Acute exercise and impaired glucose tolerance in obese humans

McClean, Conor; McNeilly, Andrea; Trinick, Tom; Murphy, Marie; Duly, Ellie; McLaughlin, James; McEneny, Jane; Burke, George; Davison, Gareth W.

doi:10.1016/j.jacl.2009.07.001

Cited by 7 publications

(6 citation statements)

References 36 publications

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“…The glucose-lowering effect of exercise found in subjects with IGT and T2D (Minuk et al 1981;Nazar et al 1987;Martin et al 1995;Kang et al 1999;McClean et al 2009) as compared to the increased plasma glucose levels during exercise and in the immediate postprandial period in NGT subjects (Nazar et al 1987;Pestell et al 1993;King et al 1995), is in accordance with previous observations. However, the finding of an unaltered postprandial glucose level following exercise in IGT subjects is in contrast to the work of Nazar et al (1987) who found decreased postprandial glucose levels immediately following exercise.…”

Section: Discussionsupporting

confidence: 86%

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The immediate effects of a single bout of aerobic exercise on oral glucose tolerance across the glucose tolerance continuum

et al. 2014

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We investigated glucose tolerance and postprandial glucose fluxes immediately after a single bout of aerobic exercise in subjects representing the entire glucose tolerance continuum. Twenty‐four men with normal glucose tolerance (NGT), impaired glucose tolerance (IGT), or type 2 diabetes (T2D; age: 56 ± 1 years; body mass index: 27.8 ± 0.7 kg/m2, P > 0.05) underwent a 180‐min oral glucose tolerance test (OGTT) combined with constant intravenous infusion of [6,6‐2H2]glucose and ingestion of [U‐13C]glucose, following 1 h of exercise (50% of peak aerobic power) or rest. In both trials, plasma glucose concentrations and kinetics, insulin, C‐peptide, and glucagon were measured. Rates (mg kg−1 min−1) of glucose appearance from endogenous (RaEndo) and exogenous (oral glucose; RaOGTT) sources, and glucose disappearance (Rd) were determined. We found that exercise increased RaEndo, RaOGTT, and Rd (all P < 0.0001) in all groups with a tendency for a greater (~20%) peak RaOGTT value in NGT subjects when compared to IGT and T2D subjects. Accordingly, following exercise, the plasma glucose concentration during the OGTT was increased in NGT subjects (P < 0.05), while unchanged in subjects with IGT and T2D. In conclusion, while a single bout of moderate‐intensity exercise increased the postprandial glucose response in NGT subjects, glucose tolerance following exercise was preserved in the two hyperglycemic groups. Thus, postprandial plasma glucose responses immediately following exercise are dependent on the underlying degree of glycemic control.

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Section: Discussionsupporting

confidence: 86%

“…; McClean et al. ) as compared to the increased plasma glucose levels during exercise and in the immediate postprandial period in NGT subjects (Nazar et al. ; Pestell et al.…”

Section: Discussionmentioning

confidence: 99%

The immediate effects of a single bout of aerobic exercise on oral glucose tolerance across the glucose tolerance continuum

et al. 2014

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“…Serum total cholesterol, HDL-C, LDL-C and TG concentration (TG) were measured using methods previously published [17]. Estimates of LDL-C concentration were calculated using the Friedewald formula [18].…”

Section: Methodsmentioning

confidence: 99%

Effect of α-lipoic acid and exercise training on cardiovascular disease risk in obesity with impaired glucose tolerance

et al. 2011

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Obese subjects with impaired glucose tolerance (IGT) are more susceptible than healthy individuals to oxidative stress and cardiovascular disease. This randomised controlled investigation was designed to test the hypothesis that α-lipoic acid supplementation and exercise training may elicit favourable clinical changes in obese subjects with IGT. All data were collected from 24 obese (BMI ≥ 30 kg/m2) IGT patients. Following participant randomisation into two groups, fasting venous blood samples were obtained at baseline, and before and following intervention. The first group consisted of 12 participants who completed a 12 week control phase followed by 12 weeks of chronic exercise at 65% HRmax for 30 minutes a day, 5 days per week, while ingesting 1 gram per day of α-lipoic acid for 12 weeks. The second group consisted of 12 participants who completed the same 12 week control phase, but this was followed by 12 weeks of 1 gram per day of α-lipoic acid supplementation only (no exercise). The main findings show a comparatively greater rate of low density lipoprotein (LDL) oxidation in the group consisting of α-lipoic acid only (p < 0.05 vs. pre intervention), although total oxidant status was lower post intervention (p < 0.05 vs. baseline) in this group. However, exercise and α-lipoic acid in combination attenuates LDL oxidation. Furthermore, in the α-lipoic acid supplement plus exercise training group, total antioxidant capacity was significantly increased (p < 0.05 vs. baseline and pre intervention). Body fat percentage and waist and hip circumference decreased following exercise training (p < 0.05 vs. post intervention). There were no selective treatment differences for a range of other clinical outcomes including glycaemic regulation (p > 0.05). These findings report that α-lipoic acid ingestion may increase the atherogenicity of LDL when ingested in isolation of exercise, suggesting that in IGT the use of this antioxidant treatment does not ameliorate metabolic disturbances, but instead may detrimentally contribute to the pathogenesis of atherosclerosis and development of CVD. However, when α-lipoic acid is combined with exercise, this atherogenic effect is abolished.

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“…Interestingly, via the convergence of NOX4 and two forms of neuronal NOS in mouse models, the resultant NO • yields peroxynitrite (ONOO − ) proposed to be involved in the signal transduction pathways for mTORC1 integral to muscle hypertrophy associated with strength/resistance training [ 66 , 67 , 68 , 69 ]. NO • itself has also been postulated to confer an intrinsic effect on the regulation of insulin secretion, and glucose transport and metabolism, which are also accentuated via exercise [ 70 , 71 ].…”

Section: Oxidative Stress and Redox Homeostasismentioning

confidence: 99%

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

McClean

Davison

2022

Antioxidants

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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.

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Acute exercise and impaired glucose tolerance in obese humans

Cited by 7 publications

References 36 publications

The immediate effects of a single bout of aerobic exercise on oral glucose tolerance across the glucose tolerance continuum

The immediate effects of a single bout of aerobic exercise on oral glucose tolerance across the glucose tolerance continuum

Effect of α-lipoic acid and exercise training on cardiovascular disease risk in obesity with impaired glucose tolerance

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

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