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Clinical Effects of Pollution
Published in William J. Rea, Kalpana D. Patel, Reversibility of Chronic Disease and Hypersensitivity, Volume 5, 2017
William J. Rea, Kalpana D. Patel
IHD is a leading cause of morbidity and mortality in the United States and other parts of the world. Despite therapeutic breakthroughs over the past decades such as coronary bypass, percutaneous coronary intervention, antiplatelet and antithrombotic therapies, and angioplasty, the prevalence of IHDs remains extremely high and constitutes a devastating factor for heart failure.610,611 This devastating prevalence is usually due to microvascular dysfunction. Among various therapeutic strategies of IHD, enormous efforts have been made to limit ischemia/reperfusion (I/R) injury, which occurs when the ischemic myocardium is reperfused with oxygen and substrate-rich blood, which paradoxically worsens heart function.611 This is often due to relief in vasospasm reinstitution of O2 extraction. Ischemic myocardium, with nutrient and oxygen deprivation and buildup of ROS, uses glycolysis as the primary source of metabolic energy. As a consequence, metabolic acidosis, hyperkalemia, and Ca2+ overload develop in cardiomyocytes after coronary artery occlusion or glucose mandated lack of O2 extraction, leading not only to cardiomyocyte apoptosis during the acute phase but also to delayed adverse myocardial remodeling, which further compromises cardiac function.611 Therefore, limiting I/R-induced myocardial ROS accumulations and apoptosis benefits both short- and long-term survival and quality of life. Although the mechanism responsible for I/R-induced cardiac abnormalities has been focused largely on necrosis and type I (apoptotic) programmed cell death,611 an intriguing and provocative paradigm has emerged recently that highlights a unique role for deregulated macroautophagy (hereafter referred to as autophagy) in the heart that may render cardiomyocytes more prone to I/R injury and long-term postinfarction cardiac remodeling.610,612It has been perceived that autophagy induced by ischemic preconditioning is essential for cardioprotection. To this end, new and innovative strategies to maintain or restore myocardial autophagy homeostasis and its attendant cardiomyocyte survival have been the subject of intensive investigation. This condition occurs to a milder degree in the periphery resulting in painful weakness and fatigue, which chemically sensitive patients frequently develop after a pollutant exposure. This pollutant-induced vascular spasm or small blood vessel leak usually results in the symptoms induced in the chemically sensitive.
IPC recovery length of 45 minutes improves muscle oxygen saturation during active sprint recovery
Published in European Journal of Sport Science, 2022
Afton D. Seeley, Kevin A. Jacobs
Ischemic preconditioning (IPC) refers to the transient imposition of ischemia via manually-imposed occlusion and reperfusion within the proximal upper or lower limbs (Incognito, Burr, & Millar, 2016). IPC typically consists of an ∼30–40-min procedure consisting of three to four rounds of 5-min occlusion/5-min reperfusion applied to the lower limbs (Salvador et al., 2016). IPC, imposed prior to an exercise bout, has been linked to improvements in cycling performance in events such as time trials (Cocking et al., 2017; Griffin, Hughes, Gissane, & Patterson, 2019), incremental maximum cycling (Crisafulli et al., 2011; de Groot, Thijssen, Sanchez, Ellenkamp, & Hopman, 2010), and repeated sprints (Patterson, Bezodis, Glaister, & Pattison, 2015). Furthermore, IPC has been postulated to enhance central motor drive and muscle fibre recruitment (Crisafulli et al., 2011; Cruz, de Aguiar, Turnes, Salvador, & Caputo, 2016) and has demonstrated improvements in local skeletal muscle oxygenation during short duration (≤ 60-s) (Patterson et al., 2015), as well as whole-body (Kido et al., 2015) endurance exercise, suggestive of lower skeletal muscle oxygen extraction and/or enhanced blood flow. Still, numerous investigations utilizing brief, intense bouts of exercise, found that IPC had no (Gibson, Mahony, Tracey, Fawkner, & Murray, 2015) or even a negative (Paixao, da Mota, & Marocolo, 2014) influence on cycling performance. While the physiological mechanisms underlying IPC are still not entirely understood, they are thought to be mediated by a complex interplay between both humoral and neural factors that, when applied appropriately, may augment local and systemic vascular reactivity and blood flow (Hausenloy & Yellon, 2008).
An examination of individual responses to ischemic preconditioning and the effect of repeated ischemic preconditioning on cycling performance
Published in European Journal of Sport Science, 2020
J.T. Slysz, H.L. Petrick, J.P. Marrow, J.F. Burr
Ischemic preconditioning (IPC) is the exposure of brief periods of circulatory occlusion and reperfusion to a limb that that activates protective mechanisms against ischemic-reperfusion injury in local and distant tissues (Addison et al., 2003; Kharbanda et al., 2002). IPC applied prior to exercise has indeed been shown to improve exercise performance, both when three or four cycles of 5 min bouts of circulatory occlusion and reperfusion are applied to exercising (Crisafulli et al., 2011; De Groot, Thijssen, Sanchez, Ellenkamp, & Hopman, 2010) and non-exercising limbs(Barbosa et al., 2015; Jean-St-Michel et al., 2011). To date, much of the reported research suggests that IPC indeed induces small, but meaningful improvements (1–4%) to endurance exercise; however, there appears to be a great variability in this response. A large between-subject variability has been reported in the exercise performance response to IPC, which confounds comparison of group-level means, and likely contributes to the large inter-study variation in response. It has been suggested that the large variability in exercise performance response within and between studies may be explained by responders and non-responders to IPC treatment (Incognito, Burr, & Millar, 2016; Koch, Della-Morte, Dave, Sacco, & Perez-Pinzon, 2014). However, few existing studies that suggest individual responses to IPC employ appropriate experimental design (Atkinson & Batterham, 2015), thereby preventing legitimate evaluation of response versus non-response to the IPC stimulus (Paradis-deschÊnes, Joanisse, & Billaut, 2018; Tomschi, Niemann, Bloch, Predel, & Grau, 2018). It is imperative to assess the within-subject variability in the exercise performance for an evaluation of true IPC response versus non-response. As the performance of an individual who undergoes an exercise trial is subject to motivational, biological, or measurement variation from bout to bout, an improvement cannot be reliably characterized as a response unless the effect is greater than the typical variation associated with the exercise task.