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 (VO2max) each separated by 2 min of recovery at 30% VO2max. 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) microM compared with 663 (46) microM at 5 min post-exercise, mean (SEM)], but fell to 572 (35) microM 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 beta-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.

To date, research has examined the physiological determinants of performance in standardized CrossFit® (CF) workouts but not without the influence of CF familiarity. Therefore, the purpose of this present study was to examine the predictive value of aerobic fitness, body composition, and total body strength on performance of two standardized CF workouts in CF-naïve participants. Twenty-two recreationally trained individuals (males = 13, females = 9) underwent assessments of peak oxygen consumption (VO2 peak), ventilatory thresholds, body composition, and one repetition maximum tests for the back squat, deadlift, and overhead press in which the sum equaled the CF Total. Participants also performed two CF workouts: a scaled version of the CF Open workout 19.1 and a modified version of the CF Benchmark workout Fran to determine scores based on total repetitions completed and time-to-completion, respectively. Simple Pearson’s r correlations were used to determine the relationships between CF performance variables (19.1 and modified Fran) and the independent variables. A forward stepwise multiple linear regression analysis was performed and significant variables that survived the regression analysis were used to create a predictive model of CF performance. Absolute VO2 peak was a significant predictor of 19.1 performance, explaining 39% of its variance (adjusted R2 = 0.39, p = 0.002). For modified Fran, CF Total was a significant predictor and explained 33% of the variance in performance (adjusted R2 = 0.33, p = 0.005). These results suggest, without any influence of CF familiarity or experience, that performance in these two CF workouts could be predicted by distinct laboratory-based measurements of fitness.

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 x 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.

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