Recovery was complete in approximately 20 min. Arterial [NH3] increased less rapidly and reached itsmaximum 2-3 min into recovery. These data demonstrate that NH3 clearance is more sensitive to the cessation of exercise than is NH3 release from skeletal muscle. Muscle [NH3] increased three to fourfold during exercise and represented 74 +/- 8% of the total net NH3 formation. Thus the change in muscle [NH3] alone underestimates the NH3 production. There was no evidence that the muscle-to-venous blood NH3 ratio shifts in accordance with the H+ data. Thus other factors must contribute to the NH3 release from active muscle. The total net NH3 formed corresponded with the intramuscular inosine 5'-monophosphate accumulation, suggesting that the NH3 was derived from AMP deamination. Changes in the known modulators of AMP deaminase (ATP, ADP, H+) were moderate, so the mechanisms initiating the deamination remain obscure.

AB - This study examined the dynamics for ammonia (NH3) metabolism in human skeletal muscle during and after intense one-legged exercise. Subjects (n = 8) performed dynamic leg extensor exercise to exhaustion (3.2 min). MuscleNH3 release increased rapidly to a maximum of 314 +/- 42 mumol/min and declined immediately on cessation of exercise. Recovery was complete in approximately 20 min. Arterial [NH3] increased less rapidly and reached itsmaximum 2-3 min into recovery. These data demonstrate that NH3 clearance is more sensitive to the cessation of exercise than is NH3 release from skeletal muscle. Muscle [NH3] increased three to fourfold during exercise and represented 74 +/- 8% of the total net NH3 formation. Thus the change in muscle [NH3] alone underestimates the NH3 production. There was no evidence that the muscle-to-venous blood NH3 ratio shifts in accordance with the H+ data. Thus other factors must contribute to the NH3 release from active muscle. The total net NH3 formed corresponded with the intramuscular inosine 5'-monophosphate accumulation, suggesting that the NH3 was derived from AMP deamination. Changes in the known modulators of AMP deaminase (ATP, ADP, H+) were moderate, so the mechanisms initiating the deamination remain obscure.

M3 - Journal article

VL - 259

SP - E170-E176

JO - American Journal of Physiology - Endocrinology and Metabolism

JF - American Journal of Physiology - Endocrinology and Metabolism

SN - 0193-1849

IS - 2

ER -