Determining female-specific high-intensity activity GPS thresholds in women's rugby union: Use of current use of male-derived absolute speed thresholds underestimates true levels.

GPS speed thresholds in women's rugby union are usually based on data derived from the men's game. However, evidence suggests the maximum speeds achieved by female players are 2-8 km.h-1 slower and the volume of high-intensity running (HIR) in women's rugby may be underestimated. The aim of the study was to examine the effect of adjusting absolute thresholds on the volume of high-intensity locomotion. GPS units recorded movement data from 58 players across 18 English Premier15 s matches. Distance in HIR and sprint (Spr) zones were calculated using male-derived criteria: AbsMale (HIR >18 km.h-1; Spr ≥21 km.h-1). Two alternative thresholds were compared: AbsFVmax (HIR >16 km.h-1; Spr ≥19 km.h-1); AbsFemale (HIR >14 km.h-1; Spr ≥17 km.h-1). Data were analysed using one-way ANOVA and effect sizes to determine differences in distances between thresholds. AbsMale HIR and Spr distances were 63 ± 71 m and 30 ± 53 m. Significantly greater distances at higher-intensity speeds were observed with female-adjusted thresholds. AbsFVmax: HIR: 139 ± 116 m (p = 0.01, ES 0.80); Spr: 60 ± 90 m (p = 0.131, ES 0.41) and AbsFemale: HIR: 239 ± 157 m (p < 0.01, ES 1.45); Spr: 137 ± 152 m (p < 0.01, ES 0.94). 24 players (41%) achieved speeds greater than the 21 km·h-1 threshold with the male-derived thresholds. At AbsFVmax threshold this increased to 44 (76%) and 100% at the AbsFemale threshold. Existing male-derived thresholds appear to underestimate high-intensity locomotion of female players. With adjusted thresholds, specifically the AbsFemale, the proportional volume of high-intensity activity in the women's game (8.2% total distance) aligns more closely to that observed during men's match-play.

Trunk Kinematics of Experienced Riders and Novice Riders During Rising Trot on a Riding Simulator.

Asymmetry of horses and humans is widely acknowledged, but the influence of one upon the other during horse riding is poorly understood. Riding simulators are popular for education of beginners and analysis of rider biomechanics. This study compares trunk kinematics and saddle forces of 10 experienced riders (ER) and 10 novice riders (NR) performing rising trot on a simulator. Markers were placed on the 4th lumbar (L4) and 7th cervical (C7) spinous processes, and both acromion processes. Displacements in three axes of motion were tracked using 10 high-speed video cameras sampling at 240 Hz. Displacement trajectories at L4 and C7 were similar between both groups, displaying an asymmetrical butterfly pattern in the frontal plane, which reversed when changing diagonal. Comparison between groups, NR displayed greater vertical displacement and higher saddle impact forces at L4 (P = .034), greater amplitude of medio-lateral displacement on the right diagonal between C7 and L4, and on the right diagonal while seated they rotated left (acromion processes) while the ER rotated right. Within group comparison demonstrated that on the right diagonal both groups produced significantly greater medio-lateral displacement at L4, and NR displayed significantly greater medio-lateral displacement between C7 and L4. On the left diagonal NR produced significantly greater vertical displacement and higher saddle impact forces. The findings of this study suggest that ER were more stable, symmetrical, and had lower impact force on the saddle. These issues could be addressed in beginners using a simulator to avoid unnecessary stresses on horses.

Putting the Boom, Boom, Boom into Physical Activity and Health: Music Festivals as a Positive Health Alternative to Couch Fandom.

Background: Despite the popularity of outdoor music festivals in the UK, no evidence exists of the volume or intensity of movement that occurs through attendance at these festivals and the potential health benefits this may provide. The aim of this study was to accurately record the amount of physical activity and movement at the Glastonbury Festival and to compare it against recommended levels. Methods: 22 attendees wore an Actigraph activity monitor and GPS data-logger to the Glastonbury Festival. Distances travelled, speeds and durations were recorded. Activity levels were identified based on step count thresholds and the total duration spent in moderate to vigorous physical activity (MVPA) was calculated. Results: Mean total distance of 66.1 km was recorded with daily distance (11.01 km), movement duration (11 h 28 min) and steps/day (15,661). Total MVPA of 927 min occurred over the festival period. Conclusions: This study objectively recorded the volume of physical activity that occurred at an outdoor UK festival. Large movement distances and MVPA six times greater than the recommended guidelines for health benefits were found. It can be suggested that attendance at large-scale festivals can be used as a modality for attaining physical activity guidelines alongside commonly suggested fitness activities.

Angiotensin type 2-receptor (AT2R) activation induces hypotension in apolipoprotein E-deficient mice by activating peroxisome proliferator-activated receptor-γ.

Angiotensin II (Ang II) modulates blood pressure and atherosclerosis development through its vascular type-1 (AT1R) and type-2 (AT2R) receptors, which have opposing effects. AT2R activation produces hypotension, and is anti-atherogenic. Targeted overexpression of AT2Rs in vascular smooth muscle cells (VSMCs) indicates that these effects are due to increased nitric oxide (NO) generation. However, the role of endogenous VSMC AT2Rs in these events is unknown. Effect of 7-day low-dose Ang II-infusion (12 µg/kg/hr) on blood pressure was tested in 9-week-old apoE((-/-)) mice fed a low or high cholesterol diet (LCD or HCD, respectively). Cardiac output was measured by echocardiography. Immunohistochemistry was performed to localize and quantify AT2Rs and p-Ser(1177)-endothelial nitric oxide synthase (eNOS) levels in the aortic arch. PD123319 and GW-9662 were used to selectively block the AT2R and peroxisome proliferator-activated receptor-γ (PPAR-γ), respectively. Ang II infusion decreased blood pressure by 12 mmHg (P < 0.001) in LCD/apoE((-/-)) mice without altering cardiac output; a response blocked by PD123319. Although, AT2R stimulation neither activated eNOS (p-Ser(1177)-eNOS) nor changed plasma NO metabolites, it caused an ~6-fold increase in VSMC PPAR-γ levels (P < 0.001) and the AT2R-mediated hypotension was abolished by GW-9662. AT2R-mediated hypotension was also inhibited by HCD, which selectively decreased VSMC AT2R expression by ~6-fold (P < 0.01). These findings suggest a novel pathway for the Ang II/AT2R-mediated hypotensive response that involves PPAR-γ, and is down regulated by a HCD.

Chlorine gas exposure disrupts nitric oxide homeostasis in the pulmonary vasculature.

Exposure to chlorine (Cl2) gas during industrial accidents or chemical warfare leads to significant airway and distal lung epithelial injury that continues post exposure. While lung epithelial injury is prevalent, relatively little is known about whether Cl2 gas also promotes injury to the pulmonary vasculature. To determine this, rats were subjected to a sub-lethal Cl2 gas exposure (400 ppm, 30 min) and then brought back to room air. Pulmonary arteries (PA) were isolated from rats at various times post-exposure and contractile (phenylephrine) and nitric oxide (NO)-dependent vasodilation (acetylcholine and mahmanonoate) responses measured ex vivo. PA contractility did not change, however significant inhibition of NO-dependent vasodilation was observed that was maximal at 24-48 h post exposure. Superoxide dismutase restored NO-dependent vasodilation suggesting a role for increased superoxide formation. This was supported by ∼2-fold increase in superoxide formation (measured using 2-hydroethidine oxidation to 2-OH-E+) from PA isolated from Cl2 exposed rats. We next measured PA pressures in anesthetized rats. Surprisingly, PA pressures were significantly (∼4 mmHg) lower in rats that had been exposed to Cl2 gas 24 h earlier suggesting that deficit in NO-signaling observed in isolated PA experiments did not manifest as increased PA pressures in vivo. Administration of the iNOS selective inhibitor 1400W, restored PA pressures to normal in Cl2 exposed, but not control rats suggesting that any deficit in NO-signaling due to increased superoxide formation in the PA, is offset by increased NO-formation from iNOS. These data indicate that disruption of endogenous NO-signaling mechanisms that maintain PA tone is an important aspect of post-Cl2 gas exposure toxicity.

Mast cell chymase limits the cardiac efficacy of Ang I-converting enzyme inhibitor therapy in rodents.

Ang I-converting enzyme (ACE) inhibitors are widely believed to suppress the deleterious cardiac effects of Ang II by inhibiting locally generated Ang II. However, the recent demonstration that chymase, an Ang II-forming enzyme stored in mast cell granules, is present in the heart has added uncertainty to this view. As discussed here, using microdialysis probes tethered to the heart of conscious mice, we have shown that chronic ACE inhibitor treatment did not suppress Ang II levels in the LV interstitial fluid (ISF) despite marked inhibition of ACE. However, chronic ACE inhibition caused a marked bradykinin/B2 receptor-mediated increase in LV ISF chymase activity that was not observed in mast cell-deficient KitW/KitW-v mice. In chronic ACE inhibitor-treated mast cell-sufficient littermates, chymase inhibition decreased LV ISF Ang II levels substantially, indicating the importance of mast cell chymase in regulating cardiac Ang II levels. Chymase-dependent processing of other regulatory peptides also promotes inflammation and tissue remodeling. We found that combined chymase and ACE inhibition, relative to ACE inhibition alone, improved LV function, decreased adverse cardiac remodeling, and improved survival after myocardial infarction in hamsters. These results suggest that chymase inhibitors could be a useful addition to ACE inhibitor therapy in the treatment of heart failure.