scholarly journals Cerebral ammonia uptake and accumulation during prolonged exercise in humans

2005 ◽  
Vol 563 (1) ◽  
pp. 285-290 ◽  
Author(s):  
Lars Nybo ◽  
Mads K. Dalsgaard ◽  
Adam Steensberg ◽  
Kirsten Møller ◽  
Niels H. Secher
1996 ◽  
Vol 270 (1) ◽  
pp. E101-E106 ◽  
Author(s):  
J. Bangsbo ◽  
B. Kiens ◽  
E. A. Richter

The present study examined NH3 (ammonia and ammonium) uptake in resting leg muscle. Six male subjects performed intermittent arm exercise at various intensities in two separate 32-min periods (part I and part II) and in one subsequent 20-min period in which one-legged exercise was also performed (part III). The arterial plasma NH3 concentration was 79.6 +/- 9.6 (SE) mumol/l at rest and 88.1 +/- 9.1, 98.1 +/- 8.1, and 210.2 +/- 7.5 mumol/l after 10 min of exercise in parts I, II, and III, respectively. The corresponding NH3 uptakes in the resting leg were 3.3 +/- 1.3 (rest), 7.8 +/- 1.5, 14.0 +/- 4.5, and 57.7 +/- 18.3 mumol/min. Throughout each exercise period a net uptake of NH3 was observed in the resting leg (P < 0.05), but uptake decreased to resting values within 5 min of termination of exercise. The muscle NH3 concentration of 195.1 +/- 15.0 mumol/kg wet wt at rest was largely unchanged throughout the experiment. The present data suggest that resting muscles extract NH3 and contribute significantly to clearance of NH3 during exercise and in early recovery from exercise. The extracted NH3 appears to be metabolized within the resting muscles.


2003 ◽  
Vol 95 (3) ◽  
pp. 1125-1131 ◽  
Author(s):  
Lars Nybo ◽  
Bodil Nielsen ◽  
Eva Blomstrand ◽  
Kirsten Møller ◽  
Niels Secher

This study examined neurohumoral alterations during prolonged exercise with and without hyperthermia. The cerebral oxygen-to-carbohydrate uptake ratio (O2/CHO = arteriovenous oxygen difference divided by arteriovenous glucose difference plus one-half lactate), the cerebral balances of dopamine, and the metabolic precursor of serotonin, tryptophan, were evaluated in eight endurance-trained subjects during exercise randomized to be with or without hyperthermia. The core temperature stabilized at 37.9 ± 0.1°C (mean ± SE) in the control trial, whereas it increased to 39.7 ± 0.2°C in the hyperthermic trial, with a concomitant increase in perceived exertion ( P < 0.05). At rest, the brain had a small release of tryptophan (arteriovenous difference of -1.2 ± 0.3 μmol/l), whereas a net balance was obtained during the two exercise trials. Both the arterial and jugular venous dopamine levels became elevated during the hyperthermic trial, but the net release from the brain was unchanged. During exercise, the O2/CHO was similar across trials, but, during recovery from the hyperthermic trial, the ratio decreased to 3.8 ± 0.3 ( P < 0.05), whereas it returned to the baseline level of ∼6 within 5 min after the control trial. The lowering of O2/CHO was established by an increased arteriovenous glucose difference (1.1 ± 0.1 mmol/l during recovery from hyperthermia vs. 0.7 ± 0.1 mmol/l in control; P < 0.05). The present findings indicate that the brain has an increased need for carbohydrates during recovery from strenuous exercise, whereas enhanced perception of effort as observed during exercise with hyperthermia was not related to alterations in the cerebral balances of dopamine or tryptophan.


1986 ◽  
Vol 60 (3) ◽  
pp. 893-900 ◽  
Author(s):  
E. Ravussin ◽  
C. Bogardus ◽  
K. Scheidegger ◽  
B. LaGrange ◽  
E. D. Horton ◽  
...  

Increased availability of circulating free fatty acids (FFA) inhibits the rate of glycolysis in heart and resting skeletal muscle (Randle effect). Whether elevated FFA may play a role in decreasing carbohydrate oxidation during prolonged exercise in humans is more controversial. Using respiratory exchange measurements, we measured substrate utilization during 2.5 h of exercise at approximately 44 +/- 1% maximal O2 uptake (VO2 max) in the presence or absence of elevated FFA levels. After 30 min of base-line determinations, 1,000 U heparin was given intravenously and a 3-h constant infusion of Intralipid 10% (150 g/h) and heparin (500 U/h) was started. After an additional 30 min of rest, subjects exercised for 2.5 h (study 1, n = 6). In another five subjects (study 2) 100 g glucose was ingested after 30 min of exercise. The same protocols (studies 1 and 2) were also performed during a 0.9%-saline infusion. During exercise, without glucose ingestion, higher FFA concentrations prevailed during the Intralipid infusion (1,122 +/- 40 vs. 782 +/- 65 mumol/l), but the relative contributions of carbohydrate (49 +/- 4 vs. 50 +/- 4%) or lipid (49 +/- 4 vs. 47 +/- 6%) oxidation to the total energy expenditure were different only during the first 30 min of exercise. Similarly, higher FFA levels (1,032 +/- 62 vs. 568 +/- 46 mumol/l) did not alter the relative contributions of carbohydrate (62 +/- 4 vs. 69 +/- 2%) or lipid (36 +/- 4 vs. 29 +/- 2%) oxidation to the total energy expenditure after glucose feeding.(ABSTRACT TRUNCATED AT 250 WORDS)


1992 ◽  
Vol 262 (6) ◽  
pp. E891-E898 ◽  
Author(s):  
L. L. Spriet ◽  
D. A. MacLean ◽  
D. J. Dyck ◽  
E. Hultman ◽  
G. Cederblad ◽  
...  

We examined the effects of a high-caffeine dose on endurance performance and muscle acetyl group metabolism during prolonged exercise. Eight subjects cycled to exhaustion at approximately 80% maximal oxygen uptake (VO2max) 1 h after ingestion of 9 mg/kg body wt dextrose (Pl) or caffeine (Caf). In the Pl trial, muscle biopsies were taken at rest (1 h postingestion) and at 15 min and exhaustion during exercise. The Caf trial followed the same protocol 1 wk later, with an additional biopsy at the time corresponding to Pl exhaustion. The subjects cycled significantly longer during the Caf trial (96.2 +/- 8.8 min) than in the Pl trial (75.8 +/- 4.8 min). Net glycogenolysis during the initial 15 min of cycling was reduced in the Caf vs. Pl trial (4.7 +/- 1.5 vs. 10.6 +/- 1.3 mmol.kg dry muscle-1.min-1; P less than 0.05). Muscle citrate concentration was increased at rest with Caf (0.59 +/- 0.07 vs. 0.37 +/- 0.05 mmol/kg dry muscle; P less than 0.05) but increased to similar values in both trials during cycling. Caf elevated the acetyl-CoA/CoA-SH ratio at rest (0.316 +/- 0.046 vs. 0.201 +/- 0.023; P less than 0.05) but had no effect on the increases in muscle acetyl-CoA and acetylcarnitine during exercise. The results indicate that Caf before exercise decreased muscle glycogenolysis by approximately 55% over the first 15 min of exercise at approximately 80% VO2max. This "spared glycogen" was available late in exercise and coincided with a prolonged time to exhaustion. Increased utilization of intramuscular triacylglycerol and/or extramuscular free fatty acids after caffeine ingestion may inhibit carbohydrate use at rest and early during exercise via elevations in muscle citrate and the acetyl-CoA/CoA-SH ratio. Muscle acetyl-CoA and acetylcarnitine were maintained above resting contents even at exhaustion when muscle glycogen was depleted.


1991 ◽  
Vol 70 (5) ◽  
pp. 2095-2103 ◽  
Author(s):  
D. A. MacLean ◽  
L. L. Spriet ◽  
E. Hultman ◽  
T. E. Graham

Plasma and muscle amino acid (AA) and ammonia (NH3) responses were measured during prolonged submaximal exercise in humans. Increased NH3 production during submaximal exercise has been attributed to the activity of the purine nucleotide cycle, without consideration of any possible contribution from AA. Six men cycled at 75% of maximal O2 uptake until exhaustion on two occasions after 2.5 days of ingestion of a high-carbohydrate or mixed diet. Plasma samples (antecubital vein) and muscle biopsies (vastus lateralis) were obtained at rest and during exercise and analyzed for plasma and muscle NH3 and AA as well as muscle metabolites. There were no significant diet effects in these parameters, so the majority of results focus on the effects of exercise. Plasma and muscle NH3 increased significantly from the onset and continued to increase throughout exercise. The total and total essential [AA] of muscle were significantly increased at exhaustion, whereas both the plasma and muscle branched-chain AA contents were unchanged. This suggests that protein catabolism was occurring during exercise and the branched-chain AA were used for energy and NH3 production.


2015 ◽  
Vol 71 (1) ◽  
pp. 9-16 ◽  
Author(s):  
Corinne Caillaud ◽  
Philippe Connes ◽  
Helmi Ben Saad ◽  
Jacques Mercier

1994 ◽  
Vol 26 (Supplement) ◽  
pp. S137
Author(s):  
Mary Jo Reiling ◽  
Kevin P. Davy ◽  
Douglas R. Seals

2004 ◽  
Vol 97 (4) ◽  
pp. 1414-1423 ◽  
Author(s):  
James A. Leppik ◽  
Robert J. Aughey ◽  
Ivan Medved ◽  
Ian Fairweather ◽  
Michael F. Carey ◽  
...  

Prolonged exhaustive submaximal exercise in humans induces marked metabolic changes, but little is known about effects on muscle Na+-K+-ATPase activity and sarcoplasmic reticulum Ca2+ regulation. We therefore investigated whether these processes were impaired during cycling exercise at 74.3 ± 1.2% maximal O2 uptake (mean ± SE) continued until fatigue in eight healthy subjects (maximal O2 uptake of 3.93 ± 0.69 l/min). A vastus lateralis muscle biopsy was taken at rest, at 10 and 45 min of exercise, and at fatigue. Muscle was analyzed for in vitro Na+-K+-ATPase activity [maximal K+-stimulated 3- O-methylfluorescein phosphatase (3- O-MFPase) activity], Na+-K+-ATPase content ([3H]ouabain binding sites), sarcoplasmic reticulum Ca2+ release rate induced by 4 chloro- m-cresol, and Ca2+ uptake rate. Cycling time to fatigue was 72.18 ± 6.46 min. Muscle 3- O-MFPase activity (nmol·min−1·g protein−1) fell from rest by 6.6 ± 2.1% at 10 min ( P < 0.05), by 10.7 ± 2.3% at 45 min ( P < 0.01), and by 12.6 ± 1.6% at fatigue ( P < 0.01), whereas 3[H]ouabain binding site content was unchanged. Ca2+ release (mmol·min−1·g protein−1) declined from rest by 10.0 ± 3.8% at 45 min ( P < 0.05) and by 17.9 ± 4.1% at fatigue ( P < 0.01), whereas Ca2+ uptake rate fell from rest by 23.8 ± 12.2% at fatigue ( P = 0.05). However, the decline in muscle 3- O-MFPase activity, Ca2+ uptake, and Ca2+ release were variable and not significantly correlated with time to fatigue. Thus prolonged exhaustive exercise impaired each of the maximal in vitro Na+-K+-ATPase activity, Ca2+ release, and Ca2+ uptake rates. This suggests that acutely downregulated muscle Na+, K+, and Ca2+ transport processes may be important factors in fatigue during prolonged exercise in humans.


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