Effect of cold air inhalation on core temperature in exercising subjects under heat stress.

Whether increasing respiratory heat loss (RHL) during exercise under heat stress can contain elevation of rectal temperature (Tre) was examined. Eight men cycled twice at 45-50% their maximum work rate until exhaustion at ambient temperature and relative humidity of 38 degrees C and 90-95%, respectively. They inspired either cold (3.6 degrees C) or ambient air in random sequence. When subjects breathed cold air during 23 min of exercise, a ninefold increase in RHL was observed vs. similar work during hot air inhalation (32.81 vs. 3.46 W). Respiratory frequency (f) and rate of rise in Tre decreased significantly (P less than or equal to 0.004 and P less than or equal to 0.002, respectively). The rise in skin temperature in each inhalant gas condition was accompanied by a parallel almost equal increase in core temperature above basal (delta Tre) for equivalent gains in skin temperature. The increase in tidal volume and decreased f in the cold condition allowed more effective physical conditioning of cold inspirate gas in the upper airways and aided RHL. Cold air inhalation also produced a significant (P less than or equal to 0.05) decrease in heart rate vs. hot air inhalation in the final stages of exercise. Insignificant changes in O2 consumption and total body fluid loss were found. These data show that cold air inhalation during exercise diminishes elevation of Tre and suggest that both the intensity and duration of work can thus be extended. The importance of the physical exchange of heat energy and any physiological mechanisms induced by the cold inspirate in producing the changes is undetermined.

The Astrand-Ryhming nomogram revisited.

Relationships among O2 uptake (VO2), heart rate, and work rate during constant-load submaximal cycle ergometry and ramp-forced exercise to exhaustion have been studied in core groups of trained (n = 15) and untrained (n = 10), 20- to 29-yr-old males. A signal aim was to improve on the accuracy of the 1954 Astrand-Ryhming (A-R) nomogram predicting maximum aerobic power from heart rate elevation at submaximum work rates. A new nomogram has been developed based on a linear relationship, established in experimental groups, between VO2 and delta HR, the latter being defined as the elevation of exercise heart rate above that reached during zero-load pedaling at 90 rpm. The delta HR variable used in a nomogram linking it and submaximum VO2 (either derived by calculation from the concomitant steady-state work rate or measured directly from respiratory gas analysis) successfully differentiated maximum aerobic power of trained from untrained subjects in core groups whose different abilities could not otherwise be distinguished by the A-R nomogram itself. In a validation group of trained (n = 5), untrained (n = 5), and moderately trained (n = 4) 20- to 29-yr-old males, the correlation measured between VO2max values and those predicted from the new nomogram was significantly better (r = 0.98) (P less than 0.05) than predictions made from the A-R nomogram (r = 0.80).

Modeling human performance in running.

This paper focuses on the characteristics of a model interpreting the effect of training on athletic performance. The model theory is presented both mathematically and graphically. In the model, a systematically quantified impulse of training produces dual responses: fitness and fatigue. In the absence of training, both decay exponentially with time. With repetitive training, these responses satisfy individual recurrence equations. Fitness and fatigue are combined in a simple linear difference equation to predict performance levels appropriate to the intensity of training being undertaken. Significant observed correlation of model-predicted performance with a measure of actual performance during both training and tapering provides validation of the model for athletes and nonathletes alike. This enables specific model parameters to be estimated and can be used to optimize future training regimens for any individual.

Optimizing athletic performance by influence curves.

Recent application of modeling techniques to physical training has opened the possibility for prediction from training. Solution of the inverse problem, determining a training program to produce a desired performance at a specific time, is also possible and may yield strategies for achieving better training and tapering (complete or relative rest for a period before competition) regimens for competitive athletes. A mathematical technique derived from model theory is described in this paper that allows the design of an optimal strategy of physical preparation for an individual to do well in a single future competitive event or cluster of events. Simulation results, using default parameters of a training model, suggest that presently accepted forms of taper for competition may remain too rigorous and short in duration to achieve the best result possible from the training undertaken.

Possible mechanisms of the anaerobic threshold. A review.

The anaerobic threshold consists of a lactate threshold and a ventilatory threshold. In some conditions there may actually be 2 ventilatory thresholds. Much of the work detailing the lactate threshold is strongly based on blood lactate concentration. Since, in most cases, blood lactate concentration does not reflect production in active skeletal muscle, inferences about the metabolic state of contracting muscle will not be valid based only on blood lactate concentration measurements. Numerous possible mechanisms may be postulated as generating a lactate threshold. However, it is very difficult to design a study to influence only one variable. One may ask, does reducing F1O2 cause an earlier occurrence of a lactate threshold during progressive exercise by reducing oxygen availability at the mitochondria? By stimulating catecholamine production? By shifting more blood flow away from tissues which remove lactate from the blood? Or by some other mechanism? Processes considered essential to the generation of a lactate threshold include: (a) substrate utilisation in which the ability of contracting muscle cells to oxidise fats reaches maximal power at lactate threshold; and (b) catecholaminergic stimulation, for without the presence of catecholamines it appears a lactate threshold cannot be generated. Other mechanisms discussed which probably enhance the lactate threshold, but are not considered essential initiators are: (a) oxygen limitation; (b) motor unit recruitment order; (c) lactate removal; (d) muscle temperature receptors; (e) metabolic stimulation; and (f) a threshold of lactate efflux. Some mechanisms reviewed which may induce or contribute to a ventilatory threshold are the effects of: (a) the carotid bodies; (b) respiratory mechanics; (c) temperature; and (d) skeletal muscle receptors. It is not yet possible to determine the hierarchy of effects essential for generating a ventilatory threshold. This may indicate that the central nervous system integrates a broad range of input signals in order to generate a non-linear increase in ventilation. Evidence indicates that the occurrence of the lactate threshold and the ventilatory threshold may be dissociated; sometimes the occurrence of the lactate threshold significantly precedes the ventilatory threshold and at other times the ventilatory threshold significantly precedes the lactate threshold. It is concluded that the 2 thresholds are not subserved by the same mechanism.

Ammonia as an indicator of exercise stress implications of recent findings to sports medicine.

The role of ammonia in exercise-induced fatigue is reviewed. Implications for integrated activity of developing hyperammoneic states, caused by various precipitating conditions such as exercise, liver dysfunction, hypoxia, hyperoxia, and chemical poisoning are described. The central role of ammonia in diverse important metabolic pathways indicates its ubiquitous role in a spectrum of activity ranging from elite exhaustive performance of sportsmen and -women to life-threatening organ dysfunction. The action of ammonia and metabolites from associated pathways in producing seemingly dangerous short term conditions, but inducing possible long term protection against degenerative processes associated with ageing (free radical-induced cellular damage) indicate the paradoxical position of ammonia and its associated metabolic pathways for health and disease processes.

Relative effects of hyperbaric oxygen on cations and catecholamine metabolism in rats: protection by lithium against seizures.

Analysis of lithium (Li+) in the brain and blood after intraperitoneal injection (i.p.) shows that initially its concentration is high in blood and negligible in the brain. Subsequently its concentration increases in the brain and disappears from the blood. Lithium itself affects neurological actions but the mechanisms remain obscure. It also modifies the toxic action of oxygen at high pressure (OHP), which causes convulsions, either suppressing or exacerbating it. These clearly separate effects correspond with the presence of Li+ in the blood (suppression) or in the brain (exacerbating). Determination of the effect of Li+ and OHP upon cations, catecholamines, ammonia, tyrosine hydroxylase, and monamine oxidase on brain and blood tissue showed that there was very little correspondence between changes in the cations either with Li+ or the toxic effects of OHP. On the other hand, OHP developed a sustained blood and brain hyperammonemia in rats which could be negatively modified by Li+ in the blood. The latter effect also corresponded with a prolongation of convulsive latency. Changes in brain catecholamines, tyrosine hydroxylase, monoamine oxidase and tyrosine were effected by Li+ and potentiated by OHP. These data suggest that Li+ and OHP mediate their effects relatively more through developing hyperammoneic states in both blood and brain than by altering cation concentrations in these tissues.

Ammonia metabolism in exercise and fatigue: a review.

Although fatigue is a well-known phenomenon and the phrase "exercised until exhaustion" is commonly understood, there is no unequivocal agreement on the fundamental nature of the fatigue process. Ammonia was linked to the development of fatigue as early as 1922, when ammonia production was observed from stimulated nerve and the question whether there could be a relationship between ammonia production and the muscle activity was raised. The immediate source of ammonia from muscle appears to be a result of the deamination of AMP and is more apparent in fast-twitch than in slow-twitch fibers. More recently, increases in blood ammonia levels have been reported in rats after swimming and in humans after arm work, maximal cycle ergometry, and treadmill exercise. Elevated blood ammonia has also been linked to a surprising variety of functional and metabolic neurological disturbances other than exercise and fatigue, including the development of hepatic coma, convulsions from ammonia toxicity precipitated by high-pressure oxygen breathing, epileptic seizures, and decreased neuronal excitability. In addition, a number of genetic disorders (inborn errors in metabolism, or IEMs) are characterized by elevated blood ammonia concentrations. Symptoms of neural disability in all of the above conditions have been related to the concentration of ammonia in blood. Although these studies do not relate to exercise or fatigue directly, it is conceivable that our understanding of the effect of high concentrations of blood ammonia in these clinical conditions may provide valuable insight into the effect of ammonia during exercise. This paper reviews the effect of ammonia production during exercise and other conditions upon purposeful activity and the development of fatigued states.

Modelling the effect of taper on performance, maximal oxygen uptake, and the anaerobic threshold in endurance triathletes.

The purpose of this study was to determine the nature of taper required to optimize performance in Ironman triathletes. Eleven triathletes (26 +/- 4 yrs, 77.0 +/- 6.5 kg) took part in 3 months of training interspersed with two taper periods, one of 10 days (Taper 1) and another six weeks later for 13 days (Taper 2). Reducing training volume by 50% in an exponential fashion (tau < or = 5 days) in one group of triathletes during Taper 1 resulted in a 46 second (4%) improvement in their 5 km criterion run time and a 23 W (5%) increase in maximal ramp power output above the same measurement at the beginning of taper. A 30% step reduction in training volume in the second group did not result in any significant improvement in physical performance on the same measures. Training volume was reduced exponentially from the end of training in both a high volume group (tau > or = 8 days) and a low volume group (tau < or = 4 days) during Taper 2. Criterion run time improved significantly by 74 seconds (6%) and 28 seconds (2%) in the high and low volume groups respectively, while maximal ramp power increased significantly by 34 W (8%) only in the low volume taper group. Maximal oxygen uptake increased progressively from 62.9 +/- 5.8 ml.kg-1.min-1 two weeks prior to taper, to a significantly higher level 68.9 +/- 4.2 ml.kg-1.min-1 during the final week of Taper 2 (p < or = 0.5). The anaerobic threshold determined by a non-invasive method was also observed to increase from 70.9% to 74.9% of a subject's maximal oxygen uptake during Taper 2. These results demonstrate that proper placement of training volume during taper is a key factor in optimizing performance for a specific competition and a high volume of training in the immediate days preceding an event may be detrimental to physical performance.

The perception of effort: an inductive approach.

A theoretical model has been proposed relating physical effort to perceived exertion. The model has been applied to a comparative investigation of the perception of various forces exerted by the adductor pollicis muscle and the quadriceps in five male subjects. The increase in perception of effort with increasing applied force in both muscle groups has been shown to increase exponentially. A force constant, defined in the paper, as the applied force at which perception of effort approximates two-thirds of maximum seems to discriminate effectively between the muscle groups concerned. The description of psychophysical data in this concise quantifiable manner may offer better insight into physiological processes contributing to the appreciation of effort.

Exercise-induced hyperammonemia: peripheral and central effects.

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 time course of brain and blood catecholamines, catechol O-methyltransferase, and amino acids in rats convulsed by oxygen at high pressure.

The time course of changes in blood and brain catecholamines, catechol O-methyltransferase (COMT), ammonia, and amino acids leading to convulsion by high pressure oxygen breathing (OHP) in rats has been investigated. Brain catecholamines were suppressed by OHP. They changed in phase with brain COMT concentration and consequently were not due to the action of this degrading enzyme. Convulsive actions seem not to be influenced by brain catecholamine concentration. Blood adrenaline concentrations are, however, significantly elevated both prior to and during convulsions. In both brain and blood, ammonia concentration increases, glutamate decreases, and glutamine-aspargine increases. It is proposed that the efficacy of the glutamate-glutamine ammonia buffering system in blood and brain is important in the prevention of the onset of convulsions but that when brain gamma-aminobutyric acid is depressed to critical levels, convulsions result.

Effects of simulated altitude training on aerobic and anaerobic power.

Five trained males aged 20-23 years undertook successive phases (2-5 weeks duration) of daily training in normoxia or hypoxia. Weekly exhaustive tests alternately in normoxia or hypoxia, throughout, assessed the comparative efficacy of the training. The relative contribution to endurance, aerobic (peak VO2) and anaerobic (deltaLa) power made by exercise or hypoxia separately was studied. In a stepwise increasing work test to exhaustion relative bradycardia developed during the first minute of exhaustive work at 1800 kgm/min in all subjects and aerobic power increased both in normoxia and hypoxia significantly by the end of the first phase hypoxic training. Endurance for exhaustive work increased in both environments as did aerobic and anaerobic power.

Effects of 6-hydroxydopamine on brain and blood catecholamines, ammonia, and amino acids in rats.

The effect of 6-hydroxydopamine (6-OHDA) upon brain and blood catecholamines, ammonia, and amino acids has been studied in rats subjected to increasing doses of the drug. Time dependent effects after injection have also been studied. Systemically injected 6-OHDA significantly, acutely reduced brain adrenaline (A), noradrenaline (NA), total catecholamines (TC), gamma-aminobutyric acid (GABA), and glutamic acid (Glu); concomitantly brain ammonia (NH3) increased. In blood, NA and TC were reduced and A and NH3 increased. The changes in brain monoamines are surprising since it has been reported that 6-OHDA does not cross the blood-brain barrier. We have proposed that these changes result from a general stress response or a reflex peripheral sympathetic response to falling blood pressure which in some manner communicates to the central nervous system. As the dose of 6-OHDA increased, brain NH3 increased and Glu decreased. A similar effect was seen from a single dose as the time after injection for sampling brain and blood constituents increased. Blood ammonia increases without change in Glu, glutamine, or asparagine. The source of NH3 may be from deamination of adenine nucleotide or catechols released from nerve terminals under the abnormal stimulus of 6-OHDA.

Effect of 6-hydroxydopamine on brain and blood catecholamine, ammonia, and amino acid metabolism in rats subjected to high pressure oxygen induced convulsions.

Effects of 6-hydroxydopamine (6-OHDA) on rat brain and blood adrenaline (A), noradrenaline (NA), ammonia (NH3), gamma-aminobutyric acid (GABA), and amino acid metabolism prior to and after high pressure oxygen (OHP) induced convulsions have been studied. 6-OHDA reduces GABA and glutamate (Glu) rior to OHP exposure in rat brain so that the concentration is even equal to that seen in nondrugged animals after convulsion. Concomitantly, 6-OHDA reduces the latency of OHP-induced convulsion significantly, and increases brain NH3, glutamine, and asparagine significantly. Although 6-OHDA, in increasing dosage, elevates blood A concentration, convulsion produces a significant further increase in A. Blood NA was not significantly changed in drugged, convulsed animals and was much less than blood NA concentrations in nondrugged convulsed animals. Increasing doses of 6-OHDA also increase NH3 in the blood significantly and convulsion increases its concentration further. Latency of convulsion seems to be related to certain monoamine levels since in some drugged animals where A and total catecholamines are still reduced 96 h after the first of two doses of 6-OHDA, NA concentrations are recovered to relatively normal and the convulsion latency time is also increased although it remains significantly abbreviated from undrugged animals' convulsion time. Low brain GABA levels seem to be a prime effector of convulsive activity.