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Context: We previously reported positive behavioral effects of both daily mantra meditation and classical music listening interventions in breast cancer survivors with cancer related cognitive complaints. Objective: The objective of this pilot study was to compare the effects of the meditation intervention to a music listening intervention on biomarkers of inflammation and cellular aging (secondary outcomes) in breast cancer survivors. Design: Randomized control trial, baseline data collection (time 1), post intervention data collection (time 2) Setting: Community-based, Central Texas Participants: 25 breast cancer survivors (BCS) who were 3 months to 6 years post chemotherapy completion and reported cognitive decline Intervention(s): Kirtan Kriya meditation (KK) or music listening (ML), 8 weeks, 12 minutes a day Main Outcome: Telomerase activity [TA], c-reactive protein [CRP], soluble IL-2 receptor alpha [sIL-2Rα], soluble IL-4 receptor [sIL-4R], soluble IL-6 receptor [sIL-6R], soluble tumor necrosis factor receptor II [sTNF-RII], VEGF receptor 2 [sVEGF-R2], and VEGF receptor 3 [sVEGF-R3] Results: Repeated measures analysis of variance models were analyzed from time 1 to time 2 by group for each biomarker. A pattern of greater telomerase activity across time in both groups (F (1,15) = 3.98, p = .06, η²p = .21); significant decreases in sIL-4R across time for both groups (F (1,22)= 6.28, p = .02, η²p = .22); group*time effect was nominally different but not statistically different for sIL-4R (F(1,22)= 3.82, p = .06, η²p = .15); and a pattern for a group*time effect with ML group showing higher levels of sVEGF-R3 at time 2 (F (1,20)=, p = .12, η²p = .11). No significant effects were found for CRP, sIL-2Rα, sIL-6R, sTNF-RII, or sVEGF-R2.

Breath-hold diving evokes a complex cardiovascular response. The degrees of hypertension induced by the diving reflex are substantial and accentuated by the underwater swimming. This condition provides a circulatory challenge to properly buffer and cushion cardiac pulsations. We determined hemodynamic changes during the diving maneuver and hypothesized that central artery compliance would be augmented during simulated breath-hold diving. A total of 20 healthy young adults were studied. Hemodynamics were measured during exercise on a cycle ergometer, apnea, face immersion in cold water (trigeminal stimulation), and simulated breath-hold diving. Arterial compliance was measured by recording the carotid artery diameter from images derived from an ultrasound machine at the cephalic portion of the common carotid artery 1–2 cm proximal to the carotid bulb, whereas arterial pressure waveforms were obtained using an arterial tonometry placed on the contralateral carotid artery and recorded on a data acquisition software. The change in diameter was divided by the change in blood pressure to calculate arterial compliance. Arterial compliance increased with simulated diving compared with rest ( P = 0.007) and was elevated compared with exercise and apnea alone ( P < 0.01). A significant increase in heart rate was observed with exercise, apnea, and facial immersion when compared with rest ( P < 0.001). However, simulated diving brought the heart rate down to resting levels. Cardiac output increased with all conditions ( P < 0.001), with an attenuated response during simulated diving compared with exercise and facial immersion ( P < 0.05). Mean blood pressure was elevated during all conditions ( P < 0.001), with a further elevation observed during simulated diving compared with exercise ( P < 0.001), apnea ( P = 0.016), and facial immersion ( P < 0.001). Total peripheral resistance was decreased during exercise and facial immersion compared with rest ( P < 0.001) but was increased during simulated diving compared with exercise ( P < 0.001), apnea ( P = 0.008), and facial immersion ( P = 0.003). We concluded that central artery compliance is augmented during simulated breath-hold diving to help buffer cardiac pulsations.

Pentraxin 3 (PTX3) has been shown to be a predictor of endothelial dysfunction in patients with increased risk of cardiovascular disease (CVD) (e.g., obesity). Circulating PTX3 concentrations are dysregulated in obese individuals and are elevated following acute aerobic exercise. High-intensity interval exercise (HIIE) has been demonstrated to be as effective as continuous moderate-intensity exercise in improving endothelial function, as indicated by brachial artery flow-mediated dilation (BAFMD), in patients with CVD. Therefore, the purpose of this study was to examine the effect of acute HIIE on plasma PTX3 and BAFMD responses in obese individuals. Eight obese and six normal-weight young males participated in acute HIIE (4 intervals of 4 min at 80–90% of VO2max; 3 min of active recovery at 50–60% VO2max). Plasma PTX3 and BAFMD were measured prior to, immediately following exercise, and one and 2 hours into recovery. Plasma PTX3 concentrations significantly increased following HIIE, yet the PTX3 response to HIIE was significantly blunted in obese compared to normal-weight participants. While the kinetic responses of BAFMD were also significantly different in obese compared to normal-weight participants, similar increases above the baseline were observed 2 hours into recovery in both groups. Finally, plasma PTX3 concentrations were not associated with BAFMD at baseline or in response to HIIE. The utilization of HIIE may serve as a time-efficient exercise prescription strategy to transiently improve endothelial function, independent of elevated plasma PTX3 concentrations, in obese individuals.

Autophagy is a critical molecular process in promoting cell survival against apoptosis. This study examined whether maximal aerobic exercise-mediated apoptosis in obesity might be underlying the involvement of autophagy in the peripheral blood mononuclear cells (PBMCs). Twelve healthy male subjects (6 obese and 6 normal-weight) were recruited to participate in a maximal graded exercise test on a treadmill. Obese subjects exhibited a significantly lower Bax, but a higher Bcl-2 protein level in conjunction with a reduced Bax/Bcl-2 AUCi compared to normal-weight subjects following exercise. Furthermore, a greater LC3-II/LC3-I ratio and LC3-II/LC3-I AUCi was observed in obese subjects compared to normal-weight subjects. LC3-II/LC3-I AUCi was also positively associated with obesity-associated parameters (BMI, waist/hip circumference, and fasting insulin level), but was negatively correlated with Bax/Bcl-2 AUCi. These findings demonstrate that maximal aerobic exercise differentially mediates the intrinsic apoptotic pathway and autophagic activity in human PBMCs isolated from obese compared to normal-weight individuals.

High consumption of low- and non-fat dairy products improves vascular dysfunction associated with elevated arterial blood pressure (BP). Currently, it is unknown if conventional full-fat dairy products improve vascular functions. To determine if adding whole milk and full-fat dairy products to the normal routine diet improves vascular function in adults with elevated BP. Sixty adults (age ± SEM; 58 ± 2 years) with elevated BP (systolic/diastolic; 120–159/

PURPOSE Reductions in skeletal muscle mass, beginning after the third decade of life, reduce maximal neuromuscular power (Pmax). Maximal aerobic power generation is also reduced. The primary purpose of this study was to investigate the effectiveness of maximal power cycling (PC) training using an inertial load ergometer on skeletal muscle mass and cardiovascular function in untrained 50- to 68-yr-old participants. METHODS The study used a pre- or postoutcome exercise intervention testing untrained 50- to 68-yr-old adults (n = 39, M = 15, mean ± SE = 58.5 ± 0.8, range = 50-68 yr). Over the course of 8 wk, participants performed 15 min of training 3 times per week. Each session involved repeated (15-30 times) 4-s sprints of PC. Measurements were thigh muscle volume, total body lean mass, Pmax, peak oxygen consumption, cardio-ankle vascular index, performance on functional tests of living (FTLChair and FTLRamp), and intermuscular fat volume. RESULTS Training for 8 wk increased thigh muscle volume (3.7% ± 0.9%, P < 0.001) and total body lean mass (1.5% ± 0.4%, P < 0.01) while increasing total body mass (TBM) (1.4% ± 0.3%, P < 0.01). Physical performance measures increased significantly (all P < 0.05) with improvements in Pmax (12.0% ± 1.5%); peak oxygen consumption (9.8% ± 1.8%), and FTL (8.5% ± 1.3% to 17.2% ± 2%). Cardio-ankle vascular index was significantly decreased -2.3% ± 1.1% (P < 0.05), indicating reduced arterial stiffness. CONCLUSIONS These results demonstrate that 8 wk of PC training at true maximal power was effective at increasing muscle mass and maximal power, as well as maximal cardiovascular capacity and functional tasks in untrained 50- to 68-yr-olds.

Swimming is a favorable and ideal modality of exercise for individuals with obesity and arthritis as it encompasses a minimal weight-bearing stress and a reduced heat load. However, the available evidence indicates that regular swimming may not be effective in reducing body weight and body fatness. A current hypothesis is that exercise in cold water stimulates appetite. We determined the effect of swimming training on appetite-related hormones. Thirty-nine adults with obesity and osteoarthritis were randomly assigned to 12 weeks of supervised swimming or cycling training. In the initial few weeks, participants exercised for 20–30 minutes/day, 3 days/week, at an exercise intensity of 40–50% of heart rate reserve (HRR). Subsequently, the intensity and duration of exercise were progressively increased to 40–45 minutes/day, 3 days/week, at an intensity of 60–70% of HRR. Fasting plasma concentrations of ghrelin, insulin, leptin, and peptide YY did not change with the swimming or cycling exercise training (p>0.05). Swimming exercise did not negatively influence appetite-related hormones in adults with obesity and osteoarthritis to impair weight loss.

Obesity may attenuate the expression of brain-derived neurotrophic factor (BDNF), thereby increasing the risk of cognitive dysfunction. High-intensity interval exercise (HIIE) has been shown to be as or more effective than continuous moderate-intensity exercise (CME) in promoting the expression of BDNF in normal-weight individuals. Therefore, the primary purpose of this study was to examine whether or not acute HIIE could be utilized as a practical model to explore the BDNF response in obese versus normal-weight subjects when compared to acute CME. The potential relationship of exercise-induced BDNF with blood lactate and cortisol was also examined. Twelve male subjects (six obese and six normal-weight) participated in a counterbalanced and caloric equated experiment: HIIE (30 min, 4 intervals of 4 min at 80%–90% of VO2max with 3 min of active recovery at 50–60% VO2max) and CME (38 min at 50%–60% VO2max). Blood samples were collected prior to, immediately following exercise, and 1 h into recovery for measurements of serum BDNF, blood lactate, and plasma cortisol. Our results showed that the BDNF response to acute HIIE was greater than CME in obese subjects when compared to normal-weight subjects. Similarly, although acute HIIE induced greater blood lactate and plasma cortisol levels than CME, obese subjects produced less blood lactate, but no difference in cortisol than normal-weight subjects. These findings suggest that acute HIIE may be a more effective protocol to upregulate BDNF expression in an obese population, independent of increased lactate and cortisol levels. Impact statement High-intensity interval exercise (HIIE) has been shown to be a time-efficient exercise strategy that provides similar or superior physiological benefits as traditional continuous moderate-intensity exercise (CME). Our previous study demonstrated an equivalent elevation on the BDNF response in both obese and normal-weight individuals following 30 min of acute CME. To discover a time-efficient exercise strategy to improve brain health in an obese population, the present study found that obese individuals elicit a greater level of BDNF following acute HIIE versus CME than normal-weight individuals. These findings indicate that acute HIIE may be an effective strategy to upregulate BDNF expression in obese individuals.

Aims Obesity is associated with lipid aggregation in adipocytes and macrophage infiltration, leading to increased oxidative stress and inflammation. Increased cell-free DNA (cfDNA) concentrations have been observed in clinical conditions of systemic inflammation. While the beneficial effects of regular physical activity on the release of circulating cfDNA still remain unknown, acute intense exercise has been shown to increase inflammatory cytokines and cfDNA concentrations in normal-weight individuals. Therefore, the primary purpose of this study was to examine the effect of acute high-intensity interval Exercise (HIIE) on plasma cfDNA and interleukin-6 (IL-6) responses in obese and normal-weight subjects. Main methods Fourteen male subjects (7 obese and 7 normal-weight) participated in an acute HIIE protocol (30 min, 4x4min @ 80% - 90% of VO2max) on a treadmill. Between HIIE intervals, subjects performed 3 min of active recovery at 50–60% VO2max. Blood samples were collected prior to, immediately following exercise, and one hour into recovery for measurements of plasma cfDNA and IL-6. Key findings Our results demonstrated a significant elevation in plasma cfDNA immediately following acute HIIE in both obese and normal-weight subjects. A comparable elevation in the concentration of plasma IL-6 was also found between two groups in response to acute HIIE. Furthermore, the level of plasma cfDNA was not correlated with IL-6 either at baseline or in response to acute HIIE. Significance These findings may support the utilization of HIIE as a time-efficient exercise protocol to understand the obesity-associated cfDNA and inflammatory responses.

BACKGROUND Recently, a novel index of arterial stiffness was developed to eliminate the placements of transducers on the carotid and femoral arteries and to make the measurement substantially easier. We evaluated the agreement of this new methodology with the well-established carotid–femoral pulse wave velocity (cfPWV). METHODS A total of 50 adults (28 men and 22 women) varying widely in age and blood pressure were studied. Heart-thigh pulse wave velocity (htPWV) and cfPWV were measured and compared. RESULTS Mean values of cfPWV and htPWV were 713 ± 145 and 699 ± 150 cm/s and were not significantly different (P = 0.43). Both cfPWV and htPWV were significantly associated with age (r = 0.80 and 0.58), body mass index (r = 0.44 and 0.31), and systolic blood pressure (r = 0.42 and 0.41). The 2 pulse wave velocity measures demonstrated a strong linear association with a Pearson correlation coefficient of 0.64 (P < 0.001). This agreement was consistent with the results of the Bland–Altman plot. CONCLUSION The automatic htPWV method, which permits the data acquisition with minimum technical skill, time, and intrusion in an operator-independent fashion, has good potential as a screening device for assessing arterial stiffness in a clinical setting.

Ischemic preconditioning can exert a powerful protection against a subsequent period of ischemia, via repeated inflation and deflation of a blood pressure cuff. Most often, damages of ischemia-reperfusion injury and benefits of preconditioning are evaluated via endothelial function. The ambulatory blood pressure monitoring constitutes repeated bouts of ischemia for 24 h. We examined whether repeated bouts of ischemia accumulated over 24 h influenced endothelial function. Twenty-two apparently healthy non-medicated middle-aged subjects 41 (8) years participated in the study. This study was registered with ClinicalTrials.gov (NCT03303404). Flow-mediated dilation (FMD) was measured as an index of endothelium-dependent vasodilation. The ambulatory blood pressure monitoring device went through an average of 110 (13) inflation/deflation cycles, which resulted in 46 (6) min of cumulative ischemic stimuli. Following 24-h of ambulatory blood pressure monitoring, FMD did not change significantly 6.6 (2.0) vs. 6.8 (2.7)%. Similarly, shear rate and reactive hyperemia were unchanged. We concluded that ambulatory blood pressure monitoring did not influence endothelium-dependent vasodilation acting via ischemic preconditioning.

BACKGROUND AND PURPOSE: Many breast cancer survivors (BCS) experience persistent cognitive and psychological changes associated with their cancer and/or treatment and that have limited treatment options. Therefore, the purpose of this study was to explore the feasibility and effects of a Kirtan Kriya meditation (KK) intervention on cognitive and psychological symptoms compared to an attention control condition, classical music listening (ML), in BCS. MATERIALS AND METHODS: A randomized control trial design was used. Participants completed eight-week interventions. Cognitive function and psychological symptoms were measured at baseline and post-intervention. Mixed analysis of variance models were examined for all cognitive and psychological outcomes. RESULTS: 27 BCS completed the study. Intervention adherence was 88%. Both groups improved in perceived cognitive impairments, cognition related quality of life, verbal memory, and verbal fluency (p’s < 0.01). There were no significant group by time effects for cognitive and psychological outcomes, except stress. The ML group reported lower stress at time 2 (p < 0.05). CONCLUSION: KK and ML are feasible, acceptable, and cost-effective interventions that may be beneficial for survivors’ cognition and psychological symptoms. Both interventions were easy to learn, low cost, and required just 12 minutes/day. Meditation or music listening could offer providers evidence-based suggestions to BCS experiencing cognitive symptoms.

Pentraxin 3 (PTX3) is mainly synthesized and released by neutrophils to help regulate innate immunity. While plasma PTX3 concentrations are associated with improved glucose metabolism and overall metabolic health, there is evidence that significant elevations in plasma glucose downregulate circulating levels of PTX3. To examine whether this relationship would be altered in response to exercise, this study investigated the kinetics of the plasma glucose and PTX3 responses following high-intensity interval exercise (HIIE) and continuous moderate-intensity exercise (CMIE). It was hypothesized that the increased concentrations of plasma glucose following HIIE compared with CMIE would be associated with an attenuated plasma PTX3 response. Eight healthy male subjects participated in both HIIE and CMIE protocols administered as a randomized, counterbalanced design. Linear mixed models for repeated measures revealed that the overall plasma glucose response was greater following HIIE compared with CMIE (protocol × time effect: p = 0.037). Although the plasma PTX3 response was higher only at 19 min into HIIE compared with CMIE (protocol × time effect: p = 0.013), no relationships were observed between plasma glucose and PTX3 either at baseline or in response to both exercise protocols, as indicated by the area under the curve “with respect to increase” analysis. Our results indicate that exercise-mediated plasma PTX3 concentrations are independent of the plasma glucose response. In addition, the present study suggests that the neutrophil-mediated innate immune response, as indicated by plasma PTX3 response, may be activated earlier during HIIE compared with CMIE.

The objective of this study was to examine whether acute aerobic exercise-mediated calprotectin in plasma would be associated with monocyte chemotactic protein-1 (MCP-1), myeloperoxidase (MPO), and interleukin-6 (IL-6) in healthy individuals. Eleven healthy participants, aged 18 to 30 years, were recruited to perform a 30-min bout of aerobic exercise at 75% maximal oxygen uptake. Acute aerobic exercise elicited a significant elevation across time in plasma calprotectin, MCP-1, MPO, and IL-6. Body mass index (BMI) was positively correlated with calprotectin area-under-the-curve with “respect to increase” (AUCi) and IL-6 AUCi. Furthermore, calprotectin AUCi was positively correlated with IL-6 AUCi and MPO AUCi, even after controlling for BMI. Although MPO AUCi was positively correlated with IL-6 AUCi, this relationship no longer existed after controlling for BMI. These results suggest that acute aerobic exercise could mediate innate immune response associated with calprotectin and its related leukocyte chemotactic and inflammatory mediators, especially in individuals with elevated BMI.

Purpose Calprotectin promotes the release of inflammatory mediators (e.g., monocyte chemoattractant protein-1 [MCP-1] and myeloperoxidase [MPO]) during the innate immune response as a mechanism to augment leukocyte chemotaxis and phagocytosis. Although plasma calprotectin is elevated with traditional continuous moderate-intensity exercise (CME) as an indicator of the inflammatory response, high-intensity interval exercise (HIIE) has been shown to attenuate systemic inflammation while providing similar improvements in cardiovascular health. Therefore, the purpose of this study was to compare plasma levels of calprotectin, MCP-1, and MPO between acute HIIE vs. CME. Methods Nine healthy males (24.67 ± 3.27 yrs) were recruited to participate in HIIE and CME on a cycle ergometer. HIIE consisted of 10 repeated 60 s of cycling at 90% max watts (Wmax) separated by 2 min of active recovery intensity of interval exercise, whereas CME consisted of 28 min of cycling at 60% Wmax. Blood samples were collected prior to, immediately post, and 30 and 60 min into recovery following exercise. Results Acute HIIE elicited a lower elevation in calprotectin and MPO compared to CME. An increase in MCP-1 was observed across time in both exercise protocols. Furthermore, our analyses did not reveal any significant correlation in percent change (baseline to immediately following exercise) among calprotectin, MCP1, and MPO in neither HIIE nor CME. However, a significant positive correlation was observed in the overall release of calprotectin and MPO across all four time points in both HIIE and CME. Conclusions Our findings indicate that acute HIIE may potentially diminish the systemic release of inflammatory mediators (calprotectin and MPO) compared to CME.