Paula J. Robson

The effects of high-intensity intermittent exercise on saliva IgA, total protein and alpha-amylase

The aim of this study was to assess the effect of an acute bout of high-intensity intermittent exercise on saliva IgA concentration and alpha-amylase activity, since this type of training is commonly incorporated into the training programmes of endurance athletes and games players. Eight well-trained male games players took part in the study. They reported to the laboratory after an overnight fast and performed a 60-min cycle exercise task consisting of twenty 1-min periods at 100% VO2max, each separated by 2 min recovery at 30% VO2max. Unstimulated whole saliva was collected over a 5-min period into pre-weighed tubes and analysed for total protein, saliva IgA and alpha-amylase. The saliva flow rate ranged from 0.08 to 1.40 ml x min(-1) at rest and was not significantly affected by the exercise. The performance of the intermittent exercise bout did not affect the saliva IgA concentration, but caused a five-fold increase in alpha-amylase activity (P<0.01 compared with pre-exercise) and a three-fold increase in total protein concentration (P<0.01). These returned to pre-exercise values within 2.5 h post-exercise. It has been suggested that IgA concentration should be expressed as the ratio to total protein concentration, to correct for any concentrating effect due to evaporative loss of saliva water when breathing through the mouth (as in strenuous exercise). The present study clearly demonstrates that this is not appropriate, since there is an increase in salivary protein secretion rate immediately after exercise (571+/-77 microg x min(-1) compared with 218+/-71 microg x min(-1) pre-exercise; P<0.05). The increased saliva alpha-amylase activity after exercise may improve the protective effect of saliva, since this enzyme is known to inhibit bacterial attachment to oral surfaces. The saliva alpha-amylase secretion rate was lower immediately pre-exercise than at any other instant, which may have been due to anticipatory psychological stress, although the subjects were all familiar with interval exercise. This emphasizes the need for true resting non-stressed control conditions in future studies of the effects of exercise on saliva constituents.

Glutamine, exercise and immune function : Links and possible mechanisms

Glutamine is the most abundant free amino acid in human muscle and plasma and is utilised at high rates by rapidly dividing cells, including leucocytes, to provide energy and optimal conditions for nucleotide biosynthesis. As such, it is considered to be essential for proper immune function.During various catabolic states including surgical trauma, infection, starvation and prolonged exercise, glutamine homeostasis is placed under stress. Falls in the plasma glutamine level (normal range 500 to 750 μmol/L after an overnight fast) have been reported following endurance events and prolonged exercise. These levels remain unchanged or temporarily elevated after short term, high intensity exercise. Plasma glutamine has also been reported to fall in patients with untreated diabetes mellitus, in diet-induced metabolic acidosis and in the recovery period following high intensity intermittent exercise. Common factors among all these stress states are rises in the plasma concentrations of cortisol and glucagon and an increased tissue requirement for glutamine for gluconeogenesis. It is suggested that increased gluconeogenesis and associated increases in hepatic, gut and renal glutamine uptake account for the depletion of plasma glutamine in catabolic stress states, including prolonged exercise.The short term effects of exercise on the plasma glutamine level may be cumulative, since heavy training has been shown to result in low plasma glutamine levels (<500 μmol/L) requiring long periods of recovery. Furthermore, athletes experiencing discomfort from the overtraining syndrome exhibit lower resting levels of plasma glutamine than active healthy controls. Therefore, physical activity directly affects the availability of glutamine to the leucocytes and thus may influence immune function. The utility of plasma glutamine level as a marker of overtraining has recently been highlighted, but a consensus has not yet been reached concerning the best method of determining the level.Since injury, infection, nutritional status and acute exercise can all influence plasma glutamine level, these factors must be controlled and/or taken into consideration if plasma glutamine is to prove a useful marker of impending overtraining.

The effects of carbohydrate supplementation on immune responses to a soccer-specific exercise protocol.

The aim of this study was to determine the effect of carbohydrate (CHO) versus placebo (PLA) beverage consumption on the immune and plasma cortisol responses to a soccer-specific exercise protocol in 8 university team soccer players. In a randomized, counterbalanced design, the players received carbohydrate or placebo beverages before, during and after two 90 min soccer-specific exercise bouts (3 days apart) designed to mimic the activities performed and the distance covered in a typical soccer match. Blood and saliva samples were collected before, during and after the exercise protocol. Plasma lactate concentration increased to approximately 4 mmol x l(-1) at 45 and 90 min of exercise in both treatments (P<0.01). Plasma glucose concentration was significantly lower after 90 min of exercise with ingestion of the placebo than the carbohydrate (PLA: 4.57+/-0.12 mmol x l(-1); CHO: 5.49+/-0.11 mmol x l(-1); P<0.01). The pattern of change in plasma cortisol, circulating lymphocyte count and saliva immunoglobulin A secretion did not differ between the carbohydrate and placebo trials. Blood neutrophil counts were 14% higher 1 h after the placebo trial than the carbohydrate trial (PLA: 4.8+/-0.5x10(9) cells x l(-1); CHO: 4.2+/-0.5x10(9) cells x l(-1); P = 0.06), but the treatment had no effect on the degranulation response of blood neutrophils stimulated by bacterial lipopolysaccharide. We conclude that, although previous studies have shown that carbohydrate feeding is effective in attenuating immune responses to prolonged continuous strenuous exercise, the same cannot be said for a soccer-specific intermittent exercise protocol. When overall exercise intensity is moderate, and changes in plasma glucose, cortisol and immune variables are relatively small, it would appear that carbohydrate ingestion has only a minimal influence on the immune response to exercise.

Nutritional aspects of immunosuppression in athletes

The literature suggests that a heavy schedule of training and competition leads to immunosuppression in athletes, placing them at a greater risk of opportunistic infection. There are many factors which influence exercise-induced immunosuppression, and nutrition undoubtedly plays a critical role. Misinterpretation of published data and misleading media reports have lead many athletes to adopt an unbalanced dietary regimen in the belief that it holds the key to improved performance. Some sports have strict weight categories, whilst in others low body fat levels are considered to be necessary for optimal performance or seen as an aesthetic advantage. This leads some athletes to consume a diet extremely low in carbohydrate content which, whilst causing rapid weight loss, may have undesirable results which include placing the athlete at risk from several nutrient deficiencies. Complete avoidance of foods high in animal fat reduces the intake of protein and several fat-soluble vitamins. On the other hand, diets with a very high carbohydrate content are usually achieved at the expense of protein.In addition, anecdotal and media reports have often promoted the supposed performance benefits of certain vitamins and minerals, yet most athletes do not realise that micronutrient supplementation is only beneficial when correcting a deficiency, and to date there is little scientific evidence to substantiate claims that micronutrients act as an ergogenic aid. Moreover, excessive intakes of micronutrients can be toxic.Deficiencies or excesses of various dietary components can have a substantial impact on immune function and may further exacerbate the immunosuppression associated with heavy training loads. This review examines the role of nutrition in exercise-induced immunosuppression and the effect of both excessive and insufficient nutrient intake on immunocompetence. As much of the present literature concerning nutrition and immune function is based on studies with sedentary participants, the need for future research which directly investigates the relationship between exercise, training, immunity and nutrition is highlighted.

The effect of severe eccentric exercise-induced muscle damage on plasma elastase, glutamine and zinc concentrations.

Abstract The aim of this study was to determine if severe exercise-induced muscle damage alters the plasma concentrations of glutamine and zinc. Changes in plasma concentrations of glutamine, zinc and polymorphonuclear elastase (an index of phagocytic cell activation) were examined for up to 10 days following eccentric exercise of the knee extensors of one leg in eight untrained subjects. The exercise bout consisted of 20 repetitions of electrically stimulated eccentric muscle actions on an isokinetic dynamometer. Subjects experienced severe muscle soreness and large increases in plasma creatine kinase activity indicative of muscle fibre damage. Peak soreness occurred at 2 days post-exercise and peak creatine kinase activity [21714 (6416) U · l−1, mean (SEM)] occurred at 3 days post-exercise (P < 0.01 compared with pre-exercise). Plasma elastase concentration was increased at 3 days post-exercise compared with pre-exercise (P < 0.05), and is presumably indicative of ongoing phagocytic leucocyte infiltration and activation in the damaged muscles. There were no significant changes in plasma zinc and glutamine concentrations in the days following eccentric exercise. We conclude that exercise-induced muscle damage does not produce changes in plasma glutamine or zinc concentrations despite evidence of phagocytic neutrophil activation.

The effects of high-intensity intermittent exercise on the plasma concentrations of glutamine and organic acids

Glutamine is an essential substrate for the proper functioning of cells of the immune system. Falls in plasma glutamine concentration after exercise may have deleterious consequences for immune cell function and render the individual more susceptible to infection. The purpose of the present study was to examine changes in plasma glutamine concentration (measured using a validated enzymatic spectrophotometric method) following an acute bout of intermittent high-intensity exercise. Eight well-trained male games players took part in the study. Subjects reported to the laboratory following an overnight fast and performed a 1-h cycle exercise task consisting of 20 1-min periods at 100% maximal O2 consumption (V˙O2max) each separated by 2 min of recovery at 30% V˙O2max. Venous blood samples were taken before exercise and at 5 min, 1 h, 2.5 h, 5 h and 24 h post-exercise. Glutamine was measured by enzymatic spectrophotometric determination of the ammonia concentration before and after treatment of the plasma with glutaminase (EC 3.5.1.2). Plasma glutamine concentration did not fall in the immediate post-exercise period [pre-exercise 681 (23) μM compared with 663 (46) μM at 5 min post-exercise, mean (SEM)], but fell to 572 (35) μM at 5 h post-exercise (P < 0.05 compared with pre-exercise). Plasma lactate concentration rose to 8.8 (1.0) mM at the end of exercise and fell to 1.8 (0.4) mM at 1 h post-exercise, but plasma concentrations of free fatty acids and β-hydroxybutyrate both rose substantially in the post-exercise period (to 240% and 400% of pre-exercise levels, respectively). The circulating leucocyte count increased significantly during exercise (P < 0.01), continued to increase in the hours following exercise and peaked at 2.5 h post-exercise (mainly due to a neutrophilia). The fall in the plasma glutamine concentration at 5 h post-exercise could be due to increased renal uptake of glutamine, which generally occurs in conditions of metabolic acidosis or due to a greater removal of glutamine from the plasma resulting from the elevated circulating leucocyte count.