Effects of physical exercise on liver ATP levels in fasted and phosphate-injected rats.
The purpose of the present study was to investigate the effects of exercise (30 min, 23 m/min, 0% grade) on the hepatic levels of ATP in fasted adrenodemedullated rats, with an intraperitoneal injection of sodium phosphate (Na (2) PO (4 ), 0.91 mM) or saline (NaCl). Sodium phosphate was injected to determine if the postulated decrease in liver ATP during exercise may be changed by providing an excess of phosphate. At the end of exercise, a piece of liver was rapidly freeze clamped and used for the enzymatic determination of ATP levels. Liver ATP, in saline-injected rats, was significantly (P < 0.05) decreased by fasting, compared to fed rats (&Xscr; +/- SE: 3. 21 +/- 0.2 vs 2.86+/- 0.2 micromol/g). Exercise in fasted rats decreased even more the ATP response in liver (2.58 +/- 0.14 micromol/g). Injection of Na (2) PO (4) did not significantly (P > 0. 05) alter the pattern of ATP response following these 3 conditions (3.35 +/- 0.14 vs 3.0 +/-0.12 vs 2.57 +/- 0.1 micromol/g), ATP levels being significantly (P <0.05) decreased by the fast and the exercise in the fasted state. Fasting and exercise resulted in a significant (P < 0.05) decrease in liver glycogen and plasma glucose concentrations and an increase in free fatty acid levels in both NaCl- and Na (2 )PO (4) -injected groups. In both injection conditions, beta-hydroxybutyrate and peripheral insulin concentrations were respectively, increased and decreased (P < 0.05) by fasting, while norepinephrine and portal glucagon were decreased (P > 0.05) following exercise. The main effect of the injection of Na ( 2) PO (4) was a stimulation (P < 0.05) of peripheral glucagon response following exercise. It is concluded that exercise results in a decrease in liver ATP levels even in fasted rats and that this decrease is not corrected by Na (2 )PO( 4) administration. The decreased liver ATP levels might be involved in the metabolic adaptations to exercise.
Département de kinésiologie, Université de Montréal, Montréal, QUE, Canada.
A
A
Ghanbari-Niaki
R
R
Bergeron
M G
MG
Latour
J M
JM
Lavoie
D000255:Adenosine Triphosphate / Q000378:metabolism*; D000313:Adrenal Medulla / Q000601:surgery; D000818:Animals; D001786:Blood Glucose / Q000378:metabolism; D002851:Chromatography, High Pressure Liquid; D004837:Epinephrine / Q000378:metabolism; D005215:Fasting / Q000378:metabolism*; D005934:Glucagon / Q000378:metabolism; D006503:Hepatic Veins; D007328:Insulin / Q000378:metabolism; D019344:Lactic Acid / Q000378:metabolism; D008099:Liver / Q000378:metabolism*; D008112:Liver Glycogen / Q000378:metabolism; D008297:Male; D009638:Norepinephrine / Q000378:metabolism; D010710:Phosphates / Q000378:metabolism / Q000494:pharmacology*; D010805:Physical Conditioning, Animal / Q000502:physiology*; D051381:Rats; D017207:Rats, Sprague-Dawley; D014280:Triglycerides / Q000378:metabolism
D001786:Blood Glucose; D007328:Insulin; D008112:Liver Glycogen; D010710:Phosphates; D014280:Triglycerides; D019344:Lactic Acid; D000255:Adenosine Triphosphate; D005934:Glucagon; C018279:sodium phosphate; D009638:Norepinephrine; D004837:Epinephrine