https://ogma.newcastle.edu.au/vital/access/ /manager/Index ${session.getAttribute("locale")} 5 https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:12681 Wed 28 Oct 2020 09:39:58 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:41127 Wed 27 Jul 2022 09:39:25 AEST ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:12753 Wed 24 Jul 2013 22:24:43 AEST ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:47410 Wed 18 Jan 2023 08:35:44 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:13385 Wed 11 Apr 2018 17:04:51 AEST ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:26424 Wed 11 Apr 2018 13:38:08 AEST ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:29291 Tue 27 Mar 2018 15:08:22 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:51313 Thu 31 Aug 2023 14:32:38 AEST ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:40967 Thu 21 Jul 2022 08:38:13 AEST ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:33214 Thu 13 Sep 2018 11:15:59 AEST ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:33212 Thu 13 Sep 2018 11:09:17 AEST ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:7708 Sat 24 Mar 2018 08:41:37 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:7671 Sat 24 Mar 2018 08:39:24 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:7056 Sat 24 Mar 2018 08:37:56 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:8031 Sat 24 Mar 2018 08:36:47 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:12722 Sat 24 Mar 2018 08:18:25 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:12700 Sat 24 Mar 2018 08:18:24 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:13287 Sat 24 Mar 2018 08:16:04 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:12662 35 mm Hg) in the rabbit, muscle blood flow did not change, although cardiac output increased. During moderate hypoxia (Po₂ 30 - 35 mm Hg) there was initial vasoconstriction in muscle, followed by a return to control values paralleling the changes in cardiac output. In severe arterial hypoxia (Po₂ < 30 mm Hg) the initial vasoconstriction was less marked, and during the 'steady state' there was a large vasodilatation and increase in muscle blood flow, at a time when the cardiac output was not elevated. 3. The early vasoconstriction in arterial hypoxia is mediated mainly through sympathetic vasoconstrictor nerves as a result of strong arterial chemoreceptor stimulation. 4. Increased secretion of adrenaline is an important factor in restoring muscle blood flow to control values during moderate arterial hypoxia, and in elevating the muscle blood flow above these values in severe hypoxia. The peripheral dilator (β-)effects of adrenaline oppose the peripheral constrictor (α-) effects resulting from increased activation of sympathetic constrictor nerves during arterial hypoxia.]]> Sat 24 Mar 2018 08:15:49 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:12260 2, respectively (P < 0.05 for 2 h runners vs controls), whereas intrinsic HR was 383 ± 3, 377 ± 2 and 346 ± 3 b.p.m., respectively (P < 0.001 for 2 h runners vs controls). Restraint stress provoked tachycardia of similar magnitude in all groups. 4. After completion of telemetric studies, haemodynamic indices and susceptibility to cardiac arrhythmias were assessed in anaesthetized animals, there were no major between-group differences in HR, arterial pressure, contractility indices or sensitivity to β-adrenoceptor stimulation (dobutamine) or blockade (atenolol). The effective refractory period in the control rats, 24 h runners and 2 h runners was 49 ± 2, 55 ± 2 and 60 ± 4 ms, respectively (P = 0.054 for 2 h runners vs controls). A significantly higher dose of aconitine was required to provoke ventricular arrhythmias in the 24 h and 2 h running groups compared with controls (489 ± 76, 505 ± 88 and 173 ± 33 μg, respectively; P < 0.05). 5. We conclude that, in rats, long-term voluntary exercise has enduring cardioprotective effects mediated at the level of both the central nervous system and the heart.]]> Sat 24 Mar 2018 08:08:11 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:11742 Sat 24 Mar 2018 08:07:49 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:16912 A receptor antagonist) into sites within a circumscribed region in the deep layers of the superior colliculus and in the central and external nuclei of the inferior colliculus evoked a response characterized by intense and highly synchronized bursts of renal sympathetic nerve activity (RSNA) and phrenic nerve activity (PNA). Each burst of RSNA had a duration of ~300–400 ms and occurred slightly later (peak to peak latency of 41 ± 8 ms) than the corresponding burst of PNA. The bursts of RSNA and PNA were also accompanied by transient increases in arterial pressure and, in most cases, heart rate. Synchronized bursts of RSNA and PNA were also evoked after neuromuscular blockade, artificial ventilation, and vagotomy and so were not dependent on afferent feedback from the lungs. We propose that the synchronized sympathetic-respiratory responses are driven by a common population of neurons, which may normally be activated by an acute threatening stimulus.]]> Sat 24 Mar 2018 07:59:52 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:18358 Sat 24 Mar 2018 07:52:40 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:18357 0.05) were covered within positions between the four different scenarios. Between scenarios, the greatest mean speed, heart rate and blood lactate responses occurred when the rules were changed, resulting in increased movement patterns (P < 0.05), most notably for batsmen and wicketkeepers. In contrast, altering the playing field size or player number did not significantly influence (P > 0.05) these responses. These results suggest that the physical demands of cricket-specific training can be increased via rule variations including hit-and-run activities, more so than field size or player number.]]> Sat 24 Mar 2018 07:52:39 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:5912 Sat 24 Mar 2018 07:46:47 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:28286 cyc) and running at 8 km/h (rHRI_run) in 13 male triathletes following two weeks of light-training (LT), two weeks of heavy-training (HT) and a two-day recovery period (RP). A five min cycling time-trial assessed performance and peak oxygen consumption (VO_2peak). Results: Performance likely decreased following HT (Effect size ± 90% confidence interval = -0.18 ± 0.09), then very likely increased following RP (0.32 ± 0.14). rHRI_cyc very likely decreased (-0.48 ± 0.24), and rHRIrun possibly decreased (-0.33 ± 0.48), following HT. Changes in both measures were unclear following RP. Steady-state HR was almost certainly lower (-0.81 ± 0.31) during rHRI_cyc than rHRI_run. A large correlation was found between reductions in performance and rHRI_run (r ± 90%; CI = 0.65 ± 0.34) from LT to HT, but was unclear for rHRI_cyc. Trivial within-subject correlations were found between rHRI and performance, but the strength of relationship between rHRI_run and performance was largely associated with VO_2peak following LT (r = -0.58 ± 0.38). Conclusions: Performance reductions were most sensitively tracked by rHRI_run following HT. This may be due to rHRI_run being assessed at a higher intensity than rHRI_cyc, inferred from a higher steady-state HR and supported by a stronger within-subject relationship between rHRI_run and performance in individuals with a lower VO_2peak, in whom the same exercise intensity would represent a greater physiological stress. rHRI assessed at relatively high exercise intensities may better track performance changes.]]> Sat 24 Mar 2018 07:41:23 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:27651 Sat 24 Mar 2018 07:38:52 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:30104 P < .05) after the first 10-min bout of basketball activity. sRPE TL was only significantly related to Lucia TRIMP (r = .66–.69; P < .05) across 0–10 and 0–20 min. Similarly, mean sprint and circuit speed were significantly correlated across 0–20 min (r = .67; P < .05). In contrast, SHRZ and Banister TRIMP were significantly related across all training doses (r = .84–.89; P < .05). Conclusions: Limited convergence exists between common TL approaches across basketball training doses lasting beyond 20 min. Thus, the interchangeability of commonly used internal and external TL approaches appears dose-dependent during basketball activity, with various psychophysiological mediators likely underpinning temporal changes.]]> Sat 24 Mar 2018 07:37:56 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:27520 Sat 24 Mar 2018 07:28:55 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:24469 0.05). The reliability for the majority of movement demands and physiological responses were moderate to high (CV: 5−17%; ICC: 0.48−1.00) within all playing positions. These results suggest that the physiological responses and movement characteristics of generic small-sided cricket games were consistent between sessions within respective playing positions.]]> Sat 24 Mar 2018 07:17:21 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:23762 2max : 43.3 ± 5.7 ml kg^-1 min^-1) volunteered to participate. Heart rate (HR) and blood lactate concentration ([BLa]) were collected across eight competitive matches. Overall and positional player activity demands were calculated across three matches using time-motion analysis methodology. Activity frequencies, total durations and total distances were determined for various activity categories. Mean (±SD) HR responses of 162±3b min^-1 (82.4±1.3% HR_max) and 136±6b min^-1 (68.6±3.1% HR_max) were evident across live and total time during matches. A mean [BLa] of 3.7 ± 1.4 mmol L^-1 was observed across competition. Player activity demands were unchanged across match periods, with 1752±186 movements performed and 5214±315m travelled across total live match time. Furthermore, 39±3%, 52±2%, 5 ± 1% and 4±1% of total live time was spent performing low-intensity, moderate-intensity, high-intensity and dribbling activity. Positional comparisons revealed backcourt players performed more ball dribbling (p<0.001) and less standing/walking (p<0.01) and running (p<0.05) than frontcourt players. Together, these findings highlight the high intermittent demands and important contributions of both anaerobic and aerobic metabolic pathways during state-level female basketball competition.]]> Sat 24 Mar 2018 07:11:08 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:24676 Sat 24 Mar 2018 07:10:51 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:37633 Mon 20 Nov 2023 15:47:52 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:53079 Fri 17 Nov 2023 11:56:47 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:32531 Fri 15 Jun 2018 10:45:14 AEST ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:35310 Fri 12 Jul 2019 11:24:18 AEST ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:55580 Fri 07 Jun 2024 11:54:12 AEST ]]>