Since a big part of the concept known as DOMS is lactic acid crystals floating about in your blood [/qoute]

Sound quite certain about a big cause of DOMS there ^^


[qoute]whether or not buffering the acidic nature of training directly helps with DOMS I cannot say for sure. I do think that the body will need to do this and so helping it will allow the body to expend more energy into repairing muscles that may well mean DOMS is less and.or last less time

health4ni wrote:@Craig & Rab: since you both know that what causes DOMS is not fully understood, then there is a possibility that acidity levels caused by training is a factor. The earth was thought to be flat once...

Muscle tenderness from exercise: mechanisms?
Uwe Proske
Department of Physiology, Monash University, Victoria, Australia
Email: uwe.proske@med.monash.edu.au


When we carry out a bout of intense exercise we can, at times, reach the point where the exercise becomes painful. But as soon as we stop, the pain subsides. However, there is one form of exercise, eccentric exercise, where there is typically no pain immediately after the exercise, but we find ourselves stiff and sore next day. The soreness can persist for 4–5 days, depending on the severity of the exercise.

The reason for the delayed soreness is that, in someone unaccustomed to eccentric exercise, it leads to localized areas of damage in muscle fibres. The present-day view is that the inflammatory response triggered by the damage leads to a sensitization of muscle nociceptors. For a review, see Proske & Morgan (2001). The soreness, referred to as delayed onset muscle soreness (DOMS), has a number of features that distinguish it from other forms of muscle pain. Incidentally, the accompanying sensation of muscle stiffness is the result of a damage-related rise in passive tension within the muscle (Whitehead et al. 2001). There is also some muscle swelling the day after the exercise. A characteristic feature of DOMS is that there is no chronic pain. So on the morning after the exercise we feel fine, until we get out of bed and take the first few tottering steps.

Pain from DOMS can be evoked by muscle contraction, stretch and palpation, all mechanical stimuli that do not evoke any sensations of pain in an unexercised individual. It is for that reason it should be referred to as a tenderness, rather than a soreness. It has led to the view that DOMS is a type of hyperalgesia and is distinct from other kinds of muscle pain such as myositis, where there is typically some chronic pain associated with tonic activity in nociceptors (Berberich et al. 1988). Because of the unusual features of DOMS and because of the debilitating effects DOMS may have on the performance of competing athletes, there has been a need to find out more about the underlying neural mechanisms. Studying pain mechanisms in human subjects is fraught with difficulties, and only limited insight can ever be achieved, especially about central mechanisms. These are circumstances where animal models can play an important role.

This issue of The Journal of Physiology contains the first description of an animal model suitable for the study of neural mechanisms underlying DOMS (Taguchi et al. 2005). The extensor digitorum longus (EDL) muscle of anaesthetized rats was contracted eccentrically numerous times and the animals were then allowed to recover. Interestingly, on recovery, the exercised rats showed no behavioural evidence of muscle tenderness. On day 2 after the exercise, one group of animals was subjected to periods of mechanical compression of the exercised muscle. Only in this group, not in the exercised animals that were not given compressions, was there evidence of up-regulation of c-Fos expression in the spinal dorsal horn, at the level of entry of afferents coming from EDL. The authors conclude that, given the diffuse and dull character of DOMS, it makes it likely to be a sensation mediated by C-fibre afferents.

However, there is evidence that the story of DOMS is not as simple as that. It has been shown that the discomfort experienced from strong mechanical compression of unexercised human calf muscles can be reduced by superimposing 80 Hz vibration on the compression. This is probably an example of the phenomenon ‘rubbing it makes it better’. If this procedure is repeated in someone with the symptoms of DOMS, the vibration exacerbates the discomfort, rather than alleviating it (Weerakkody et al. 2003). The result raises a number of issues. Presumably as a result of the exercise, there has been a change in the central processing of the vibration-evoked afferent signals. Vibration frequencies of up to 120 Hz reduced the pain threshold (Weerakkody et al. 2003). It makes it unlikely that the afferents involved are in the C-fibre range, given the long refractory period for unmyelinated fibres. Other potential candidates for the vibration response are mechanically sensitive group III afferents (Paintal, 1960). It has also been shown that the pain threshold to mechanical pressure in someone with DOMS rises if the large muscle afferents, within the group I–II range, are blocked (Barlas et al. 2000; Weerakkody et al. 2003). It raises the possibility that large muscle afferents can contribute to DOMS and that DOMS could be seen to have features of a secondary hyperalgesia and allodynia. Direct evidence for mechanisms of this kind can now be sought in animal models of the type described by Taguchi et al. (2005).

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1456053/" onclick="window.open(this.href);return false;" onclick="window.open(this.href);return false;" onclick="window.open(this.href);return false;" onclick="window.open(this.href);return false;" onclick="window.open(this.href);return false;

Delayed muscle soreness. The inflammatory response to muscle injury and its clinical implications.

MacIntyre DL, Reid WD, McKenzie DC.

School of Rehabilitation Sciences, University of British Columbia, Vancouver, Canada.

Delayed onset muscle soreness (DOMS) is a sensation of discomfort that occurs 1 to 2 days after exercise. The soreness has been reported to be most evident at the muscle/tendon junction initially, and then spreading throughout the muscle. The muscle activity which causes the most soreness and injury to the muscle is eccentric activity. The injury to the muscle has been well described but the mechanism underlying the injury is not fully understood. Some recent studies have focused on the role of the cytoskeleton and its contribution to the sarcomere injury. Although little has been confirmed regarding the mechanisms involved in the production of delayed muscle soreness, it has been suggested that the soreness may occur as a result of mechanical factors or it may be biochemical in nature. To date, there appears to be no relationship between the development of soreness and the loss of muscle strength, in that the timing of the two events is different. Loss of muscle force has been observed immediately after the exercise. However, by collecting data at more frequent intervals a second loss of force has been reported in mice 1 to 3 days post-exercise. Future studies with humans may find this second loss of force to be related to DOMS. The role of inflammation during exercise-induced muscle injury has not been clearly defined. It is possible that the inflammatory response may be responsible for initiating, amplifying, and/or resolving skeletal muscle injury. Evidence from the literature of the involvement of cytokines, complement, neutrophils, monocytes and macrophages in the acute phase response are presented in this review. Clinically, DOMS is a common but self-limiting condition that usually requires no treatment. Most exercise enthusiasts are familiar with its symptoms. However, where a muscle has been immobilised or debilitated, it is not known how that muscle will respond to exercise, especially eccentric activity.

http://www.ncbi.nlm.nih.gov/pubmed/7481 ... rom=pubmed" onclick="window.open(this.href);return false;" onclick="window.open(this.href);return false;" onclick="window.open(this.href);return false;" onclick="window.open(this.href);return false;" onclick="window.open(this.href);return false;

The emerging role of free radicals in delayed onset muscle soreness and contraction-induced muscle injury.

Close GL, Ashton T, McArdle A, Maclaren DP.

Division of Cellular and Metabolic Medicine, School of Clinical Sciences, University of Liverpool, Liverpool L69 3GA, UK. gclose@liv.ac.uk

The first reported reference to delayed onset muscle soreness (DOMS) was that by Theodore Hough in 1902. Hough stated that when an untrained skeletal muscle performed exercise, it often resulted in discomfort that did not manifest until 8-10 h post-exercise, and concluded that this could not be solely attributed to fatigue. Since Hough's initial observation there has been a proliferation in research into DOMS, and despite this, the exact aetiology remains unclear. This review explores the concept of DOMS in relation to the likely causative factors and also discusses possible reasons for the equivocal findings in the literature. Free radicals are unquestionably produced during and following various forms of contractile activity and are known to result in skeletal muscle damage. Given the link between DOMS and contraction-induced muscle damage, post-exercise free radical production has been associated with DOMS; however, the precise nature of this relationship remains unsubstantiated. This review will address free radical production during and following exercise, discuss methods of assessing their generation, and critically evaluate their relationship with DOMS. There is increasing literature to suggest that free radicals act as signalling molecules, specifically activating redox sensitive transcription factors, which are necessary for muscle regeneration and adaptation following damage. Consequently free radicals may play a key physiological role in the aetiology of DOMS as opposed to a pathological role. Evidence for and against free radicals causing DOMS will be presented, and finally a suggested role of free radicals in DOMS will be proposed.

http://www.ncbi.nlm.nih.gov/pubmed/1615 ... rom=pubmed" onclick="window.open(this.href);return false;" onclick="window.open(this.href);return false;" onclick="window.open(this.href);return false;" onclick="window.open(this.href);return false;" onclick="window.open(this.href);return false;

Eccentric exercise, isokinetic muscle torque and delayed onset muscle soreness: the role of reactive oxygen species.

Close GL, Ashton T, Cable T, Doran D, MacLaren DP.

Research Institute for Sport and Exercise Sciences, Liverpool John Moores University, Henry Cotton Campus, 15-21 Webster Street, L3 2ET, Liverpool, UK. hhsgclos@livjm.ac.uk

There is growing evidence that reactive oxygen species (ROS) are involved in the muscular damage and soreness that is observed following strenuous or unaccustomed exercise. This study investigated the relationship between delayed onset muscle soreness (DOMS), muscle function and ROS following downhill running using electron spin resonance (ESR) spectroscopy and plasma malonaldehyde (MDA) concentrations. Eight physically active male subjects participated in two trials consisting of 30 min of running at approximately 65% VO(2max) on the flat (FLA) or a 15% downhill (DWN) gradient. Venous blood samples were drawn before, immediately after, and then 24, 48 and 72 h post exercise, and at the same time DOMS and muscle function were assessed. Blood was analysed for markers of ROS, total and differential white blood cell count, and creatine kinase. Muscle function was measured on an isokinetic dynamometer, whilst DOMS was assessed using a visual analogue scale. An increase in ROS, detected via ESR spectroscopy and MDA, was observed following DWN ( P<0.05) but not following FLA. Increased DOMS and loss of muscle function were observed following DWN ( P<0.05) but not following FLA ( P>0.05). DWN resulted in a transient leukocytosis ( P<0.05) occurring immediately post-exercise but returning to pre-exercise levels by 24 h. Although DWN resulted in an increase in ROS production, the increase occurred after the peak decline in muscle function and DOMS, suggesting that there may be a disassociation in the temporal relationship between ROS, loss of muscle function and DOMS.

http://www.ncbi.nlm.nih.gov/pubmed/1468 ... inalpos=11" onclick="window.open(this.href);return false;" onclick="window.open(this.href);return false;" onclick="window.open(this.href);return false;" onclick="window.open(this.href);return false;" onclick="window.open(this.href);return false;

Mechanisms of exercise-induced delayed onset muscular soreness: a brief review.

Armstrong RB.

Delayed-onset muscular soreness (DOMS), the sensation of pain and stiffness in the muscles that occurs from 1 to 5 d following unaccustomed exercise, can adversely affect muscular performance, both from voluntary reduction of effort and from inherent loss of capacity of the muscles to produce force. This reduction in performance is temporary; permanent impairment does not occur. A number of clinical correlates are associated with DOMS, including elevations in plasma enzymes, myoglobinemia, and abnormal muscle histology and ultrastructure; exertional rhabdomyolysis appears to be the extreme form of DOMS. Presently, the best treatment for DOMS appears to be muscular activity, although the sensation again returns following the exercise. Training for the specific contractile activity that causes DOMS reduces the soreness response. The etiology and cellular mechanisms of DOMS are not known, but a number of hypotheses exist to explain the phenomenon. The following model may be proposed: 1) high tensions (particularly those associated with eccentric exercise) in the contractile/elastic system of the muscle result in structural damage; 2) cell membrane damage leads to disruption of Ca++ homeostasis in the injured fibers, resulting in necrosis that peaks about 2 d post-exercise; and 3) products of macrophage activity and intracellular contents accumulate in the interstitium, which in turn stimulate free nerve endings of group-IV sensory neurons in the muscles leading to the sensation of DOMS.

http://www.ncbi.nlm.nih.gov/pubmed/6392 ... inalpos=19" onclick="window.open(this.href);return false;" onclick="window.open(this.href);return false;" onclick="window.open(this.href);return false;" onclick="window.open(this.href);return false;" onclick="window.open(this.href);return false;

Delayed onset muscle soreness : treatment strategies and performance factors.

Cheung K, Hume P, Maxwell L.

School of Community Health and Sports Studies, Auckland University of Technology, Auckland, New Zealand.

Delayed onset muscle soreness (DOMS) is a familiar experience for the elite or novice athlete. Symptoms can range from muscle tenderness to severe debilitating pain. The mechanisms, treatment strategies, and impact on athletic performance remain uncertain, despite the high incidence of DOMS. DOMS is most prevalent at the beginning of the sporting season when athletes are returning to training following a period of reduced activity. DOMS is also common when athletes are first introduced to certain types of activities regardless of the time of year. Eccentric activities induce micro-injury at a greater frequency and severity than other types of muscle actions. The intensity and duration of exercise are also important factors in DOMS onset. Up to six hypothesised theories have been proposed for the mechanism of DOMS, namely: lactic acid, muscle spasm, connective tissue damage, muscle damage, inflammation and the enzyme efflux theories. However, an integration of two or more theories is likely to explain muscle soreness. DOMS can affect athletic performance by causing a reduction in joint range of motion, shock attenuation and peak torque. Alterations in muscle sequencing and recruitment patterns may also occur, causing unaccustomed stress to be placed on muscle ligaments and tendons. These compensatory mechanisms may increase the risk of further injury if a premature return to sport is attempted.A number of treatment strategies have been introduced to help alleviate the severity of DOMS and to restore the maximal function of the muscles as rapidly as possible. Nonsteroidal anti-inflammatory drugs have demonstrated dosage-dependent effects that may also be influenced by the time of administration. Similarly, massage has shown varying results that may be attributed to the time of massage application and the type of massage technique used. Cryotherapy, stretching, homeopathy, ultrasound and electrical current modalities have demonstrated no effect on the alleviation of muscle soreness or other DOMS symptoms. Exercise is the most effective means of alleviating pain during DOMS, however the analgesic effect is also temporary. Athletes who must train on a daily basis should be encouraged to reduce the intensity and duration of exercise for 1-2 days following intense DOMS-inducing exercise. Alternatively, exercises targeting less affected body parts should be encouraged in order to allow the most affected muscle groups to recover. Eccentric exercises or novel activities should be introduced progressively over a period of 1 or 2 weeks at the beginning of, or during, the sporting season in order to reduce the level of physical impairment and/or training disruption. There are still many unanswered questions relating to DOMS, and many potential areas for future research.

http://www.ncbi.nlm.nih.gov/pubmed/12617692" onclick="window.open(this.href);return false;" onclick="window.open(this.href);return false;" onclick="window.open(this.href);return false;" onclick="window.open(this.href);return false;" onclick="window.open(this.href);return false;

Evidence for myofibril remodeling as opposed to myofibril damage in human muscles with DOMS: an ultrastructural and immunoelectron microscopic study.

Yu JG, Carlsson L, Thornell LE.

Department of Integrative Medical Biology, Section for Anatomy, Umeå University, 901 87 Umeå, Sweden.

The myofibrillar and cytoskeletal alterations observed in delayed onset muscle soreness (DOMS) caused by eccentric exercise are generally considered to represent damage. By contrast our recent immunohistochemical studies suggested that the alterations reflect myofibrillar remodeling (Yu and Thornell 2002; Yu et al. 2003). In the present study the same human muscle biopsies were further analyzed with transmission electron microscopy and immunoelectron microscopy. We show that the ultrastructural hallmarks of DOMS, Z-disc streaming, Z-disc smearing, and Z-disc disruption were present in the biopsies and were significantly more frequent in biopsies taken 2-3 days and 7-8 days after exercise than in those from controls and 1 h after exercise. Four main types of changes were observed: amorphous widened Z-discs, amorphous sarcomeres, double Z-discs, and supernumerary sarcomeres. We confirm by immunoelectron microscopy that the main Z-disc protein alpha-actinin is not present in Z-disc alterations or in the links of electron-dense material between Z-discs in longitudinal register. These alterations were related to an increase of F-actin and desmin, where F-actin was present within the strands of amorphous material. Desmin, on the other hand, was seen in less dense regions of the alterations. Our results strongly support that the myofibrillar and cytoskeletal alterations, considered to be the hallmarks of DOMS, reflect an adaptive remodeling of the myofibrils.

Copyright 2004 Springer-Verlag

http://www.ncbi.nlm.nih.gov/pubmed/1499 ... t=Abstract" onclick="window.open(this.href);return false;" onclick="window.open(this.href);return false;" onclick="window.open(this.href);return false;" onclick="window.open(this.href);return false;" onclick="window.open(this.href);return false;

Biochemistry of exercise-induced metabolic acidosis
Robert A. Robergs,1 Farzenah Ghiasvand,1 and Daryl Parker2

1Exercise Physiology Laboratories, Exercise Science Program, Department of Physical Performance and Development, The University of New Mexico, Albuquerque, New Mexico 87131; and 2Exercise Science Program, California State University-Sacramento, Sacramento, California 95819

The development of acidosis during intense exercise has traditionally been explained by the increased production of lactic acid, causing the release of a proton and the formation of the acid salt sodium lactate. On the basis of this explanation, if the rate of lactate production is high enough, the cellular proton buffering capacity can be exceeded, resulting in a decrease in cellular pH. These biochemical events have been termed lactic acidosis. The lactic acidosis of exercise has been a classic explanation of the biochemistry of acidosis for more than 80 years. This belief has led to the interpretation that lactate production causes acidosis and, in turn, that increased lactate production is one of the several causes of muscle fatigue during intense exercise. This review presents clear evidence that there is no biochemical support for lactate production causing acidosis. Lactate production retards, not causes, acidosis. Similarly, there is a wealth of research evidence to show that acidosis is caused by reactions other than lactate production. Every time ATP is broken down to ADP and Pi, a proton is released. When the ATP demand of muscle contraction is met by mitochondrial respiration, there is no proton accumulation in the cell, as protons are used by the mitochondria for oxidative phosphorylation and to maintain the proton gradient in the intermembranous space. It is only when the exercise intensity increases beyond steady state that there is a need for greater reliance on ATP regeneration from glycolysis and the phosphagen system. The ATP that is supplied from these nonmitochondrial sources and is eventually used to fuel muscle contraction increases proton release and causes the acidosis of intense exercise. Lactate production increases under these cellular conditions to prevent pyruvate accumulation and supply the NAD+ needed for phase 2 of glycolysis. Thus increased lactate production coincides with cellular acidosis and remains a good indirect marker for cell metabolic conditions that induce metabolic acidosis. If muscle did not produce lactate, acidosis and muscle fatigue would occur more quickly and exercise performance would be severely impaired.

metabolism; skeletal muscle; lactate; acid-base; lactic acidosis

Alex wrote:Rab, if DOM's are severe enough to hamper training that muscle group again then in theory they could effect growth if you continuously breakdown muscle tissue and don't allow enough time for regrowth. Hopefully most of us recognise this through loss of strength and muscle fatigue but this fact does remain.

Sometimes this isn't a bad thing and can be advantageous in small bursts as I think the resulting adaptation can help with better gains later on.

health4ni wrote:@Craig & Rab: since you both know that what causes DOMS is not fully understood, then there is a possibility that acidity levels caused by training is a factor. The earth was thought to be flat once...

Rilla wrote:

health4ni wrote:@Craig & Rab: since you both know that what causes DOMS is not fully understood, then there is a possibility that acidity levels caused by training is a factor. The earth was thought to be flat once...

By that logic, there's also a possibility that porridge+blue shorts is a factor.
While your idea may be valid, your logic is so far off on this one. You must've been in a hurry as you always seem to back up your posts with well thought out ideas/scientific stuff.

health4ni wrote:^^ he's being a rogue at the mo as he's not sleeping AT ALL between 11pm & 4am; Thurs, Fri & Sat he didn't sleep at all from midnight to 6am! Killer.

I'm on good quality Holy Basil supps to help me out. Might get some Rhodiola Rosea too.

health4ni wrote:^^ he's being a rogue at the mo as he's not sleeping AT ALL between 11pm & 4am; Thurs, Fri & Sat he didn't sleep at all from midnight to 6am! Killer.

I'm on good quality Holy Basil supps to help me out. Might get some Rhodiola Rosea too.