Effect Of Ischemic Preconditioning Research Articles

Ischemic Preconditioning Blunts Loss of Knee Extensor Torque Complexity with Fatigue.

ABSTRACTIntroductionNeuromuscular fatigue reduces the temporal structure, or complexity, of muscle torque output, purportedly through an effect on motor unit behavior. Ischemic preconditioning (IPC), an emerging ergogenic aid, has been demonstrated to have a potent effect on muscular output and endurance. We therefore tested the hypothesis that IPC would attenuate the fatigue-induced loss of muscle torque complexity.MethodsTen healthy participants (6 males/4 females) performed intermittent isometric knee extension contractions (6 s contraction, 4 s rest) to task failure at 40% maximal voluntary contraction. Contractions were preceded by either IPC (three bouts of 5 min proximal thigh occlusion at 225 mm Hg, interspersed with 5 min rest) or SHAM (as IPC, but occlusion at only 20 mm Hg) treatments. Torque and EMG signals were sampled continuously. Complexity and fractal scaling were quantified using approximate entropy (ApEn) and the detrended fluctuation analysis (DFA) α scaling exponent. Muscle oxygen consumption (mV˙O2) was determined using near-infrared spectroscopy.ResultsIPC increased time to task failure by 43% ± 13% (mean ± SEM, P = 0.047). Complexity decreased in both trials (decreased ApEn, increased DFA α; both P < 0.001), although the rate of decrease was significantly lower after IPC (ApEn, −0.2 ± 0.1 vs –0.4 ± 0.1, P = 0.013; DFA α, 0.2 ± 0.1 vs 0.3 ± 0.1, P = 0.037). Similarly, the rates of increase in EMG amplitude (P = 0.022) and mV˙O2 (P = 0.043) were significantly slower after IPC.ConclusionThese results suggest that the ergogenic effect of IPC observed here is of neural origin and accounts for the slowing of the rates of change in torque complexity, EMG amplitude, and mV˙O2 as fatigue develops.

Time-related metabolomics study in the rat plasma after global cerebral ischemia and reperfusion: Effect of ischemic preconditioning.

Cardiac arrest is one of the major causes of death and disability. The aim of the study was to identify dynamic time-dependent metabolomic changes reflected in rat plasma induced by cerebral ischemia and reperfusion with the focus on the protective effect of ischemic preconditionig. Global cerebral ischemia in rats was induced by the four-vessel occlusion. Blood plasma was collected in three reperfusion times: an early post-acute 3 hr, then 24 hr, as an incipient time for delayed neuronal death induction and 72 hr as prolonged reperfusion period. The metabolomic measurements were conducted via untargeted nuclear magnetic resonance spectroscopy. Plasma of ischemized rats manifested dynamic metabolomic changes over the reperfusion time, such as increased levels of ketone bodies, decreased levels of pyruvate, alanine, and citrate. All three branched chain amino acids showed common pattern during reperfusion time: a decrease in 3 hr compared to sham, then a highest level in 24 hr and decrease in 72 hr reperfusion time, similar to their corresponding ketoacids. The protective effect of ischemic preconditioning was demonstrated by a faster tendency of plasma metabolites to normalize. Results also proved the remarkable metabolomic differences between the control (naïve) and sham-operated anesthetized animals, what warrants for critical evaluation of surgery/anaesthesy in the algorithm of metabolomic animal studies.

90 days impacts of remote ischemic preconditioning on patients undergoing open total aortic arch replacement: a post-hoc analysis of previous trial

BackgroundIn the previous randomized controlled trial by our research group, we evaluated the effect of remote ischemic preconditioning (RIPC) in 130 patients (65 per arm) on acute kidney injury (AKI) within 7 days of open total aortic arch replacement. Significantly fewer RIPC-treated patients than sham-treated patients developed postoperative AKI, and, epically, RIPC significantly reduced serious AKI (stage II–III). However, the long-term effect of RIPC in patients undergoing open total aortic arch replacement is unclear.MethodsThis study was a post-hoc analysis. We aimed to assess the roles of RIPC in major adverse kidney events (MAKE), defined as consisting persistent renal dysfunction, renal replacement therapy and mortality, within 90 days after surgery in patients receiving open total aortic arch replacement.ResultsIn this 90-day follow-up study, data were available for all study participants. We found that RIPC failed to improve the presence of MAKE within 90 days after surgery (RIPC: 7 of 65[10.8%]) vs sham: 15 of 65[23.1%]; P = 0.061). In those patients who developed AKI after surgery, we found that the rate of MAKE within 90 days after surgery differed between the RIPC group and the sham group (RIPC: 4 of 36[11.2%]; sham: 14 of 48[29.2%]; P = 0.046).ConclusionsAt 90 days after open total aortic arch replacement, we failed to find a difference between the renoprotective effects of RIPC and sham treatment. The effectiveness or ineffectiveness of RIPC should be further investigated in a large randomized sham-controlled trial.Trial registrationThis study was approved by the Ethics Committee of Fuwai Hospital (No. 2016–835) and our previous study was registered at clinicaltrials.gov before patient enrollment (NCT03141385; principal investigator: G.W.; date of registration: March 5, 2017).

Effects of ischemic preconditioning on indirect markers of exercise-induced muscle damage: protocol for a randomized placebo-controlled trial

Background: Ischemic preconditioning (IPC) has been used to improve exercise performance, but its role in protecting against exercise-induced muscle damage (EIMD) is still unclear. Objective: To investigate the effects of IPC on the indirect markers of EIMD when compared to placebo. Methods: 30 healthy young men, with no recent experience in lower limb strength training, will be recruited. Subjects will be allocated randomly into two groups: IPC or placebo. The IPC group will undergo 4 x 5 min of occlusion (with individualized total occlusion pressure), interspersed with 5 min of reperfusion. The placebo group will be submitted to the same protocol, but with minimum pressure (10mmHg) being applied during the occlusion period. After the interventions, volunteers will be submitted to muscle damage induced by isokinetic exercise (10 sets of 12 maximum eccentric repetitions) in the non-dominant femoral quadriceps. The primary outcome will be isometric peak torque, measured both before and up to 72 hours after exercise. Secondary outcomes include rate of torque development, muscle soreness, knee range of motion, thigh circumference and blood levels of creatine kinase. Discussion: The results of this trial will indicate whether the effects of IPC are superior to placebo in the protection against EIMD

Role of Remote Ischemic Preconditioning in Hepatic Ischemic Reperfusion Injury.

The effect of remote ischemic preconditioning (RIPC) has been proposed that mediates the protective response in ischemia reperfusion injury (IRI) of various organs. In this study, we investigated the effect of RIPC in hepatic IRI, by assessing biomarker of oxidative stress and inflammatory cytokines. Moreover, we intended to demonstrate any such protective effect through nitric oxide (NO). Twenty-five rats were divided into the 5 groups: (1) Sham; (2) RIPC; (3) hepatic IRI; (4) RIPC + hepatic IRI; (5) C-PTIO, 2-(4-carboxyphenyl)-4,5dihydro-4,4,5,5-tetramethyl-1H-imidazolyl-1-oxy-3oxide, + RIPC + hepatic IRI. RIPC downregulated the level of aspartate aminotransferase (AST), alanine aminotransferase (ALT), histologic damage, and activity of Malondialdehyde (MDA). However, there was no significant reduction in the level of tumor necrosis factor-alpha (TNF-α) and nuclear factor kappa B (NF-κB). AST and ALT levels, and hepatic tissue morphology in the C-PTIO group showed a significant improvement compared to those of the RIPC + hepatic IRI group. The application of RIPC before hepatic ischemia downregulated the oxidative stress, not the inflammatory cytokines. Moreover, these protective effect of RIPC would be mediated through the activation of NO as well as anti-oxidant effect.

Ischemic Preconditioning Of Thigh Muscles: Number Of Proper Repetitions And Effectiveness

Ischemic preconditioning (IPC) was introduced after it was demonstrated that repetitions of short-term ischemia and reperfusion of coronary arteries can reduce the myocardial damage following prolonged ischemia (direct IPC). It was later shown that the IPC of coronary arteries also protects remote cardiac tissue not directly exposed to IPC (remote IPC). Several studies suggested that the IPC of a limb may protect remote organs against an ischemic incident. Because of the intermittent nature of blood flow during intense muscle actions, it was proposed that IPC prior to exercise could increase muscular performance. Although most of the prior exercise studies used an IPC protocol involving four cycles of 5-min circulatory occlusion followed by a 5-min reperfusion period, the optimal number of repetitions of IPC has been unknown. PURPOSE: We examined the effects of direct IPC on thigh strength and sought to determine the optimal repetitions of IPC for successful results. METHODS: In a randomized cross-over study, 12 healthy young males (19.8 ± 2.1 yrs, body mass index: 22.1 ± 2.7 kg/m2) performed maximal knee extension (Biodex System 3; New York, USA) of the right leg preceded by direct IPC at four different repetitions (1, 2, 3, and 4 sets) and a control intervention. One IPC consisted of 5-min circulatory occlusion by 1.3-times systolic blood pressure and 5-min reperfusion. RESULTS: There was no significant difference in the maximal voluntary torque of knee extension between the control and any number of repetitions of the IPC, as shown below.MVT, maximal voluntary torque; Nm, newton meter. Data are mean ± SD (n=12). CONCLUSIONS: These data indicate that direct IPC for the thigh muscles could not improve maximal strength regardless of the number of repetitions. The application of pre-exercise IPC for improving performance should be further carefully examined concerning the optimal protocol and its indications, such as exercise types and target muscles.

The Effect Of Ischemic Preconditioning And Hypoxia On Neuromuscular Function During Intense Exercise

Ischemic preconditioning (IPC) has been proposed to preserve neural drive during fatiguing exercise, however the underlying mechanism of this response remains unclear. Previous research has shown exercises impairing local tissue oxygenation to be more favourable in eliciting the humoral effects of IPC. PURPOSE: To determine whether IPC mediated effects on neuromuscular function are dependent on tissue oxygenation. METHODS: Eleven resistance-trained males completed four exercise trials (6 sets of 11 repetitions of maximal effort dynamic single-leg extensions) in either normoxic (fraction of inspired oxygen (FiO2): 21%) or hypoxic (FiO2: 14%) conditions, preceded by treatments of either IPC (3 x 5 min bilateral leg occlusions at 220 mmHg) or sham (3 x 5 min at 20 mmHg). Femoral nerve stimulation was utilized to assess voluntary activation and potentiated twitch characteristics during maximal voluntary contractions (MVCs) performed at baseline, prior to the exercise task and after each set of the exercise task. Tissue oxygenation (via near-infrared spectroscopy), blood oxygenation (via pulse oximetry) and surface electromyography activity was measured throughout the exercise task. RESULTS: MVC and twitch torque declined 62% and 54%, respectively (MVC: 96 ± 24 Nm, 95% CI = 73 to 119 Nm, Cohen’s d = 2.9, p < 0.001; twitch torque: 37 ± 11 Nm, 95% CI = 26 to 48 Nm, d = 1.6, p < 0.001), between pre- and post-exercise measurements without reductions in voluntary activation (mean decrease 0.2 ± 6.2%, 95% CI = -5.7 to 6.1%, d = 0.05, p > 0.21); there were no differences between conditions. Hypoxia reduced both blood and tissue oxygenation by 5% and 6%, respectively, compared to normoxic conditions (blood oxygenation: 4.8 ± 0.3%, 95% CI = 4.7 to 5.0%, d = 1.9, p < 0.001; tissue oxygenation: 3.5 ± 1.5%, 95% CI 2.6 to 4.4%, d = 2.4, p < 0.001), with a further 3% reduction in tissue saturation evident in the hypoxic IPC compared to hypoxic sham trial (mean decrease 1.8 ± 0.7%, 95% CI = 0.5 to 3.5%, d = 1.0, p < 0.05). CONCLUSION: IPC did not affect any measure of neuromuscular function regardless of tissue oxygenation. A reduction in FiO2 did invoke a humoral response and improved muscle O2 extraction during exercise, however it did not manifest into any performance benefit.

Ischemic Preconditioning Protects Against Hepatic Ischemia-Reperfusion Injury Under Propofol Anesthesia in Rats

BackgroundPropofol is widely used in general anesthesia, and it has been reported to protect various organs against ischemia-reperfusion injury (IRI), including liver. To evaluate the hepatoprotective effects of ischemic preconditioning (IP) under propofol anesthesia, we investigated the possible underlying mechanisms in rats. MethodsMale Sprague–Dawley rats were randomly assigned to 3 groups: sham group (n = 5), non-IP group (n = 9; 45 minutes of hepatic ischemia followed by 2 hours of reperfusion), and IP group (n = 9; IP applied as 10 minutes of hepatic ischemia followed by 15 minutes of reperfusion before 45 minutes of ischemia). Anesthesia was maintained with intravenous (IV) infusion of propofol (800 μg/kg/min). Liver enzymes, histopathological changes, and cytokine expression were examined. ResultsThe IP group showed significantly lower liver enzyme levels (aspartate aminotransferase, P = .045; alanine aminotransferase, P = .006) and reduced the histologic grades of hepatic injury 2 hours after reperfusion (P = .004) compared to the non-IP group. Lactate dehydrogenase activity (P < .001) and interleukin-6 mRNA levels were significantly higher in the non-IP group than in the sham and IP groups (P = .002, both groups). ConclusionsOur results demonstrate that IP under propofol anesthesia significantly attenuated hepatic IRI. The principal mechanism of the protective effects appeared to involve reduced expression of the IL-6 pro-inflammatory cytokine and subsequent reduction of the degree of necrosis.

Ischemic preconditioning improves performance and accelerates the heart rate recovery.

Previous studies have assessed the effects of ischemic preconditioning (IPC) on exercise performance and physiological variables, such as lactate and muscle deoxygenation. In this study, we verified the IPC effects on performance and heart rate during and immediately after a maximal incremental cycling test (ICT). Eighteen recreationally trained cyclists (28±4 years) were allocated to one of three groups: IPC, SHAM and Control. After the first visit to familiarization, cyclists attended the laboratory on two separate occasions to perform an ICT: in the 1st visit they performed the reference test (baseline), and in 2nd the test ischemic preconditioning (2 cycles of 5-min occlusion [at 50 mm Hg above systolic arterial pressure]/ 5-min reperfusion), SHAM (identical to ischemic preconditioning, but at 20 mm Hg) or control (no occlusion) interventions (post intervention). During the ICT, heart rate, power output and perceived exertion were measured and the heart rate was monitored throughout the recovery. Only ischemic preconditioning group improved performance time by 4.9±4.0% and decreased heart rate at submaximal point during ICT, of 170±8 to 166±8 bpm (P<0.05). Also, IPC promoted faster heart rate recovery, mainly on first minute (from 151±9 to 145±8 bpm; P<0.05), compared to baseline. No differences for other parameters were found. Two cycles of five minutes of ischemia were relevant to produce positive effects on performance and alter the heart rate during and soon after ICT.

Protective effects of ischemic preconditioning against neuronal apoptosis and dendritic injury in the hippocampus are age-dependent.

Ischemic preconditioning with non-lethal ischemia can be protective against lethal forebrain ischemia. We hypothesized that aging may aggravate ischemic susceptibility and reduce brain plasticity against preconditioning. Magnetic resonance diffusion tensor imaging (DTI) is a sensitive tool to detect brain integrity and white matter architecture. This study used DTI and histopathology to investigate the effect of aging on ischemic preconditioning. In this study, adult and middle-aged male Mongolian gerbils were subjected to non-lethal 5-min forebrain ischemia (ischemic preconditioning) or sham-operation, followed by 3days of reperfusion, and then lethal 15-min forebrain ischemia. A 9.4-Tesla MR imaging system was used to study DTI indices, namely fractional anisotropy (FA), mean diffusivity (MD), and intervoxel coherence (IC) in the hippocampal CA1 and dentate gyrus (DG) areas. In situ expressions of microtubule-associated protein 2 (MAP2, dendritic marker protein) and apoptosis were also examined. The 5-min ischemia did not cause dendritic and neuronal injury and any significant change in DTI indices and MAP2 in adult and middle-aged gerbils. The 15-min ischemia-induced significant delayed neuronal apoptosis and early dendritic injury evidenced by DTI and MAP2 studies in both CA1 and DG areas with more severe injury in middle-aged gerbils than adult gerbils. Ischemic preconditioning could improve neuronal apoptosis in CA1 area and dendritic integrity in both CA1 and DG areas with better improvement in adult gerbils than middle-aged gerbils. This study thus suggests an age-dependent protective effect of ischemic preconditioning against both neuronal apoptosis and dendritic injury in hippocampus after forebrain ischemia.

A RANDOMIZED COMPARATIVE STUDY BETWEEN REMOTE ISCHEMIC PRECONDITIONING AND PHARMACOLOGICAL PRECONDITIONING IN MAJOR AORTIC SURGERIES

Background: Cardiopulmonary bypass (CPB) remains an essential element of the surgical correction of most majorcardiovascular lesions. CPB is complicated by multisystem injury, the mechanisms of which include ischemia–reperfusion injury (IRI) and a detrimental systemic inflammatory response. Cardiac, pulmonary and neuronal injury and dysfunction remain important clinical problems after CPB. Aim of the study: The aim of this study was to compare and evaluate the effectiveness of remote ischemic preconditioning and pharmacological preconditioning in reducing cardiac injury inducedby cardiopulmonary bypass in adult patients undergoing major aortic surgeries. Patients and Methods: This study included (42) patients, divided into two groups 21 patients each, Group R: Remote Ischemic Preconditioning (cycles of ischemia and reperfusion of lower limb using blood pressure cuff) and Group P: pharmacological preconditioning (administration of sevoflurane and dexmedetomidine). Results: The current studyshowed postoperative lower elevation in CK total enzyme, CK MB enzyme and troponin I enzyme and decreased inotropic support(adrenaline infusion) requirements post-operatively along with shorter duration of postoperative intubation and postoperative ICU stay in group Pcompared to group R. Conclusion: Pharmacological preconditioning using sevoflurane and dexmedetomidine hasmyocardial protective effect after CPB in adult patients undergoing major aortic surgeries more than remote ischemic preconditioning as reflected by lower elevation in CK total enzyme, CK MB enzyme and troponin I enzyme and decreased inotropic support (adrenaline infusion) requirements postoperatively along with shorter duration of both postoperative intubation and postoperative ICU stay.

Remote ischemic preconditioning for prevention of contrast-induced nephropathy – A randomized control trial

BackgroundThere is a lack of sufficient data regarding the protective effects of remote ischemic preconditioning (RIPC) in patients at risk of developing contrast-induced nephropathy (CIN). Thus, this study was conducted to determine whether RIPC as an adjunct to standard therapy prevents CIN in high-risk patients undergoing coronary intervention. MethodsIn a single-center, double-blinded, randomized controlled trial, 162 patients who were at risk of CIN received standard hydration combined with RIPC or hydration with sham preconditioning. RIPC was accomplished by four cycles of 5 min ischemia and 5 min reperfusion of the forearm. The primary endpoint was a rise in serum creatinine (>0.5 mg/dL or >25%) from baseline to serum creatinine 48–72 h after contrast administration. ResultsOf the 162 patients, 81 were randomly allocated to receive sham preconditioning and 81 to receive RIPC. Significantly reduced serum creatinine levels were observed in patients with a Mehran moderate risk allocated to sham group compared to the RIPC group (0.070 ± 0.16 mg/dL vs. 0.107 ± 0.13 mg/dL, p = 0.001). With regards to the primary endpoint, a significantly higher change in serum creatinine from baseline to 48–72 h was observed in the sham group compared to the RIPC group (0.023 ± 0.2 μmol/L vs −0.064 ± 0.1 μmol/L, p < 0.001). ConclusionRIPC as an alternative to standard therapy, improved serum creatinine levels after contrast administration in patients at risk of CIN. However, present data indicate that RIPC might have beneficial effects in patients with a moderate or high risk of CIN.

Ischemic Preconditioning Attenuates Rating of Perceived Exertion But Does Not Improve Maximal Oxygen Consumption or Maximal Power Output.

ter Beek, F, Jokumsen, PS, Sloth, BN, Thomas Stevenson, AJ, and Larsen, RG. Ischemic preconditioning attenuates rating of perceived exertion but does not improve maximal oxygen consumption or maximal power output. J Strength Cond Res 36(9): 2479-2485, 2022-Brief consecutive periods of limb ischemia and reperfusion, known as ischemic preconditioning (IPC), have been reported to increase maximal power output (MPO) during cycling. However, the underlying mechanisms are unclear. Therefore, the purpose of the study was to investigate the effects of IPC on MPO, maximal oxygen consumption (V̇ o2 max), muscle oxygenation, and rating of perceived exertion (RPE) during an incremental cycling test. Fourteen healthy young men participated in this double-blinded, randomized crossover study, involving IPC (250 mm Hg; four 5-minute cycles of ischemia) and sham (20 mm Hg) treatment followed by an incremental cycling test to exhaustion. During the cycling test, V̇ o2 , RPE, heart rate (HR), blood lactate (BL), and muscle oxygenation and deoxygenation (near-infrared spectroscopy) were measured. MPO, V̇ o2 max, HRmax, and muscle deoxygenation did not change with IPC (all p -values > 0.13). Furthermore, IPC had no significant effect on V̇ o2 , HR, or muscle oxygenation during the incremental cycling test (all p -values > 0.18). However, IPC attenuated RPE during cycling at 210 W (IPC: median 17.0 [interquartile range 15.3-19.0]; sham: 17.5 [17.0-19.0]; p = 0.007) and 245 W (IPC: 18.0 [17.0-18.8]; sham: 19.0 [18.0-19.8]; p = 0.011). A single session of IPC did not improve MPO, V̇ o2 max, or measures of oxygen consumption during the cycling test. However, IPC lowered RPE at 210 and 245 W, suggesting that IPC may attenuate the perception of effort at higher submaximal exercise intensities.

Cardioprotective effects of remote ischemic preconditioning and its challenges in clinical application

Remote ischemic preconditioning (RIPC) is a novel preventative treatment approach that is proposed in recent years. It is a non-invasive and clinically relevant preventative strategy of cardiac muscles, that is, to carry out acute transient ischemia in the distant limb before surgery, so as to possibly relieve ischemia/perfusion injury (I/RI) in distant organs (including the heart and brain, etc.). A large number of animal studies and human clinical trials have demonstrated that remote ischemic preconditioning can reduce myocardial infarction size to prevent reperfusion injury. Unfortunately, it is difficult to transform from experiments to clinical application and finally benefit patients. Therefore, the efficient and effective method has yet to be developed. In this review, now analyzed the studies concerning cardioprotective effects by RIPC and summarized the difficulties of clinical practice. Key words: Remote ischemic preconditioning; Myocardial protection; Ischemia/reperfusion injury; Clinical application

Protective effects of remote ischemic preconditioning against spinal cord ischemia–reperfusion injury in rats

ObjectivesWe aimed to investigate the protective effect of remote ischemic preconditioning against spinal cord ischemia and find a clue to its mechanism by measuring glutamate concentrations in the spinal ventral horn. MethodsMale Sprague-Dawley rats were divided into 5 groups (n = 6 in each group) as follows: sham; SCI (only spinal cord ischemia); RIPC/SCI (perform remote ischemic preconditioning before spinal cord ischemia); MK-801/RIPC/SCI (administer MK-801, N-methyl-D-aspartate receptor antagonist, before remote ischemic preconditioning); and MK-801/SCI (administer MK-801 without remote ischemic preconditioning). Remote ischemic preconditioning was achieved by brief limb ischemia 80 minutes before spinal cord ischemia. MK-801 (1 mg/kg, intravenous) was administered 60 minutes before remote ischemic preconditioning. The glutamate concentration in the ventral horn was measured by microdialysis for 130 minutes after spinal cord ischemia. Immunofluorescence was also performed to evaluate the expression of N-methyl-D-aspartate receptor 2B subunit in the ventral horn 130 minutes after spinal cord ischemia. ResultsThe glutamate concentrations in the spinal cord ischemia group were significantly higher than in the sham group at all time points (P < .01). Remote ischemic preconditioning attenuated the spinal cord ischemia–induced glutamate increase. When MK-801 was preadministered before remote ischemic preconditioning, glutamate concentration was increased after spinal cord ischemia (P < .01). Immunofluorescence showed that remote ischemic preconditioning prevented the increase in the expression of N-methyl-D-aspartate receptor 2B subunit on the surface of motor neurons (P = .047). ConclusionsOur results showed that remote ischemic preconditioning prevented spinal cord ischemia–induced extracellular glutamate increase in ventral horn and suppressed N-methyl-D-aspartate receptor 2B subunit expression.

Effects of Ischemic Preconditioning on Maximal Exercise and Metaboreflex Activation

Ischemic preconditioning is a manipulation that uses short bouts of ischemia in order to “condition” the tissue and protect from future damage related to a lack of blood and oxygen delivery. While it is known that IPC has benefits in medical settings such as cardiothoracic surgery, its application to exercise as an ergogenic aid is newer and rapidly evolving. The relative hypoxic environment of skeletal muscle during high‐intensity exercise may be similar to that of ischemic conditions, which IPC can be used to protect against. Here, we tested the hypothesis that IPC improves maximal cycle exercise performance (maximum watts) and increases maximal aerobic capacity (VO2max, oxygen consumption) in healthy, young subjects. Given the relationship between exercise capacity and metaboreflex activation, we also tested the hypothesis that IPC attenuates muscle metaboreflex activation. Healthy, young, men and women (n=8, 22.5 ± 5.5 yrs) participated in counterbalanced experimental visits, each consisting of two protocols: one to test the effects of IPC on the metaboreflex, and one that investigated the effects of IPC on maximal cycle exercise. First, subjects underwent a 40‐minute IPC session (4 × 5 min thigh cuff inflation on each leg at a pressure of 200 mmHg). On the sham visit, cuffs were inflated to 10mmHg so that leg blood flow was not affected by the intervention. Next, in order to test IPC’s effects on the metaboreflex, subjects performed 2 minutes of continuous static handgrip exercise, at 40% of their max contraction weight. Ten seconds prior to exercise cessation, a standard blood pressure cuff was rapidly inflated to 200mmHg on the exercising arm in order to trap metabolites, stimulate afferent nerves, and trigger the metaboreflex. Systemic hemodynamics including heart rate (ECG) and non‐invasive beat‐to‐beat pressure (Finometer) were monitored throughout. Compared to the sham conditions, IPC attenuated the increase in MAP (mean ± s.d) from rest to static contraction (Δ2.8 ± 2.2 mmHg vs. Δ1.6 ± 1.5 mmHg; p=0.03) and from rest to the final minute of post‐exercise occlusion (Δ2.6 ± 2.5 mmHg vs Δ1.1 ± 2.5 mmHg; p=0.017). In order to test IPC’s effect on maximal‐effort exercise, subjects performed a maximal exercise test on an electronically‐braked ergometer (Velotron) and indirect calorimetry was performed to collect breath‐by‐breath metabolic measurements (True One 2400, Parvo). IPC did not significantly affect exercise performance as measured by max wattage output (260 ± 49W vs 258 ± 49W; p=0.68), or VO2 max (41.6 ± 10.2 mL/Kg/min vs 43.5 ± 10.5 mL/Kg/min; p=0.53). While IPC did not impact maximal exercise, the finding that IPC can attenuate the body’s metaboreflex is of interest. Given we tested a young, healthy population, it is possible that the metaboreflex was not limiting exercise performance. Therefore, it may be of interest to investigate the potential benefit of IPC in diseased populations where an exaggerated metaboreflex activation can contribute to limitations in exercise capacity.Support or Funding InformationAmerican Physiological Society, UGSRF (SAL)University of Dayton University Honors Program (SAL)

Effect of Remote Ischemic Preconditioning Conducted in Living Liver Donors on Postoperative Liver Function in Donors and Recipients Following Liver Transplantation: A Randomized Clinical Trial.

This study aimed to assess the effects of remote ischemic preconditioning (RIPC) on liver function in donors and recipients after living donor liver transplantation (LDLT). Ischemia reperfusion injury (IRI) is known to be associated with graft dysfunction after liver transplantation. RIPC is used to lessen the harmful effects of IRI. A total of 148 donors were randomly assigned to RIPC (n = 75) and control (n = 73) groups. RIPC involves 3 cycles of 5-minute inflation of a blood pressure cuff to 200 mm Hg to the upper arm, followed by 5-minute reperfusion with cuff deflation. The primary aim was to assess postoperative liver function in donors and recipients and the incidence of early allograft dysfunction and graft failure in recipients. RIPC was not associated with any differences in postoperative aspartate aminotransferase (AST) and alanine aminotransferase levels after living donor hepatectomy, and it did not decrease the incidence of delayed graft hepatic function (6.7% vs 0.0%, P = 0.074) in donors. AST level on postoperative day 1 [217.0 (158.0, 288.0) vs 259.5 (182.0, 340.0), P = 0.033] and maximal AST level within 7 postoperative days [244.0 (167.0, 334.0) vs 296.0 (206.0, 395.5), P = 0.029) were significantly lower in recipients who received a preconditioned graft. No differences were found in the incidence of early allograft dysfunction (4.1% vs 5.6%, P = 0.955) or graft failure (1.4% vs 5.6%, P = 0.346) among recipients. RIPC did not improve liver function in living donor hepatectomy. However, RIPC performed in liver donors may be beneficial for postoperative liver function in recipients after living donor liver transplantation.

Early Maladaptive Cardiovascular Responses are Associated with Mortality in a Porcine Model of Hemorrhagic Shock.

Hemorrhage is a leading cause of death on the battlefield. Current methods for predicting hemodynamic deterioration during hemorrhage are of limited accuracy and practicality. During a study of the effects of remote ischemic preconditioning in pigs that underwent hemorrhage, we noticed arrhythmias among all pigs that died before the end of the experiment but not among surviving pigs. The present study was designed to identify and characterize the early maladaptive hemodynamic responses (tachycardia in the presence of hypotension without a corresponding increase in cardiac index or mean arterial blood pressure) and their predictive power for early mortality in this experimental model. Controlled hemorrhagic shock was induced in 16 pigs. Hemodynamic parameters were monitored continuously for 7 h following bleeding. Changes in cardiovascular and laboratory parameters were analyzed and compared between those that had arrhythmia and those that did not. All animals had similar changes in parameters until the end of the bleeding phase. Six animals developed arrhythmias and died early, while 10 had no arrhythmias and survived longer than 6 h or until euthanasia. Unlike survivors, those that died did not compensate for cardiac output (CO), diastolic blood pressure (DBP), and stroke volume (SV). Oxygen delivery (DO2) and mixed venous saturation (SvO2) remained low in animals that had arrhythmia, while achieving certain measures of recuperation in animals that did not. Serum lactate increased earlier and continued to rise in all animals that developed arrhythmias. No significant differences in hemoglobin concentrations were observed between groups. Despite similar initial changes in variables, we found that low CO, DBP, SV, DO2, SvO2, and high lactate are predictive of death in this animal model. The results of this experimental study suggest that maladaptive responses across a range of cardiovascular parameters that begin early after hemorrhage may be predictive of impending death, particularly in situations where early resuscitative treatment may be delayed.

Changes in the quadriceps spinal reflex pathway after repeated sprint cycling are not influenced by ischemic preconditioning.

We examined the effect of ischemic preconditioning (IPC) on changes in muscle force, activation, and the spinal reflex pathway during and after repeated sprint cycling. Eight recreationally active men (high-intensity cardiorespiratory training > 3 times per week, > 6months) completed two exercise sessions (5 sets of 5 cycling sprints, 150% max W), preceded by either IPC (3 × 5min leg occlusions at 220mmHg) or SHAM (3 × 5min at 20mmHg). Knee extensor maximal force and rate of force were measured before (PRE), immediately post (POST), 1H, and 24H after cycling. Twitch interpolation and resting potentiated twitches were applied to estimate voluntary activation and muscle contractility, respectively. Quadriceps H-reflex recruitment curves were collected at all time-points using 10Hz doublet stimulation to allow estimation of H-reflex post-activation depression. Surface electromyograms and tissue oxygenation (via near-infrared spectroscopy) were continuously recorded during cycling. IPC did not affect any measure of neuromuscular function or performance during cycling. Maximal force and muscle contractility were significantly lower at POST and 1H compared to PRE and 24H by up to 50% (p < 0.01). Maximal force was lower than PRE at 24H by 8.7% (p = 0.028). Voluntary activation and rate of force were unchanged. A rightwards shift was observed for the H-reflex recruitment curve POST, and post-activation depression was higher than all other time-points at 24H (p < 0.05). Muscle activation and oxygenation decreased during cycling. IPC has a nominal effect on mechanisms associated with neuromuscular function during and after exercise in healthy populations.

Ischemic Preconditioning Improves Resistance Training Session Performance.

da Silva Novaes, J, da Silva Telles, LG, Monteiro, ER, da Silva Araujo, G, Vingren, JL, Silva Panza, P, Reis, VM, Laterza, MC, and Vianna, JM. Ischemic preconditioning improves resistance training session performance. J Strength Cond Res 35(11): 2993-2998, 2021-The aim of this study was to investigate the acute effect of ischemic preconditioning (IPC) in a resistance exercise (RE) training session on the number of repetitions performed, total volume, and rating of perceived exertion in recreationally trained and normotensive men. Sixteen recreationally trained and normotensive men completed 3 RE sessions in a counterbalanced and randomized order: (a) IPC protocol using 220 mm Hg followed by RE (IPC), (b) IPC cuff control protocol with 20 mm Hg followed by RE (CUFF), and (c) no IPC (control) followed by RE (CON). RE was performed with 3 sets of each exercise (bench press, leg press, lateral pulldown, hack machine squat, shoulder press, and Smith back squat) until concentric muscular failure, at 80% of one repetition maximum, with 90 seconds of rest between sets and 2 minutes of rest between exercises. Ischemic preconditioning and CUFF consisted of 4 cycles of 5 minutes of occlusion/low pressure alternating with 5 minutes of no occlusion (0 mm Hg) using a pneumatic tourniquet applied around the subaxillary region of the upper arm. For each condition, the number of repetitions completed, total volume of work performed, and rating of perceived exertion were determined. No significant difference was found for rating of perceived exertion between any experimental protocol. Ischemic preconditioning significantly (p < 0.05) increased the number of repetitions across exercises. Consequently, total volume performed (sum of total number of repetitions x load for each exercise) was significantly higher in IPC (46,170 kg) compared with CON (34,069 kg) and CUFF (36,590 kg) across all exercises. This work may have important implications for athletic populations because it demonstrates increase in muscle performance outcomes during a single RE session. Therefore, performing IPC before RE could be an important exercise prescription recommendation to increase maximum repetition performance and total volume of work performed and thus potentially increase desired training adaptations (i.e., strength and hypertrophy).