Dude, turbo -- are you trying to assert yourself as the alpha-male of the bunch or what with that bod-pic? Are we all supposed to take our shirts off and compare?
[huh]
I think you should go with higher dose ALCAR + RALA. Maybe even add some NAC? Like I've suggested before, that would probably be most beneficial for you if you consider yourself a "body builder" type. If you exercise intensively, your glutathione and other natural endogenous antioxidant's levels are probably lower than normal.
Exerc Immunol Rev. 2004;10:129-41.
Neutrophil activation, antioxidant supplements and exercise-induced oxidative stress.
Peake J, Suzuki K.
School of Human Sciences and Consolidated Research Institute for Advanced Science and Medical Care, Waseda University.
Neutrophils produce free radicals known as reactive oxygen species (ROS), which assist in the clearance of damaged host tissue. Tissue damage may occur during exercise due to muscle damage, thermal stress and ischaemia/reperfusion. When produced in excess, neutrophil-derived ROS mayoverwhelm the body's endogenous antioxidant defence mechanisms, and this can lead to oxidative stress.
There is increasing evidence for links between oxidative stress and a variety of pathological disorders such as cardiovascular diseases, cancer, chronic inflammatory diseases and post-ischaemic organ injury. A small number of studies have investigated whether there is a link between neutrophil activation and oxidative stress during exercise. In this review, we have summarised the findings of these studies. Exercise promotes the release of neutrophils into the circulation, and some evidence suggests that neutrophils mobilised after exercise have an enhanced capacity to generate some forms of ROS when stimulated in vitro. Neutrophil activation during exercise may challenge endogenous antioxidant defence mechanisms, but does not appear to increase lipid markers of oxidative stress to any significant degree, at least in the circulation. Antioxidant supplements such as N-acetylcysteine are effective at attenuating increases in the capacity of neutrophils to generate ROS when stimulated in vitro, whereas vitamin E reduces tissue infiltration of neutrophils during exercise. Free radicals generated during intense exercise may lead to DNA damage in leukocytes, but it is unknown if this damage is the result of neutrophil activation. Exercise enhances the expression of inducible haem (heme)-oxygenase (HO-1) in neutrophils after exercise, however, it is uncertain whether oxidative stress is the stimulus for this response.
Publication Types:
Review
PMID: 15633591 [PubMed - indexed for MEDLINE]
Mol Cell Biochem. 1999 Jun;196(1-2):31-42.
Glutathione homeostasis in response to exercise training and nutritional supplements.
Sen CK.
Environmental Energies Technologies Division, University of California at Berkeley, 94720, USA.
Glutathione plays a central role in the maintenance of tissue antioxidant defenses and in the regulation of redox sensitive signal transduction. In muscle cells, the level and redox status of GSH regulates activity of the redox sensitive transcription factor NF-kappaB. Physical exercise may cause oxidation of GSH in tissues such as the blood, skeletal muscle and liver. Endurance training strengthened GSH dependent tissue antioxidant defenses in most studies. Although studies investigating the effect of sprint training are few, current results show that sprint training may also have a beneficial effect on tissue GSH homeostasis. Skeletal muscle GSH level appears to be tightly regulated by the state of physical activity. Regular exercise enhances and chronic inactivity decreases the level of GSH in this tissue.
N-acetyl-L-cysteine (NAC) and alpha-lipoic acid (LA) are two antioxidant dietary supplements that are able to enhance cellular GSH levels. Because LA can be recycled to its potent dithiol form, dihydrolipoate, by enzymes present in the human cell it has a clear advantage over NAC. Recently an improved form of LA, a positively charged analogue (LA-Plus), has been discovered. LA-Plus has more potent immuno-modulatory activity compared to LA. Both LA and NAC have been shown to have beneficial effects in protecting tissue GSH homeostasis against exercise induced oxidative stress.
Publication Types:
Review
PMID: 10448900 [PubMed - indexed for MEDLINE]
Am J Clin Nutr. 2000 Aug;72(2 Suppl):653S-69S.
Thiol homeostasis and supplements in physical exercise.
Sen CK, Packer L.
Departments of Surgery and Molecular & Cellular Biochemistry, The Ohio State University Medical Center, Columbus, OH 43210-1252, USA. sen-1@medctr.osu.edu
Thiols are a class of organic sulfur derivatives (mercaptans) characterized by the presence of sulfhydryl residues. In biological systems, thiols have numerous functions, including a central role in coordinating the antioxidant defense network.
Physical exercise may induce oxidative stress. In humans, a consistent marker of exercise-induced oxidative stress is blood glutathione oxidation. Physical training programs have specific effects on tissue glutathione metabolism that depend on the work program and the type of tissue. Experimental studies show that glutathione metabolism in several tissues sensitively responds to an exhaustive bout of exercise. Study of glutathione-deficient animals clearly indicates the central importance of having adequate tissue glutathione to protect against exercise-induced oxidative stress. Among the various thiol supplements studied, N-acetyl-L-cysteine and alpha-lipoic acid hold the most promise. These agents may have antioxidant effects at the biochemical level but are also known to influence redox-sensitive cell signaling.
Publication Types:
Review
Rev Pneumol Clin. 2005 Feb;61(1 Pt 1):16-21.
[Oxidative stress in bronchopulmonary disease: contribution of N-acetylcysteine (NAC)]
[Article in French]
Guerin JC, Leophonte P, Lebas FX, Liard F, Terrioux P, Boulanger P.
Service de Pneumologie, Hopital de la Croix-Rousse, 103, grande-rue de la Croix-Rousse, 69317 Lyon Cedex 04. jean-claude.guerin@chu-lyon.fr
Oxidative stress is a frequent mechanism involved in the pathogenesis of bronchopulmonary disease. The cause can be exogenous, in particular related to to atmospheric pollution and tobacco smoke, or endogenous, related to mobilization of inflammatory cells (macrophages and polymorphonuclear neutrophils). In this general review, we present work demonstrating this oxidative stress and activation of inflammatory cells. We discuss the effect of oxidative stress on the bronchial tree and the need to maintain an adequate balance between oxidants and anti-oxidants.
This reviews focuses on experimental studies proving the anti-oxidant effect of NAC on glutathione synthesis and on different pharmacological models. We then discuss human trials, initially experimental then in different bronchopulmonary pathologies related to oxidative stress. Acetaminophen intoxication and pulmonary fibrosis are models for use of NAC.Recent work on COPD appears to show a decrease in exacerbations, improvement in symptoms and quality-of-life, and perhaps a reduction in the alteration of ventilatory function.
Publication Types:
Review
PMID: 15772575 [PubMed - indexed for MEDLINE]
Cell Mol Life Sci. 2003 Jan;60(1):6-20.
Molecular mechanisms of N-acetylcysteine actions.
Zafarullah M, Li WQ, Sylvester J, Ahmad M.
Departement de Medecine, Centre de Recherche du Centre Hospitalier de l'Universite de Montreal, Lab. K-5255 Mailloux, Hopital Notre-Dame du CHUM, 1560 Sherbrooke est, Montreal, Quebec H2L 4M1, Canada. Muhammad.Zafarullah@umontreal.ca
Oxidative stress generated by an imbalance between reactive oxygen species (ROS) and antioxidants contributes to the pathogenesis of arthritis, cancer, cardiovascular, liver and respiratory diseases. Proinflammatory cytokines and growth factors stimulate ROS production as signaling mediators.
Antioxidants such as N-acetylcysteine (NAC) have been used as tools for investigating the role of ROS in numerous biological and pathological processes. NAC inhibits activation of c-Jun N-terminal kinase, p38 MAP kinase and redox-sensitive activating protein-1 and nuclear factor kappa B transcription factor activities regulating expression of numerous genes. NAC can also prevent apoptosis and promote cell survival by activating extracellular signal-regulated kinase pathway, a concept useful for treating certain degenerative diseases. NAC directly modifies the activity of several proteins by its reducing activity. Despite its nonspecificity, ability to modify DNA and multiple molecular modes of action, NAC has therapeutic value for reducing endothelial dysfunction, inflammation, fibrosis, invasion, cartilage erosion, acetaminophen detoxification and transplant prolongation.
Publication Types:
Review
Altern Med Rev. 1998 Apr;3(2):114-27.
Clinical applications of N-acetylcysteine.
Kelly GS.
Alternative Medicine Review, Greenwich, CT.
N-acetylcysteine (NAC), the acetylated variant of the amino acid L-cysteine, is an excellent source of sulfhydryl (SH) groups, and is converted in the body into metabolites capable of stimulating glutathione (GSH) synthesis, promoting detoxification, and acting directly as free radical scavengers. Administration of NAC has historically been as a mucolytic agent in a variety of respiratory illnesses; however, it appears to also have beneficial effects in conditions characterized by decreased GSH or oxidative stress, such as HIV infection, cancer, heart disease, and cigarette smoking. An 18-dose oral course of NAC is currently the mainstay of treatment for acetaminophen-induced hepatotoxicity. N-acetylcysteine also appears to have some clinical usefulness as a chelating agent in the treatment of acute heavy metal poisoning, both as an agent capable of protecting the liver and kidney from damage and as an intervention to enhance elimination of the metals.
Publication Types:
Review
PMID: 9577247 [PubMed - indexed for MEDLINE]
