Characterization of Individualized Glycemic Excursions during a Standardized Bout of Hypoglycemia-Inducing Exercise and Subsequent Hypoglycemia Treatment-A Pilot Study.
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SUBMITTER: Broz J
PROVIDER: S-EPMC8619071 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description:During exercise, there is coordination between various hormonal systems to ensure glucoregulation. This study examined if hypoglycemia occurs during moderate-intensity exercise in non-obese and obese individuals with and without type 2 diabetes (T2D). Eighteen non-obese, 18 obese, and 10 obese with T2D completed 2 study days that included a meal at 1,800 h followed by rest (NOEX) or exercise (PMEX; 45 min/55% of VO2 max 2 h post meal). Glucose, insulin, and glucagon concentrations were measured throughout this 5.5 h period. Subjects with T2D had elevated glucose responses to the meal on both study days, compared to non-obese and obese subjects (P < 0.05). During evening exercise (PMEX), subjects with T2D had a greater drop in glucose concentration (-98.4 ± 13.3 mg/dL) compared to obese (-44.8 ± 7.1 mg/dL) and non-obese (-39.3 ± 6.1 mg/dL; P < 0.01) subjects. Glucose levels decreased more so in females than males in both conditions (P < 0.01). Nadir glucose levels <70 mg/dL were observed in 33 subjects during NOEX and 39 subjects during PMEX. Obese males had a larger exercise-induced insulin drop than obese females (P = 0.01). During PMEX, peak glucagon concentrations were elevated compared to NOEX (P < 0.001). Male participants with T2D had an increased glucagon response during NOEX and PMEX compared to females (P < 0.01). In conclusion, in individuals with varying glucose tolerance, there is a dramatic drop in glucose levels during moderate-intensity exercise, despite appropriate insulin concentrations prior to exercise, and glucagon levels rising during exercise. Moderate-intensity exercise can result in low glucose concentrations (<60 mg/dL), and yet many of these individuals will be asymptomatic.
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Project description:Vitamin D is necessary for musculoskeletal health, however, the supplementation of vitamin D above the sufficiency level does not bring additional bone mass density (BMD), unlike physical exercise which enhances the bone formatting process. Regular physical activity has been shown to upregulate VDR expression in muscles and to increase circulating vitamin D. Here we investigate whether a single bout of exercise might change 25(OH)D3 blood concentration and how it affects metabolic response to exercise. Twenty-six boys, 13.8 years old (SD ± 0.7) soccer players, participated in the study. The participants performed one of two types of exercise: the first group performed the VO2max test until exhaustion, and the second performed three times the repeated 30 s Wingate Anaerobic Test (WAnT). Blood was collected before, 15 min and one hour after the exercise. The concentration of 25(OH)D3, parathyroid hormone (PTH), interleukin-6 (IL-6), lactate, non-esterified fatty acids (NEFA) and glycerol were determined. 25(OH)D3 concentration significantly increased after the exercise in all boys. The most prominent changes in 25(OH)D3, observed after WAnT, were associated with the rise of PTH. The dimensions of response to the exercises observed through the changes in the concentration of 25(OH)D3, PTH, NEFA and glycerol were associated with the significant increases of IL-6 level. A single bout of exercise may increase the serum's 25(OH)D3 concentration in young trained boys. The intensive interval exercise brings a more potent stimulus to vitamin D fluctuations in young organisms. Our results support the hypothesis that muscles may both store and release 25(OH)D3.
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Project description:Research in human subjects suggests that acute exercise can improve memory performance, but the qualities of the exercise necessary to promote improved memory, and the signaling pathways that mediate these effects are unknown. Brain-derived neurotrophic factor (Bdnf), noradrenergic signaling, and post-translational modifications to AMPA receptors have all been implicated in the enhancement of memory following emotional or physical arousal; however, it is not known if a single bout of exercise is sufficient to engage these pathways. Here we use a rodent model to investigate the effects of acute and chronic exercise on hippocampal transcript-specific Bdnf expression and phosphorylation of the GluR1 subunit of the AMPA-type glutamate receptor. A single bout of treadmill exercise was insufficient to mimic the increased expression of GluR1 protein and phosphorylation at Ser845 observed following 1 month of voluntary wheel running. However, acute exercise was sufficient to increase Bdnf transcript IV messenger RNA (mRNA) expression in sedentary subjects, but not subjects housed for 1 month with a running wheel. High-intensity acute exercise increased total Bdnf mRNA in sedentary mice, but not above levels observed following chronic access to the running wheel. Although depletion of central noradrenergic signaling with DSP-4 reduced Bdnf IV mRNA, the effect of acute exercise on Bdnf mRNA persisted. Our characterization of the effects of acute exercise on Bdnf expression and persistence in the absence of noradrenergic modulation may inform strategies to employ physical activity to combat cognitive aging and mental health disorders.
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Project description:BackgroundThere is a knowledge gap in the physiological effects of short-term yoga exercise interventions.ObjectiveTo evaluate the feasibility of a randomized controlled trial (RCT) assessing the acute effects of a yoga exercise protocol practiced at 2 intensities (high or moderate) on temporal responses of a battery of systemic circulatory cytokines in healthy yoga-naïve adults.MethodsThis study was a three-arm, pre-post pilot-RCT employing a single bout of yoga exercise intervention. Groups were high-intensity yoga (HY, n = 10), moderate-intensity yoga (MY, n = 10), and a sedentary, no-intervention control group (CON, n = 10). Blood samples were collected at baseline and post-intervention at 6 timepoints (0-, 30-, 60-, 120-, 180-minutes, and 24-hours post-intervention) and were processed with a pre-defined inflammatory panel of 13 cytokines. Heart rate (HR) was assessed with a Polar H10® device. The PROMIS Pain intensity Questionnaire was used to assess body soreness.ResultsWe demonstrate feasibility of recruitment, randomization, and retention of participants based upon predetermined metrics, including: proportion of eligible to enrolled participants (55%); recruitment period (11-months); participant retention (97%); completion rate for questionnaires (99%); completion of physiological measures (98%); and adherence to the yoga exercise protocol (88%). Cytokine levels over time were heterogeneous within and between groups. Responses of a subset of cytokines were positively correlated with 1 another in high- and moderate-intensity yoga exercise groups but not in the control group. Median values for HR were 91 (IQR: 71-95) in the HY, 95 (IQR: 88-100) in the MY, and 73 (IQR: 72-75) in the CON. Pre-post changes in body soreness after the yoga exercise intervention were most evident in the HY group.ConclusionAlong with observed trends in select cytokines, findings encourage a more definitive trial aimed at understanding the short-term effects of yoga exercise on inflammatory immune markers and pain in sedentary healthy adults. Clinicaltrials.gov ID# NCT04444102.
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