The Effect of Glutamine in Modulating Exertional Heat Stress Response of Intestinal Cells in Trained and Untrained Runners

Glutamine is the preferred substrate of intestinal cells and is required for the protection of intestinal cells integrity, helping to prevent exercise-induced endotoxin leakage from the intestine during stressful conditions. Increased endotoxins in the blood circulation (also known as endotoxaemia) has been shown to trigger systemic inflammation which is implicated in exertional heat stroke. This study examined firstly whether orally administered glutamine helps to reduce intestinal injury following an acute high intensity exercise session in hot conditions and secondly whether there is a different outcome according to fitness levels in runners. A randomized, double-blinded crossover study design was utilized. Twelve runners unacclimatised to heat, divided into trained [T; n=6; maximal oxygen uptake (VO2max) = 61.2 ± 1.0 ml∙kg-1∙min-1] and untrained (UT; n=6; VO2max = 51.0 ± 0.7 ml∙kg-1∙min-1) groups, ingested either a placebo or glutamine dipeptide supplement (L-alanyl-L-glutamine; 0.2 g/kg bodyweight/day) for 5 consecutive days before running at 70%VO2max in a climate chamber (30°C, 40% relative humidity) for 1 hour. Cardiac output, stroke volume, heart rates, sweat loss, percent dehydration, rectal and skin surface temperatures were measured. Venous blood samples at baseline, immediately after completion of run and 1-hour post run were analysed for endotoxins and intestinal fatty acid binding proteins (I-FABP) as markers of intestinal injury. Intestinal permeability was measured at pre and post exercise using dual sugar probes (L-R; lactulose and rhamnose). No significant difference was observed in all responses for training status. L-R ratios remained unchanged with or without glutamine. However, a significant main effect for time and treatment was observed for plasma I-FABP (

Lymphocyte and Monocyte Hsp72 Responses to Exercise in Athletes with Prior Exertional Heat Illness

ABSTRACT Introduction. Exertional heatstroke is a serious disorder that can be fatal especially if treatment is delayed. Heat shock protein 72 (Hsp72) is strongly induced by heat, and can be protective against a subsequent stress that may be the same or of a different form. In animal models it has been shown that upregulation of Hsp72 is protective against heatstroke. There is a natural variability in the amount and/or inducibility of Hsp72 in cells and tissues between individuals, and it is possible that impaired expression levels could make some athletes more prone to heat illness. The purpose of this study was to examine Hsp72 expression in lymphocytes and monocytes of young (\u3c40 years) athletes who had previously experienced, but recovered from serious heatstroke during exercise in the heat. Methods. Fourteen athletes ran on a treadmill for 60 min at 72% maximal oxygen uptake (o2max) in warm conditions (30°C, 40% relative humidity). One group consisted of athletes who had a previous history of exertional heat illness (EHI), while the control group (CON) had no previous history of EHI. Both groups were of similar age (29.7 ± 1.2 and 29.1 ± 2 years, CON vs EHI) and fitness (o2max 65.7 ± 2 and 64.5 ± 3 ml.kg-1.min-1, CON vs EHI). Rectal temperature was measured using a thermistor inserted to a depth of 10 cm past the anal sphincter. Hsp72 levels were measured in both monocytes and lymphocytes by flow cytometry before and immediately after the 60-min run, then after 60 min of recovery at an ambient temperature of 24°C. Results. Rectal temperature increased during the exercise period but there was no difference between groups, demonstrating that the EHI group had recovered from their heat illness and were not heat intolerant. Lymphocyte Hsp72 was lower in the EHI group after 60 min of exercise (p\u3c0.05), while monocyte Hsp72 was not different between groups. Conclusion. Our study found a lower lymphocyte Hsp72 concentration during exercise in athletes who had previously collapsed with serious EHI. Further research is needed to determine whether lower lymphocyte Hsp72 is a factor that may predispose athletes to develop EHI

The effect of ice-slushy consumption on plasma vasoactive intestinal peptide during prolonged exercise in the heat

The aim of this study was to determine the effect of exercise in the heat on thermoregulatory responses and plasma vasoactive intestinal peptide concentration (VIP) and whether it is modulated by ice-slushy consumption. Ten male participants cycled at 62% View the MathML sourceV̇O2max for 90 min in 32 °C and 40% relative humidity. A thermoneutral (37 °C) or ice-slushy (−1 °C) sports drink was given at 3.5 ml kg−1 body mass every 15 min during exercise. VIP and rectal temperature increased during exercise (mean±standard deviation: 4.6±4.4 pmol L−1, P=0.005; and 1.3±0.4 °C, P\u3c0.001 respectively) and were moderately associated (r=0.35, P=0.008). While rectal temperature and VIP were not different between trials, ice-slushy significantly reduced heat storage (P=0.010) and skin temperature (timextrial interaction P=0.038). It appears that VIP does not provide the signal linking cold beverage ingestion and lower skin temperature in the heat

Effects of sprint training on extrarenal potassium regulation with intense exercise in Type 1 diabetes

Effects of sprint training on plasma K+ concentration ([K+]) regulation during intense exercise and on muscle Na+-K+-ATPase were investigated in subjects with Type 1 diabetes mellitus (T1D) under real-life conditions and in nondiabetic subjects(CON). Eight subjects with T1D and seven CON undertook 7 wk of sprint cycling training. Before training, subjects cycled to exhaustion at 130% peak O2 uptake. After training, identical work was performed. Arterialized venous blood was drawn at rest, during exercise, and at recovery and analyzed for plasma glucose, [K+], Na+ concentration ([Na+]), catecholamines, insulin, and glucagon. A vastus lateralis biopsy was obtained before and after training and assayed for Na+-K+-ATPase content ([3H]ouabain binding). Pretraining, Na+-K+-ATPase content and the rise in plasma [K+] (Δ[K+]) during maximal exercise were similar in T1D and CON. However, after 60 min of recovery in T1D, plasma [K+], glucose, and glucagon/insulin were higher and plasma [Na+] was lower than in CON. Training increased Na+-K+-ATPase content and reduced Δ[K+] in both groups (P \u3c 0.05). These variables were correlated in CON (r = –0.65, P \u3c 0.05) but not in T1D. This study showed first that mildly hypoinsulinemic subjects with T1D can safely undertake intense exercise with respect to K+ regulation; however, elevated [K+] will ensue in recovery unless insulin is administered. Second, sprint training improved K+ regulation during intense exercise in both T1D and CON groups; however, the lack of correlation between plasma Δ[K+] and Na+-K+-ATPase content in T1D may indicate different relative contributions of K+-regulatory mechanisms

Skeletal muscle metabolic and ionic adaptations during intense exercise following sprint training in humans

The effects of sprint training on muscle metabolism and ion regulation during intense exercise remain controversial. We employed a rigorous methodological approach, contrasting these responses during exercise to exhaustion and during identical work before and after training. Seven untrained men undertook 7 wk of sprint training. Subjects cycled to exhaustion at 130% pretraining peak oxygen uptake before (PreExh) and after training (PostExh), as well as performing another posttraining test identical to PreExh (PostMatch). Biopsies were taken at rest and immediately postexercise. After training in PostMatch, muscle and plasma lactate (Lac−) and H+ concentrations, anaerobic ATP production rate, glycogen and ATP degradation, IMP accumulation, and peak plasma K+ and norepinephrine concentrations were reduced ( P &lt; 0.05). In PostExh, time to exhaustion was 21% greater than PreExh ( P &lt; 0.001); however, muscle Lac− accumulation was unchanged; muscle H+concentration, ATP degradation, IMP accumulation, and anaerobic ATP production rate were reduced; and plasma Lac−, norepinephrine, and H+ concentrations were higher ( P &lt; 0.05). Sprint training resulted in reduced anaerobic ATP generation during intense exercise, suggesting that aerobic metabolism was enhanced, which may allow increased time to fatigue. </jats:p