Thermoregulatory Adaptations following Sprint Interval Training

Traditional endurance training typically involves weeks of long-duration (60–90 min) exercise performed at a moderate to vigorous intensity. An alternative paradigm, sprint interval training, is characterized by multiple bouts of short-duration, high-intensity exercise. Similar fitness benefits from the two paradigms have been demonstrated, but whether sprint interval training—like traditional endurance training—induces heat acclimation remains unclear. Purpose To test the hypothesis that sprint interval training performed over six sessions results in measureable thermoregulatory and cardiovascular adaptations consistent with heat acclimation. Methods Seven untrained men [mean ± SD, 13 ± 5% body fat, 22 ± 3 y, 3.1 ± 0.3 L/min peak oxygen uptake (V̇O2peak)] performed 6 sprint interval training sessions over 12 days with 48­–72 h between sessions. Sessions consisted of 4–6 thirty-second Wingate Anaerobic Tests separated by ~4 min. Before and after the two-week training protocol, participants cycled for 30 min at 65% V̇O2peak in 25 °C to assess the effects of sprint interval training on heat acclimation. Results Main outcome variables (onset of sweating, sweat sensitivity, heart rate at end of exercise, percent change in plasma volume, and core temperature change from pre- to post-exercise) were not different from pre- to post-training (all p \u3e 0.05). Conclusion Two weeks of sprint interval training performed under the conditions specified does not result in heat acclimation

The Heritability of Amyotrophic Lateral Sclerosis in a Clinically Ascertained United States Research Registry

The genetic basis of amyotrophic lateral sclerosis (ALS) is not entirely clear. While there are families with rare highly penetrant mutations in Cu/Zn superoxide dismutase 1 and several other genes that cause apparent Mendelian inheritance of the disease, most ALS occurs in families without another affected individual. However, twin studies suggest that all ALS has a substantial genetic basis. Herein, we estimate the genetic contribution to ALS in a clinically ascertained case series from the United States.We used the database of the Emory ALS Center to ascertain individuals with ALS along with their family histories to determine the concordance among parents and offspring for the disease. We found that concordance for all parent-offspring pairs was low (<2%). With this concordance we found that ALS heritability, or the proportion of the disease explained by genetic factors, is between 40 and 45% for all likely estimates of ALS lifetime prevalence.We found the lifetime risk of ALS is 1.1% in first-degree relatives of those with ALS. Environmental and genetic factors appear nearly equally important for the development of ALS

Enhancing Discovery of Genetic Variants for Posttraumatic Stress Disorder Through Integration of Quantitative Phenotypes and Trauma Exposure Information

Funding Information: This work was supported by the National Institute of Mental Health / U.S. Army Medical Research and Development Command (Grant No. R01MH106595 [to CMN, IL, MBS, KJRe, and KCK], National Institutes of Health (Grant No. 5U01MH109539 to the Psychiatric Genomics Consortium ), and Brain & Behavior Research Foundation (Young Investigator Grant [to KWC]). Genotyping of samples was provided in part through the Stanley Center for Psychiatric Genetics at the Broad Institute supported by Cohen Veterans Bioscience . Statistical analyses were carried out on the LISA/Genetic Cluster Computer ( https://userinfo.surfsara.nl/systems/lisa ) hosted by SURFsara. This research has been conducted using the UK Biobank resource (Application No. 41209). This work would have not been possible without the financial support provided by Cohen Veterans Bioscience, the Stanley Center for Psychiatric Genetics at the Broad Institute, and One Mind. Funding Information: MBS has in the past 3 years received consulting income from Actelion, Acadia Pharmaceuticals, Aptinyx, Bionomics, BioXcel Therapeutics, Clexio, EmpowerPharm, GW Pharmaceuticals, Janssen, Jazz Pharmaceuticals, and Roche/Genentech and has stock options in Oxeia Biopharmaceuticals and Epivario. In the past 3 years, NPD has held a part-time paid position at Cohen Veterans Bioscience, has been a consultant for Sunovion Pharmaceuticals, and is on the scientific advisory board for Sentio Solutions for unrelated work. In the past 3 years, KJRe has been a consultant for Datastat, Inc., RallyPoint Networks, Inc., Sage Pharmaceuticals, and Takeda. JLM-K has received funding and a speaking fee from COMPASS Pathways. MU has been a consultant for System Analytic. HRK is a member of the Dicerna scientific advisory board and a member of the American Society of Clinical Psychopharmacology Alcohol Clinical Trials Initiative, which during the past 3 years was supported by Alkermes, Amygdala Neurosciences, Arbor Pharmaceuticals, Dicerna, Ethypharm, Indivior, Lundbeck, Mitsubishi, and Otsuka. HRK and JG are named as inventors on Patent Cooperative Treaty patent application number 15/878,640, entitled “Genotype-guided dosing of opioid agonists,” filed January 24, 2018. RP and JG are paid for their editorial work on the journal Complex Psychiatry. OAA is a consultant to HealthLytix. All other authors report no biomedical financial interests or potential conflicts of interest. Funding Information: This work was supported by the National Institute of Mental Health/ U.S. Army Medical Research and Development Command (Grant No. R01MH106595 [to CMN, IL, MBS, KJRe, and KCK], National Institutes of Health (Grant No. 5U01MH109539 to the Psychiatric Genomics Consortium), and Brain & Behavior Research Foundation (Young Investigator Grant [to KWC]). Genotyping of samples was provided in part through the Stanley Center for Psychiatric Genetics at the Broad Institute supported by Cohen Veterans Bioscience. Statistical analyses were carried out on the LISA/Genetic Cluster Computer (https://userinfo.surfsara.nl/systems/lisa) hosted by SURFsara. This research has been conducted using the UK Biobank resource (Application No. 41209). This work would have not been possible without the financial support provided by Cohen Veterans Bioscience, the Stanley Center for Psychiatric Genetics at the Broad Institute, and One Mind. This material has been reviewed by the Walter Reed Army Institute of Research. There is no objection to its presentation and/or publication. The opinions or assertions contained herein are the private views of the authors and are not to be construed as official or as reflecting true views of the U.S. Department of the Army or the Department of Defense. We thank the investigators who comprise the PGC-PTSD working group and especially the more than 206,000 research participants worldwide who shared their life experiences and biological samples with PGC-PTSD investigators. We thank Mark Zervas for his critical input. Full acknowledgments are in Supplement 1. MBS has in the past 3 years received consulting income from Actelion, Acadia Pharmaceuticals, Aptinyx, Bionomics, BioXcel Therapeutics, Clexio, EmpowerPharm, GW Pharmaceuticals, Janssen, Jazz Pharmaceuticals, and Roche/Genentech and has stock options in Oxeia Biopharmaceuticals and Epivario. In the past 3 years, NPD has held a part-time paid position at Cohen Veterans Bioscience, has been a consultant for Sunovion Pharmaceuticals, and is on the scientific advisory board for Sentio Solutions for unrelated work. In the past 3 years, KJRe has been a consultant for Datastat, Inc. RallyPoint Networks, Inc. Sage Pharmaceuticals, and Takeda. JLM-K has received funding and a speaking fee from COMPASS Pathways. MU has been a consultant for System Analytic. HRK is a member of the Dicerna scientific advisory board and a member of the American Society of Clinical Psychopharmacology Alcohol Clinical Trials Initiative, which during the past 3 years was supported by Alkermes, Amygdala Neurosciences, Arbor Pharmaceuticals, Dicerna, Ethypharm, Indivior, Lundbeck, Mitsubishi, and Otsuka. HRK and JG are named as inventors on Patent Cooperative Treaty patent application number 15/878,640, entitled ?Genotype-guided dosing of opioid agonists,? filed January 24, 2018. RP and JG are paid for their editorial work on the journal Complex Psychiatry. OAA is a consultant to HealthLytix. All other authors report no biomedical financial interests or potential conflicts of interest. Publisher Copyright: © 2021 Society of Biological PsychiatryBackground: Posttraumatic stress disorder (PTSD) is heritable and a potential consequence of exposure to traumatic stress. Evidence suggests that a quantitative approach to PTSD phenotype measurement and incorporation of lifetime trauma exposure (LTE) information could enhance the discovery power of PTSD genome-wide association studies (GWASs). Methods: A GWAS on PTSD symptoms was performed in 51 cohorts followed by a fixed-effects meta-analysis (N = 182,199 European ancestry participants). A GWAS of LTE burden was performed in the UK Biobank cohort (N = 132,988). Genetic correlations were evaluated with linkage disequilibrium score regression. Multivariate analysis was performed using Multi-Trait Analysis of GWAS. Functional mapping and annotation of leading loci was performed with FUMA. Replication was evaluated using the Million Veteran Program GWAS of PTSD total symptoms. Results: GWASs of PTSD symptoms and LTE burden identified 5 and 6 independent genome-wide significant loci, respectively. There was a 72% genetic correlation between PTSD and LTE. PTSD and LTE showed largely similar patterns of genetic correlation with other traits, albeit with some distinctions. Adjusting PTSD for LTE reduced PTSD heritability by 31%. Multivariate analysis of PTSD and LTE increased the effective sample size of the PTSD GWAS by 20% and identified 4 additional loci. Four of these 9 PTSD loci were independently replicated in the Million Veteran Program. Conclusions: Through using a quantitative trait measure of PTSD, we identified novel risk loci not previously identified using prior case-control analyses. PTSD and LTE have a high genetic overlap that can be leveraged to increase discovery power through multivariate methods.publishersversionpublishe

Rare coding variants in PLCG2, ABI3, and TREM2 implicate microglial-mediated innate immunity in Alzheimer's disease

We identified rare coding variants associated with Alzheimer’s disease (AD) in a 3-stage case-control study of 85,133 subjects. In stage 1, 34,174 samples were genotyped using a whole-exome microarray. In stage 2, we tested associated variants (P<1×10-4) in 35,962 independent samples using de novo genotyping and imputed genotypes. In stage 3, an additional 14,997 samples were used to test the most significant stage 2 associations (P<5×10-8) using imputed genotypes. We observed 3 novel genome-wide significant (GWS) AD associated non-synonymous variants; a protective variant in PLCG2 (rs72824905/p.P522R, P=5.38×10-10, OR=0.68, MAFcases=0.0059, MAFcontrols=0.0093), a risk variant in ABI3 (rs616338/p.S209F, P=4.56×10-10, OR=1.43, MAFcases=0.011, MAFcontrols=0.008), and a novel GWS variant in TREM2 (rs143332484/p.R62H, P=1.55×10-14, OR=1.67, MAFcases=0.0143, MAFcontrols=0.0089), a known AD susceptibility gene. These protein-coding changes are in genes highly expressed in microglia and highlight an immune-related protein-protein interaction network enriched for previously identified AD risk genes. These genetic findings provide additional evidence that the microglia-mediated innate immune response contributes directly to AD development

Comparison of bioelectrical impedance analysis and dual-energy x-ray absorptiometry for estimating bone mineral content

The purpose of this study was to validate single-frequency hand-to-foot bioelectrical impedance analysis (HFBIA) for estimating bone mineral content (BMC) using dual-energy X-ray absorptiometry as the criterion measure in healthy men and women aged 18-40 years. A total of 80 men and women participated in this study. BMC was estimated on the same day using HFBIA and dual-energy X-ray absorptiometry. The HFBIA device provided higher mean BMC values in men and the entire sample, but not in women. A smaller standard error of estimate was observed in women (0.20, corresponding to 8% of the mean reference BMC values) compared with men (0.39, corresponding to 12% of the mean reference BMC values) and the combined sample (0.31). HFBIA provided a smaller constant error and individual estimation error indicated by the 95% limits of agreement in women (-0.05 ± 0.39) compared with men (-0.16 ± 0.78) and the entire sample (-0.10 ± 0.63). In conclusion, although BMC values were found to be more accurate in women, HFBIA overestimated BMC compared with dual-energy X-ray absorptiometry, especially in individuals with lower values. Given these results, using HFBIA to measure BMC would be inappropriate for diagnostic purposes

An Evaluation of Select Physical Activity Exercise Classes on Bone Metabolism

International Journal of Exercise Science 11(2): 452-461, 2018. Weight-bearing physical activity can optimize bone mass early in life and prevent the development of osteoporosis. However, less is known about the potential benefits of non-weight-bearing activities. The purpose of this study was to assess the efficacy of structured physical activity classes on bone metabolism. Twenty-eight premenopausal women, aged 18–35 years who were either enrolled in a yoga class (n=14) or cardio-kickboxing class (n=14) voluntarily consented to participate. Both classes were introductory classes meeting twice per week for 50 min per session for 12 weeks. Anteroposterior spine (L1-L4), hip (dual femur), and total body bone mineral density (BMD) was measured in both groups pre and post intervention using dual-energy X-ray absorptiometry (DXA). Pre and post blood samples were drawn for measurement of serum osteocalcin (OC) by enzyme-linked immunosorbent assay (ELISA) in each group. Baseline subject characteristics including age, height, weight, body fat percentage, and lean body mass did not differ between groups. BMD levels did not increase but were held stable over the course of the intervention. Yoga increased OC by 68% (P \u3c 0.001) and cardio-kickboxing increased OC by 67% (P \u3c 0.001) over the course of the 12-week classes. While 12 weeks of yoga and cardio-kickboxing were insufficient to induce BMD changes, OC levels reflect the bone formation process was initiated, but not yet complete. Increased OC levels suggest the selected physical activity classes provided enough of a stimulus to precipitate a future response of bone growth, assuming exercise training remains constant

Acute Effect of Lower-Body Vibration as a Recovery Method After Fatiguing Exercise

The purpose of this study was to compare three recovery methods: control (CON), lower-body vibration (LBV) and LBV+ local muscle cooling (LBVC) on lower-body performance, perceived recovery, and muscle soreness. Physically active male volunteers (n=8) in a repeated-measures, counterbalanced design, completed three sets of squats to fatigue, each recovery treatment, and two Wingate Anaerobic Tests. Rating of perceived exertion (RPE), and heart rate (HR) were measured after fatiguing exercise, recovery treatment and Wingate Anaerobic tests. Peak and mean power, fatigue index, Delayed Onset Muscle Soreness (DOMS), and comfort levels were compared between each treatment. In Wingate 1, no significant differences (p=0.42) were found among CON, LBV, or LBVC regarding peak power (1119±239, 1097±225, and 1146±260 W, respectively), mean power (p=0.32), or fatigue index (p=0.47). In Wingate 2, no significant (p=0.17) differences were found among CON, LBV, or LBVC regarding peak power (1042±228, 1078±233, and 1110±268 W, respectively), mean power (p=0.38), or fatigue index (p=0.15). A significantly better (p=0.01) perceived recovery was observed after LBV (6±1) and LBVC (6±1) compared to CON (4±1). The study findings support psychological but not performance enhancing benefits after the use of LBV and LBVC as recovery methods

Articles in PresS

ABSTRACT 25 The influence of thermoreceptors in human facial skin on thermoeffector responses is equivocal; 26 furthermore, the presence of thermoreceptors in the respiratory tract and their involvement in 27 thermal homeostasis has not been elucidated. This study tested the hypothesis that hot air 28 directed on the face and inhaled during whole-body passive heat stress elicits an earlier onset and 29 greater sensitivity of cutaneous vasodilation and sweating than that directed on an equal skin 30 surface area away from the face. Six men and 2 women completed 2 trials separated by ~1 31 week. Participants were passively heated (water-perfused suit; core temperature increase ~0.9 32 °C) while hot air was directed on either the face or on the lower leg (counterbalanced). Skin 33 blood flux (laser-Doppler flowmetry) and local sweat rate (capacitance hygrometry) were 34 measured at the chest and one forearm. During hot-air heating, local temperatures of the cheek 35 and leg were 38.4 ± 0.8 °C and 38.8 ± 0.6 °C, respectively (p=0.18). Breathing hot air combined 36 with facial heating did not affect mean body temperature onsets (p=0.97 and 0.27 for arm and 37 chest sites, respectively) or slopes of cutaneous vasodilation (p=0.49 and 0.43 for arm and chest 38 sites, respectively), or the onsets (p=0.89 and 0.94 for arm and chest sites, respectively) or slopes 39 of sweating (p=0.48 and 0.65 for arm and chest sites, respectively). Based on these findings, 40 respiratory tract thermoreceptors-if present in humans-and selective facial skin heating do not 41 modulate thermoeffector responses during passive heat stress. 4