Ibuprofen ingestion does not affect markers of post-exercise muscle inflammation

PURPOSE: We investigated if oral ingestion of ibuprofen influenced leucocyte recruitment and infiltration following an acute bout of traditional resistance exercise Methods: Sixteen male subjects were divided into two groups that received the maximum over-the-counter dose of ibuprofen (1200mg d(-1)) or a similarly administered placebo following lower body resistance exercise. Muscle biopsies were taken from m.vastus lateralis and blood serum samples were obtained before and immediately after exercise, and at 3 and 24 h after exercise. Muscle cross-sections were stained with antibodies against neutrophils (CD66b and MPO) and macrophages (CD68). Muscle damage was assessed via creatine kinase and myoglobin in blood serum samples, and muscle soreness was rated on a ten-point pain scale. RESULTS: The resistance exercise protocol stimulated a significant increase in the number of CD66b(+) and MPO(+) cells when measured 3 h post exercise. Serum creatine kinase, myoglobin and subjective muscle soreness all increased post-exercise. Muscle leucocyte infiltration, creatine kinase, myoglobin and subjective muscle soreness were unaffected by ibuprofen treatment when compared to placebo. There was also no association between increases in inflammatory leucocytes and any other marker of cellular muscle damage. CONCLUSION: Ibuprofen administration had no effect on the accumulation of neutrophils, markers of muscle damage or muscle soreness during the first 24 h of post-exercise muscle recovery

Leucocytes, cytokines and satellite cells: what role do they play in muscle damage and regeneration following eccentric exercise?

Exercise-induced muscle damage is an important topic in exercise physiology. However several aspects of our understanding of how muscles respond to highly stressful exercise remain unclear In the first section of this review we address the evidence that exercise can cause muscle damage and inflammation in otherwise healthy human skeletal muscles. We approach this concept by comparing changes in muscle function (i.e., the force-generating capacity) with the degree of leucocyte accumulation in muscle following exercise. In the second section, we explore the cytokine response to 'muscle-damaging exercise', primarily eccentric exercise. We review the evidence for the notion that the degree of muscle damage is related to the magnitude of the cytokine response. In the third and final section, we look at the satellite cell response to a single bout of eccentric exercise, as well as the role of the cyclooxygenase enzymes (COX1 and 2). In summary, we propose that muscle damage as evaluated by changes in muscle function is related to leucocyte accumulation in the exercised muscles. 'Extreme' exercise protocols, encompassing unaccustomed maximal eccentric exercise across a large range of motion, generally inflict severe muscle damage, inflammation and prolonged recovery (> 1 week). By contrast, exercise resembling regular athletic training (resistance exercise and downhill running) typically causes mild muscle damage (myofibrillar disruptions) and full recovery normally occurs within a few days. Large variation in individual responses to a given exercise should, however be expected. The link between cytokine and satellite cell responses and exercise-induced muscle damage is not so clear The systemic cytokine response may be linked more closely to the metabolic demands of exercise rather than muscle damage. With the exception of IL-6, the sources of systemic cytokines following exercise remain unclear The satellite cell response to severe muscle damage is related to regeneration, whereas the biological significance of satellite cell proliferation after mild damage or non-damaging exercise remains uncertain. The COX enzymes regulate satellite cell activity, as demonstrated in animal models; however the roles of the COX enzymes in human skeletal muscle need further investigation. We suggest using the term 'muscle damage' with care. Comparisons between studies and individuals must consider changes in and recovery of muscle force-generating capacity

ACUTE AND LONG-TERM EFFECTS OF BLOOD FLOW RESTRICTED TRAINING ON HEAT SHOCK PROTEINS: FAILURE versus NON-FAILURE PROTOCOL

Introduction: The stress imposed on muscle fibres during low-load blood flow restricted resistance exercise (BFRRE) performed to failure seems to preferentially stress type I fibres (Cumming et al., 2014). Therefore, the aim of this study was to compare the effect of a failure (FA) vs non-failure (NON-FA) BFRRE protocol on heat-shock protein responses in the exercising muscles. Methods: Sixteen untrained men (18-45yrs) completed 14 BFRRE sessions divided into 2 blocks of 7 sessions in 5 days, interspersed by 10 days of rest. Legs were randomly assigned to either FA (4 sets to voluntary failure) or NO protocol (30-, 15-, 15-, 15 reps) using unilateral knee extensions at 20% of 1RM with 30s rest between sets. BFRRE was conducted with partial blood flow restriction (100 mmHg) induced by a 15cm wide pressure cuff. Muscle biopsies were collected before, during and post intervention and analysed for aB-crystallin (aBc), HSP70 and MHC by immunofluorescence

Cardiovascular Effects of Vena-Venous Bypass during Hepatic Transplantation

(J. Extra-Corpor. Technol. 19[3] p. 268-273 Fall 1987, 12 ref). A series of 42 orthotopic hepatic transplant patients were reviewed retrospectively to determine the cardiovascular effects of heparinless venavenous bypass using a constrained vortex pump. Pump flows and cardiac outputs fell progressively during bypass. During the bypass period the vascular volume became hemoconcentrated as indicated by increases in hematocrit, colloid osmotic pressure, serum osmolality, and serium sodium. The changes in colloid osmotic pressure were inversely related to the bypass pump flow. Transient hemodynamics occurring at the onset of bypass included decreases in temperature, heart rate, arterial pressure, and increases in pulmonary artery pressure, central venous pressure and T wave amplitude. Core temperature changed at the rate of -0.89°C per hour during the bypass period as compared to -0.31°C during the previous phase of the procedure. Veno-venous bypass may improve hemodynamic stability during the anhepatic phase of the procedure, but the abdomen and lower extremities may be less than optimally perfused

Comparaison de deux protocoles d'entraînement de force par occlusion vasculaire (à l'épuisement versus sous-maximal) sur la réponse des protéines de stress

INTRODUCTION: The stress imposed to muscle fibers during blood flow restricted resistance exercise (BFRRE) is poorly investigated. Therefore, we aimed to compare the effect of a failure (FA) vs submaximal (SU) BFRRE protocol on heat-shock protein responses in the exercising muscles. METHODS: Sixteen untrained men (18-45 yrs) completed 14 BFRRE sessions divided into 2 blocks of 7 sessions in 5 days, interspersed by 10 days of rest. Legs were randomly assigned to either FA (4 sets to voluntary failure) or SU protocol (30-, 15-, 15-, 15 reps) using unilateral knee extensions at 20% of 1 repetition maximum with 30s rest between sets. BFRRE was conducted with partial blood flow restriction (100 mmHg) induced by a 15 cm wide pressure cuff. Biopsies from the m. vastus lateralis were collected before, during and post intervention. The HSP response investigated was changes in αB-crystallin staining intensity on muscle cross sections analyzed by immunofluorescence. RESULTS: Relative to pre-exercise, a significant increase in αB-crystallin staining intensity (reflecting cytoskeletal bound proteins) was observed 2h after the first session in both legs (129 ± 18%, p<0.001 and 77 ± 10%, p<0.05; FA and SU, respectively). There were no significant difference between protocols at any time point, but these changes tended to be larger in FA legs than SU legs. During the rest period and 10 days post intervention, αB-crystallin staining intensity gradually decreased to baseline values. CONCLUSION: The αB-crystallin immunostaining analyses suggest that cytoskeletal proteins are highly stressed after the first session of both FA and SU BFRRE protocols

Antioxidants in Translational Medicine

Significance: It is generally accepted that reactive oxygen species (ROS) scavenging molecules or antioxidants exert health-promoting effects and thus their consumption as food additives and nutraceuticals has been greatly encouraged. Antioxidants may be beneficial in situations of subclinical deficiency and increased demand or acutely upon high-dose infusion. However, to date, there is little clinical evidence for the long-term benefit of most antioxidants. Alarmingly, recent evidence points even to health risks, in particular for supplements of lipophilic antioxidants. Recent Advances: The biological impact of ROS depends not only on their quantities but also on their chemical nature, (sub)cellular and tissue location, and the rates of their formation and degradation. Moreover, ROS serve important physiological functions; thus, inappropriate removal of ROS may cause paradoxical reductive stress and thereby induce or promote disease. Critical Issues: Any recommendation on antioxidants must be based on solid clinical evidence and patient-relevant outcomes rather than surrogate parameters. Future Directions: Such evidence-based use may include site-directed application, time-limited high dosing, (functional) pharmacological repair of oxidized biomolecules, and triggers of endogenous antioxidant response systems. Ideally, these approaches need guidance by patient stratification through predictive biomarkers and possibly imaging modalities. Antioxid. Redox Signal. 23, 1130–1143