bluuebunny/crossref_metadata_2025_split huggingface dataset:
The Effect of Varying Plyometric Volume on Stretch-Shortening Cycle Capability in Collegiate Male Rugby Players
Authors: Jeffreys Mark A. , De Ste Croix Mark B.A. , Lloyd Rhodri S. , Oliver Jon L. , Hughes Jonathan D. 
Published: April 2017

Abstract
Jeffreys, MA, De Ste Croix, MBA, Lloyd, RS, Oliver, JL, and Hughes, JD. The effect of varying plyometric volume on stretch-shortening cycle capability in collegiate male rugby players. J Strength Cond Res 33(1): 139–145, 2019—The purpose of this study was to identify the effectiveness of low and high volume plyometric loads on developing stretch-shortening cycle capability in collegiate rugby players. A between-group repeated measures design was used. Thirty-six subjects (age 20.3 ± 1.6 years, mass 91.63 ± 10.36 kg, stature 182.03 ± 5.24 cm) were randomly assigned to one of 3 groups: a control group (CG), a low volume plyometric group (LPG), or a high volume plyometric group (HPG). Data were collected from a force plate, and measures of reactive strength index (RSI) and leg stiffness were calculated from jump height, contact time, and flight time. A significant between-group × time (F = 4.01, p ≤ 0.05) interaction effect for RSI was observed. Bonferroni post hoc analysis indicated that both the LPG training group (p = 0.002) and HPG training group (p = 0.009) were significantly higher than the control group. No significant interaction effect between time × group was observed for leg stiffness (F = 1.39, p = 0.25). This study has demonstrated that it is possible to improve reactive strength capabilities through the use of a low volume plyometric program. The low volume program elicited the same performance improvement in RSI as a high volume program while undertaking a lower dose. This suggests that strength and conditioning coaches may be able to benefit from the ability to develop more time-efficient and effective plyometric programs.
The Effects of a Cycling Warm-up Including High-Intensity Heavy-Resistance Conditioning Contractions on Subsequent 4-km Time Trial Performance
Authors: Chorley Alan , Lamb Kevin L. 
Published: April 2017

Abstract
Chorley, A and Lamb, KL. The effects of a cycling warm-up including high-intensity heavy-resistance conditioning contractions on subsequent 4-km time trial performance. J Strength Cond Res 33(1): 57–65, 2019—Previous exercise has been shown to improve subsequent performance through different mechanisms. Sport-specific conditioning contractions can be used to exploit the “post-activation potentiation” (PAP) phenomenon to enhance performance although this has rarely been investigated in short endurance events. The aim of this study was to compare a cycling warm-up with PAP-inducing conditioning contractions (CW) with a moderate-intensity warm-up (MW) on performance and physiological outcomes of a 4-km time trial. Ten well-trained male endurance cyclists (

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max 65.3 ± 5.6 ml·kg−1·min−1) performed two 4-km cycling time trials after a 5-minute recovery after a warm-up at 60% of

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max for 6.5 minutes (MW), and a warm-up with conditioning contractions (CW) consisting of 5 minutes at 60% of

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max then 3 × 10-second at 70% of peak power interspersed with a 30-second recovery. Blood lactate concentrations were measured before and after time trial. Expired gases were analyzed along with time, power output (PO), and peak forces over each 500 m split. After CW, mean completion time was reduced (1.7 ± 3.5 seconds p > 0.05), PO increased (5.1 ± 10.5 W p > 0.05) as did peak force per pedal stroke (5.7 ± 11 N p > 0.05) when compared with MW.

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increased (1.4 ± 1.6 ml·kg−1·min−1
p ≤ 0.05) after CW, whereas respiratory exchange ratio (RER) decreased (0.05 ± 0.02 p ≤ 0.05). Physiological and performance differences after CW were greatest over the first 1,500 m of the trials. The results suggest that a PAP-inducing warm-up alters

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kinetics and can lead to performance improvements in short endurance cycling but work and recovery durations should be optimized for each athlete.
A Field-Based Cycling Test to Assess Predictors of Endurance Performance and Establishing Training Zones
Authors: Sanders Dajo , Taylor Richard J. , Myers Tony , Akubat Ibrahim 
Published: April 2017

Abstract
Sanders, D, Taylor, RJ, Myers, T, and Akubat, I. A field-based cycling test to assess predictors of endurance performance and establishing training zones. J Strength Cond Res 34(12): 3482–3488, 2020—This study evaluates the relationship between a field-based 8-minute time trial (8MTT) and physiological endurance variables assessed with an incremental laboratory test. Second, lactate thresholds assessed in the laboratory were compared with estimated functional threshold power (FTP) from the 8MTT. Nineteen well-trained road cyclists (aged 22 ± 2 years, height 185.9 ± 4.5 cm, body mass 72.8 ± 4.6 kg, V̇o
2max 64 ± 4 ml·min−1·kg−1) participated. Linear regression revealed that mean 8MTT power output (PO) was strongly to very strongly related to PO at 4 mmol·L−1, PO at initial rise of 1.00 mmol·L−1, PO at Dmax and modified (mDmax) (r = 0.61–0.82). Mean 8MTT PO was largely to very largely different compared with PO at fixed blood lactate concentration of 2 mmol·L−1 (ES = 3.20) and 4 mmol·L−1 (ES = 1.90), PO at initial rise 1.00 mmol·L−1 (ES = 2.33), PO at Dmax (ES = 3.47) and mDmax (ES = 1.79) but only trivially different from maximal PO (W
max) (ES = 0.09). The 8MTT based estimated FTP was moderate to very largely different compared with PO at initial rise of 1 mmol·L−1 (ES = 1.37), PO at Dmax (ES = 2.42), PO at mDmax (ES = 0.77) and PO at 4 mmol·L−1 (ES = 0.83). Therefore, even though the 8MTT can be valuable as a performance test in cycling shown through its relationships with predictors of endurance performance, coaches should be cautious when using FTP and PO at laboratory-based thresholds interchangeably to inform training prescription.
Impact of Endurance Exercise in Hypoxia on Muscle Damage, Inflammatory and Performance Responses
Authors: Sumi Daichi , Kojima Chihiro , Goto Kazushige 
Published: April 2017

Abstract
Sumi, D, Kojima, C, and Goto, K. Impact of endurance exercise in hypoxia on muscle damage, inflammatory and performance responses. J Strength Cond Res 32(4): 1053–1062, 2018—This study evaluated muscle damage and inflammatory and performance responses after high-intensity endurance exercise in moderate hypoxia among endurance athletes. Nine trained endurance athletes completed 2 different trials on different days: exercise under moderate hypoxia (H trial, FiO2 = 14.5%) and normoxia (N trial, FiO2 = 20.9%). They performed interval exercises (10 × 3-minute running at 95% of V̇o
2max with 60-second of active rest at 60% of V̇o
2max) followed by 30-minute of continuous running at 85% of V̇o
2max under either hypoxic or normoxic conditions. Venous blood samples were collected 4 times: before exercise, 0, 60, and 120-minute after exercise. The time to exhaustion (TTE) during running at 90% of V̇o
2max was also determined to evaluate endurance capacity 120-minute after the training session. The H trial induced a significantly greater exercise-induced elevation in the blood lactate concentration than did the N trial (p = 0.02), whereas the elevation in the exercise-induced myoglobin concentration (muscle damage marker) was significantly greater in the N trial than in the H trial (p = 0.005). There was no significant difference in plasma interleukin-6 (inflammatory marker) concentration between the H and N trials. The TTE was shorter in the N trial (613 ± 65 seconds) than in the H trial (783 ± 107 seconds, p = 0.02). In conclusion, among endurance athletes, endurance exercise under moderate hypoxic conditions did not facilitate an exercise-induced muscle damage response or cause a further reduction in the endurance capacity compared with equivalent exercise under normoxic conditions.
Strength and Conditioning for Netball: A Needs Analysis and Training Recommendations
Authors: Thomas Christopher , Comfort Paul , Jones Paul A. , Dos'Santos Thomas 
Published: April 2017

ABSTRACT
THERE IS A LACK OF STRENGTH AND CONDITIONING RESEARCH INTO THE DEMANDS AND THE SPECIFIC AREAS OF DEVELOPMENT REQUIRED TO OPTIMIZE PERFORMANCE AND REDUCE THE RISK OF COMMON INJURIES IN FEMALE NETBALL ATHLETES. NETBALL IS PREDOMINANTLY ANAEROBIC, CHARACTERIZED BY FREQUENT HIGH-INTENSITY MOVEMENTS THAT REQUIRE HIGH LEVELS OF STRENGTH, POWER, AND LOWER LIMB CONTROL. HOWEVER, THERE IS LIMITED RESEARCH IN THE PREPARATION OF FEMALE NETBALL PLAYERS FOR TRAINING AND COMPETITION. IN THIS REVIEW, WE PRESENT THE PHYSIOLOGICAL DEMANDS OF TRAINING AND COMPETITION, COMMON CAUSES OF INJURY, AND STRENGTH AND CONDITIONING TRAINING RECOMMENDATIONS TO ENHANCE PERFORMANCE AND REDUCE THE LIKELIHOOD OF INJURY IN FEMALE NETBALL PLAYERS.
Bridging the Performance Gap: Interdisciplinary Collaboration With Sports Dietitians
Authors: Potter Shelby , Boyd Joni M. 
Published: April 2017

ABSTRACT
ATHLETES AND COACHES ARE AWARE OF THE IMPORTANCE OF ADEQUATE NUTRITION FOR ATHLETIC PERFORMANCE; HOWEVER, MOST LACK ADEQUATE NUTRITION KNOWLEDGE. ATHLETES EXPRESS INTEREST IN LEARNING MORE ABOUT NUTRITION FOR PERFORMANCE BUT CONSISTENTLY CONSULT SOURCES WITH LITTLE NUTRITION KNOWLEDGE. SPORTS DIETITIANS CAN ASSIST ATHLETES IN MEETING NUTRITION NEEDS BUT ARE OFTEN UNDERUTILIZED FOR ATHLETIC PERFORMANCE. THIS ARTICLE DISCUSSES THE CURRENT NEEDS OF ATHLETES, DIFFERENCES IN NUTRITION TITLES, CURRENT STATE OF SPORTS DIETITIANS, AND THE BENEFIT OF USING A SPORTS DIETITIAN.
Densin-180 Controls the Trafficking and Signaling of L-Type Voltage-Gated Cav1.2 Ca2+Channels at Excitatory Synapses
Authors: Wang Shiyi , Stanika Ruslan I. , Wang Xiaohan , Hagen Jussara , Kennedy Mary B. , Obermair Gerald J. , Colbran Roger J. , Lee Amy 
Published: April 2017

Voltage-gated Cav1.2 and Cav1.3 (L-type) Ca2+channels regulate neuronal excitability, synaptic plasticity, and learning and memory. Densin-180 (densin) is an excitatory synaptic protein that promotes Ca2+-dependent facilitation of voltage-gated Cav1.3 Ca2+channels in transfected cells. Mice lacking densin (densin KO) exhibit defects in synaptic plasticity, spatial memory, and increased anxiety-related behaviors—phenotypes that more closely match those in mice lacking Cav1.2 than Cav1.3. Therefore, we investigated the functional impact of densin on Cav1.2. We report that densin is an essential regulator of Cav1.2 in neurons, but has distinct modulatory effects compared with its regulation of Cav1.3. Densin binds to the N-terminal domain of Cav1.2, but not that of Cav1.3, and increases Cav1.2 currents in transfected cells and in neurons. In transfected cells, densin accelerates the forward trafficking of Cav1.2 channels without affecting their endocytosis. Consistent with a role for densin in increasing the number of postsynaptic Cav1.2 channels, overexpression of densin increases the clustering of Cav1.2 in dendrites of hippocampal neurons in culture. Compared with wild-type mice, the cell surface levels of Cav1.2 in the brain, as well as Cav1.2 current density and signaling to the nucleus, are reduced in neurons from densin KO mice. We conclude that densin is an essential regulator of neuronal Cav1 channels and ensures efficient Cav1.2 Ca2+signaling at excitatory synapses.SIGNIFICANCE STATEMENTThe number and localization of voltage-gated CavCa2+channels are crucial determinants of neuronal excitability and synaptic transmission. We report that the protein densin-180 is highly enriched at excitatory synapses in the brain and enhances the cell surface trafficking and postsynaptic localization of Cav1.2 L-type Ca2+channels in neurons. This interaction promotes coupling of Cav1.2 channels to activity-dependent gene transcription. Our results reveal a mechanism that may contribute to the roles of Cav1.2 in regulating cognition and mood.
A Presynaptic Group III mGluR Recruits Gβγ/SNARE Interactions to Inhibit Synaptic Transmission by Cone Photoreceptors in the Vertebrate Retina
Authors: Van Hook Matthew J. , Babai Norbert , Zurawski Zack , Yim Yun Young , Hamm Heidi E. , Thoreson Wallace B. 
Published: April 2017

G-protein βγ subunits (Gβγ) interact with presynaptic proteins and regulate neurotransmitter release downstream of Ca2+influx. To accomplish their roles in sensory signaling, photoreceptor synapses use specialized presynaptic proteins that support neurotransmission at active zone structures known as ribbons. While several G-protein coupled receptors (GPCRs) influence synaptic transmission at ribbon synapses of cones and other retinal neurons, it is unknown whether Gβγ contributes to these effects. We tested whether activation of one particular GPCR, a metabotropic glutamate receptor (mGluR), can reduce cone synaptic transmission via Gβγ in tiger salamander retinas. In recordings from horizontal cells, we found that an mGluR agonist (L-AP4) reduced cone-driven light responses and mEPSC frequency. In paired recordings of cones and horizontal cells, L-AP4 slightly reduced cone ICa(∼10%) and caused a larger reduction in cone-driven EPSCs (∼30%). Proximity ligation assay revealed direct interactions between SNAP-25 and Gβγ subunits in retinal synaptic layers. Pretreatment with the SNAP-25 cleaving protease BoNT/A inhibited L-AP4 effects on synaptic transmission, as did introduction of a peptide derived from the SNAP-25 C terminus. Introducing Gβγ subunits directly into cones reduced EPSC amplitude. This effect was inhibited by BoNT/A, supporting a role for Gβγ/SNAP-25 interactions. However, the mGluR-dependent reduction in ICawas not mimicked by Gβγ, indicating that this effect was independent of Gβγ. The finding that synaptic transmission at cone ribbon synapses is regulated by Gβγ/SNAP-25 interactions indicates that these mechanisms are shared by conventional and ribbon-type synapses. Gβγ liberated from other photoreceptor GPCRs is also likely to regulate synaptic transmission.SIGNIFICANCE STATEMENTDynamic regulation of synaptic transmission by presynaptic G-protein coupled receptors shapes information flow through neural circuits. At the first synapse in the visual system, presynaptic metabotropic glutamate receptors (mGluRs) regulate cone photoreceptor synaptic transmission, although the mechanisms and functional impact of this are unclear. We show that mGluRs regulate light response encoding across the cone synapse, accomplished in part by triggering G-protein βγ subunits (Gβγ) interactions with SNAP-25, a core component of the synaptic vesicle fusion machinery. In addition to revealing a role in visual processing, this provides the first demonstration that Gβγ/SNAP-25 interactions regulate synaptic function at a ribbon-type synapse, contributing to an emerging picture of the ubiquity of Gβγ/SNARE interactions in regulating synaptic transmission throughout the nervous system.
Alcohol Dependence Disrupts Amygdalar L-Type Voltage-Gated Calcium Channel Mechanisms
Authors: Varodayan Florence P. , de Guglielmo Giordano , Logrip Marian L. , George Olivier , Roberto Marisa 
Published: April 2017

L-type voltage-gated calcium channels (LTCCs) are implicated in several psychiatric disorders that are comorbid with alcoholism and involve amygdala dysfunction. Within the amygdala, the central nucleus (CeA) is critical in acute alcohol's reinforcing actions, and its dysregulation in human alcoholics drives their negative emotional state and motivation to drink. Here we investigated the specific role of CeA LTCCs in the effects of acute alcohol at the molecular, cellular physiology, and behavioral levels, and their potential neuroadaptation in alcohol-dependent rats. Alcohol increases CeA activity (neuronal firing rates and GABA release) in naive rats by engaging LTCCs, and intra-CeA LTCC blockade reduces alcohol intake in nondependent rats. Alcohol dependence reduces CeA LTCC membrane abundance and disrupts this LTCC-based mechanism; instead, corticotropin-releasing factor type 1 receptors (CRF1s) mediate alcohol's effects on CeA activity and drive the escalated alcohol intake of alcohol-dependent rats. Collectively, our data indicate that alcohol dependence functionally alters the molecular mechanisms underlying the CeA's response to alcohol (from LTCC- to CRF1-driven). This mechanistic switch contributes to and reflects the prominent role of the CeA in the negative emotional state that drives excessive drinking.SIGNIFICANCE STATEMENTThe central amygdala (CeA) plays a critical role in the development of alcohol dependence. As a result, much preclinical alcohol research aims to identify relevant CeA neuroadaptions that promote the transition to dependence. Here we report that acute alcohol increases CeA neuronal activity in naive rats by engaging L-type calcium channels (LTCCs) and that intra-CeA LTCC blockade reduces alcohol intake in nondependent rats. Alcohol dependence disrupts this LTCC-based mechanism; instead, corticotropin-releasing factor type 1 receptors (CRF1s) mediate alcohol's effects on CeA activity and drive the escalated alcohol intake of alcohol-dependent rats. This switch reflects the important role of the CeA in the pathophysiology of alcohol dependence and represents a new potential avenue for therapeutic intervention during the transition period.
Synaptotagmin2 (Syt2) Drives Fast Release Redundantly with Syt1 at the Output Synapses of Parvalbumin-Expressing Inhibitory Neurons
Authors: Bouhours Brice , Gjoni Enida , Kochubey Olexiy , Schneggenburger Ralf 
Published: April 2017

Parvalbumin-expressing inhibitory neurons in the mammalian CNS are specialized for fast transmitter release at their output synapses. However, the Ca2+sensor(s) used by identified inhibitory synapses, including the output synapses of parvalbumin-expressing inhibitory neurons, have only recently started to be addressed. Here, we investigated the roles of Syt1 and Syt2 at two types of fast-releasing inhibitory connections in the mammalian CNS: the medial nucleus of the trapezoid body to lateral superior olive glycinergic synapse, and the basket/stellate cell-Purkinje GABAergic synapse in the cerebellum. We used conditional and conventional knock-out (KO) mouse lines, with viral expression of Cre-recombinase and a light-activated ion channel for optical stimulation of the transduced fibers, to produce Syt1-Syt2 double KO synapsesin vivo. Surprisingly, we found that KO of Syt2 alone had only minor effects on evoked transmitter release, despite the clear presence of the protein in inhibitory nerve terminals revealed by immunohistochemistry. We show that Syt1 is weakly coexpressed at these inhibitory synapses and must be genetically inactivated together with Syt2 to achieve a significant reduction and desynchronization of fast release. Thus, our work identifies the functionally relevant Ca2+sensor(s) at fast-releasing inhibitory synapses and shows that two major Syt isoforms can cooperate to mediate release at a given synaptic connection.SIGNIFICANCE STATEMENTDuring synaptic transmission, the influx of Ca2+into the presynaptic nerve terminal activates a Ca2+sensor for vesicle fusion, a crucial step in the activity-dependent release of neurotransmitter. Synaptotagmin (Syt) proteins, and especially Syt1 and Syt2, have been identified as the Ca2+sensor at excitatory synapses, but the Ca2+sensor(s) at inhibitory synapses in native brain tissue are not well known. We found that both Syt1 and Syt2 need to be genetically inactivated to cause a significant reduction of activity-evoked release at two types of fast inhibitory synapses in mouse brain. Thus, we identify Syt2 as a functionally important Ca2+sensor at fast-releasing inhibitory synapses, and show that Syt1 and Syt2 can redundantly control transmitter release at specific brain synapses.
Blood Pressure Regulation by the Rostral Ventrolateral Medulla in Conscious Rats: Effects of Hypoxia, Hypercapnia, Baroreceptor Denervation, and Anesthesia
Authors: Wenker Ian C. , Abe Chikara , Viar Kenneth E. , Stornetta Daniel S. , Stornetta Ruth L. , Guyenet Patrice G. 
Published: April 2017

Current understanding of the contribution of C1 neurons to blood pressure (BP) regulation derives predominantly from experiments performed in anesthetized animals or reducedex vivopreparations. Here, we use ArchaerhodopsinT3.0 (ArchT) loss-of-function optogenetics to explore BP regulation by C1 neurons in intact, unanesthetized rats. Using a lentivirus that expresses ArchT under the Phox2b-activated promoter PRSx8 (PRSx8-ArchT), ∼65% of transduced neurons were C1 (balance retrotrapezoid nucleus, RTN). Other rats received CaMKII-ArchT3.0 AAV2 (CaMKII-ArchT), which transduced C1 neurons and larger numbers of unidentified glutamatergic and GABAergic cells. Under anesthesia, ArchT photoactivation reduced sympathetic nerve activity and BP and silenced/strongly inhibited most (7/12) putative C1 neurons. In unanesthetized PRSx8-ArchT-treated rats breathing room air, bilateral ArchT photoactivation caused a very small BP reduction that was only slightly larger under hypercapnia (6% FiCO2), but was greatly enhanced during hypoxia (10 and 12% FiO2), after sino-aortic denervation, or during isoflurane anesthesia. The degree of hypotension correlated with percentage of ArchT-transduced C1 neurons. ArchT photoactivation produced similar BP changes in CaMKII-ArchT-treated rats. Photoactivation in PRSX8-ArchT rats reduced breathing frequency (FR), whereasFRincreased in CaMKII-ArchT rats. We conclude that the BP drop elicited by ArchT activation resulted from C1 neuron inhibition and was unrelated to breathing changes. C1 neurons have low activity under normoxia, but their activation is important to BP stability during hypoxia or anesthesia and contributes greatly to the hypertension caused by baroreceptor deafferentation. Finally, C1 neurons are marginally activated by hypercapnia and the large breathing stimulation caused by this stimulus has very little impact on resting BP.SIGNIFICANCE STATEMENTC1 neurons are glutamatergic/peptidergic/catecholaminergic neurons located in the medulla oblongata, which may operate as a switchboard for differential, behavior-appropriate activation of selected sympathetic efferents. Based largely on experimentation in anesthetized or reduced preparations, a rostrally located subset of C1 neurons may contribute to both BP stabilization and dysregulation (hypertension). Here, we used Archaerhodopsin-based loss-of-function optogenetics to explore the contribution of these neurons to BP in conscious rats. The results suggest that C1 neurons contribute little to resting BP under normoxia or hypercapnia, C1 neuron discharge is restrained continuously by arterial baroreceptors, and C1 neuron activation is critical to stabilize BP under hypoxia or anesthesia. This optogenetic approach could also be useful to explore the role of C1 neurons during specific behaviors or in hypertensive models.