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Departments of Pathological Biochemistry (J.M.R.G., M.J.C., C.J.P.) and Medicine (W.R.F.), Glasgow Royal Infirmary, Glasgow, Scotland G31 2ER, United Kingdom; and Department of Human Nutrition (C.M., F.T., D.M.), University of Glasgow, Glasgow, Scotland G12 8QQ, United Kingdom
Address all correspondence and requests for reprints to: Dr. Jason M. R. Gill, Division of Neuroscience and Biomedical Systems, Institute of Biomedical and Life Sciences, West Medical Building, University of Glasgow, Glasgow, G12 8QQ, United Kingdom. E-mail: j.gill{at}bio.gla.ac.uk.
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Abstract |
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Introduction |
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More recently it has become evident that endothelial function, particularly in conduit vessels, is impaired in the postprandial state, with the postprandial impairment in function related to the postprandial rise in triglyceride (TG) concentration (3, 4, 5). Recent studies have also shown that, in healthy subjects, plasma concentrations of inflammatory cytokines and adhesion molecules are increased following the ingestion of high-fat, but not high-carbohydrate, meals (6), suggesting that fat ingestion promotes a transient proinflammatory state. Impaired endothelial function and an increased level of inflammation have been implicated in the atherosclerotic disease process by a number of mechanisms and are associated with an increase in cardiovascular risk (7, 8, 9). Thus, the perturbations to metabolism occurring in the postprandial state are likely to influence atherosclerotic progression through novel nonlipid mechanistic pathways as well as the classical direct lipid and lipoprotein effects.
Trained endurance athletes and regular exercisers have low levels of postprandial lipaemia (10). However, this favorable metabolic situation is rapidly reversed when training is interrupted; stopping training for just 60 h has been reported to increase postprandial TG concentrations by over one third (11). This change in lipids is evident long before other changes associated with detraining, such as an increase in body fat or a decrease in cardiorespiratory fitness, can occur. Thus, the early detraining period provides an excellent model for studying the effects of changes in postprandial TG metabolism on endothelial function and inflammatory processes in the absence of changes to body composition that could confound the interpretation of longer-term dietary or exercise intervention studies.
The purpose of this study was therefore to determine the effects of a 7-d detraining period on postprandial lipid metabolism, vascular function and inflammation in endurance-trained men. This would increase understanding about the interrelationships between metabolism, vascular function, and inflammation in the postprandial state.
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Subjects and Methods |
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Eight endurance-trained men aged 27.8 ± 12.1 yr (mean ± SD), with body mass index 23.6 ± 1.0 kg/m-2, waist circumference 79.3 ± 4.1 cm, and percentage body fat [estimated from the sum of bicep, tricep, subscapular, and suprailiac skinfolds (12)] 16.9 ± 3.2% volunteered to participate in this study. Three were distance runners, two were triathletes, two were swimmers, and one was a cyclist. They had been training regularly for 4–10 yr and typically performed 4–8 h of endurance training per week. Six subjects competed regularly at regional or national level, and the other two participants were serious recreational athletes. All were apparently healthy normotensive nonsmokers, and none was taking any drug therapies. The study was conducted with the approval of North Glasgow University Hospitals National Health Service Trust Ethics Committee and subjects gave written informed consent before participation.
Study design
Each subject participated in two oral fat tolerance tests; one during a period of normal training, the other immediately following 1 wk of detraining. Subjects were requested to maintain their normal training program during the week leading up to their first fat tolerance test (trained state), ensuring that they trained on the day preceding the test, and keep a training diary during this week. Subjects then refrained from all training until their second fat tolerance test 1 wk later (detrained state). Subjects weighed and recorded their dietary intake and refrained from alcohol consumption for the 2 d preceding their oral fat tolerance test in the trained state and replicated this intake during the 2 d preceding their test in the detrained state.
On the morning of the oral fat tolerance tests, subjects reported to the laboratory between 0800 and 0900 h after a 12-h fast. Forearm microvascular function was assessed using laser Doppler imaging with iontophoresis (see Assessment of microvascular function for description). A venous cannula was then inserted and, after an interval of 10 min, a baseline blood sample was obtained. Subjects then consumed a high-fat test meal comprising whipping cream, fruit, cereal, nuts, and chocolate that provided 80 g fat, 80 g carbohydrate, 11.4 g protein, and 4.5 MJ energy. Further blood samples were obtained 30, 60, 90, 120, 240, and 360 min after completion of the meal. Microvascular function was assessed again 4 h postprandially to coincide with maximal plasma TG concentrations. Subjects rested throughout this day and consumed only water. This was provided ad libitum during the test in the trained state, and water intake was replicated during the trial in the detrained state.
Assessment of microvascular function
Microvascular function was assessed using laser Doppler imaging to quantify vasodilator responses to iontophoresis of acetylcholine (ACh, endothelium dependent) and sodium nitroprusside (SNP, endothelium independent). This method has been validated and described in detail previously (13, 14). Subjects lay in a semirecumbent position in a temperature-controlled room, with their noncannulated forearm supported by an armrest. Perspex iontophoresis chambers (ION 6, Moor Instruments Ltd., Axminster, UK) were attached to the volar aspect of the forearm and 1% solutions of ACh and SNP introduced into the anodal and cathodal chambers, respectively. Drug delivery was achieved using a constant-current iontophoresis controller (MIC-1ev; Moor Instruments Ltd.) with current increasing incrementally from 5–20 µA, providing a total charge of 8 mC. Voltage across the chambers was measured to enable calculation of the electrical resistance of the skin. Noninvasive measurement of skin perfusion was performed using a laser Doppler imager (Moor Instruments Ltd.) equipped with a red laser, positioned 30 cm above the chambers. The laser was scanned in a raster fashion over both chambers and the backscattered light was converted into a signal proportional to perfusion in arbitrary perfusion (flux) units. Twenty repetitive scans, each taking 50 sec, were performed; a control scan with no current, 14 scans during the incremental iontophoresis protocol, and five further scans with no current administration. For each scan, median flux values within each chamber were determined using the imager manufacturer’s image analysis software. Perfusion values were corrected for variation in skin resistance (13) and the area under the corrected flux vs. time curve over the 20 scans was defined as the microvascular response. The within-day and between-day coefficients of variation for this method are both less than 10% (13).
Analytical procedures
Blood samples were collected into potassium EDTA tubes and lithium heparin tubes (BD Vacutainer Systems, Becton, Dickinson, and Co., Plymouth, UK) and placed on ice. Plasma was separated within 15 min of collection. Plasma for lipoprotein analyses (EDTA) was stored at 4 C, and the remainder was divided into aliquots and stored at -70 C.
Plasma very LDL (VLDL) cholesterol, LDL cholesterol, and HDL cholesterol concentrations were determined in the fasted state according to the Lipid Research Clinics Program Manual of Laboratory Operations (15). Chylomicron (Sf > 400) and VLDL (Sf 
20–400) lipoproteins were isolated from plasma collected in the fasted and postprandial states using sequential density-flotation ultracentrifugation (16). TG and cholesterol was determined the chylomicron and VLDL fractions, as well as in whole plasma using commercially available enzymatic colorimetric kits (Roche Diagnostics Corp., Lewes, UK). Apolipoprotein B (apo B) was determined in the VLDL fraction and whole plasma using a commercially available immunoturbidimetric kit (chylomicron apo B was not determined as concentrations were too low to be detected by this method) (Roche Diagnostics Corp.). It is recognized that the VLDL fraction in postprandial samples will include some small chylomicron particles.
Glucose and nonesterified fatty acid (NEFA) concentrations were determined in EDTA plasma by enzymatic colorimetric methods using commercially available kits (Roche Diagnostics GmbH, Mannheim, Germany and Wako Chemicals USA, Inc., Richmond, VA). Insulin was analyzed in lithium heparin plasma by an in-house immunoradiometric assay using a radiolabeled mouse monoclonal antiinsulin and solid phase guinea pig antiinsulin (both antibodies supplied by Scottish Antibody Production Unit) (17). Concentrations of soluble intracellular adhesion molecule-1, soluble vascular cell adhesion molecule-1, IL-6, and TNF-
were determined in EDTA plasma using commercially available ELISAs (R&D Systems Inc., Oxon, UK). High-sensitivity assays were used for IL-6 and TNF-. Other than lipoprotein analyses, which were performed on fresh plasma, all samples for each subject were analyzed in the same run. Coefficients of variation were less than 5% for all non-ELISAs and less than 10% all for ELISAs.
Data analysis
The time-averaged postprandial concentration—defined as the trapezium rule-derived area under the plasma or lipoprotein fraction concentration vs. time curve, divided by the duration of postprandial observation period (6 h)—was used as a summary measure of the postprandial responses. The postprandial rise in concentration was defined as the time-averaged postprandial concentration minus the fasting concentration (i.e. the incremental area under the concentration vs. time curve, divided by 6 h). NEFA suppression was calculated by subtracting the lowest postprandial NEFA concentration (usually 1 h postprandial) from the fasting NEFA concentration. The number of TG molecules per apo B containing particle in the VLDL fraction was calculated by converting apo B concentrations to mmol/liter-1 and dividing the VLDL TG concentration by the VLDL apo B concentration. Homeostasis model assessment was used as a validated surrogate index of insulin sensitivity (18). Fasting plasma concentrations and summary postprandial responses were compared using paired Student’s t tests. Two-way ANOVA with repeated measures on both factors and post hoc least significant difference tests were used to determine changes in variables with time during each trial and differences between the two trials. Data for TG and TNF- concentrations and for microvascular function were normalized by logarithmic transformation before statistical analysis. Significance was accepted at the P < 0.05 level and data are presented as mean ± SEM unless otherwise stated.
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Results |
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Fasting plasma TG concentrations increased by 35% with detraining (P = 0.002), with the majority of this increase accounted for by a 50% rise in VLDL TG concentrations (P = 0.001) (see Fig. 1
). VLDL apo B increased by 25% with detraining (trained, 3.04 ± 0.52 mg/dl-1; detrained, 3.79 ± 0.32 mg/dl-1, P = 0.03), but total apo B (trained, 63.9 ± 5.3 mg/dl-1; detrained, 62.8 ± 4.9 mg/dl-1, P = 0.69), LDL cholesterol [trained, 87 ± 9 mg/dl-1 (2.26 ± 0.24 mmol/liter-1); detrained, 85 ± 7 mg/dl-1 (2.20 ± 0.19 mmol/liter-1), P = 0.73] and HDL cholesterol [trained, 48 ± 2 mg/dl-1 (1.24 ± 0.06 mmol/liter-1); detrained, 46 ± 4 mg/dl-1 (1.18 ± 0.10 mmol/liter-1), P = 0.23] were not significantly altered by the training cessation. Fasting insulin concentrations increased by 39% with detraining (P = 0.03); fasting glucose concentrations were unchanged (P = 0.74) (see Fig. 1 for both). Homeostasis model assessment-estimated insulin resistance increased significantly with detraining (trained, 0.91 ± 0.08; detrained, 1.28 ± 0.14, P = 0.03). Fasting NEFA concentrations were 50% lower in the detrained state compared with the trained state (P = 0.0009) (Fig. 1). Fasting concentrations of IL-6 and TNF- did not differ significantly between the two conditions, although TNF- tended to be higher in the detrained state (P = 0.10) (see Fig. 2).
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Both the time-averaged postprandial plasma TG concentration [trained, 123 ± 17 mg/dl-1 (1.39 ± 0.19 mmol/liter-1); detrained, 188 ± 21 mg/dl-1 (2.12 ± 0.24 mmol/liter-1), P = 0.002] and the postprandial rise in plasma TG [trained, 55 ± 12 mg/dl-1 (0.62 ± 0.13 mmol/liter-1); detrained, 93 ± 14 mg/dl-1 (1.05 ± 0.16 mmol/liter-1), P = 0.004] increased significantly with detraining (see Fig. 1
). This was accounted for by significantly higher time-averaged postprandial chylomicron TG [trained, 35 ± 9 mg/dl-1 (0.40 ± 0.10 mmol/liter-1); detrained, 59 ± 9 mg/dl-1 (0.67 ± 0.10 mmol/liter-1), P = 0.02] and VLDL TG concentrations [trained, 50 ± 8 mg/dl-1 (0.57 ± 0.09 mmol/liter-1); detrained, 76 ± 10 mg/dl-1 (0.86 ± 0.11 mmol/liter-1), P = 0.005] in the detrained condition, although the postprandial rise in VLDL TG concentration did not differ significantly between the trained and detrained conditions [trained, 15 ± 2 mg/dl-1 (0.17 ± 0.04 mmol/liter-1); detrained, 23 ± 5 mg/dl-1 (0.26 ± 0.06 mmol/liter-1), P = 0.10] (see Fig. 2). Time-averaged postprandial VLDL apo B concentrations (trained, 3.35 ± 0.52 mg/dl-1; detrained, 4.21 ± 0.32 mg/dl-1, P = 0.02) and molecules of TG per apo B-containing VLDL particle (trained, 8728 ± 648; detrained, 10316 ± 996, P = 0.02) were also significantly higher in the detrained than the trained condition, implying detraining-induced increases in both the number of VLDL particles and the amount of TG contained in each VLDL particle. Time-averaged postprandial total apo B concentrations did not differ between the trained and detrained conditions (trained, 64.1 ± 5.0 mg/dl-1; detrained, 63.3 ± 4.8 mg/dl-1, P = 0.76).
Both the time-averaged postprandial insulin concentration (trained, 12.3 ± 1.1 µU/ml-1; detrained, 17.0 ± 1.3 µU/ml-1, P = 0.003) and the postprandial rise in insulin concentration (trained, 8.2 ± 1.0 µU/ml-1; detrained, 11.3 ± 1.0 µU/ml-1, P = 0.01) increased markedly with detraining, but there was no difference between trials in either the time-averaged postprandial glucose concentration (P = 0.80) or the postprandial rise in glucose concentration (P = 0.66) (see Fig. 1). The postprandial suppression of plasma NEFA was reduced with detraining [trained, 0.34 ± 0.07 mEq/liter-1; detrained, 0.15 ± 0.05 mEql/liter-1, P = 0.0009 (1 mEq/liter-1 
1 mmol/liter-1)] although the time-averaged postprandial NEFA concentration was lower (trained, 0.39 ± 0.04 mEq/liter-1; detrained, 0.15 ± 0.05 mEq/liter-1, P = 0.02) in the detrained state compared with the trained state (Fig. 1).
Inflammatory and adhesion molecule response to the test meal
Plasma concentrations of IL-6 increased linearly during the postprandial period with values at 4 and 6 h being significantly higher than fasting values in both the trained and detrained conditions (P < 0.01). There were, however, no differences between the two trials for either the time-averaged postprandial IL-6 concentration or the postprandial rise in IL-6 concentration. There was no significant postprandial change in TNF- concentrations in either trial; however, the time-averaged postprandial TNF- concentration was 35% higher in the detrained trial than the trained trial (trained, 1.05 ± 0.08 pg/ml-1; detrained, 1.42 ± 0.13 pg/ml-1, P = 0.02). Concentrations of soluble intracellular adhesion molecule-1 and soluble vascular cell adhesion molecule-1 did not differ between the trained and detrained conditions in either the fasted or the postprandial state and did not change significantly following ingestion of the test meal in either trial (data not shown).
Microvascular responses to ACh and SNP in the fasted state and after ingestion of the test meal
Figure 3 shows the skin perfusion responses to iontophoresis of ACh and SNP, in the fasted state and 4 h postprandially in the two experimental trials. These data are presented as flux vs. cumulative charge, essentially a cumulative dose-response relationship as increasing charge leads to increasing drug delivery with consequentially greater skin perfusion. In both the trained and detrained trials, the ACh response (i.e. area under the flux vs. time curve) was significantly lower in the postprandial state compared with the fasted state [by 17% (P = 0.03) and 22% (P = 0.03) respectively], but neither the fasting (trained, 17414 ± 1985 U; detrained, 18717 ± 2708 U, not significant) nor the postprandial (trained, 14390 ± 2613 U; detrained, 14617 ± 2508 U, not significant) ACh responses differed significantly between the trained and detrained trials. There were no significant differences in the SNP responses between the fasted and postprandial states or between the trained and detrained trials.
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Discussion |
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The values for the fasting and postprandial ACh responses in the present subjects were 40–50% higher than those seen in nonsmoking untrained men of similar age and body mass index studied in our laboratory [untrained men (n = 7) age 35.7 ± 2.3 yr, body mass index 25.0 ± 1.6 kg/m-2, fasting ACh response: 12,459 ± 1,363 U; postprandial ACh response, 9,961 ± 2,348 U (Gill, J. M. R., and W. R. Ferrell, unpublished data)]. However, whereas values for the postprandial plasma TG concentration in the present subjects were low in the trained condition, their postprandial TG concentrations after 1 wk of detraining were comparable to those seen in our studies of untrained middle-aged men (19), emphasizing the acute nature of exercise-induced changes to TG metabolism.
Release of nitric oxide (NO), and other vasodilator substances, from the vascular endothelium plays an important role in the regulation of vascular tone and impairment of this process is associated with atherosclerotic progression (9). It is probable that the decrement in endothelial function following fat ingestion results from a disruption of this pathway but the precise mechanism responsible has not been elucidated. One suggestion is that postprandial lipoproteins, particularly remnants of chylomicrons and VLDL, induce oxygen radical generation at the endothelial surface quenching NO, thereby reducing its bioavailability (8). In addition, postprandial lipoproteins and their remnants can penetrate the endothelial barrier (20), where they are cytotoxic (21) and thus may directly promote endothelial damage. However, it is also likely that other nonlipoprotein changes to metabolism occurring after fat ingestion could contribute to the postprandial impairment endothelial function. Some of these possibilities are discussed below.
Detraining induced two complementary shifts to TG metabolism: increasing the fasting TG concentrations, and augmenting the postprandial rise in TG concentration seen following meal ingestion. The former change was largely due to increases in VLDL (Sf 20–400) particles, whereas the latter effect was predominantly the result of increases in large chylomicron (Sf > 400) particles—there was no significant effect of detraining on the postprandial rise in VLDL TG. The fact that increasing the postprandial concentration of chylomicron TG by over two thirds did not influence the postprandial decrement in endothelial function is consistent with the observation that nascent chylomicron particles are too large to directly interact with the vascular wall (20). Thus, although fat ingestion appears to be necessary to induce postprandial endothelial dysfunction—as ingestion of a low-fat meal does not seem to induce this effect (3)—it seems likely that factors other than the influx of large lipoprotein particles, which accounts for the majority of the postprandial rise in TG, mediate this effect.
Postprandial changes to VLDL could conceivably have contributed to the postprandial decrement in endothelial function. Concentrations of TG and apo B in the VLDL fraction increased postprandially and, like the postprandial change in endothelial function, did not differ between the trained and detrained states. This is consistent with reports that postprandial increases in remnant-like lipoprotein particles—which fall into the VLDL density range—contribute to postprandial endothelial dysfunction (22). However, changes in VLDL cannot fully explain the results on endothelial function seen in the present study; detraining increased VLDL TG concentrations by 50% in the fasted state, yet did not influence fasting endothelial function.
Both exercise training and meal ingestion induce a number of integrated changes to metabolism—influencing glucose, fatty acid, and insulin, as well as lipoprotein concentrations—and it has been suggested that NEFA (23) and glucose (24) can impair, and insulin (23) can facilitate, endothelial function. Whereas NEFA, glucose, and insulin concentrations measured 4 h postprandially were similar in the trained and detrained conditions (see Fig. 1) and thus, probably unlikely to have influenced postprandial endothelial function differently between the two experimental trials, significant differences in fasting insulin and NEFA concentrations existed between the trained and detrained conditions. The net effect on endothelial function of the detraining-induced increase in fasting insulin is difficult to interpret as this increase in concentration probably reflects a decrease in insulin sensitivity. Thus, the potential vasodilator effect of a higher insulin concentration would likely be offset by altered insulin signaling within the vascular wall (e.g. decreased activation of the phosphatidyl 3-kinase pathway) reducing effectiveness of insulin to mediate NO release (23). Interestingly, detraining decreased fasting NEFA concentrations despite increasing concentrations of lipoprotein TG. This altered relationship between circulating concentrations of lipoprotein TG and NEFA is noteworthy, as in a number of circumstances which lead to elevated TG concentrations, such as insulin resistance or obesity, there is a parallel elevation in NEFA concentrations (25). The higher fasting NEFA concentrations in the trained state probably reflect a combination of increased spill-over into the circulation of fatty acids released from lipoproteins following the action of lipoprotein lipase and increased hormone-sensitive lipase-mediated release of fatty acids from adipose tissue stores (26). This is desirable for the regulation of body mass as it serves to direct fatty acids away from away from long-term storage in adipose tissue toward other tissues, such as skeletal muscle, for oxidation and to replenish depleted substrate stores. However, it is conceivable that these elevated fasting NEFA concentrations in the trained state may impair endothelial function through direct effects on the endothelial NO system (23) or indirectly by increasing the toxicity of VLDL to endothelial cells (27). This could potentially offset any training-induced vascular benefits resulting from lower fasting lipoprotein TG concentrations or increased insulin sensitivity.
It has recently been reported that circulating concentrations of inflammatory cytokines, adhesion molecules, and neutrophils increase following fat ingestion (6, 28), and this may contribute to the functional impairment of endothelium-dependent dilatation observed postprandially as increased inflammatory activity has been implicated as a cause of endothelial dysfunction (28, 29, 30). In the present study we observed a marked postprandial elevation in IL-6 concentrations, and this may have contributed to the postprandial decrement in endothelial function as IL-6 is one of a number of cytokines shown to impair the integrity and function of the endothelium (29, 30, 31). Concentrations of IL-6 did not differ between the trained and detrained conditions in accord with our finding that the postprandial decrement in endothelial function was similar in both conditions. Thus, we could speculate that changes to circulating concentrations of inflammatory cytokines, such as IL-6, rather than direct effects of TG-rich lipoproteins, might mediate the postprandial endothelial dysfunction observed following fat ingestion. There is some indirect support for this concept in the literature. Coingestion of antioxidant vitamins with fat, which abolishes the postprandial decrement in endothelial function seen when fat is ingested alone (32, 33), also virtually eliminates the postprandial increase in cytokine concentrations seen following fat ingestion (6). This postulated interrelationship between fat ingestion, cytokine production, and endothelial function clearly warrants further investigation.
Although IL-6 is released from a number of cell types (34), it seems likely that adipose tissue contributed to the postprandial rise in plasma IL-6 concentrations as the cytokine is released in large amounts from adipose tissue in vivo (35), and its concentration in adipose tissue interstitial fluid is increased postprandially (36). By contrast, TNF- is not released into the circulation by sc adipose tissue (35) or significantly increased in adipose tissue interstitial fluid following meal ingestion (36), in line with our present findings showing no postprandial elevation in TNF-. However, although IL-6 release from adipose tissue is likely to have contributed to the postandial rise in systemic IL-6 concentrations, it should be noted that IL-6 is also released by the endothelial cells (37); thus, the postprandial increase in IL-6 may, to some extent, simply reflect endothelial activation and therefore be a consequence as well as a cause of the observed postprandial decrement in endothelial function. It has also recently been demonstrated that IL-6 is produced and released into the circulation by exercising muscle (38); however, this seems unlikely to have been a major contributor to the postprandial rise in circulating IL-6 in the present study as concentrations did not differ between the trained state, when subjects had recently exercised, and the detrained state, when subjects had not exercised for 1 wk.
Interestingly, plasma concentrations of the proinflammatory cytokine TNF were higher in the detrained than the trained state, suggesting that regular training has an antiinflammatory effect. This was evident despite the subjects being in heavy training during the test undertaken in the trained state and thus probably exhibiting some degree of inflammatory muscle soreness and damage. Whereas others have shown that programs of endurance training can reduce plasma concentrations of TNF (39, 40), this study adds to the literature by revealing that, even in trained athletes, this antiinflammatory effect diminishes rapidly with exercise cessation. Thus, in common with effects on lipoprotein metabolism and insulin sensitivity, beneficial effects of exercise training on inflammatory processes may be relatively short-lived, further highlighting the importance of frequent exercise to maximize potential health benefits.
In the present study, we assessed endothelial function in the cutaneous microcirculation using the novel technique of laser Doppler imaging with iontophoresis. This well-tolerated and noninvasive method assesses resistance vessel function and therefore differs from a number of previous reports which have shown that fat ingestion impairs flow-mediated dilatation-assessed endothelial function in conduit vessels (3, 4, 5). The evidence suggesting that resistance vessel endothelial function—assessed using invasive venous occlusion plethysmography—is impaired following fat ingestion is much more limited (41), and findings on this have been inconsistent (42, 43). Our findings therefore add important information to the literature, demonstrating that endothelial function in the resistance vasculature is impaired following fat ingestion and that this can be assessed using a simple, noninvasive method.
In conclusion, this study confirms previous reports demonstrating that ingestion of a high-fat meal induces transient endothelial dysfunction. However, our findings suggest that factors other the postprandial rise in TG are responsible for this effect as 1 wk of detraining—which induced a substantial increase in postprandial lipemia in these endurance-trained men—did not alter the effects of fat ingestion on endothelial function. Thus, interventions that alter TG metabolism do not necessarily have a concomitant effect on endothelial function.
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Footnotes |
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Received February 12, 2003.
Accepted May 29, 2003.
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References |
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, in vivo. J Clin Endocrinol Metab 82:4196–4200 system and insulin sensitivity during an exercise training program in obese women with normal and impaired glucose tolerance. Eur J Endocrinol 145:273–280[Abstract]
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