86 research outputs found
Oxidative stress and apoptosis in a pig model of brain death (BD) and living donation (LD)
Creatine ingestion augments dietary carbohydrate mediated muscle glycogen supercomposition during the initial 24 hrs of recovery following prolonged exhaustive exercise in humans
Muscle glycogen availability can limit endurance exercise performance. We previously demonstrated 5 days of creatine (Cr) and carbohydrate (CHO) ingestion augmented post-exercise muscle glycogen storage compared to CHO feeding alone in healthy volunteers. Here we aimed to characterise the time-course of this Cr-induced response under more stringent and controlled experimental conditions and identify potential mechanisms underpinning this phenomenon. Fourteen healthy, male volunteers cycled to exhaustion at 70% VO2peak. Muscle biopsies were obtained at rest immediately post-exercise and after 1, 3 and 6 days of recovery, during which Cr or placebo supplements (20g.day-1) were ingested along with a prescribed high CHO diet (37.5 kcal.kg body mass-1.day-1, >80% calories CHO). Oral-glucose tolerance tests (oral-GTT) were performed pre-exercise and after 1, 3 and 6 days of Cr and placebo supplementation. Exercise depleted muscle glycogen content to the same extent in both treatment groups. Creatine supplementation increased muscle total-Cr, free-Cr and phosphocreatine (PCr) content above placebo following 1, 3 and 6 days of supplementation (all P<0.05). Creatine supplementation also increased muscle glycogen content noticeably above placebo after 1 day of supplementation (P<0.05), which was sustained thereafter. This study confirmed dietary Cr augments post-exercise muscle glycogen super-compensation, and demonstrates this occurred during the initial 24 h of post-exercise recovery (when muscle total-Cr had increased by <10%). This marked response ensued without apparent treatment differences in muscle insulin sensitivity (oral-GTT, muscle GLUT4 mRNA), osmotic stress (muscle c-fos and HSP72 mRNA) or muscle cell volume (muscle water content) responses, such that another mechanism must be causative
Eccentric Exercise Activates Novel Transcriptional Regulation of Hypertrophic Signaling Pathways Not Affected by Hormone Changes
Unaccustomed eccentric exercise damages skeletal muscle tissue, activating mechanisms of recovery and remodeling that may be influenced by the female sex hormone 17β-estradiol (E2). Using high density oligonucleotide based microarrays, we screened for differences in mRNA expression caused by E2 and eccentric exercise. After random assignment to 8 days of either placebo (CON) or E2 (EXP), eighteen men performed 150 single-leg eccentric contractions. Muscle biopsies were collected at baseline (BL), following supplementation (PS), +3 hours (3H) and +48 hours (48H) after exercise. Serum E2 concentrations increased significantly with supplementation (P<0.001) but did not affect microarray results. Exercise led to early transcriptional changes in striated muscle activator of Rho signaling (STARS), Rho family GTPase 3 (RND3), mitogen activated protein kinase (MAPK) regulation and the downstream transcription factor FOS. Targeted RT-PCR analysis identified concurrent induction of negative regulators of calcineurin signaling RCAN (P<0.001) and HMOX1 (P = 0.009). Protein contents were elevated for RND3 at 3H (P = 0.02) and FOS at 48H (P<0.05). These findings indicate that early RhoA and NFAT signaling and regulation are altered following exercise for muscle remodeling and repair, but are not affected by E2
The Hsp72 and Hsp90α mRNA responses to hot downhill running are reduced following a prior bout of hot downhill running, and occur concurrently within leukocytes and the vastus lateralis
The leukocyte heat shock response (HSR) is used to determine individual’s
thermotolerance. The HSR and thermotolerance are enhanced following interventions
such as preconditioning and/or acclimation/acclimatization. However, it is unclear
whether the leukocyte HSR is an appropriate surrogate for the HSR in other tissues
implicated within the pathophysiology of exertional heat illnesses (e.g., skeletal muscle),
and whether an acute preconditioning strategy (e.g., downhill running) can improve
subsequent thermotolerance. Physically active, non-heat acclimated participants were
split into two groups to investigate the benefits of hot downhill running as preconditioning
strategy. A hot preconditioning group (HPC; n = 6) completed two trials (HPC1HOTDOWN
and HPC2HOTDOWN) of 30 min running at lactate threshold (LT) on −10% gradient in
30◦C and 50% relative humidity (RH) separated by 7 d. A temperate preconditioning
group (TPC; n = 5) completed 30 min running at LT on a −1% gradient in 20◦C and
50% (TPC1TEMPFLAT) and 7 d later completed 30 min running at LT on −10% gradient
in 30◦C and 50% RH (TPC2HOTDOWN). Venous blood samples and muscle biopsies
(vastus lateralis; VL) were obtained before, immediately after, 3, 24, and 48 h after each
trial. Leukocyte and VL Hsp72, Hsp90a, and Grp78 mRNA relative expression was
determined via RT-QPCR. Attenuated leukocyte and VL Hsp72 (2.8 to 1.8 fold and 5.9
to 2.4 fold; p < 0.05) and Hsp90a mRNA (2.9 to 2.4 fold and 5.2 to 2.4 fold; p < 0.05) responses accompanied reductions (p < 0.05) in physiological strain [exercising rectal
temperature (−0.3◦C) and perceived muscle soreness (∼ −14%)] during HPC2HOTDOWN
compared to HPC1HOTDOWN (i.e., a preconditioning effect). Both VL and leukocyte Hsp72
and Hsp90a mRNA increased (p < 0.05) simultaneously following downhill runs and
demonstrated a strong relationship (p <0.01) of similarmagnitudes with one another. Hot
downhill running is an effective preconditioning strategy which ameliorates physiological
strain, soreness and Hsp72 and Hsp90a mRNA responses to a subsequent bout.
Leukocyte and VL analyses are appropriate tissues to infer the extent to which the HSR
has been augmented
Hypoxic Air Inhalation and Ischemia Interventions Both Elicit Preconditioning Which Attenuate Subsequent Cellular Stress In vivo Following Blood Flow Occlusion and Reperfusion
schemic preconditioning (IPC) is valid technique which elicits reductions in femoral blood flow occlusion mediated reperfusion stress (oxidative stress, Hsp gene transcripts) within the systemic blood circulation and/or skeletal muscle. It is unknown whether systemic hypoxia, evoked by hypoxic preconditioning (HPC) has efficacy in priming the heat shock protein (Hsp) system thus reducing reperfusion stress following blood flow occlusion, in the same manner as IPC. The comparison between IPC and HPC being relevant as a preconditioning strategy prior to orthopedic surgery. In an independent group design,
18 healthy men were exposed to 40 min of (1) passive whole-body HPC (FiO2 = 0.143; no ischemia. N = 6), (2) IPC (FiO2 = 0.209; four bouts of 5 min ischemia and 5 min reperfusion. n = 6), or (3) rest (FiO2 = 0.209; no ischemia. n = 6). The interventions were administered 1 h prior to 30 min of tourniquet derived femoral blood flow occlusion and were followed by 2 h subsequent reperfusion. Systemic blood samples were taken pre- and post-intervention. Systemic blood and gastrocnemius skeletal muscle samples were obtained pre-, 15 min post- (15PoT) and 120 min (120PoT) post-tourniquet deflation. To determine the cellular stress response gastrocnemius and leukocyte Hsp72 mRNA and Hsp32 mRNA gene transcripts were determined by RT-qPCR. The plasma oxidative stress response (protein carbonyl, reduced glutathione/oxidized glutathione ratio) was measured utilizing commercially available kits. In comparison to control, at 15PoT a significant difference in gastrocnemius Hsp72 mRNA was seen in HPC (−1.93-fold; p = 0.007) and IPC (−1.97-fold; p = 0.006). No significant differences were observed in gastrocnemius Hsp32 and Hsp72 mRNA, leukocyte Hsp72 and Hsp32 mRNA, or oxidative stress markers (p > 0.05) between HPC and IPC. HPC provided near identical amelioration of blood flow occlusion mediated gastrocnemius stress response (Hsp72 mRNA), compared to an established IPC protocol. This was seen independent of changes in systemic oxidative stress, which likely explains the absence of change in Hsp32 mRNA transcripts within leukocytes and the gastrocnemius. Both the established IPC and novel HPC interventions facilitate a priming of the skeletal muscle, but not leukocyte, Hsp system prior to femoral blood flow occlusion. This response demonstrates a localized tissue specific adaptation which may ameliorate reperfusion stress
Der entscheidende Einfluß der Gesetzgebung und der staatlichen Einrichtungen der römischen Republik auf die universale Bedeutung des römischen Privatrechtes : Rectoratsrede im Studienj. 1879/80 an d. Innsbrucker Univ. gehalten
von V. Puntschart(VLID)346521
Das "Inwärts-Eigen" im österreichischen Dienstrecht des Mittelalters : Ein Beitrag zur Eigentumstheorie
Festrede zur Saecularfeier der Geburt Friedrich Karl von Savigny's gehalten in der Aula der Innsbrucker Universität am 21. Februar 1879
gehalten von V. Puntschart(VLID)347512
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