This article [Iellamo et al., 2002: (http://circ.ahajournals.org/cgi/reprint/105/23/2719)(http://www.ncbi.nlm.nih.gov/pubmed/12057984?dopt=Abstract)] is interesting, and it gives the reader at least some sense of the capacity of high-intensity exercise to produce quite different cardiovascular effects than low-intensity, aerobic exercise produces. There's a popular notion that aerobic exercise is the "heart-healthy" form of exercise and that weight training/resistance exercise is just about "muscle-building" or who knows what. The article by Iellamo et al. (2002) shows that high-intensity exercise tends to increase beta-adrenoreceptor responsiveness more than lower-intensity exercise, but the authors seem to evidently still be under the impression that this is "bad." There are just lots of problems with research in exercise. I know it's apparently impossible to research the effects of weight training in rodents, because they can only run on wheels, etc. But researchers keep doing studies on people who are in really pretty decent shape to begin with and then finding no changes or minimal changes in variables related to adrenergic functioning. In general, in my opinion, based on the information from many articles, resistance exercise produces more of an enhancement of beta-adrenoreceptor sensitivity but does not cause some kind of "pressor" effect, and endurance exercise is well-known to produce more of a pronounced increase in vagal (vagus nerve), or parasympathetic, tone, and this is not always purely beneficial to people. Sigal et al. (2004) [Sigal et al., 2004: (http://care.diabetesjournals.org/cgi/content/full/27/10/2518)(http://www.ncbi.nlm.nih.gov/pubmed/15451933)] discuss the fact that, during aerobic (endurance, lower-intensity) exercise, the regulation of glucose availability is primarily driven by these sort of subtle changes in neuroendocrine activity, and endurance exercise tends to decrease insulin levels and cause either unchanged or, actually, decreased plasma glucose levels, during exercise. In contrast, the increases in free fatty acids and plasma glucose that occur during resistance exercise are driven primarily by strong, sympathetic activation and can elevate adrenaline (epinephrine) levels by 15-fold, significantly elevate plasma growth hormone (GH) levels, and increase cortisol meaningfully, etc. So resistance exercise has a very different effect, and, in my opinion, "high-intensity" endurance exercise is not going to mimic those effects very effectively, if at all, in the long term. Reading various articles, one would think that no one has any problem with diminished sympathetic (I'm referring to adrenergic) tone, in terms of the vasoconstriction that is required for venous return to the heart, but this article discusses the high degree of prevalence of postural tachycardia (syncope can result from severe postural tachycardia/postural hypotension, and they're really talking about postural tachycardia and orthostatic intolerance in this article) [Van Lieshout et al., 2003: (http://jap.physiology.org/cgi/reprint/94/3/833)(http://www.ncbi.nlm.nih.gov/pubmed/12571122?dopt=Abstract)]. The authors discuss the fact that improving the strength of leg muscles can improve these symptoms significantly (postural tachycardia manifests itself as dizziness or as an inappropriate and prolonged increase in heart rate upon standing, etc.) and that the venous return to the heart plays a role in maintaining cerebral blood flow, etc.
It's well-known that pilots who fly some types of aircraft experience high G-forces can experience blackouts or "grayouts" tunnel vision, because of transiently diminished cerebral blood flow, and it's well known that resistance training, much more than endurance training, can reduce these symptoms by improving venous return, and Van Lieshout et al. (2003) mention some of that. The baroreflex that normally prevents orthostatic tachycardia or hypotension has multiple components and is really complex, but it's discussed, in much of the literature, as if everyone will benefit from an increase in vagal tone and that the vagal component of the baroreflex is the only relevant one. It's not, and the adrenergic activation that occurs in the brain is likely to be substantially more pronounced, in my opinion, during resistance exercise than during aerobic exercise.
The firing of muscle spindle afferent neurons increases during exercise and contributes to the activation of sympathetic neurons in the medulla, in the brainstem, and higher plasma adrenaline levels (which are obviously much higher during resistance exercise, in general, than during endurance exercise) correlate positively with larger amounts of noradrenaline release in the prefrontal cortex, in exercising rats [Pagliari et al., 1995: (http://www.ncbi.nlm.nih.gov/pubmed/7665408)]. The increases in plasma epinephrine result primarily from increases in the sympathetic outflow from the brain. The direct sympathetic innervation of the adrenal medulla allows epinephrine to be rapidly released during high-intensity exercise. ACTH is also released from the anterior pituitary gland during exercise and stimulates the release of cortisol from the adrenal cortex, during high-intensity exercise. Resistance exercise can induce prolonged elevations in plasma cortisol, at essentially all times during the increases and decreases in plasma cortisol that normally occur throughout the day. This can gradually contribute, over days, to an upregulation of beta-adrenoreceptor density and responsiveness and lead to changes in the magnitude and effects of the acute, exercise-induced increases in plasma epinephrine. Increases in plasma pCO2, during exercise, may also contribute to the activation of noradrenergic neurons in the A1/A2 adrenergic cell groups and the locus ceruleus, in the brain, during exercise [Bailey et al., 2003: (http://www.ncbi.nlm.nih.gov/pubmed/14513913)].
The release of noradrenaline in the prefrontal cortex is almost certainly a result, mainly, of increases in the firing rates of noradrenergic neurons whose cell bodies are in the locus ceruleus, although the other noradrenergic cell groups probably contribute more indirectly to that effect. The central noradrenergic activity, during exercise, is also required for brain-derived neurotrophic factor production in response to exercise, in the brain [Ivy et al., 2003 : (http://www.ncbi.nlm.nih.gov/pubmed/12759116), cited and discussed here: (http://hardcorephysiologyfun.blogspot.com/2008/12/noradrenergic-regulation-of-bdnf.html)], etc. There's a popular belief that increases in plasma beta-endorphin levels, which can occur during exercise, produce an opioidergic or morphine-like effect on the brain, etc., but an increase in plasma beta-endorphin levels is really an indication of a generalized stress response [Farrell et al., 1982: (http://www.ncbi.nlm.nih.gov/pubmed/7096149)]. To produce some kind of opioidergic reward, opioid peptides released into the blood would have to cross the blood-brain barrier, back into the brain, and somehow act selectively on opioidergic pathways that are involved in the mesolimbic reward system, and this isn't really likely to occur. There's a great deal of evidence that the increase in noradrenergic transmission, in the brain, during exercise is more likely to be a major factor regulating the subjective effects or mood elevation in response to exercise. Exercise can also increase dopamine release in the striatum (http://scholar.google.com/scholar?num=100&hl=en&lr=&q=exercise+dopamine+release), and the catecholaminergic effects of exercise are likely to be crucially important for many of its effects.
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