T-cell counts in response to acute cardiorespiratory or resistance exercise in physically active or physically inactive older adults: a randomized crossover study.

T cells often undergo age-related changes, which may be offset by regular exercise training. However, the majority of literature is derived from cardiorespiratory exercise studies. The purpose of this study was to examine the effects of acute cardiorespiratory exercise and acute resistance exercise on the T-cell response among physically active (PA) older adults compared with physically inactive (PI) older adults. Twenty-four healthy older adults [PA n = 12; PI n = 12; means ± SD; age (years) PA 62 ± 5, PI 64 ± 5; body mass index (BMI; kg/m2) PA 23.9 ± 3.0, PI 25.6 ± 3.5] completed one bout each of matched intensity cardiorespiratory exercise and resistance exercise in a randomized order. Blood samples drawn preexercise, postexercise, and 1 h postexercise (recovery) were analyzed by flow cytometry for T cells and T-cell subsets. Resistance exercise mobilized more T-cell subsets in PI (10 of the measured types, including total T cells; CD45RA+ CD62L+, CD45RA- CD62L+, CD45RA- CD62L-, and CD45RA+ CD62L- T cells), whereas cardiorespiratory exercise mobilized more subsets in PA (CD45RA+ CD62L- and CD57+ CD45RA+ CD62L- CD4+ T cells). Both cardiorespiratory exercise and resistance exercise elicited a significant (P < 0.05) mobilization of highly differentiated (CD45RA+ CD62L-; CD57+ CD45RA+ CD62L-) CD8+ T cells into the circulation postexercise in both PA and PI groups. Furthermore, cardiorespiratory exercise resulted in a decrease in the number of circulating Th17 cells postexercise, whereas resistance exercise increased Th17 cell mobilization compared with the cardiorespiratory exercise response. There are differences between cardiorespiratory exercise and resistance exercise on the immune responses of T cells, particularly in PI individuals. This research study was registered at clinicaltrials.gov NCT03794050. NEW & NOTEWORTHY A bout of resistance exercise did not elicit the same T-cell responses as a bout of walking on a treadmill, and the response was also not the same for people who participate in regular exercise compared with those who do not. Although there were several similarities, these potential differences underscore the importance of careful selection of exercise protocol based on the population studied and the desired T-cell response to exercise outcome.

A Short-Term Paleolithic Dietary Intervention Does Not Alter Adipokines Linked to Adiposity.

The Paleolithic diet, characterized by an emphasis on hunter-gatherer type foods accompanied by an exclusion of grains, dairy products, and highly processed food items, is often promoted for weight loss and a reduction in cardiometabolic disease risk factors. Specific adipokines, such as adiponectin, omentin, nesfatin, and vaspin are reported to be dysregulated with obesity and may respond favorably to diet-induced fat loss. We aimed to evaluate the effects of an eight-week Paleolithic dietary intervention on circulating adiponectin, omentin, nesfatin, and vaspin in a cohort of physically inactive, but otherwise healthy adults. METHODS: Seven inactive adults participated in eight weeks of adherence to the Paleolithic Diet. Fasting blood samples, anthropometric, and body composition data were collected from each participant pre-and post-intervention. Serum adiponectin, omentin, nesfatin, and vaspin were measured. RESULTS: After eight weeks of following the Paleolithic diet, there were reductions (p<0.05) in relative body fat (-4.4%), waist circumference (- 5.9 cm), and sum of skinfolds (-36.8 mm). No changes were observed in waist to hip ratio (WHR), or in adiponectin, omentin, and nesfatin (p>0.05), while serum vaspin levels for all participants were undetectable. CONCLUSIONS: It is possible that although eight weeks resulted in modest body composition changes, short-term fat loss will not induce changes in adiponectin, omentin, and nesfatin in apparently healthy adults. Larger, long-term intervention studies that examine Paleolithic diet-induced changes across sex, body composition, and in populations with metabolic dysregulation are warranted.

ß2-Adrenergic receptor signaling mediates the preferential mobilization of differentiated subsets of CD8+ T-cells, NK-cells and non-classical monocytes in response to acute exercise in humans.

Acute exercise preferentially mobilizes cytotoxic T-cells, NK-cells and non-classical monocytes to the bloodstream under the influence of hemodynamic forces and/or ß2-adrenergic receptor (ß2-AR) signaling. However, the relative contribution of these mechanisms to the redeployment of the most exercise-responsive cell types is largely unknown. We determined the lymphocyte and monocyte subtypes mobilized to blood during exercise via ß2-AR signaling whilst controlling for ß1-AR mediated reductions in hemodynamic forces. In a randomized, double blind, complete cross-over design, 14 healthy cyclists exercised for 30-minutes at +10% of blood lactate threshold after ingesting: (1) a placebo, (2) a ß1-preferential antagonist (10 mg bisoprolol), or (2) a non-preferential ß1 + ß2-antagonist (80 mg nadolol) across three trials separated by >7-days. Bisoprolol was administered to reduce hemodynamic forces (heart rate and blood pressure) during exercise to levels comparable with nadolol but without blocking ß2-ARs. The mobilization of total NK-cells, terminally differentiated (CD57+) NK-cells, central memory, effector memory and CD45RA+ effector memory CD8+ T-cells; non-classical monocytes; and γδ T-cells were significantly blunted or abrogated under nadolol compared to both bisoprolol and placebo, indicating that the exercise-induced mobilization of these cell types to the blood is largely influenced by ß2-AR signaling. Nadolol failed to inhibit the mobilization of classical monocytes, CD4+ T-cells (and their subsets) or naïve CD8+ T-cells, indicating that these cell types are mobilized with exercise independently of the ß2-AR. We conclude that the preferential mobilization of NK-cells, non-classical monocytes and differentiated subsets of CD8+ T-cells with exercise is largely dependent on catecholamine signaling through the ß2-AR. These findings provide mechanistic insights by which distinct lymphocyte and monocyte subtypes are preferentially mobilized to protect the host from anticipated injury or infection in response to an acute stress response.

Vigorous exercise mobilizes CD34+ hematopoietic stem cells to peripheral blood via the ß2-adrenergic receptor.

Acute dynamic exercise mobilizes CD34+ hematopoietic stem cells (HSCs) to the bloodstream, potentially serving as an economical adjuvant to boost the collection of HSCs from stem cell transplant donors. The mechanisms responsible for HSC mobilization with exercise are unknown but are likely due to hemodynamic perturbations, endogenous granulocyte-colony stimulating factor (G-CSF), and/or ß2-adrenergic receptor (ß2-AR) signaling. We characterized the temporal response of HSC mobilization and plasma G-CSF following exercise, and determined the impact of in vivo ß-AR blockade on the exercise-induced mobilization of HSCs. Healthy runners (n = 15) completed, in balanced order, two single bouts of steady state treadmill running exercise at moderate (lasting 90-min) or vigorous (lasting 30-min) intensity. A separate cohort of healthy cyclists (n = 12) completed three 30-min cycling ergometer trials at vigorous intensity after ingesting: (i) 10 mg bisoprolol (ß1-AR antagonist); (ii) 80 mg nadolol (ß1 + ß2-AR antagonist); or (iii) placebo, in balanced order with a double-blind design. Blood samples collected before, during (runners only), immediately after, and at several points during exercise recovery were used to determine circulating G-CSF levels (runners only) and enumerate CD34+ HSCs by flow cytometry (runners and cyclists). Steady state vigorous but not moderate intensity exercise mobilized HSCs, increasing the total blood CD34+ count by ∼4.15 ±â€¯1.62 Δcells/µl (+202 ±â€¯92%) compared to resting conditions. Plasma G-CSF increased in response to moderate but not vigorous exercise. Relative to placebo, nadolol and bisoprolol lowered exercising heart rate and blood pressure to comparable levels. The number of CD34+ HSCs increased with exercise after the placebo and bisoprolol trials, but not the nadolol trial, suggesting ß2-AR signaling mediated the mobilization of CD34+ cells [Placebo: 2.10 ±â€¯1.16 (207 ±â€¯69.2%), Bisoprolol 1.66 ±â€¯0.79 (+163 ±â€¯29%), Nadolol: 0.68 ±â€¯0.54 (+143 ±â€¯36%) Δcells/µL]. We conclude that the mobilization of CD34+ HSCs with exercise is not dependent on circulating G-CSF and is likely due to the combined actions of ß2-AR signaling and hemodynamic shear stress.

Exercise and the Regulation of Immune Functions.

Exercise has a profound effect on the normal functioning of the immune system. It is generally accepted that prolonged periods of intensive exercise training can depress immunity, while regular moderate intensity exercise is beneficial. Single bouts of exercise evoke a striking leukocytosis and a redistribution of effector cells between the blood compartment and the lymphoid and peripheral tissues, a response that is mediated by increased hemodynamics and the release of catecholamines and glucocorticoids following the activation of the sympathetic nervous system and the hypothalamic-pituitary-adrenal axis. Single bouts of prolonged exercise may impair T-cell, NK-cell, and neutrophil function, alter the Type I and Type II cytokine balance, and blunt immune responses to primary and recall antigens in vivo. Elite athletes frequently report symptoms associated with upper respiratory tract infections (URTI) during periods of heavy training and competition that may be due to alterations in mucosal immunity, particularly reductions in secretory immunoglobulin A. In contrast, single bouts of moderate intensity exercise are "immuno-enhancing" and have been used to effectively increase vaccine responses in "at-risk" patients. Improvements in immunity due to regular exercise of moderate intensity may be due to reductions in inflammation, maintenance of thymic mass, alterations in the composition of "older" and "younger" immune cells, enhanced immunosurveillance, and/or the amelioration of psychological stress. Indeed, exercise is a powerful behavioral intervention that has the potential to improve immune and health outcomes in the elderly, the obese, and patients living with cancer and chronic viral infections such as HIV.

Body composition assessment in overweight women: validation of air displacement plethysmography.

PURPOSE: The purpose of this study was to evaluate the validity and reliability of air displacement plethysmography (ADP) compared to a dual energy x-ray absorptiometry (DXA) criterion for body composition measurement in overweight and obese women (BMI ≥ 25·0 kg m(2) ). SUBJECTS/METHODS: Twenty-four overweight and obese women (Mean ± SD; Age: 36·6 ± 12·0 years; Height: 166·4 ± 5·8 cm; Weight: 86·5 ± 14·2 kg; Body Fat: 38·5 ± 3·7%; BMI: 31·3 ± 5·5 kg m(2) ) were tested after an 8-h fast. Fat mass (FM), fat-free mass (FFM) and percent body fat (%BF) were measured by ADP and compared to values determined by the DXA criterion. FFM from DXA was calculated as lean mass plus bone mineral content. A paired samples t-test was used to test for significant differences in the body composition variables between methods. A one-way ANOVA along with intraclass correlation coefficient (ICC), SEM,%SEM and MD was used to represent reliability. RESULTS: Validity data comparing ADP and DXA demonstrated no significant difference in FM (ADP-DXA FM = 0·99 kg; P = 0·113), FFM (0·98 kg; P = 0·115) and %BF (1·56%; P = 0·540). Reliability data for ADP between the first and second trials showed no significant difference in FM (P = 0·168; ICC = 0·994; SEM = 0·668), FFM (P = 0·058; ICC = 0·973; SEM = 0·892) or %BF (P = 0·121; ICC = 0·971; SEM = 0·813). CONCLUSIONS: For overweight and obese women, ADP was found to be a valid measure of FM, FFM and %BF when compared with DXA. The reliability of ADP was supported for all body composition variables.

Photoelectrochemical complexes for solar energy conversion that chemically and autonomously regenerate.

Naturally occurring photosynthetic systems use elaborate pathways of self-repair to limit the impact of photo-damage. Here, we demonstrate a complex consisting of two recombinant proteins, phospholipids and a carbon nanotube that mimics this process. The components self-assemble into a configuration in which an array of lipid bilayers aggregate on the surface of the carbon nanotube, creating a platform for the attachment of light-converting proteins. The system can disassemble upon the addition of a surfactant and reassemble upon its removal over an indefinite number of cycles. The assembly is thermodynamically metastable and can only transition reversibly if the rate of surfactant removal exceeds a threshold value. Only in the assembled state do the complexes exhibit photoelectrochemical activity. We demonstrate a regeneration cycle that uses surfactant to switch between assembled and disassembled states, resulting in an increased photoconversion efficiency of more than 300% over 168 hours and an indefinite extension of the system lifetime.

A mechanochemical model of growth termination in vertical carbon nanotube forests.

Understanding the mechanisms by which vertical arrays of carbon nanotube (CNT) forests terminate their growth may lead to the production of aligned materials of infinite length. We confirm through calculation of the Thiele modulus that several prominent systems reported in the literature to date are not stunted by diffusion limitations. Evidence also suggests that, for many systems, the growth-termination mechanism is spatially correlated among nanotubes, making spontaneous, random catalytic poisoning unlikely as a dominant mechanism. We propose that a mechanical coupling of the top surface of the film creates an energetic barrier to the relative displacement between neighboring nanotubes. A Monte Carlo simulation based on this premise is able to qualitatively reproduce characteristic deflections of the top surface of single- and doubled-walled CNT (SWNT and DWNT) films near the edges and corners. The analysis asserts that the coupling is limited by the enthalpy of the carbon-forming reaction. We show that for patterned domains, the resulting top surface of the pillars is approximately conic with hyperbolic cross sections that allow for empirical calculation of a threshold force (F(max) = 34-51 nN for SWNTs, 25-27 nN for DWNTs) and elastic constant (k, 384-547 N/m for SWNTs and 157-167 N/m for DWNTs) from the images of experimentally synthesized films. Despite differences in nanotube type and precursor chemistry, the values appear consistent supporting the validity of the model. The possible origin of the mechanical coupling is discussed.