Comprehensive Physical Activity Assessment During U.S. Army Basic Combat Training.

ABSTRACT: Alemany, JA, Pierce, JR, Bornstein, DB, Grier, TL, Jones, BH, and Glover, SH. Comprehensive physical activity assessment during U.S. Army Basic Combat Training. J Strength Cond Res 36(12): 3505-3512, 2022-Physical activity (PA) volume, intensity, and qualitative contextual information regarding activity type and loads carried are limited during U.S. Army Basic Combat Training (BCT). The purpose of this study was to characterize daily (05:00-20:00 hours) PA during BCT using a comprehensive approach. During 2 10-week BCT cycles ( n = 40 trainees per cycle), pedometers, accelerometers, and direct observation were used to estimate daily step count, PA volume, and intensity. Physical activity intensity was categorized by metabolic equivalents (METs) such as "sedentary" (1-2 METs), "light" (2-3 METs), "moderate" (3-6 METs), or "vigorous" (≥6 METs). Daily PA data were analyzed longitudinally using linear mixed models, with significance set at p ≤ 0.05. The mean daily step count was 13,459 ± 4,376 steps, and the mean daily accelerometer-assessed PA volume and intensity were as follows: sedentary: 505 ± 98 minutes, light: 190 ± 78 minutes, moderate: 168 ± 51 minutes, and vigorous: 14 ± 14 minutes, with no differences between cycles for all measures ( p > 0.50). Cumulative time on feet (∼50%) and sitting (20-25%) accounted for most daily activity types during both cycles. Trainees, on average, carried between 3 and 9 kg, and ≥9 kg, for 60% and 10% of the monitored day, respectively. Basic Combat Training's physical demands are high, where trainees achieved 1.7 to 2.7 times greater daily ambulation and 6 times the recommended weekly moderate-to-vigorous PA compared with civilian counterparts and performed weight-bearing load carriage for nearly half of the day. Basic Combat Training-associated PA may increase injury risk among trainees unaccustomed to arduous PA and exercise. Implementing national PA policies to improve physical fitness and facilitate acclimatization to BCT's high physical demands could reduce public health burdens and military nonreadiness.

Innate immunity receptor CD36 promotes cerebral amyloid angiopathy.

Deposition of amyloid-ß (Aß) in cerebral arteries, known as cerebral amyloid angiopathy (CAA), occurs both in the setting of Alzheimer's disease and independent of it, and can cause cerebrovascular insufficiency and cognitive deficits. The mechanisms leading to CAA have not been established, and no therapeutic targets have been identified. We investigated the role of CD36, an innate immunity receptor involved in Aß trafficking, in the neurovascular dysfunction, cognitive deficits, and amyloid accumulation that occurs in mice expressing the Swedish mutation of the amyloid precursor protein (Tg2576). We found that Tg2576 mice lacking CD36 have a selective reduction in Aß1-40 and CAA. This reduced vascular amyloid deposition was associated with preservation of the Aß vascular clearance receptor LRP-1, and protection from the deleterious effects of Aß on cerebral arterioles. These beneficial vascular effects were reflected by marked improvements in neurovascular regulation and cognitive performance. Our data suggest that CD36 promotes vascular amyloid deposition and the resulting cerebrovascular damage, leading to neurovascular dysfunction and cognitive deficits. These findings identify a previously unrecognized role of CD36 in the mechanisms of vascular amyloid deposition, and suggest that this scavenger receptor is a putative therapeutic target for CAA and related conditions.

IL-15 concentrations in skeletal muscle and subcutaneous adipose tissue in lean and obese humans: local effects of IL-15 on adipose tissue lipolysis.

Animal/cell investigations indicate that there is a decreased adipose tissue mass resulting from skeletal muscle (SkM) IL-15 secretion (e.g., SkM-blood-adipose tissue axis). IL-15 could regulate fat mass accumulation in obesity via lipolysis, although this has not been investigated in humans. Therefore, the purpose was to examine whether SkM and/or subcutaneous adipose tissue (SCAT) IL-15 concentrations were correlated with SCAT lipolysis in lean and obese humans and determine whether IL-15 perfusion could induce lipolysis in human SCAT. Local SkM and abdominal SCAT IL-15 (microdialysis) and circulating IL-15 (blood) were sampled in lean (BMI: 23.1 ± 1.9 kg/m(2); n = 10) and obese (BMI: 34.7 ± 3.5 kg/m(2); n = 10) subjects at rest/during 1-h cycling exercise. Lipolysis (SCAT interstitial glycerol concentration) was compared against local/systemic IL-15. An additional probe in SCAT was perfused with IL-15 to assess direct lipolytic responses. SkM IL-15 was not different between lean and obese subjects (P = 0.45), whereas SCAT IL-15 was higher in obese vs. lean subjects (P = 0.02) and was correlated with SCAT lipolysis (r = 0.45, P = 0.05). Exercise increased SCAT lipolysis in lean and obese (P < 0.01), but exercise-induced SCAT lipolysis changes were not correlated with exercise-induced SCAT IL-15 changes. Microdialysis perfusion resulting in physiological IL-15 concentrations in the adipose tissue interstitium increased lipolysis in lean (P = 0.04) but suppressed lipolysis in obese (P < 0.01). Although we found no support for a human IL-15 SkM-blood-adipose tissue axis, IL-15 may be produced in/act on the abdominal SCAT depot. The extent to which this autocrine/paracrine IL-15 action regulates human body composition remains unknown.

Human Performance Optimization Metrics: Consensus Findings, Gaps, and Recommendations for Future Research.

Human performance optimization (HPO) is defined as "the process of applying knowledge, skills and emerging technologies to improve and preserve the capabilities of military members, and organizations to execute essential tasks." The lack of consensus for operationally relevant and standardized metrics that meet joint military requirements has been identified as the single most important gap for research and application of HPO. In 2013, the Consortium for Health and Military Performance hosted a meeting to develop a toolkit of standardized HPO metrics for use in military and civilian research, and potentially for field applications by commanders, units, and organizations. Performance was considered from a holistic perspective as being influenced by various behaviors and barriers. To accomplish the goal of developing a standardized toolkit, key metrics were identified and evaluated across a spectrum of domains that contribute to HPO: physical performance, nutritional status, psychological status, cognitive performance, environmental challenges, sleep, and pain. These domains were chosen based on relevant data with regard to performance enhancers and degraders. The specific objectives at this meeting were to (a) identify and evaluate current metrics for assessing human performance within selected domains; (b) prioritize metrics within each domain to establish a human performance assessment toolkit; and (c) identify scientific gaps and the needed research to more effectively assess human performance across domains. This article provides of a summary of 150 total HPO metrics across multiple domains that can be used as a starting point-the beginning of an HPO toolkit: physical fitness (29 metrics), nutrition (24 metrics), psychological status (36 metrics), cognitive performance (35 metrics), environment (12 metrics), sleep (9 metrics), and pain (5 metrics). These metrics can be particularly valuable as the military emphasizes a renewed interest in Human Dimension efforts, and leverages science, resources, programs, and policies to optimize the performance capacities of all Service members.

Walking as a method for epistemic justice in sustainability.

We argue that walking as a method provides an integrative approach to advance epistemic justice in sustainability research. The theory and practice of walking as a method has grown quickly within the social sciences and arts but remains underrepresented in sustainability research, where walking is typically an object of study (e.g., urban walkability). We argue that walking should be valued as an important mode of knowledge production that simultaneously widens sustainability knowledge, integrates diverse knowledge systems, and supports transdisciplinary sustainability solutions. In this perspective article, we consider the following questions: (1) Why is walking important to sustainability knowledge? (2) How can walk-based methods advance epistemic justice in sustainability knowledge? (3) What outcomes might we expect from cultivating walking as a method for sustainability knowledge? We reflect on how walking as a method centers equity and the contributions of walk-based sustainability knowledge for research and policy.

COX-1-derived PGE2 and PGE2 type 1 receptors are vital for angiotensin II-induced formation of reactive oxygen species and Ca(2+) influx in the subfornical organ.

Regulation of blood pressure by angiotensin II (ANG II) is a process that involves the reactive oxygen species (ROS) and calcium. We have shown that ANG-II type 1 receptor (AT1R) and prostaglandin E2 (PGE2) type 1 receptors (EP1R) are required in the subfornical organ (SFO) for ROS-mediated hypertension induced by slow-pressor ANG-II infusion. However, the signaling pathway associated with this process remains unclear. We sought to determine mechanisms underlying the ANG II-induced ROS and calcium influx in mouse SFO cells. Ultrastructural studies showed that cyclooxygenase 1 (COX-1) codistributes with AT1R in the SFO, indicating spatial proximity. Functional studies using SFO cells revealed that ANG II potentiated PGE2 release, an effect dependent on AT1R, phospholipase A2 (PLA2) and COX-1. Furthermore, both ANG II and PGE2 increased ROS formation. While the increase in ROS initiated by ANG II, but not PGE2, required the activation of the AT1R/PLA2/COX-1 pathway, both ANG II and PGE2 were dependent on EP1R and Nox2 as downstream effectors. Finally, ANG II potentiated voltage-gated L-type Ca(2+) currents in SFO neurons via the same signaling pathway required for PGE2 production. Blockade of EP1R and Nox2-derived ROS inhibited ANG II and PGE2-mediated Ca(2+) currents. We propose a mechanism whereby ANG II increases COX-1-derived PGE2 through the AT1R/PLA2 pathway, which promotes ROS production by EP1R/Nox2 signaling in the SFO. ANG II-induced ROS are coupled with Ca(2+) influx in SFO neurons, which may influence SFO-mediated sympathoexcitation. Our findings provide the first evidence of a spatial and functional framework that underlies ANG-II signaling in the SFO and reveal novel targets for antihypertensive therapies.

IGF-I measurement across blood, interstitial fluid, and muscle biocompartments following explosive, high-power exercise.

Insulin-like growth factor-I (IGF-I) resides across different biocompartments [blood, interstitial fluid (ISF), and muscle]. Whether circulating IGF-I responses to exercise reflect local events remains uncertain. We measured the IGF-I response to plyometric exercise across blood, ISF, and muscle biopsy from the vastus lateralis. Twenty volunteers (8 men, 12 women, 22 ± 1 yr) performed 10 sets of 10 plyometric jump repetitions at a 40% 1-repetition maximum. Blood, ISF, and muscle samples were taken pre- and postexercise. Circulating IGF-I increased postexercise: total IGF-I (preexercise = 546 ± 42, midexercise = 585 ± 43, postexercise = 597 ± 45, +30 = 557 ± 42, +60 = 536 ± 40, +120 = 567 ± 42 ng/ml; midexercise, postexercise, and +120 greater than preexercise, P < 0.05); Free IGF-I (preexercise = 0.83 ± 0.09, midexercise = 0.78 ± 0.10, postexercise = 0.79 ± 0.11, +30 = 0.93 ± 0.10, +60 = 0.88 ± 0.10, + 120 = 0.91 ± 0.11 ng/ml; +30 greater than all other preceding time points, P < 0.05). No exercise-induced changes were observed for ISF IGF-I (preexercise = 2.35 ± 0.29, postexercise = 2.46 ± 0.35 ng/ml). No changes were observed for skeletal muscle IGF-I protein, although IGF-I mRNA content increased ∼40% postexercise. The increase in circulating total and free IGF-I was not correlated with increases in ISF IGF-I or muscle IGF-I protein content. Our data indicate that exercise-induced increases in circulating IGF-I are not reflective of local IGF-I signaling.

New insights into the role of hilar ectopic granule cells in the dentate gyrus based on quantitative anatomic analysis and three-dimensional reconstruction.

The dentate gyrus is one of two main areas of the mammalian brain where neurons are born throughout adulthood, a phenomenon called postnatal neurogenesis. Most of the neurons that are generated are granule cells (GCs), the major principal cell type in the dentate gyrus. Some adult-born granule cells develop in ectopic locations, such as the dentate hilus. The generation of hilar ectopic granule cells (HEGCs) is greatly increased in several animal models of epilepsy and has also been demonstrated in surgical specimens from patients with intractable temporal lobe epilepsy (TLE). Herein we review the results of our quantitative neuroanatomic analysis of HEGCs that were filled with Neurobiotin following electrophysiologic characterization in hippocampal slices. The data suggest that two types of HEGCs exist, based on a proximal or distal location of the cell body relative to the granule cell layer, and based on the location of most of the dendrites, in the molecular layer or hilus. Three-dimensional reconstruction revealed that the dendrites of distal HEGCs can extend along the transverse and longitudinal axis of the hippocampus. Analysis of axons demonstrated that HEGCs have projections that contribute to the normal mossy fiber innervation of CA3 as well as the abnormal sprouted fibers in the inner molecular layer of epileptic rodents (mossy fiber sprouting). These data support the idea that HEGCs could function as a "hub" cell in the dentate gyrus and play a critical role in network excitability.

Insulin-like growth factor-I biocompartmentalization across blood, interstitial fluid and muscle, before and after 3 months of chronic resistance exercise.

This investigation examined the influence of 12-week ballistic resistance training programs on the IGF-I system in circulation, interstitial fluid, and skeletal muscle, at rest and in response to acute exercise. Seventeen college-aged subjects (11 women/6 men; 21.7 ± 3.7 yr) completed an acute ballistic exercise bout before and after the training program. Blood samples were collected pre-, mid-, and postexercise and analyzed for serum total IGF-I, free IGF-I, and IGF binding proteins (IGFBPs) 1-4. Dialysate and interstitial free IGF-I were analyzed in vastus lateralis (VL) interstitial fluid collected pre- and postexercise via microdialysis. Pre- and postexercise VL muscle biopsies were analyzed for IGF-I protein expression, IGF-I receptor phosphorylation (p-IGF-IR), and AKT phosphorylation (p-AKT). Following training, basal serum IGF-I, free IGF-I, IGFBP-2, and IGFBP-3 decreased whereas IGFBP-1 and IGFBP-4 increased. Training reduced basal dialysate and interstitial free IGF-I but had no effect on basal skeletal muscle IGF-I, p-IGF-IR, or p-AKT. Acute exercise elicited transient changes in IGF-I system concentrations and downstream anabolic signaling both pre- and posttraining; training did not affect this acute exercise response. Posttraining, acute exercise-induced changes in dialysate/interstitial free IGF-I were strongly correlated with the changes in intramuscular IGF-I expression, p-IGF-IR, and p-AKT. The divergent influence of resistance training on circulating/interstitial and skeletal muscle IGF-I demonstrates the importance of concurrent, multiple biocompartment analysis when examining the IGF-I system. As training elicited muscle hypertrophy, these findings indicate that IGF-I's anabolic effects on skeletal muscle are mediated by local, rather than systemic mechanisms.NEW & NOTEWORTHY In the first investigation to assess resistance training's effects on the IGF-I system in serum, interstitial fluid, and skeletal muscle, training decreased basal circulating and interstitial IGF-I but did not alter basal intramuscular IGF-I protein activity. Posttraining, acute exercise-induced interstitial IGF-I increases were strongly correlated with intramuscular IGF-I expression and signaling. These findings highlight the importance of multibiocompartment measurement when analyzing IGF-I and suggest that IGF-I's role in hypertrophic adaptations is locally mediated.

Growth Hormone and Insulin-like Growth Factor-I Molecular Weight Isoform Responses to Resistance Exercise Are Sex-Dependent.

Purpose: To determine if acute resistance exercise-induced increases in growth hormone (GH) and insulin-like growth factor-I (IGF-I) were differentially responsive for one or more molecular weight (MW) isoforms and if these responses were sex-dependent. Methods: College-aged men (n = 10) and women (n = 10) performed an acute resistance exercise test (ARET; 6 sets, 10 repetition maximum (10-RM) squat, 2-min inter-set rest). Serum aliquots from blood drawn Pre-, Mid-, and Post-ARET (0, +15, and +30-min post) were processed using High Performance Liquid Chromatography (HPLC) fractionation and pooled into 3 MW fractions (Fr.A: >60; Fr.B: 30-60; Fr.C: <30 kDa). Results: We observed a hierarchy of serum protein collected among GH fractions across all time points independent of sex (Fr.C > Fr.A > Fr.B, p ≤ 0.03). Sex × time interactions indicated that women experienced earlier and augmented increases in all serum GH MW isoform fraction pools (p < 0.05); however, men demonstrated delayed and sustained GH elevations (p < 0.01) in all fractions through +30-min of recovery. Similarly, we observed a sex-independent hierarchy among IGF-I MW fraction pools (Fr.A > Fr.B > Fr.C, p ≤ 0.01). Furthermore, we observed increases in IGF-I Fr. A (ternary complexes) in men only (p ≤ 0.05), and increases in Fr.C (free/unbound IGF-I) in women only (p ≤ 0.05) vs. baseline, respectively. Conclusions: These data indicate that the processing of GH and IGF-I isoforms from the somatotrophs and hepatocytes are differential in their response to strenuous resistance exercise and reflect both temporal and sex-related differences.

Relationship of Anthropometric Measures on Female Trainees' and Active Duty Soldiers' Performance of Common Soldiering Tasks.

INTRODUCTION: This study compared the relationship between height (HT), body mass (BM), and body mass index (BMI) of female trainees and active duty female soldiers and their performance on simulated common soldiering tasks (CSTs) with high physical demands. METHODS: Female trainees (n = 133) and soldiers (n = 229) completed the following CSTs: sandbag carry, move under fire, casualty drag, casualty evacuation, and road march. Quartiles were created among HT, BM, and BMI by which task performance was compared using ANOVAs with Tukey post hoc comparisons. RESULTS: For both trainees and soldiers, HT, BM, and BMI were positively associated with improved road march, casualty drag, casualty evacuation, and sandbag carry performance. On the move under fire task, only soldier HT was positively associated with improved performance. CONCLUSION: Female trainees and soldiers who are taller and heavier with a higher BMI may demonstrate better performance on CSTs required of all soldiers. In addition to task-specific training, performance of CSTs may be enhanced in tasks requiring strength and power by recruiting and retaining taller and heavier females with a higher BMIs. Allowances should be considered for soldiers and trainees who can successfully perform soldiering tasks with high physical demands despite less desirable anthropometric measurements.

Microdialysis-Assessed Exercised Muscle Reveals Localized and Differential IGFBP Responses to Unilateral Stretch Shortening Cycle Exercise.

Microdialysis allows for a preview into local muscle metabolism and can provide physiological insight that blood measurements cannot. Purpose: To examine the potential differential IGF-I system regulation in interstitial fluid during unilateral stretch shortening cycle exercise. Methods: 10 men (26 ± 7 year) performed unilateral jumping [stretch shortening cycle (SSC) exercise at 50% of optimal jump height] until volitional fatigue on a sled apparatus. Biological sampling took place using a catheter inserted into an antecubital vein (serum), and 100 kDa microdialysis probes inserted into the thigh muscle of each exercise/control leg (dialysate). Serum was drawn before (Pre; -3 h) and after SSC [Post I (+0 h), II (+3 h), or III (+20 h)]; dialysate was sampled for 2 h before (Pre), during/immediately after (Ex), and 3 h into recovery (Rec) following SSC. IGF-I system parameters (free/total IGF-I and IGFBPs 1-6) were measured with immunoassays. Interstitial free IGF-I was estimated from dialysate IGF-I and relative recovery (ethanol) correction. Data were analyzed with repeated measures ANOVA. Results: Serum total IGF-I remained elevated +3 h (Post II: 182.8 ± 37.6 vs. Pre: 168.3 ± 35.0 ng/mL, p < 0.01), but returned to baseline by +20 h (Post III vs. Pre, p = 0.31). No changes in serum free IGF-I were noted. Serum BP-1 and -3 increased over baseline, but not until + 20 h after SSC (Post III vs. Pre: 7.6 ± 4.9 vs. 3.7 ± 2.3 and 1,048.6 ± 269.2 vs. 891.4 ± 171.2 ng/mL, respectively). We observed a decreased serum BP-6 +3 h after SSC (p < 0.01), followed by a return to baseline at +20 h (p = 0.64 vs. Pre). There were no exercise-induced changes in serum BP-2, -4, or -5. Unlike serum, there were no changes in dialysate or interstitial free IGF-I in either leg (p > 0.05). Dialysate BP-1 remained increased in both exercise and control legs through 3 h into recovery (Rec vs. Pre, p < 0.01). Dialysate BP-3 also demonstrated a prolonged elevation over Pre SSC concentrations, but in the exercise leg only (Ex and Rec vs. Pre, p < 0.04). We observed a prolonged decrease in dialysate BP-5 (Ex and Rec vs. Pre, p < 0.03) and an increase in BP-4 IP in the exercise leg only. There were no changes relative to Pre SSC in dialysate BP-2 or -6. Conclusions: Unilateral exercise drives differential regulation of the IGF-I system at both local and systemic levels. More specifically, this is the first study to demonstrate that localized exercise increases IGFBP-3, IGFBP-4 and decreases in IGFBP-5 in muscle interstitial fluid.

The neurokinin-3 (NK3) and the neurokinin-1 (NK1) receptors are differentially targeted to mesocortical and mesolimbic projection neurons and to neuronal nuclei in the rat ventral tegmental area.

Tonic activation of neurokinin-3 (NK(3)) receptors in dopamine neurons of the ventral tegmental area (VTA) has been implicated in the pathophysiology of schizophrenia. This psychiatric disorder is associated with a dysfunctional activity in VTA projection neurons that can affect cognitive function at the level of the medial prefrontal cortex (mPFC) as well as motor and motivational states controlled in part by mesolimbic output to the nucleus accumbens (Acb). To determine the relevant sites for NK(3) receptor activation within this neuronal network, we used confocal and electron microscopy to examine NK(3) receptors (Cy5; immunogold) and retrograde labeling of fluorogold (FG, FITC; immunoperoxidase) in the VTA of rats receiving either Acb or mPFC injections of FG. Comparison was made with neurokinin-1 (NK(1)) receptors, which are also present, but less abundant then NK(3) receptors, in dopaminergic and GABAergic VTA neurons. There were no observable differences between NK(3) and NK(1) receptors in their primary locations in the cytoplasm and on the plasma membrane of VTA somata and dendrites with or without FG. Dendrites labeled with FG retrogradely transported from mPFC, however, contained more NK(3) or less NK(1) immunogold particles (plasmalemmal + cytoplasmic) then those retrogradely labeled following FG injection in the Acb. Moreover, only the NK(3) receptors were detected in neuronal nuclei in the VTA and in the nuclei of human HEK-293T NK(3)-transfected cells. The enrichment of NK(3) receptors in mesocortical projection neurons and nuclear distribution of these receptors may provide insight for understanding the selective antipsychotic effectiveness of NK(3) antagonists.

Effects of exercise training on the matrix metalloprotease response to acute exercise.

Matrix metalloproteases (MMPs) in the circulation are thought to modulate the activation of growth factors, cytokines, and angiogenesis, facilitating physiological adaptations to exercise training. The purpose of this work was to characterize serum MMP-1, MMP-2, MMP-3, and MMP-9 concentrations pre- and post-eight weeks of exercise training. We tested the hypothesis that exercise training would influence serum MMP concentrations in response to an acute resistance exercise test (ARET). Participants were randomized into an 8-week training program (5 days per week) that emphasized callisthenic (CT, N = 8) or resistance (RT, N = 8) exercise. Serum MMP concentrations (MMP-1, -2, -3, -9) were assessed in men (N = 16) in response to an acute bout of high-intensity resistance exercise (six sets of 10-RM squats with 2-min inter-set rest periods) both before and after 8 weeks of training. Training resulted in a temporal shift in the peak MMP-1 concentration from post-ARET to mid-ARET in both groups. Post-training, MMP-9 concentrations were increased immediately after the ARET in the CT group as compared to pre-training ARET concentrations. RT did not alter MMP-3 and -9 concentrations. These data suggest that the mode of exercise training influences the MMP response to an acute bout of exercise, revealing a possible role of MMPs in initiating training-specific adaptations.

Characterization of growth hormone disulfide-linked molecular isoforms during post-exercise release vs nocturnal pulsatile release reveals similar milieu composition.

OBJECTIVE: To characterize the influence of mode (aerobic/resistance) and volume of exercise (moderate/high) on circulating GH immediately post-exercise as well as following the onset of sleep. DESIGN: This study used repeated measures in which subjects randomly completed 5 separate conditions: control (no exercise), moderate volume resistance exercise (MR), high-volume resistance exercise (HR), moderate volume aerobic exercise (MA), and high volume aerobic exercise (HA). METHODS: Subjects had two overnight stays on each of the 5 iterations. Serial blood draws began as soon as possible after the completion of the exercise session. Blood was obtained every 20 min for 24-h. GH was measured using a chemiluminescent immunoassay. Pooled samples representing post exercise (PE) and first nocturnal pulse (NP) were divided into two aliquots. One of these aliquots was chemically reduced by adding 10 mM glutathione (GSH) to break down disulfide-linked aggregates. RESULTS: No differences were observed when pooling GH response at post-exercise (2.02 ±â€¯0.21) and nocturnal pulse (2.63 ±â€¯0.51; p = .32). Pairwise comparisons revealed main effect differences between controls (1.19 ±â€¯0.29) and both MA (2.86 ±â€¯0.31; p = .009) and HA (3.73 ±â€¯0.71; p = .001). Both MA (p = .049) and HA (p = .035) responses were significantly larger than the MR stimulus (1.96 ±â€¯0.28). With GSH reduction, controls significantly differed from MA (p = .018) and HA (p = .003) during PE, but only differed from HA (p = .003) during NP. CONCLUSIONS: This study demonstrated similar GH responses to exercise and nocturnal pulse, indicating that mode and intensity of exercise does not proportionately affect GH dimeric isoform concentration.

Exercise Effects on Adipose Tissue Postprandial Lipolysis and Blood Flow in Children.

Poor suppression of lipolysis and blunted increase in blood flow after meal ingestion in obese adults may indicate resistance to the antilipolytic action of insulin. Exercise may be used to normalize lipolytic responses to food intake by increasing insulin sensitivity. PURPOSE: To determine if acute bouts of aerobic exercise and/or excise training alter lipolytic and blood flow responses to food intake in lean (LN) and obese (OB) children. METHODS: Sixty-five children (9-11 yr) were randomized into acute exercise (EX: 16 LN and 28 OB) or control (CON: 9 LN and 12 OB) groups that exercised (EX), or rested (CON) between standardized breakfast and lunch. Microdialysis probes were inserted into the subcutaneous abdominal adipose tissue to monitor interstitial glycerol (lipolysis) and blood flow. Changes in interstitial glycerol and nutritive flow were calculated from dialysate samples before and after each meal. A subgroup (OB = 15 and LN = 9) from the acute exercise group underwent 16 wk of aerobic exercise training. RESULTS: Poor suppression of lipolysis and a blunted increase in adipose tissue nutritive blood flow in response to breakfast was associated with BMI percentile (r = 0.3, P < 0.05). These responses were normalized at lunch in the OB in the EX (P < 0.05), but not in OB in the CON. Sixteen weeks of exercise training did not improve meal-induced blood flow and marginally altered the antilipolytic response to the two meals (P = 0.06). CONCLUSIONS: Daily bouts of acute aerobic exercise should be used to improve the antilipolytic and nutritive blood flow response to a subsequent meal in obese children.

Mossy cell axon synaptic contacts on ectopic granule cells that are born following pilocarpine-induced seizures.

Granule cell neurogenesis increases following seizures, and some newly born granule cells develop at abnormal locations within the hilus. These ectopic granule cells (EGCs) demonstrate regular bursts of action potentials that are synchronized with CA3 pyramidal cell burst discharges and the bursts of hilar neurons, including mossy cells. Such findings suggest that mossy cells may participate in circuits that activate EGCs. Electron microscopic immunolabeling was therefore used to determine if mossy cell axon terminals form synapses with hilar EGC dendrites, using animals that underwent pilocarpine-induced status epilepticus. Pilocarpine was administered to adult male rats, and those which developed status epilepticus were perfused 5-7 months later, after the period of EGC genesis. Hippocampal sections were processed for dual electron microscopic immunolabeling (using calcitonin gene-related peptide (CGRP) as a marker for mossy cells and calbindin (CaBP) as a marker for EGCs). Light microscopic analysis revealed large CGRP-immunoreactive cells in the hilus, with the appearance and distribution of mossy cells. Electron microscopic analysis revealed numerous CaBP-immunoreactive dendrites in the hilus, some of which were innervated by CGRP-immunoreactive terminals. The results suggest that mossy cells participate in the excitatory circuits which activate EGCs, providing further insight into the network rearrangements that accompany seizure-induced neurogenesis in this animal model of epilepsy.

Body mass index predicts selected physical fitness attributes but is not associated with performance on military relevant tasks in U.S. Army Soldiers.

OBJECTIVES: Army body composition standards are based upon validated criteria; however, certain field-expedient methodologies (e.g., weight-for-height, body mass index [BMI]) may disqualify individuals from service who may otherwise excel on physical performance and military-relevant tasks. The purpose was to assess soldier physical performance and military-specific task/fitness performance stratified by BMI. DESIGN: Cross-sectional observational study. METHODS: Male (n=275) and female (n=46) soldiers performed a wide-array of physical fitness tests and military-specific tasks, including the Army physical fitness test (APFT). Within-sex performance data were analyzed by BMI tertile stratification or by Army Body Composition Program (ABCP) weight-for-height (calculated BMI) screening standards using ANOVA/Tukey post-hoc or independent t-tests, respectively. RESULTS: BMI stratification (higher vs. lower BMI) was associated with significant improvements in muscular strength and power, but also with decrements in speed/agility in male and female soldiers. Within the military specific tasks, a higher BMI was associated with an increased APFT 2-Mile Run time; however, performance on a 1600-m Loaded March or a Warrior Task and Battle Drill obstacle course was not related to BMI in either sex. Male and Female soldiers who did not meet ABCP screening standards demonstrated a slower 2-Mile Run time; however, not meeting the ABCP BMI standard only affected a minimal number (∼6%) of soldiers' ability to pass the APFT. CONCLUSIONS: Military body composition standards require a careful balance between physical performance, health, and military readiness. Allowances should be considered where tradeoffs exist between body composition classifications and performance on physical tasks with high military relevance.

Growth hormone and muscle function responses to skeletal muscle ischemia.

We examined the effects of ischemia (ISC) alone and with low-intensity exercise (ISC+EX) on growth hormone (GH) and muscle function responses. Nine men (22 +/- 0.7 yr) completed 3 study days: an ISC day (thigh cuff inflated five times, 5 min on, 3 min off), an ISC+EX day [knee extension at 20% maximal voluntary contraction (MVC) with ISC], and a control day. MVCs and submaximal contraction tasks (15 and 30% MVC) were performed before and following the perturbations. Surface electromyogram signals were collected from thigh muscles and analyzed for median frequency and root mean square alterations. Blood samples were collected every 10 min (190 min total) and analyzed for GH concentrations. Peak GH concentrations and GH area under the curve were highest (P < 0.01) on the ISC+EX day (7.5 microg/l and 432 microg.l(-1).min(-1), respectively) compared with the ISC (0.9 microg/l and 76.4 microg.l(-1).min(-1)), and CON (1.1 microg/l and 83.8 microg.l(-1).min(-1)) days. A greater GH pulse amplitude, mass/pulse, and production rate were also observed on the ISC+EX day (P < 0.05). Following the intervention, force production decreased on the ISC and ISC+EX days by 16.1 and 55.8%, respectively, and did not return to baseline values within 5 min of recovery. During the submaximal contractions, median frequency shifted to lower frequencies for most of the muscles examined, and root mean square electromyogram was consistently elevated for ISC+EX day. In conclusion, ISC coupled with resistance exercise acutely increases GH levels and reduces MVC, whereas ISC alone decreases force capacity, without alterations in GH levels.

Sensory-Derived Glutamate Regulates Presynaptic Inhibitory Terminals in Mouse Spinal Cord.

Circuit function in the CNS relies on the balanced interplay of excitatory and inhibitory synaptic signaling. How neuronal activity influences synaptic differentiation to maintain such balance remains unclear. In the mouse spinal cord, a population of GABAergic interneurons, GABApre, forms synapses with the terminals of proprioceptive sensory neurons and controls information transfer at sensory-motor connections through presynaptic inhibition. We show that reducing sensory glutamate release results in decreased expression of GABA-synthesizing enzymes GAD65 and GAD67 in GABApre terminals and decreased presynaptic inhibition. Glutamate directs GAD67 expression via the metabotropic glutamate receptor mGluR1ß on GABApre terminals and regulates GAD65 expression via autocrine influence on sensory terminal BDNF. We demonstrate that dual retrograde signals from sensory terminals operate hierarchically to direct the molecular differentiation of GABApre terminals and the efficacy of presynaptic inhibition. These retrograde signals comprise a feedback mechanism by which excitatory sensory activity drives GABAergic inhibition to maintain circuit homeostasis.