Potential physiological responses contributing to the ergogenic effects of acute ischemic preconditioning during exercise: A narrative review.
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SUBMITTER: O'Brien L
PROVIDER: S-EPMC9742576 | biostudies-literature | 2022
REPOSITORIES: biostudies-literature
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Potential physiological responses contributing to the ergogenic effects of acute ischemic preconditioning during exercise: A narrative review.
Frontiers in physiology 20221128
Ischemic preconditioning (IPC) has been reported to augment exercise performance, but there is considerable heterogeneity in the magnitude and frequency of performance improvements. Despite a burgeoning interest in IPC as an ergogenic aid, much is still unknown about the physiological mechanisms that mediate the observed performance enhancing effects. This narrative review collates those physiological responses to IPC reported in the IPC literature and discusses how these responses may contribut ...[more]
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Project description:This study evaluated the acute effect of ischemic preconditioning (IPC) on a high-intensity intermittent exercise performance and physiological indicators in amateur soccer players. Thirteen players (21.5 ± 2 yrs) attended three trials separated by 3-5 days in a counterbalanced randomized cross-over design: IPC (4 × 5-min occlusion 220 mmHg/reperfusion 0 mmHg) in each thigh; SHAM (similar to the IPC protocol but "occlusion" at 20 mmHg) and control (seated during the same time of IPC). After 6-min of each trial (IPC, SHAM or control), the players performed the YoYo Intermittent Endurance Test level 2 (YoYoIE2). The distance covered in the YoYoIE2 (IPC 867 ± 205 m; SHAM 873 ± 212 m; control 921 ± 206 m) was not different among trials (p = 0.10), furthermore, lactate concentration and rate of perceived exertion did not differ (P > 0.05) among protocols. There were also no significant differences in either mean heart rate (HR) or peak HR (p > 0.05) for both IPC and SHAM compared to control. Therefore, we conclude that acute IPC does not influence high-intensity intermittent exercise performance in amateur soccer players and that rate of perceived exertion, heart rate and lactate do not differ between the intervention IPC, SHAM and control.
| S-EPMC5712465 | biostudies-literature
Project description:BackgroundRemote ischemic preconditioning (RIPC) has emerged as an attractive strategy in clinical settings. Despite convincing evidence of the critical role played by circulating humoral mediators, their actual identities remain unknown. In this study, we aimed to identify RIPC-induced humoral mediators using a proteomic approach.Methodsand Results Rats were exposed to 10-min limb ischemia followed by 5- (RIPC 5') or 10-min (RIPC 10') reperfusion prior to blood sampling. The control group only underwent blood sampling. Plasma samples were analyzed using surface-enhanced laser desorption and ionization - time of flight - mass spectrometry (SELDI-TOF-MS). Three protein peaks were selected for their significant increase in RIPC 10'. They were identified and confirmed as apolipoprotein A-I (ApoA-I). Additional rats were exposed to myocardial ischemia-reperfusion (I/R) and assigned to one of the following groups RIPC+myocardial infarction (MI) (10-min limb ischemia followed by 10-min reperfusion initiated 20 minutes prior to myocardial I/R), ApoA-I+MI (10 mg/kg ApoA-I injection 10 minutes before myocardial I/R), and MI (no further intervention). In comparison with untreated MI rats, RIPC reduced infarct size (52.2±3.7% in RIPC+MI vs. 64.9±2.6% in MI; p<0.05). Similarly, ApoA-I injection decreased infarct size (50.9±3.8%; p<0.05 vs. MI).ConclusionsRIPC was associated with a plasmatic increase in ApoA-I. Furthermore, ApoA-I injection before myocardial I/R recapitulated the cardioprotection offered by RIPC in rats. This data suggests that ApoA-I may be a protective blood-borne factor involved in the RIPC mechanism.
| S-EPMC3796499 | biostudies-literature
Project description:BackgroundCarbohydrate (CHO) ingestion has an ergogenic effect on endurance training performance. Less is known about the effect of acute CHO ingestion on resistance training (RT) performance and equivocal results are reported in the literature.ObjectiveThe current systematic review and meta-analysis sought to determine if and to what degree CHO ingestion influences RT performance.MethodsPubMed, MEDLINE, SportDiscus, Scopus, and CINAHL databases were searched for peer-reviewed articles written in English that used a cross-over design to assess the acute effect of CHO ingestion on RT performance outcomes (e.g., muscle strength, power, and endurance) in healthy human participants compared to a placebo or water-only conditions. The Cochrane Collaboration's risk of bias tool and GRADE approaches were used to assess risk of bias and certainty of evidence, respectively. Random effects meta-analyses were performed for total training session volume and post-exercise blood lactate and glucose. Sub-group meta-analysis and meta-regression were performed for categorical (session and fast durations) and continuous (total number of maximal effort sets, load used, and CHO dose) covariates, respectively.ResultsTwenty-one studies met the inclusion criteria (n = 226 participants). Pooled results revealed a significant benefit of CHO ingestion in comparison to a placebo or control for total session training volume (standardised mean difference [SMD] = 0.61). Sub-group analysis revealed a significant benefit of CHO ingestion during sessions longer than 45 min (SMD = 1.02) and after a fast duration of 8 h or longer (SMD = 0.39). Pooled results revealed elevated post-exercise blood lactate (SMD = 0.58) and blood glucose (SMD = 2.36) with CHO ingestion. Meta-regression indicated that the number of maximal effort sets, but not CHO dose or load used, moderates the effect of CHO ingestion on RT performance (beta co-efficient [b] = 0.11). Carbohydrate dose does not moderate post-exercise lactate accumulation nor do maximal effort sets completed, load used, and CHO dose moderate the effect of CHO ingestion on post-exercise blood glucose.ConclusionsCarbohydrate ingestion has an ergogenic effect on RT performance by enhancing volume performance, which is more likely to occur when sessions exceed 45 min and where the fast duration is ≥ 8 h. Further, the effect is moderated by the number of maximal effort sets completed, but not the load used or CHO dose. Post-exercise blood lactate is elevated following CHO ingestion but may come at the expense of an extended time-course of recovery due to the additional training volume performed. Post-exercise blood glucose is elevated when CHO is ingested during RT, but it is presently unclear if it has an impact on RT performance.Protocol registrationThe original protocol was prospectively registered on the Open Science Framework (Project identifier: https://doi.org/10.17605/OSF.IO/HJFBW ).
| S-EPMC9584980 | biostudies-literature
Project description:Exercise preconditioning (EP) has a good myocardial protective effect. This study explored whether EP improves electrocardiographic (ECG) signs of myocardial ischemic/hypoxic injury and the occurrence of malignant arrhythmia after exhaustive exercise. A total of 120 male SD rats were randomly divided into the control group (group C), early exercise preconditioning group (group EEP), late exercise preconditioning group (group LEP), exhaustive exercise group (group EE), early exercise preconditioning + exhaustive exercise group (group EEP + EE) and late exercise preconditioning + exhaustive exercise group (group LEP + EE). Changes in heart rate (HR), ST segment, T wave and QT corrected (QTc) intervals on ECG; hematoxylin-basic fuchsin-picric acid (HBFP) staining; and cTnI levels were used to study myocardial injury and the protective effect of EP. Compared with those in group C, the levels of plasma markers of myocardial injury, HBFP staining and ECG in group EE were significantly increased (P < 0.05). Compared with those in group EE, the levels of plasma markers of myocardial injury, HBFP staining and ECG in group EEP + EE and group LEP + EE were significantly decreased (P < 0.05). The results suggested that EP improved ECG signs of myocardial ischemic/hypoxic injury and malignant arrhythmias that occur after exhaustive exercise. The ST segment and T wave could also serve as indexes for evaluating exhaustive exercise-induced myocardial ischemia/hypoxia.
| S-EPMC9637115 | biostudies-literature
Project description:Repeated sprint exercise (RSE) acutely impairs post-exercise heart rate (HR) recovery (HRR) and time-domain heart rate variability (i. e., RMSSD), likely in part, due to lactic acidosis-induced reduction of cardiac vagal reactivation. In contrast, ischemic preconditioning (IPC) mediates cardiac vagal activation and augments energy metabolism efficiency during prolonged ischemia followed by reperfusion. Therefore, we investigated whether IPC could improve recovery of cardiac autonomic control from RSE partially via improved energy metabolism responses to RSE. Fifteen men team-sport practitioners (mean ± SD: 25 ± 5 years) were randomly exposed to IPC in the legs (3 × 5 min at 220 mmHg) or control (CT; 3 × 5 min at 20 mmHg) 48 h, 24 h, and 35 min before performing 3 sets of 6 shuttle running sprints (15 + 15 m with 180° change of direction and 20 s of active recovery). Sets 1 and 2 were followed by 180 s and set 3 by 360 s of inactive recovery. Short-term HRR was analyzed after all sets via linear regression of HR decay within the first 30 s of recovery (T30) and delta from peak HR to 60 s of recovery (HRR60s). Long-term HRR was analyzed throughout recovery from set 3 via first-order exponential regression of HR decay. Moreover, RMSSD was calculated using 30-s data segments throughout recovery from set 3. Energy metabolism responses were inferred via peak pulmonary oxygen uptake ( V ˙ O 2 peak), peak carbon dioxide output ( V ˙ O 2 peak), peak respiratory exchange ratio (RERpeak), first-order exponential regression of V ˙ O 2 decay within 360 s of recovery and blood lactate concentration ([Lac-]). IPC did not change T30, but increased HRR60s after all sets (condition main effect: P = 0.03; partial eta square (η2 p ) = 0.27, i.e., large effect size). IPC did not change long-term HRR and RMSSD throughout recovery, nor did IPC change any energy metabolism parameter. In conclusion, IPC accelerated to some extent the short-term recovery, but did not change the long-term recovery of cardiac autonomic control from RSE, and such accelerator effect was not accompanied by any IPC effect on surrogates of energy metabolism responses to RSE.
| S-EPMC6212507 | biostudies-literature
Project description:Although urgently needed in clinical practice, a cardioprotective therapeutic approach against myocardial ischemia/ reperfusion injury remains to be established. Remote ischemic preconditioning (rIPC) and ischemic preconditioning (IPC) represent promising tools comprising three entities: the generation of a protective signal, the transfer of the signal to the target organ, and the response to the transferred signal resulting in cardioprotection. However, in light of recent scientific advances, many controversies arise regarding the efficacy of the underlying signaling. We here show methods for the generation of the signaling cascade by rIPC as well as IPC in a mouse model for in vivo myocardial ischemia/ reperfusion injury using highly reproducible approaches. This is accomplished by taking advantage of easily applicable preconditioning strategies compatible with the clinical setting. We describe methods for using laser Doppler perfusion imaging to monitor the cessation and recovery of perfusion in real time. The effects of preconditioning on cardiac function can also be assessed using ultrasound or magnetic resonance imaging approaches. On a cellular level, we confirm how tissue injury can be monitored using histological assessment of infarct size in conjunction with immunohistochemistry to assess both aspects in a single specimen. Finally, we outline, how the rIPC-associated signaling can be transferred to the target cell via conservation of the signal in the humoral (blood) compartment. This compilation of experimental protocols including a conditioning regimen comparable to the clinical setting should proof useful to both beginners and experts in the field of myocardial infarction, supplying information for the detailed procedures as well as troubleshooting guides.
| S-EPMC5218813 | biostudies-literature
Project description:BACKGROUND:Remote ischemic preconditioning (RIPC) of a limb has been reported to protect against ischemic stroke. Our previous results demonstrated that the RIPC-mediated neuroprotection is associated with alterations in circulating immune cell populations. Here, we evaluated the effect of the spleen, the largest reservoir of immune cells, on RIPC-mediated neuroprotection against stroke. METHODS:Noninvasive RIPC was achieved by four repeated cycles of 5-min blood flow constriction in the hindlimbs using a tourniquet. The blood and spleens were collected before and 1 h and 3 days after preconditioning to analyze the effect of RIPC on the spleen and the correlation between splenic and peripheral lymphocytes. Moreover, spleen weight and splenic lymphocytes were compared in stroke rats with or without RIPC. Finally, splenectomy was made 1 day or 2 weeks before RIPC and 90-min middle cerebral artery occlusion (MCAO). The infarct areas and deficits were assessed. Blood was collected 1 h after RIPC and 3 days after MCAO to explore the impact of splenectomy on RIPC-induced neuroprotection and immune changes. The contralateral and ipsilateral hemispheres were collected 3 days after MCAO to detect the infiltration of immune cells after RIPC and splenectomy. RESULTS:Flow cytometry analysis demonstrated that the RIPC promptly increased the percentages of CD3+CD8+ cytotoxic T (Tc) cells in the spleen with a relatively delayed elevation in CD3+CD161+ natural killer T (NKT) and CD3-CD45RA+ B lymphocytes. The percentages of circulating lymphocytes are positively correlated with the percentages of splenic lymphocytes in normal rats. Interestingly, RIPC resulted in negative correlations between the percentages of splenic and circulating T lymphocytes, while the correlation between splenic and circulating B lymphocytes remained positive. For animals subjected to RIPC followed by MCAO, RIPC increased splenic volume with an expansion of splenic lymphocytes 3 days after MCAO. Furthermore, the removal of the spleen 1 day or 2 weeks before RIPC and MCAO reduced the protective effect of RIPC on ischemic brain injury and reversed the effects of RIPC on circulating immune cell composition. RIPC significantly reduced brain infiltration of Tc and NKT cells. Prior splenectomy showed no effect on immune cell infiltration after RIPC and stroke. CONCLUSION:These results reveal an immunomodulatory effect of the spleen, effecting mainly the spleen-derived lymphocytes, during RIPC-afforded neuroprotection against cerebral ischemia.
| S-EPMC5972448 | biostudies-literature
Project description:Ischemic preconditioning (IPC) is a robust neuroprotective phenomenon in which a brief period of cerebral ischemia confers transient tolerance to subsequent ischemic challenge. Research on IPC has implicated cellular, molecular, and systemic elements of the immune response in this phenomenon. Potent molecular mediators of IPC include innate immune signaling pathways such as Toll-like receptors and type 1 interferons. Brain ischemia results in release of pro- and anti-inflammatory cytokines and chemokines that orchestrate the neuroinflammtory response, resolution of inflammation, and transition to neurological recovery and regeneration. Cellular mediators of IPC include microglia, the resident central nervous system immune cells, astrocytes, and neurons. All of these cell types engage in cross-talk with each other using a multitude of signaling pathways that modulate activation/suppression of each of the other cell types in response to ischemia. As the postischemic neuroimmune response evolves over time there is a shift in function toward provision of trophic support and neuroprotection. Peripheral immune cells infiltrate the central nervous system en masse after stroke and are largely detrimental, with a few subtypes having beneficial, protective effects, though the role of these immune cells in IPC is largely unknown. The role of neural progenitor cells in IPC-mediated neuroprotection is another active area of investigation as is the role of microglial proliferation in this setting. A mechanistic understanding of these molecular and cellular mediators of IPC may not only facilitate more effective direct application of IPC to specific clinical scenarios, but also, more broadly, reveal novel targets for therapeutic intervention in stroke.
| S-EPMC5081114 | biostudies-literature
Project description:Remote ischemic preconditioning (RIPC) by repeated brief cycles of limb ischemia/reperfusion may reduce myocardial ischemia/reperfusion injury and improve patients' prognosis after elective coronary artery bypass graft (CABG) surgery. The signal transducer and activator of transcription (STAT)5 activation in left ventricular myocardium is associated with RIPC´s cardioprotection. Cytokines and growth hormones typically activate STATs and could therefore act as humoral transfer factors of RIPC´s cardioprotection. We here determined arterial plasma concentrations of 25 different cytokines, growth hormones, and other factors which have previously been associated with cardioprotection, before (baseline)/after RIPC or placebo (n = 23/23), respectively, and before/after ischemic cardioplegic arrest in CABG patients. RIPC-induced protection was reflected by a 35% reduction of serum troponin I release. With the exception of interleukin-1α, none of the humoral factors changed in their concentrations after RIPC or placebo, respectively. Interleukin-1α, when normalized to baseline, increased after RIPC (280 ± 56%) but not with placebo (97 ± 15%). The interleukin-1α concentration remained increased until after ischemic cardioplegic arrest and was also higher than with placebo in absolute concentrations (25 ± 6 versus 16 ± 3 pg/mL). Only interleukin-1α possibly fulfills the criteria which would be expected from a substance to be released in response to RIPC and to protect the myocardium during ischemic cardioplegic arrest.
| S-EPMC5627278 | biostudies-literature
Project description:The timing of macronutrient ingestion in relation to exercise is a purported strategy to augment muscle accretion, muscle and athletic performance, and recovery. To date, the majority of macronutrient nutrient timing research has focused on carbohydrate and protein intake. However, emerging research suggests that the strategic ingestion of various ergogenic aids and micronutrients may also have beneficial effects. Therefore, the purpose of this narrative review is to critically evaluate and summarize the available literature examining the timing of ergogenic aids (caffeine, creatine, nitrates, sodium bicarbonate, beta-alanine) and micronutrients (iron, calcium) on muscle adaptations and exercise performance. In summary, preliminary data is available to indicate the timing of caffeine, nitrates, and creatine monohydrate may impact outcomes such as exercise performance, strength gains and other exercise training adaptations. Furthermore, data is available to suggest that timing the administration of beta-alanine and sodium bicarbonate may help to minimize known untoward adverse events while maintaining potential ergogenic outcomes. Finally, limited data indicates that timed ingestion of calcium and iron may help with the uptake and metabolism of these nutrients. While encouraging, much more research is needed to better understand how timed administration of these nutrients and others may impact performance, health, or other exercise training outcomes.
| S-EPMC6721335 | biostudies-literature