Exercise acutely increases vitamin D receptor expression in T lymphocytes in vitamin D-deficient men, independent of age.

NEW FINDINGS: What is the central question of this study? Does exercise affect vitamin D receptor expression in T lymphocytes in young, middle-aged and older adults? What is the main finding and its importance? Moderate-intensity cycling exercise increases vitamin D receptor expression in vitamin D-deficient men, independent of age, presenting a strategy to combat the prevalence of vitamin D deficiency. ABSTRACT: Vitamin D plays a key role in the modulation of the immune system, mediated through the intracellular vitamin D receptor (VDR). Exercise has been shown to influence the activity and availability of the VDR. The aim of this study was to investigate the effect of age on basal immune cell (T-lymphocyte) VDR expression and the subsequent effect of acute aerobic exercise to modulate VDR expression in peripheral T cells. Thirty-five men were included in the study (mean ± SD: age 44 ± 17 years and body mass index 25.7 ± 3.1 kg/m2 ), separated into three age groups: 18-30 (n = 12), 31-45 (n = 11) and 60-75 years (n = 12). Participants completed two trials [control (CON) and aerobic exercise (AE)], with blood samples collected pre- and postexercise (0, 1 and 3 h). Peripheral blood T cells were isolated and analysed for VDR expression by flow cytometry. The results show that advanced age is associated with lower VDR expression in T cells (882 ± 274, 796 ± 243 and 594 ± 174 geomean in the 18-30, 31-45 and 60-75 year age groups, respectively). Acute AE was successful at acutely increasing VDR expression in T cells, irrespective of age. Advanced age corresponds to a lower T-cell VDR expression, which might be responsible for age-associated development of chronic conditions and autoimmunity. Exercise was successful in increasing VDR expression in T cells irrespective of age and independent of exercise-induced T-cell mobilization.

Circulating hormone and cytokine response to low-load resistance training with blood flow restriction in older men.

It has been suggested that circulating hormones and cytokines are important in the adaptive response to low-load resistance training (LLRT) with blood flow restriction (BFR); however, their response following this type of training in older men is unclear. Seven healthy older men (age 71.0 ± 6.5 year, height 1.77 ± 0.05 m, body mass 80.0 ± 7.5 kg; mean ± SD) performed five sets of unilateral LLRT knee extensions (20 % 1-RM) of both limbs, with or without BFR in a counterbalanced order. For the BFR condition, a pressure cuff was applied on the upper thigh and inflated to ~110 mmHg. Venous blood samples were taken at rest and 30-, 60- and 120-min post-exercise and measured for plasma concentrations of growth hormone (GH), insulin-like growth factor 1 (IGF-1), vascular endothelial growth factor (VEGF), cortisol and interleukin-6 (IL-6). GH increased (P < 0.05) from rest to 30-min post-exercise and was greater (P < 0.05) during LLRT with BFR than without. VEGF was significantly (P < 0.05) elevated from resting levels at 30-, 60- and 120-min post-exercise following LLRT with BFR with no change seen following LLRT without BFR. IL-6 increased (P < 0.05) from 30- to 60-min post-exercise and remained elevated at 120-min post-exercise in both conditions. Cortisol and IGF-1 were unaffected following exercise. In conclusion, a single bout of LLRT with BFR increases the circulating concentrations of GH and VEGF in older men and may explain the skeletal muscle and peripheral vascular adaptations observed following training with BFR.

The Effect of a Single Bout of High Intensity Intermittent Exercise on Glucose Tolerance in Non-diabetic Older Adults.

Our aim was to investigate the acute effects of a single bout of high intensity intermittent training (HIIT) on glucose tolerance and other physiological and metabolic markers in non-diabetic older adults. Fourteen healthy older adults (age, 64 ± 2 y; BMI, 25.7 ± 2.8 kg·m-2) performed two acute exercise trials: continuous moderate intensity exercise (MOD) and HIIT, with the response to an oral glucose tolerance test (OGTT) determined <24 hours after. Inflammatory, haematological, and lipid parameters were also assessed the day after each trial. There was an effect of the trials on the insulin response to an OGTT (P=0.047), but not the glucose response. Following an acute bout of HIIT, insulin concentration during an OGTT was elevated at 60 min compared to the control trial (P=0.045), indicating more insulin was secreted, but glucose concentration was unchanged in all trials. The study findings demonstrate that a single bout of HIIT affects the insulin response but not the glycaemic response to a glucose load, proffering a potential benefit for metabolic health in older adults.

The combined effect of high-intensity intermittent training and vitamin D supplementation on glycemic control in overweight and obese adults.

High-intensity intermittent training (HIIT) has been shown to reduce the risk of chronic conditions including the development of type 2 diabetes mellitus (T2DM). Independently, a low vitamin D status has also been linked to the prevalence of T2DM. The aim of this study was to investigate if there was a synergistic metabolic effect of HIIT and vitamin D supplementation on glycemic control. A total of 20 male and female participants (age, 34 ± 9 year; BMI, 31.4 ± 2.8 kg·m-2 ) completed 6 weeks HIIT, and were randomized to ingest 100 µg·day-1 of vitamin D3 or placebo. Response to an oral glucose tolerance test (OGTT) was determined at baseline and at 72 h postintervention. Glucose tolerance was improved as a result of the HIIT intervention, shown through a reduction in glucose and insulin concentrations during the OGTT, accompanied by a decrease in glucose (829 ± 110 to 786 ± 139 mmol·h-1 ·L-1 ; P = 0.043) and insulin (8101 ± 4755-7024 ± 4489 mU·h-1 ·L-1 ; P = 0.049) area under the curve (AUC). Supplementation increased 25-hydroxyvitamin D3 concentration by 120% to a sufficiency status (P < 0.001). However, the consumption of vitamin D3 seemed to attenuate the glucose response during an OGTT. Triglyceride content was lowered following the intervention (P = 0.025). There was no effect of the intervention on insulin sensitivity (IS) indices: ISIMatsuda and HOMA-IR. Our findings demonstrate that HIIT improves glucose tolerance in nondiabetic overweight and obese adults; however vitamin D3 supplementation did not proffer any additional positive effects on the measured indices of metabolic health.

Subclinical diastolic dysfunction in young adults with Type 2 diabetes mellitus: a multiparametric contrast-enhanced cardiovascular magnetic resonance pilot study assessing potential mechanisms.

AIMS: To assess the cardiac, vascular, anthropometric, and biochemical determinants of subclinical diastolic dysfunction in younger adults with Type 2 diabetes mellitus (T2DM) using multiparametric contrast-enhanced cardiovascular magnetic resonance (CMR) imaging. METHODS AND RESULTS: Twenty adults <40 years with T2DM [mean age 31.8(6.6) years, T2DM duration 4.7(4.0) years] and 20 age and sex-matched controls [10 obese non-diabetic controls and 10 lean controls (LC)] were studied. Cardiac volumes and function, circumferential strain and peak early diastolic strain rate (PEDSR), myocardial perfusion reserve, aortic stiffness (distensibility, pulse-wave velocity), focal fibrosis on late gadolinium enhancement, and pre- and post-contrast T1 mapping for contrast agent partition coefficient (subset, n = 26) were determined by CMR. In the T2DM cohort, mean aortic distensibility correlated with PEDSR (r = 0.564, P = 0.023) and diabetes duration correlated inversely with PEDSR (r = -0.534, P = 0.015) on univariate analysis. There was a close association between PEDSR and peak systolic strain (r = -0.580, P = 0.007). CONCLUSION: In young adults with T2DM, diabetes duration and aortic distensibility were associated with diastolic dysfunction. Interventional studies are required to assess whether cardiac dysfunction can be reversed in this phenotype of patients.

Determination of inflammatory and prominent proteomic changes in plasma and adipose tissue after high-intensity intermittent training in overweight and obese males.

This study aimed to determine whether 2 wk of high-intensity intermittent training (HIIT) altered inflammatory status in plasma and adipose tissue in overweight and obese males. Twelve participants [mean (SD): age 23.7 (5.2) yr, body mass 91.0 (8.0) kg, body mass index 29.1 (3.1) kg/m(2)] undertook six HIIT sessions over 2 wk. Resting blood and subcutaneous abdominal adipose tissue samples were collected and insulin sensitivity determined, pre- and posttraining. Inflammatory proteins were quantified in plasma and adipose tissue. There was a significant decrease in soluble interleukin-6 receptor (sIL-6R; P = 0.050), monocyte chemotactic protein-1 (MCP-1, P = 0.047), and adiponectin (P = 0.041) in plasma posttraining. Plasma IL-6, intercellular adhesion molecule-1 (ICAM-1), tumor necrosis factor-α (TNF-α), IL-10, and insulin sensitivity did not change. In adipose tissue, IL-6 significantly decreased (P = 0.036) and IL-6R increased (P = 0.037), while adiponectin tended to decrease (P = 0.056), with no change in ICAM-1 posttraining. TNF-α, MCP-1, and IL-10 were not detectable in adipose tissue. Adipose tissue homogenates were then resolved using one-dimensional gel electrophoresis, and major changes in the adipose tissue proteome, as a consequence of HIIT, were evaluated. This proteomic approach identified significant reductions in annexin A2 (P = 0.046) and fatty acid synthase (P = 0.016) as a response to HIIT. The present investigation suggests 2 wk of HIIT is sufficient to induce beneficial alterations in the resting inflammatory profile and adipose tissue proteome of an overweight and obese male cohort.

The response of interleukin-6 and soluble interleukin-6 receptor isoforms following intermittent high intensity and continuous moderate intensity cycling.

As interleukin-6 (IL-6), its soluble receptor (sIL-6R), and the IL-6/sIL-6R complex is transiently elevated in response to prolonged moderate-intensity exercise, this study investigated how these levels would be modulated by an acute bout of high-intensity intermittent (HIIT) exercise in comparison to continuous moderate-intensity exercise (MOD). This study also investigated the expression of the differentially spliced sIL-6R (DS-sIL-6R) in response to exercise. Eleven healthy males completed two exercise trials matched for external work done (582 ± 82 kJ). During MOD, participants cycled at 61.8 (2.6)% VO(2peak) for 58.7 (1.9) min, while HIIT consisted of ten 4-min intervals cycling at 87.5 (3.4)% [Formula: see text] separated by 2-min rest. Blood samples were collected pre-exercise, post-exercise, and 1.5, 6, and 23 h post-exercise. Plasma IL-6, sIL-6R, IL-6/sIL-6R complex, and DS-sIL-6R levels were measured by enzyme-linked immunosorbent assay. HIIT caused a significantly greater increase in IL-6 than MOD (P = 0.018). Both MOD and HIIT resulted in an increase in sIL-6R and IL-6/sIL-6R complex (P < 0.001), however, this was not significantly different between trials. Soluble IL-6R peaked at 6 h post-exercise in both trials. DS-sIL-6R increased significantly with exercise (P = 0.02), representing 0.49% of the total sIL-6R increase. This investigation has demonstrated that the IL-6 response is greater after intermittent high-intensity exercise than comparable moderate-intensity exercise; however, increased IL-6/sIL-6R complex nor sIL-6R was different between HIIT and MOD. The current study has shown for the first time that elevated sIL-6R after HIIT exercise is derived from both proteolytic cleavage and differential splicing.

Individual responsiveness to exercise-induced fat loss is associated with change in resting substrate utilization.

Fat loss in response to exercise training varies between individuals, even when differences in compliance to the exercise program are accounted for. The purpose of this study was to investigate whether individual variation in change in fasting respiratory quotient (RQ) after exercise training contributes to this interindividual variability. Fifty-five premenopausal women participated in a 7-week endurance-type exercise training program; and fitness, body composition, and resting substrate utilization and metabolic rate in the fasted state were assessed at baseline and postintervention. Total net energy expenditure of the exercise intervention (exEE) was determined from heart rate obtained in all exercise sessions and individualized calibration of the heart rate vs oxygen uptake relationship. Dietary intake and physical activity (by constant heart rate monitoring) were assessed at baseline and during the final week of the intervention. Mean change in fat mass for the group was -0.97 kg (range, +2.1 to -5.3 kg). The strongest correlate of change in fat mass was exEE (r = 0.60, P < .0005). Change in fasting RQ correlated significantly (r = -0.26, P = .05) with the residual for change in fat mass after adjusting for the effects of both exEE and change in energy intake, explaining 7% of the variance. In multiple regression analysis, exEE (P < .0005) and change in fasting RQ (P = .02) were the only statistically significant independent predictors of change in fat mass, together explaining 40.2% of the variance. Thus, fat loss in response to exercise training depends not only on exercise energy expenditure but also on exercise training-induced changes in RQ at rest. This suggests that development of strategies to maximize the change in resting fat oxidation in response to an exercise training program may help individuals to maximize exercise-induced fat loss.