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No.
Overreaching refers to a fairly short-term drop in performance that clears up in an equally short time (talking weeks). One might deliberately over-reach to (try to) induce supercompensation.
Overtraining refers to a longer term drop in performance that takes an equally long time (months) to clear up.
one isn't necessarily local vs. systemic.
you could locally overtrain a muscle, lots and lots of negatives leading to major muscle damage, causing decreased performance, that takes weeks to recover from.
you could locally overtrain a joint, lots of heavy work that caused joint inflammation causing decreased performance that took a long time to clear up. think tendonitis.
you can systemically overtrain, as well. lots of intensive (neurally) work could systemically overtrain the nervous system.
hihg volume overtraining tends to cause endocrine problems.
there are some models trying to link local factors (such as chronic inflammation of muscular or connective tissues) to the systemic factors (the compounds formed by the inflammation, various cytokines and such affect neural function).
Lyle
*** 1: Med Sci Sports Exerc 2000 Feb;32(2):317-31
Cytokine hypothesis of overtraining: a physiological adaptation to excessive stress?
Smith LL.
Department of Health, Leisure, and Exercise Science, Appalachian State University, Boone, NC 28608, USA.
Overtraining syndrome (OTS) is a condition wherein an athlete is training excessively, yet performance deteriorates. This is usually accompanied by mood/behavior changes and a variety of biochemical and physiological alterations. Presently, there is no global hypothesis to account for OTS. The present paper will attempt to provide a unifying paradigm that will integrate previous research under the rubric of the cytokine hypothesis of overtraining. It is argued that high volume/intensity training, with insufficient rest, will produce muscle and/or skeletal and/or joint trauma. Circulating monocytes are then activated by injury-related cytokines, and in turn produce large quantities of proinflammatory IL-1beta, and/or IL-6, and/or TNF-alpha, producing systemic inflammation. Elevated circulating cytokines then co-ordinate the whole-body response by: a) communicating with the CNS and inducing a set of behaviors referred to as 'sickness' behavior, which involves mood and behavior changes that support resolution of systemic inflammation: b) adjusting liver function, to support the up-regulation of gluconeogenesis, as well as de novo synthesis of acute phase proteins, and a concomitant hypercatabolic state; and c) impacting on immune function. Theoretically, OTS is viewed as the third stage of Selye's general adaptation syndrome, with the focus being on recovery/survival, and not adaptation, and is deemed to be 'protective,' occurring in response to excessive physical/physiological stress. Recommendations are made for potential markers of OTS, based on a systemic inflammatory condition.
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