Exercise, type 1 diabetes mellitus and blood glucose: The implications of exercise timing.

The scientific literature shows that exercise has many benefits for individuals with type 1 diabetes. Yet, several barriers to exercise in this population exist, such as post-exercise hypoglycaemia or hyperglycaemia. Several studies suggest that the timing of exercise may be an important factor in preventing exercise-induced hypoglycaemia or hyperglycaemia. However, there is a paucity of evidence solely focused on summarising findings regarding exercise timing and the impact it has on glucose metabolism in type 1 diabetes. This report suggests that resistance or high-intensity interval exercise/training (often known as HIIT) may be best commenced at the time of day when an individual is most likely to experience a hypoglycaemic event (i.e., afternoon/evening) due to the superior blood glucose stability resistance and HIIT exercise provides. Continuous aerobic-based exercise is advised to be performed in the morning due to circadian elevations in blood glucose at this time, thereby providing added protection against a hypoglycaemic episode. Ultimately, the evidence concerning exercise timing and glycaemic control remains at an embryonic stage. Carefully designed investigations of this nexus are required, which could be harnessed to determine the most effective, and possibly safest, time to exercise for those with type 1 diabetes.

Oxidative Stress and Exercise.

It is now well-established that regular moderate-intensity exercise training can activate salient cell adaptive properties, leading to a state of oxidative eustress [...].

Circadian Clocks, Redox Homeostasis, and Exercise: Time to Connect the Dots?

Compelling research has documented how the circadian system is essential for the maintenance of several key biological processes including homeostasis, cardiovascular control, and glucose metabolism. Circadian clock disruptions, or losses of rhythmicity, have been implicated in the development of several diseases, premature ageing, and are regarded as health risks. Redox reactions involving reactive oxygen and nitrogen species (RONS) regulate several physiological functions such as cell signalling and the immune response. However, oxidative stress is associated with the pathological effects of RONS, resulting in a loss of cell signalling and damaging modifications to important molecules such as DNA. Direct connections have been established between circadian rhythms and oxidative stress on the basis that disruptions to circadian rhythms can affect redox biology, and vice versa, in a bi-directional relationship. For instance, the expression and activity of several key antioxidant enzymes (SOD, GPx, and CAT) appear to follow circadian patterns. Consequently, the ability to unravel these interactions has opened an exciting area of redox biology. Exercise exerts numerous benefits to health and, as a potent environmental cue, has the capacity to adjust disrupted circadian systems. In fact, the response to a given exercise stimulus may also exhibit circadian variation. At the same time, the relationship between exercise, RONS, and oxidative stress has also been scrutinised, whereby it is clear that exercise-induced RONS can elicit both helpful and potentially harmful health effects that are dependent on the type, intensity, and duration of exercise. To date, it appears that the emerging interface between circadian rhythmicity and oxidative stress/redox metabolism has not been explored in relation to exercise. This review aims to summarise the evidence supporting the conceptual link between the circadian clock, oxidative stress/redox homeostasis, and exercise stimuli. We believe carefully designed investigations of this nexus are required, which could be harnessed to tackle theories concerned with, for example, the existence of an optimal time to exercise to accrue physiological benefits.

"Take My Bone Away?" Hypoxia and bone: A narrative review.

To maintain normal cellular and physiological function, sufficient oxygen is required. Recently, evidence has suggested that hypoxia, either pathological or environmental, may influence bone health. It appears that bone cells are distinctly responsive to hypoxic stimuli; for better or worse, this is still yet to be elucidated. Hypoxia has been shown to offer potentially therapeutic effects for bone by inducing an osteogenic-angiogenic response, although, others have noted excessive osteoclastic bone resorption instead. Much evidence suggests that the hypoxic-inducible pathway is integral in mediating the changes in bone metabolism. Furthermore, many factors associated with hypoxia including changes in energy metabolism, acid-base balance and the increased generation of reactive oxygen species, are known to influence bone metabolism. This review aims to examine some of the putative mechanisms responsible for hypoxic-induced alterations of bone metabolism, with regard to osteoclasts and osteoblasts, both positive and negative.

DNA Damage Following Acute Aerobic Exercise: A Systematic Review and Meta-analysis.

BACKGROUND: Exercise is widely recognised for its health enhancing benefits. Despite this, an overproduction of reactive oxygen and nitrogen species (RONS), outstripping antioxidant defence mechanisms, can lead to a state of (chronic) oxidative stress. DNA is a vulnerable target of RONS attack and, if left unrepaired, DNA damage may cause genetic instability. OBJECTIVE: This meta-analysis aimed to systematically investigate and assess the overall effect of studies reporting DNA damage following acute aerobic exercise. METHODS: Web of Science, PubMed, MEDLINE, EMBASE, and Scopus were searched until April 2019. Outcomes included (1) multiple time-points (TPs) of measuring DNA damage post-exercise, (2) two different quantification methods (comet assay and 8-oxo-2'-deoxyguanosine; 8-OHdG), and (3) protocols of high intensity (≥ 75% of maximum rate of oxygen consumption; VO2-max) and long distance (≥ 42 km). RESULTS: Literature search identified 4316 non-duplicate records of which 35 studies were included in the meta-analysis. The evidence was strong, showcasing an increase in DNA damage immediately following acute aerobic exercise with a large-effect size at TP 0 (0 h) (SMD = 0.875; 95% CI 0.5, 1.25; p < 0.05). When comparing between comet assay and 8-OHdG at TP 0, a significant difference was observed only when using the comet assay. Finally, when isolating protocols of long-distance and high-intensity exercise, increased DNA damage was only observed in the latter. (SMD = 0.48; 95% CI - 0.16, 1.03; p = 0.15 and SMD = 1.18; 95% CI 0.71, 1.65; p < 0.05 respectively). CONCLUSIONS: A substantial increase in DNA damage occurs immediately following acute aerobic exercise. This increase remains significant between 2 h and 1 day, but not within 5-28 days post-exercise. Such an increase was not observed in protocols of a long-distance. The relationship between exercise and DNA damage may be explained through the hormesis theory, which is somewhat one-dimensional, and thus limited. The hormesis theory describes how exercise modulates any advantageous or harmful effects mediated through RONS, by increasing DNA oxidation between the two end-points of the curve: physical inactivity and overtraining. We propose a more intricate approach to explain this relationship: a multi-dimensional model, to develop a better understanding of the complexity of the relationship between DNA integrity and exercise.

Correction to: DNA Damage Following Acute Aerobic Exercise: A Systematic Review and Meta-analysis.

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Preceding exercise and postprandial hypertriglyceridemia: effects on lymphocyte cell DNA damage and vascular inflammation.

BACKGROUND: Exercise has proved effective in attenuating the unfavourable response normally associated with postprandial hypertriglyceridemia (PHTG) and accompanying oxidative stress. Yet, the acute effects of prior exercise and PHTG on DNA damage remains unknown. The purpose of this study was to examine if walking alters PHTG-induced oxidative damage and the interrelated inflammatory mechanisms. METHODS: Twelve apparently healthy, recreationally active, male participants (22.4 ± 4.1 years; 179.2 ± 6 cm; 84.2 ± 14.7 kg; 51.3 ± 8.6 ml·kg- 1·min- 1) completed a randomised, crossover study consisting of two trials: (1) a high-fat meal alone (resting control) or (2) a high-fat meal immediately following 1 h of moderate exercise (65% maximal heart rate). Venous blood samples were collected at baseline, immediately post-exercise or rest, as well as at 2, 4 and 6 h post-meal. Biomarkers of oxidative damage (DNA single-strand breaks, lipid peroxidation and free radical metabolism) and inflammation were determined using conventional biochemistry techniques. RESULTS: DNA damage, lipid peroxidation, free radical metabolism and triglycerides increased postprandially (main effect for time, p < 0.05), regardless of completing 1 h of preceding moderate intensity exercise. Plasma antioxidants (α-tocopherol and γ-tocopherol) also mobilised in response to the high-fat meal (main effect for time, p < 0.05), but no changes were detected for retinol-binding protein-4. CONCLUSION: The ingestion of a high fat meal induces postprandial oxidative stress, inflammation and a rise in DNA damage that remains unaltered by one hour of preceding exercise.

Metabolomic Response to Acute Hypoxic Exercise and Recovery in Adult Males.

Metabolomics is a relatively new "omics" approach used to characterize metabolites in a biological system at baseline and following a diversity of stimuli. However, the metabolomic response to exercise in hypoxia currently remains unknown. To examine this, 24 male participants completed 1 h of exercise at a workload corresponding to 75% of pre-determined O2max in hypoxia (Fio2 = 0.16%), and repeated in normoxia (Fio2 = 0.21%), while pre- and post-exercise and 3 h post-exercise metabolites were analyzed using a LC ESI-qTOF-MS untargeted metabolomics approach in serum samples. Exercise in hypoxia and in normoxia independently increased metabolism as shown by a change in a combination of twenty-two metabolites associated with lipid metabolism (p < 0.05, pre vs. post-exercise), though hypoxia per se did not induce a greater metabolic change when compared with normoxia (p > 0.05). Recovery from exercise in hypoxia independently decreased seventeen metabolites associated with lipid metabolism (p < 0.05, post vs. 3 h post-exercise), compared with twenty-two metabolites in normoxia (p < 0.05, post vs. 3 h post-exercise). Twenty-six metabolites were identified as responders to exercise and recovery (pooled hypoxia and normoxia pre vs. recovery, p < 0.05), including metabolites associated with purine metabolism (adenine, adenosine and hypoxanthine), the amino acid phenylalanine, and several acylcarnitine molecules. Our novel data provides preliminary evidence of subtle metabolic differences to exercise and recovery in hypoxia and normoxia. Specifically, exercise in hypoxia activates metabolic pathways aligned to purine and lipid metabolism, but this effect is not selectively different from exercise in normoxia. We also show that exercise per se can activate pathways associated with lipid, protein and purine nucleotide metabolism.

Extremely short duration interval exercise improves 24-h glycaemia in men with type 2 diabetes.

PURPOSE: Reduced-exertion high-intensity interval training (REHIT) is a genuinely time-efficient exercise intervention that improves aerobic capacity and blood pressure in men with type 2 diabetes. However, the acute effects of REHIT on 24-h glycaemia have not been examined. METHODS: 11 men with type 2 diabetes (mean ± SD: age, 52 ± 6 years; BMI, 29.7 ± 3.1 kg/m2; HbA1c, 7.0 ± 0.8%) participated in a randomised, four-trial crossover study, with continual interstitial glucose measurements captured during a 24-h dietary-standardised period following either (1) no exercise (CON); (2) 30 min of continuous exercise (MICT); (3) 10 × 1 min at ~ 90 HRmax (HIIT; time commitment, ~ 25 min); and (4) 2 × 20 s 'all-out' sprints (REHIT; time commitment, 10 min). RESULTS: Compared to CON, mean 24-h glucose was lower following REHIT (mean ± 95%CI: - 0.58 ± 0.41 mmol/L, p = 0.008, d = 0.55) and tended to be lower with MICT (- 0.37 ± 0.41 mmol/L, p = 0.08, d = 0.35), but was not significantly altered following HIIT (- 0.37 ± 0.59 mmol/L, p = 0.31, d = 0.35). This seemed to be largely driven by a lower glycaemic response (area under the curve) to dinner following both REHIT and MICT (- 11%, p < 0.05 and d > 0.9 for both) but not HIIT (- 4%, p = 0.22, d = 0.38). Time in hyperglycaemia appeared to be reduced with all three exercise conditions compared with CON (REHIT: - 112 ± 63 min, p = 0.002, d = 0.50; MICT: -115 ± 127 min, p = 0.08, d = 0.50; HIIT - 125 ± 122 min, p = 0.04, d = 0.54), whilst indices of glycaemic variability were not significantly altered. CONCLUSION: REHIT may offer a genuinely time-efficient exercise option for improving 24-h glycaemia in men with type 2 diabetes and warrants further study.

The acute effects of walking exercise intensity on systemic cytokines and oxidative stress.

PURPOSE: Oxidative stress is associated with tissue cytokine secretion although the precise mechanism(s) underpinning this relationship during high intensity intermittent exercise remains unclear. This study investigates the acute response to a bout of high intensity intermittent walking (HIIW), compared to continuous moderate intensity walking (CMW), on various cytokines and biomarkers of oxidative stress. METHODS: Seventeen (n = 17) apparently healthy male participants (aged 22.6 ± 4.6 years; [Formula: see text]: 53.7 ± 7.1 ml kg-1 min-1) undertook a randomised crossover study consisting of two exercise trials: (1) HIIW requiring 3 × 5 min bursts at 80% [Formula: see text] (each separated by 5 min of walking at 30% [Formula: see text]) and (2) CMW (60% [Formula: see text] for 30 min). Each trial was separated by 7 days. Venous blood samples were obtained pre-exercise, post-exercise and at 2, 4, 24 and 48 h post-exercise for determination of systemic inflammation (IL-6 and TNF-α), lipid soluble antioxidants and oxidative stress (LOOH, H2O2 and the ascorbyl free radical). RESULTS: Both IL-6 and TNF-α increased immediately post exercise, regardless of intensity and remained elevated until at least 4 h (main effect for time; p < 0.05). While there was no change in either lipid peroxidation or free radical metabolism (Asc· and H2O2), α-tocopherol increased (pooled HIIW and CMW, p < 0.05), whereas lycopene decreased at 2 h post HIIW (p < 0.05). CONCLUSION: Bouts of both HIIW and CMW promote cytokine secretion post exercise, and this seems to be independent of oxidative stress. Further investigation is required to assess how such changes may underpin some of the transient health benefits of exercise.

Effects of Exercise Intensity on Postexercise Endothelial Function and Oxidative Stress.

PURPOSE: To measure endothelial function and oxidative stress immediately, 90 minutes, and three hours after exercise of varying intensities. METHODS: Sixteen apparently healthy men completed three exercise bouts of treadmill running for 30 minutes at 55% V̇O(2max) (mild); 20 minutes at 75% V̇O(2max) (moderate); or 5 minutes at 100% V̇O(2max) (maximal) in random order. Brachial artery flow-mediated dilation (FMD) was assessed with venous blood samples drawn for measurement of endothelin-1 (ET-1), lipid hydroperoxides (LOOHs), and lipid soluble antioxidants. RESULTS: LOOH increased immediately following moderate exercise (P < 0.05). ET-1 was higher immediately after exercise and 3 hours after exercise in the mild trial compared to maximal one (P < 0.05). Transient decreases were detected for ΔFMD/Shear(AUC) from baseline following maximal exercise, but it normalised at 3 hours after exercise (P < 0.05). Shear rate was higher immediately after exercise in the maximal trial compared to mild exercise (P < 0.05). No changes in baseline diameter, peak diameter, absolute change in diameter, or FMD were observed following any of the exercise trials (P > 0.05). CONCLUSIONS: Acute exercise at different intensities elicits varied effects on oxidative stress, shear rate, and ET-1 that do not appear to mediate changes in endothelial function measured by FMD.

A Systematic Review of the Acute Effects of Exercise on Immune and Inflammatory Indices in Untrained Adults.

BACKGROUND: Cardiovascular disease (CVD) is the leading cause of global mortality. Although the incidence may be reduced with regular exercise, the health benefits of a single bout of exercise on selected CVD risk factors are not well understood. The primary objective of this review is to consider the transient effects of exercise on immune (neutrophil count) and inflammatory (interleukin-6 [IL-6], C-reactive protein [CRP]) markers in untrained adults. METHODS: MEDLINE, EMBASE, CINAHL, Sports Discus and Cochrane were searched for relevant studies published from January 1946 to May 2013. Randomised controlled or crossover studies which measured any of these parameters in untrained but otherwise healthy participants in the 48 h following about of exercise, less than 1 h in duration were included. RESULTS: Ten studies met the inclusion criteria. The results indicate a single bout of aerobic or resistance exercise of moderate to high intensity promotes an increase in IL-6 (145 %) and neutrophil counts (51 %). It appears that 30-60 min of moderate to high intensity exercise is necessary to elicit such changes although variables such as the mode, intensity and pattern of exercise also affect the response. The acute response of CRP within the included studies is equivocal. CONCLUSIONS: Although responses to CRP are inconsistent, a single bout of exercise can increase the activity of both circulating IL-6 and neutrophil counts in untrained adults. These immune and inflammatory responses to a single bout of exercise may be linked to a range of health benefits.

Effects of α-lipoic acid on mtDNA damage after isolated muscle contractions.

INTRODUCTION: Although pharmacological antioxidants have previously been investigated for a prophylactic effect against exercise oxidative stress, it is not known if α-lipoic acid supplementation can protect against DNA damage after high-intensity isolated quadriceps exercise. This randomized controlled investigation was designed to test the hypothesis that 14 d of α-lipoic acid supplementation can attenuate exercise-induced oxidative stress. METHODS: Twelve (n = 12) apparently healthy male participants (age = 28 ± 10 yr, stature = 177 ± 12 cm and body mass = 81 ± 15 kg) were randomly assigned to receive either a daily supplement of 1000 mg of α-lipoic acid (2 × 500-mg tablets) for 14 d (n = 6) or receive no supplement (n = 6) in a double-blinded experimental approach. Blood and muscle biopsy tissue samples were taken at rest and after the completion of 100 isolated and continuous maximal knee extension (minimum force = 200 N, speed of contraction = 60° · s(-1)). RESULTS: Exercise increased mitochondrial 8-hydroxy-2-deoxyguanosine (8-OHdG) concentration in both groups (P < 0.05 vs rest) with a concomitant decrease in total antioxidant capacity (P < 0.05 vs rest). There was a marked increase in blood total antioxidant capacity after oral α-lipoic acid supplementation (P < 0.05 vs nonsupplemented), whereas DNA damage (Comet assay and 8-OHdG), lipid peroxidation, and hydrogen peroxide increased after exercise in the nonsupplemented group only (P < 0.05 vs supplemented). Exercise increased protein oxidation in both groups (P < 0.05 vs rest). CONCLUSIONS: These findings suggest that short-term α-lipoic acid supplementation can selectively protect DNA (but not in muscle mitochondria) and lipids against exercise-induced oxidative stress.

Exercise training and impaired glucose tolerance in obese humans.

Individuals with impaired glucose tolerance (IGT) are at greater risk of developing diabetes than in normoglycaemia. The aim of this study was to examine the effects of 12-weeks exercise training in obese humans with IGT. Eleven participants (6 males and 5 females; 49±9 years; mean Body Mass Index (BMI) 32.4 kg · m(-2)), completed a 12-week brisk walking intervention (30 min per day, five days a week (d · wk(-1)), at 65% of age-predicted maximal heart rate (HR(max)). Anthropometric measurements, dietary intake, pulse wave velocity (PWV, to determine arterial stiffness) and blood pressure (BP) were examined at baseline and post intervention. Fasting blood glucose, glycosylated haemoglobin, insulin, blood lipids, indices of oxidative stress and inflammation (lipid hydroperoxides; superoxide dismutase; multimeric adiponectin concentration and high-sensitivity C-reactive protein) were also determined. Post intervention, PWV (9.08±1.27 m · s(-1) vs. 8.39±1.21 m · s(-1)), systolic BP (145.4±14.5 vs. 135.8±14.9 mmHg), triglycerides (1.52±0.53 mmol · L(-1) vs. 1.31±0.54 mmol · L(-1)), lipid hydroperoxides (1.20±0.47 µM · L(-1) vs. 0.79±0.32 µM · L(-1)) and anthropometric measures decreased significantly (P < 0.05). Moderate intensity exercise training improves upper limb vascular function in obese humans with IGT, possibly by improving triglyceride metabolism, which may subsequently reduce oxidative stress. These changes were independent of multimeric adiponectin modification and alterations in other blood biomarkers.

Effect of cinnamon on gastric emptying, arterial stiffness, postprandial lipemia, glycemia, and appetite responses to high-fat breakfast.

BACKGROUND: Cinnamon has been shown to delay gastric emptying of a high-carbohydrate meal and reduce postprandial glycemia in healthy adults. However, it is dietary fat which is implicated in the etiology and is associated with obesity, type 2 diabetes and cardiovascular disease. We aimed to determine the effect of 3 g cinnamon (Cinnamomum zeylanicum) on GE, postprandial lipemic and glycemic responses, oxidative stress, arterial stiffness, as well as appetite sensations and subsequent food intake following a high-fat meal. METHODS: A single-blind randomized crossover study assessed nine healthy, young subjects. GE rate of a high-fat meal supplemented with 3 g cinnamon or placebo was determined using the 13C octanoic acid breath test. Breath, blood samples and subjective appetite ratings were collected in the fasted and during the 360 min postprandial period, followed by an ad libitum buffet meal. Gastric emptying and 1-day fatty acid intake relationships were also examined. RESULTS: Cinnamon did not change gastric emptying parameters, postprandial triacylglycerol or glucose concentrations, oxidative stress, arterial function or appetite (p < 0.05). Strong relationships were evident (p < 0.05) between GE Thalf and 1-day palmitoleic acid (r = -0.78), eiconsenoic acid (r = -0.84) and total omega-3 intake (r = -0.72). The ingestion of 3 g cinnamon had no effect on GE, arterial stiffness and oxidative stress following a HF meal. CONCLUSIONS: 3 g cinnamon did not alter the postprandial response to a high-fat test meal. We find no evidence to support the use of 3 g cinnamon supplementation for the prevention or treatment of metabolic disease. Dietary fatty acid intake requires consideration in future gastrointestinal studies. TRIAL REGISTRATION NUMBER: at http://www.clinicaltrial.gov: NCT01350284.

The impact of acute moderate intensity exercise on arterial regional stiffness, lipid peroxidation, and antioxidant status in healthy males.

There is a paucity of research examining the influence of acute exercise on pulse wave velocity (PWV) and oxidative stress. The purpose of this study was to examine the effects of acute moderate aerobic exercise on PWV and oxidative stress in healthy males. Eight apparently healthy males (age 23.6 ± 2.8 yrs; stature 181.4 ± 8.1 cm; weight 83.4 ± 16.2 kg; all data mean ±SD) participated in a randomized crossover design consisting of (i) a one hour bout of moderate aerobic exercise and (ii) a control trial of one hour rest. Pre- and post-exercise blood samples were drawn for the determination of lipid hydroperoxides (LOOHs) and lipid-soluble antioxidants (lycopene, retinol, and ß-carotene). Exercise had no effect on stiffness and LOOHs (P > 0.05). Retinol and lycopene were increased following exercise (P < 0.05). These findings suggest that acute moderate exercise has no effect on PWV and LOOHs, but it can increase systemic antioxidants, which may be of benefit to health.

Acute exercise and impaired glucose tolerance in obese humans.

BACKGROUND: Individuals with impaired glucose tolerance (IGT) have a greater risk of developing diabetes and cardiovascular disease compared with those with normal glycemic control. The aim of this study was to examine the effects of acute aerobic exercise on glycemia, regional arterial stiffness, and oxidative stress in obese subjects with IGT. DESIGN: Twelve obese subjects (7 men and 5 women; 48.0±9.4 years; body mass index 32.4±7.0kg/m(2)) with IGT participated in a 30-minute bout of walking at 65% of maximum predicted heart rate. Pulse wave velocity (PWV, for determination of arterial stiffness) and blood pressure were examined before and after exercise, whereas venous blood samples were drawn for the determination of glucose, blood lipids, and indices of oxidative stress and inflammation (lipid hydroperoxides; superoxide dismutase; high-sensitivity C-reactive protein). RESULTS: After exercise PWV (9.1±1.2m/s vs. 8.6±1.0m/s), glucose (5.7±0.6 mmol·L(-1) vs. 5.4±0.6 mmol·L(-1)), and diastolic blood pressure (94±14mm Hg vs. 86±13mm Hg) decreased, respectively (P < .05). A correlation was observed between PWV and glucose (r=0.544, P < .05). There were no changes in lipid hydroperoxides, superoxide dismutase, high-sensitivity C-reactive protein, or blood lipids (P > .05). CONCLUSIONS: These findings suggest that acute aerobic exercise can reduce regional arterial stiffness in obese subjects with IGT by possibly improving glucose metabolism, independent of changes in oxidative stress.

Exercise and postprandial lipaemia: effects on peripheral vascular function, oxidative stress and gastrointestinal transit.

Postprandial lipaemia may lead to an increase in oxidative stress, inducing endothelial dysfunction. Exercise can slow gastric emptying rates, moderating postprandial lipaemia. The purpose of this study was to determine if moderate exercise, prior to fat ingestion, influences gastrointestinal transit, lipaemia, oxidative stress and arterial wall function. Eight apparently healthy males (age 23.6 +/- 2.8 yrs; height 181.4 +/- 8.1 cm; weight 83.4 +/- 16.2 kg; all data mean +/- SD) participated in the randomised, crossover design, where (i) subjects ingested a high-fat meal alone (control), and (ii) ingested a high-fat meal, preceded by 1 h of moderate exercise. Pulse Wave Velocity (PWV) was examined at baseline, post-exercise, and in the postprandial period. Gastric emptying was measured using the 13C-octanoic acid breath test. Measures of venous blood were obtained prior to and following exercise and at 2, 4 and 6 hours post-ingestion. PWV increased (6.5 +/- 1.9 m/sec) at 2 (8.9 +/- 1.7 m/sec) and 4 hrs (9.0 +/- 1.6 m/sec) post-ingestion in the control group (time x group interaction, P < 0.05). PWV was increased at 2 hrs post-ingestion in the control compared to the exercise trial; 8.9 +/- 1.7 vs. 6.2 +/- 1.5 m/sec (time x group interaction, P < 0.05). Lipid hydroperoxides increased over time (pooled exercise and control data, P < 0.05). Serum triacylglycerols were elevated postprandially (pooled exercise and control data, P < 0.05). There were no changes in gastric emptying, cholesterol, or C-reactive protein levels. These data suggest that acute exercise prior to the consumption of a high-fat meal has the potential to reduce vascular impairments.