Ammonia metabolism in exercise and fatigue

Mutch, Barbara J. C.; Banister, E. W.

doi:10.1249/00005768-198315010-00009

Cited by 124 publications

(116 citation statements)

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“…However, whether this finding reflects a similar reduction in TAN loss in both conditions, in view of the fact that the pH gradient between tissues determines their relative ammonia concentrations and the -202 -direction of ammonia movement between intra-and extracellular compartments (Mutch and Banister, 1983;Harris and Dudley 1 1989), it can be argued. Nevertheless, the high plasma ammonia concentrations found in the present study do suggest that considerable reduction in TAN must have occurred during this type of exercise, irrespective of condition.…”

Section: Discussionmentioning

confidence: 97%

Human muscle metabolism during intermittent maximal exercise

Gaitanos

Williams

Boobis

et al. 1993

Journal of Applied Physiology

756

591

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Eight male subjects volunteered to take part in this study. The exercise protocol consisted of ten 6-s maximal sprints with 30 s of recovery between each sprint on a cycle ergometer. Needle biopsy samples were taken from the vastus lateralis muscle before and after the first sprint and 10 s before and immediately after the tenth sprint. The energy required to sustain the high mean power output (MPO) that was generated over the first 6-s sprint (870.0 +/- 159.2 W) was provided by an equal contribution from phosphocreatine (PCr) degradation and anaerobic glycolysis. Indeed, within the first 6-s bout of maximal exercise PCr concentration had fallen by 57% and muscle lactate concentration had increased to 28.6 mmol/kg dry wt, confirming significant glycolytic activity. However, in the tenth sprint there was no change in muscle lactate concentration even though MPO was reduced only to 73% of that generated in the first sprint. This reduced glycogenolysis occurred despite the high plasma epinephrine concentration of 5.1 +/- 1.5 nmol/l after sprint 9. In face of a considerable reduction in the contribution of anaerobic glycogenolysis to ATP production, it was suggested that, during the last sprint, power output was supported by energy that was mainly derived from PCr degradation and an increased aerobic metabolism.

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Section: Discussionmentioning

confidence: 97%

Human muscle metabolism during intermittent maximal exercise

Gaitanos

Williams

Boobis

et al. 1993

Journal of Applied Physiology

756

591

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show abstract

“…Peripheral muscle dysfunction and, in particular, impaired energy metabolism may prove an important remediable source of exercise intolerance in this population despite largely irreversible lung impairment. In healthy subjects, training increases ammonia workload threshold [31] and a reduction in blood ammonia concentration appears to delay onset of fatigue and increase the duration of intense exercise [11,31]. It is feasible that similar results with training could be achieved in COPD patients who have an observed ammonia increase with exercise.…”

Section: Discussionmentioning

confidence: 99%

“…In young healthy adults, blood ammonia concentration has been shown to increase during incremental exercise only when high intensities are reached [9,10]. This has been implicated in the development of fatigue and physical exhaustion [11]. Although plasma ammonia has been shown to closely reflect muscle adenine nucleotide metabolism in healthy subjects [11], the ammonia response to exercise in subjects with COPD has not been reported.…”

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confidence: 99%

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The plasma ammonia response to cycle exercise in COPD

Calvert¹,

Singh²,

Greenhaff³

et al. 2007

Eur Respir J

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The plasma ammonia response to exercise in chronic obstructive pulmonary disease (COPD) was examined and the relationship between plasma ammonia concentration and muscle adenine nucleotide metabolism was explored.In total, 25 stable COPD patients and 13 similar-aged controls underwent incremental and constant-work rate cycle exercise tests. Arterialised venous blood was sampled at rest, at 1-min intervals during exercise and f5 min after exercise for ammonia and lactate concentration.Peak incremental work rate was significantly less in COPD subjects (67¡21 W) than similar-aged controls (156¡46 W). In COPD and control subjects, plasma ammonia concentration increased during incremental exercise until 2 min post-exercise and then declined by 5 min post-exercise. However, two distinct patterns were seen in COPD subjects. In one group (n516), ammonia increased (42.8¡3.3 mmol?L ). In the second COPD group (n59), no ammonia increase was observed despite a similar lactate increase. Ammonia change with incremental and constant-work rate exercise strongly correlated in COPD subjects. Plasma ammonia increase correlated with muscle inosine-59-monophosphate formation after constant-work rate exercise.Plasma ammonia concentration increases during incremental and constant-work rate cycle exercise in chronic obstructive pulmonary disease subjects at lower absolute work rates compared with similar-aged controls. The plasma ammonia response may provide useful information about adenine nucleotide metabolism and, therefore, muscle fatigue during exercise in patients with chronic obstructive pulmonary disease.

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“…Indeed, rainbow trout refused to perform repetitive bouts of burst exercise when plasma lactate concentration exceeded 13·mmol·l -1 (Stevens and Black, 1966) and a poorer repeat Ucrit was found for sockeye salmon Oncorhynchus nerka when plasma lactate concentration was >10·mmol·l -1 . In mammals, elevated plasma Tamm has been implicated in exercise fatigue (reviewed by Mutch and Banister, 1983) due to inhibitory influences on anaerobic metabolism (Zaleski and Bryla, 1977;Su and Storey, 1994), aerobic metabolism (McKhann and Tower, 1961;Avillo et al, 1981) and neuromuscular coordination (Binstock and Lecar, 1969;O'Neill and O'Donovan, 1979). Plasma Tamm also increases in rainbow trout during exercise (Turner et al, 1983;Wang et al, 1994; but see Beaumont et al, 1995a,b).…”

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confidence: 99%

Influence of seasonal temperature on the repeat swimming performance of rainbow troutOncorhynchus mykiss

Jain

Farrell

2003

Journal of Experimental Biology

161

116

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). Given that metabolic recovery in skeletal muscle (muscle lactate, ATP and glycogen, but not PCr) occurs more rapidly at warm than cold temperatures in exhausted rainbow trout Oncorhynchus mykiss and Atlantic salmon Salmo salar (Kieffer et al., 1994;Wilkie et al., 1997;Kieffer, 2000), the expectation is that swimming performance is restored faster at a higher temperature. This expectation would be consistent with the known increase in both maximum oxygen uptake and maximum cardiac output with temperature (e.g. Butler et al., 1992;Farrell, 1997;Taylor et al., 1997) because an improved oxygen delivery system could support a more rapid recovery of the metabolic debt incurred with exhaustive exercise. However, when Atlantic salmon were angled rather than chased to exhaustion, muscle glycogen, intracellular pH and lactate were restored more rapidly under cold conditions than warm conditions (Wilkie et al., While the temperature dependence of exercise performance in fishes is reasonably well documented, information on the temperature dependence of metabolic recovery and reperformance is scant. This study examined the recovery of swimming performance after exhaustive exercise in rainbow trout Oncorhynchus mykiss at seasonal temperatures ranging from 5 to 17°C and explored the relationship between performance and preceding metabolic state. The primary objective of the study was to test the hypothesis that increased temperature increases the capability of rainbow trout to repeat a critical swimming speed (U crit), as assessed by two consecutive critical swimming speed tests separated by a 40·min rest interval. An additional expectation was that certain plasma ionic, metabolic and humoral parameters would be correlated with how well fish reperformed and so plasma levels of lactate, potassium, ammonia, osmolality, sodium and cortisol, as well as hematocrit, were monitored before, during and after the swim challenges via an indwelling cannula in the dorsal aorta. As expected, performance in the first Ucrit test (Ucrit1) was positively related to temperature. However, the relationship between Ucrit1 and reperformance (Ucrit2) was not dependent on acclimation temperature in a simple manner. Contrary to our expectations, Ucrit2 was less than Ucrit1 for warmacclimated fish (14.9±1.0°C), whereas Ucrit2 equaled Ucrit1 for cold-acclimated fish (8.4±0.9°C). Cold-acclimated fish also exhibited a lower Ucrit1 and less metabolic disruption compared with warm-acclimated fish. Thus, while warm acclimation conferred a faster Ucrit1, a similar swimming speed could not be attained on subsequent swim after a 40·min recovery period. This finding does not support the hypothesis that the ability of rainbow trout to reperform on U crit test is improved with temperature. Both plasma lactate and plasma potassium levels were strongly correlated with Ucrit1 performance. Therefore, the higher Ucrit1 of warm-acclimated fish may have been due in part to a greater anaerobic swimming effort compared with cold-acclimated fish. In fact, a significant co...

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Ammonia metabolism in exercise and fatigue

Cited by 124 publications

References 0 publications

Human muscle metabolism during intermittent maximal exercise

Human muscle metabolism during intermittent maximal exercise

The plasma ammonia response to cycle exercise in COPD

Influence of seasonal temperature on the repeat swimming performance of rainbow troutOncorhynchus mykiss

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