The intent of this paper is to review the recent literature on exercise-induced hyperammonemia (EIH) and to compare the current interpretations of ammonia accumulation during exercise with the recognized clinical symptoms of progressive ammonia toxicity. In doing so, we will speculate on possible exercise-induced symptoms of CNS dysfunction which could result from elevated ammonia during intense short-duration or prolonged exercise. Ammonia is a ubiquitous metabolic product producing multiple effects on physiological and biochemical systems. Its concentration in several body compartments is elevated during exercise, predominantly by increased activity of the purine nucleotide cycle (PNC) in skeletal muscle. Depending on the intensity and duration of exercise, muscle ammonia may be elevated to the extent that it leaks (diffuses) from muscle to blood, and thereby can be carried to other organs. The direction of movement of ammonia or the ammonium ion is dependent on concentration and pH gradients between tissues. In this manner, ammonia can also cross the blood-brain barrier (BBB), although the rate of diffusion of ammonia from blood to brain during exercise is unknown. It seems reasonable to assume that exhaustive exercise may induce a state of acute ammonia toxicity which, although transient and reversible relative to disease states, may be severe enough in critical regions of the CNS to affect continuing coordinated activity. Regional differences in brain ammonia content, detoxification capacity, and specific sensitivity may account for the variability of precipitating factors and latency of response in CNS-mediated dysfunction arising from an exercise stimulus, e. g., motor incoordination, ataxia, stupor. There have been numerous suggestions that elevated ammonia is associated with, or perhaps is responsible for, exercise fatigue, although evidence for this relies extensively on temporal relationships. Fatigue may become manifest both as a peripheral organ or central nervous system phenomenon, or combination of both. Thus, we must examine the sequential or concomitant changes in ammonia concentration occurring in the periphery, the central nervous system (CNS), and the cerebrospinal fluid (CSF) induced by any effector, not only exercise, to interpret and rationalize the diverse physical, physiological, biochemical, and clinical symptoms produced by hyperammonemic states. Since more is known about elevated brain ammonia during other diverse conditions such as disease states, chemically induced convulsion, and hyperbaric hyperoxia, some of these relevant data are discussed.

The aim of this study was to measure serial changes in the rate of blood lactate clearance (gamma2) in response to sequential periods of training and detraining in four male triathletes aged 22-44 years. There were two major phases of training and taper, each lasting 4-5 weeks (training 1 = 5 weeks, taper 1 = 2 weeks, training 2 = 4 weeks and taper 2 = 2 weeks), in preparation for a triathlon competition. The training stimulus absorbed by each subject was carefully quantified from the duration and intensity of the training exercise. A serial weekly measure of each trainee's physical response to training was evaluated as the peak power, termed a 'criterion performance', developed by a subject during a 30 W x min(-1) ramp cycle ergometer test to exhaustion each week. During 30 min of recovery after this test, 13 samples of venous blood were drawn sequentially from a subject to measure the blood lactate recovery curve. The rate constant of blood lactate clearance was estimated by a non-linear least-squares regression technique. In addition, the concurrent time to peak lactate concentration and the peak lactate concentration were also estimated to help define changing lactate kinetics. The criterion performance generally declined throughout each period of incremental training and improved during each taper period, rising iteratively in this way to be clearly above baseline by the end of the second taper. The blood lactate clearance rate increased transiently in early training before declining from the middle of the first training period to the middle of the first taper; thereafter, gamma2 increased above baseline in each trainee throughout the remaining first taper and the major portion of the second training period, decreasing only in the final criterion performance test. The time to peak lactate declined from baseline throughout all phases of training and taper. Peak blood lactate increased in all subjects to the end of the first taper before declining by the end of the second training period, rising again to baseline levels during the second taper. The change in gamma2 was examined relative to the work rate achieved in cycle ergometry above an initial baseline score (deltaCP) and against concurrent peak blood lactate. There was a clear upward shift in gamma2 above baseline throughout the first and second training and taper in two subjects; this was less clear in the remaining two subjects, each of whom had a lower deltaCP. We conclude that this indicates improved lactate clearance, manifest by the change in gamma2 induced by endurance training.

A number of studies have identified the existence of two ventilation thresholds during ramp or incremental exercise to exhaustion on the cycle ergometer. This study was undertaken to investigate whether two threshold turnpoints could be identified in blood lactate concentration data collected at such times. Five trained athletes provided serial blood samples on several occasions each during a 3-month period of training. Blood lactate concentration was analysed by fitting models with no, one or two turnpoints. Ordinary residuals from the first two models were often found to exhibit an oscillatory behaviour consistent with the existence of two turnpoints in lactate concentration. A comparative analysis of goodness of fit of these models revealed that the model with two turnpoints was significantly better than either of the simpler models. This suggests that two transitions exist, which divide the time domain for blood lactate concentration in ramp exercise into three regions. These two transitions may correspond to the two ventilation thresholds.

A study was conducted to demonstrate IGF-1 gene expression in porcine ovarian tissue. Using northern blot analysis, IGF-1 messenger ribonucleic acid (mRNA) transcripts could not be consistently detected in total RNA. Authentic mRNA transcripts were detected in polyadenylated RNA-enriched RNA with sizes of 8.0, 3.6 and 2.3 bases, and possibly 0.8–1.1 kbases. Key words: Ovary, IGF-1, pig, mRNA

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