A B S T R A C TThe aim of the present study was to establish whether gastro-intestinal (GI) complaints observed during and after ultra-endurance exercise are related to gut ischaemia-associated leakage of endotoxins [lipopolysaccharide (LPS)] into the circulation and associated cytokine production. Therefore we collected blood samples from 29 athletes before, immediately after, and 1, 2 and 16 h after a long-distance triathlon for measurement of LPS, tumour necrosis factor-α and interleukin-6 (IL-6). As the cytokine response would trigger an acute-phase response, characteristic variables of these responses were also measured, along with creatine kinase (CK) to obtain an indicator of muscle damage. There was a high incidence (93 % of all participants) of GI symptoms ; 45 % reported severe complaints and 7 % of the participants abandoned the race because of severe GI distress. Mild endotoxaemia (5-15 pg/ml) was evident in 68 % of the athletes immediately after the race, as also indicated by a reduction in IgG anti-LPS levels. In addition, we observed production of IL-6 (27-fold increase immediately after the race), leading to an acutephase response (20-fold increase in C-reactive protein and 12 % decrease in pre-albumin 16 h after the race). The extent of endotoxaemia was not correlated with the GI complaints or the IL-6 response, but did show a correlation with the elevation in C-reactive protein (r s 0.389 ; P l 0.037). Creatine kinase levels were increased significantly immediately post-race, and increased further in the follow-up period. Creatine kinase levels did not correlate with those of either IL-6 or C-reactive protein. It is therefore concluded that LPS does enter the circulation after ultra-endurance exercise and may, together with muscle damage, be responsible for the increased cytokine response and hence GI complaints in these athletes.

The effect of addition of different dosages of caffeine (Caf) to a carbohydrate-electrolyte solution (CES) on metabolism, Caf excretion, and performance was examined. Subjects (n = 15) ingested 8 ml/kg of water placebo (Pla-W), 7% CES (Pla-CES), or 7% CES with 150, 225, and 320 mg/l Caf (CES-150, CES-225, and CES-320, respectively) during a warm-up protocol (20 min) and 3 ml/kg at one-third and two-thirds of a 1-h time trial. Performance was improved with Caf supplementation: 62.5 +/- 1.3, 61.5 +/- 1.1, 60.4 +/- 1.0, 58.9 +/- 1.0, and 58.9 +/- 1.2 min for Pla-W, Pla-CES, CES-150, CES-225, and CES-320, respectively. The postexercise urinary Caf concentration (range 1.3-2.5 microg/ml) was dose dependent and always far below the doping level of the International Olympic Committee (12 microg/ml) in all subjects. Sweat Caf excretion during exercise exceeded postexercise early-void urinary Caf excretion. Caffeinated CES did not enhance free fatty acid availability, ruling out the fact that performance improvement resulted from enhanced fat oxidation. It is concluded that addition of relatively low amounts of Caf to CES improves performance and that postexercise urinary Caf concentration remained low.

Fat and carbohydrate are the principal substrates that fuel aerobic ATP synthesis in skeletal muscle. Endogenous carbohydrates, mainly stored as muscle and liver glycogen, represent less than 5 % of total energy storage in an average man. The vast majority of our energy reserves is stored as fat, mainly deposited as triacylglycerol (TG) in subcutaneous and deep visceral adipose tissue. Smaller quantities of TG are present in circulating lipoprotein particles and in lipid droplets inside the muscle fibres, intramyocellular triacylglycerol (IMTG;Hoppeler et al. 1985). The latter has recently regained much attention due to the proposed functional relationship between IMTG accumulation and the development of insulin resistance (Boden et al. 2001). It is speculated that elevated free fatty acid (FFA) delivery and/or impaired FA oxidation result in intramyocellular accumulation of TG and FA metabolites, which could induce defects in the insulin signalling cascade, causing skeletal muscle insulin resistance. The progressive accumulation of IMTG in sedentary, obese and/or type 2 diabetes patients should therefore form a major therapeutic target and efforts should be made to develop interventions that prevent excess IMTG accretion by stimulating their rate of oxidation. However, the latter is complicated by the fact that information on the regulation of IMTG metabolism is scarce.Several studies applying FA isotope tracers have shown that during moderate intensity exercise ~40-60 % of total fat oxidation is accounted for by plasma derived FFA oxidation in endurance trained male subjects following an overnight fast (Romijn et al. 1993;Sidossis et al. 1998;Coyle et al. 2001;van Loon et al. 2001). This implies that other fat sources can contribute substantially to total fat oxidation during exercise. However, the relative contribution of these other fat sources to energy expenditure has been shown to depend on exercise Both stable isotope methodology and fluorescence microscopy were applied to define the use of intramuscular triglyceride (IMTG) stores as a substrate source during exercise on a whole-body as well as on a fibre type-specific intramyocellular level in trained male cyclists. Following an overnight fast, eight subjects were studied at rest, during 120 min of moderate intensity exercise (60 % maximal oxygen uptake capacity (◊J ,max )) and 120 min of post-exercise recovery. Continuous infusions of [U-13 C]palmitate and [6,6-2 H 2 ]glucose were administered at rest and during subsequent exercise to quantify whole-body plasma free fatty acid (FFA) and glucose oxidation rates and the contribution of other fat sources (sum of muscle-plus lipoprotein-derived TG) and muscle glycogen to total energy expenditure. Fibre type-specific intramyocellular lipid content was determined in muscle biopsy samples collected before, immediately after and 2 h after exercise. At rest, fat oxidation provided 66 ± 5 % of total energy expenditure, with FFA and other fat sources contributing 48 ± 6 and 17 ± 3 %, respectively. FFA oxidation r...

The purposes of this study were 1) to investigate the effect of carbohydrate (CHO) ingestion on endogenous glucose production (EGP) during prolonged exercise, 2) to study whether glucose appearance in the circulation could be a limiting factor for exogenous CHO oxidation, and 3) to investigate whether large CHO feedings can reduce muscle glycogen oxidation during exercise. Six well-trained subjects exercised three times for 120 min at 50% maximum workload while ingesting water (FAST), a 4% glucose solution (LO-Glc), or a 22% glucose solution (HI-Glc). A primed continuous intravenous [6,6-2H2]glucose infusion was given, and the ingested glucose was enriched with [U-13C]glucose. Glucose ingestion significantly elevated CHO oxidation as well as the rates of appearance (Ra) and disappearance. Ra glucose equaled Ra of glucose in gut (Ra gut) during HI-Glc, whereas EGP was completely suppressed. During LO-Glc, EGP was partially suppressed, whereas Ra gut provided most of the total glucose Ra. We conclude that 1) high rates of CHO ingestion can completely block EGP, 2) Ra gut may be a limiting factor for exogenous CHO oxidation, and 3) muscle glycogen oxidation was not reduced by large glucose feedings.

No abstract