Scaredypants:

Influence of recombinant human erythropoietin treatment on pulmonary O2 uptake kinetics during exercise in humans.

Wilkerson DP, Rittweger J, Berger NJ, Naish PF, Jones AM.

J Physiol. 2005 Oct 15;568(Pt 2):639-52. Epub 2005 Aug 4.

Abstract

We hypothesized that 4 weeks of recombinant human erythropoietin (RhEPO) treatment would result in a significant increase in haemoglobin concentration ([Hb]) and arterial blood O(2)-carrying capacity and that this would (1) increase peak pulmonary oxygen uptake during ramp incremental exercise, and (2) speed kinetics during ‘severe’-, but not ‘moderate’- or ‘heavy’-intensity, step exercise. Fifteen subjects (mean +/- s.d. age 25 +/- 4 years) were randomly assigned to either an experimental group which received a weekly subcutaneous injection of RhEPO (150 IU kg(-1); n = 8), or a control group (CON) which received a weekly subcutaneous injection of sterile saline (10 ml; n = 7) as a placebo, for four weeks. The subjects and the principal researchers were both blind with respect to the group assignment. Before and after the intervention period, all subjects completed a ramp test for determination of the gas exchange threshold (GET) and , and a number of identical ‘step’ transitions from ‘unloaded’ cycling to work rates requiring 80% GET (moderate), 70% of the difference between the GET and (heavy), and 105% (severe) as determined from the initial ramp test. Pulmonary gas exchange was measured breath-by-breath. There were no significant differences between the RhEPO and CON groups for any of the measurements of interest ([Hb], kinetics) before the intervention. Four weeks of RhEPO treatment resulted in a 7% increase both in [Hb] (from 15.8 +/- 1.0 to 16.9 +/- 0.7 g dl(-1); P < 0.01) and (from 47.5 +/- 4.2 to 50.8 +/- 10.7 ml kg(-1).min(-1); P < 0.05), with no significant change in CON. RhEPO had no significant effect on kinetics for moderate (Phase II time constant, from 28 +/- 8 to 28 +/- 7 s), heavy (from 37 +/- 12 to 35 +/- 11 s), or severe (from 33 +/- 15 to 35 +/- 15 s) step exercise. Our results indicate that enhancing blood O(2)-carrying capacity and thus the potential for muscle O(2) delivery with RhEPO treatment enhanced the peak but did not influence kinetics, suggesting that the latter is principally regulated by intracellular (metabolic) factors, even during exercise where the requirement is greater than the , at least in young subjects performing upright cycle exercise.

Also:

Influence of blood donation on O2 uptake on-kinetics, peak O2 uptake and time to exhaustion during severe-intensity cycle exercise in humans.

Burnley M, Roberts CL, Thatcher R, Doust JH, Jones AM.

Exp Physiol. 2006 May;91(3):499-509. Epub 2006 Jan 23.

Abstract

We hypothesized that the reduction of O2-carrying capacity caused by the withdrawal of approximately 450 ml blood would result in slower phase II O2 uptake (VO2) kinetics, a lower VO2peak and a reduced time to exhaustion during severe-intensity cycle exercise. Eleven healthy subjects (mean +/- S.D. age 23 +/- 6 years, body mass 77.2 +/- 11.0 kg) completed ‘step’ exercise tests from unloaded cycling to a severe-intensity work rate (80% of the difference between the predetermined gas exchange threshold and the VO2peak) on two occasions before, and 24 h following, the voluntary donation of approximately 450 ml blood. Oxygen uptake was measured breath-by-breath, and VO2 kinetics estimated using non-linear regression techniques. The blood withdrawal resulted in a significant reduction in haemoglobin concentration (pre: 15.4 +/- 0.9 versus post: 14.7 +/- 1.3 g dl(-1); 95% confidence limits (CL): -0.04, -1.38) and haematocrit (pre: 44 +/- 2 versus post: 41 +/- 3%; 95% CL: -1.3, -5.1). Compared to the control condition, blood withdrawal resulted in significant reductions in VO2peak (pre: 3.79 +/- 0.64 versus post: 3.64 +/- 0.61 l min(-1); 95% CL: -0.04, – 0.27) and time to exhaustion (pre: 375 +/- 129 versus post: 321 +/- 99 s; 95% CL: -24, -85). However, the kinetic parameters of the fundamental VO2 response, including the phase II time constant (pre: 29 +/- 8 versus post: 30 +/- 6 s; 95% CL: 5, -3), were not altered by blood withdrawal. The magnitude of the VO2 slow component was significantly reduced following blood donation owing to the lower VO2peak attained. We conclude that a reduction in blood O2-carrying capacity, achieved through the withdrawal of approximately 450 ml blood, results in a significant reduction in VO2peak and exercise tolerance but has no effect on the fundamental phase of the VO2 on-kinetics during severe-intensity exercise.

Jon

p.s. I am not selling rhEPO or blood donations!

Paper 1. Not athletes? Were they even used to regular exercise, I wonder

Our results indicate that enhancing blood O(2)-carrying capacity and thus the potential* for muscle O(2) delivery with RhEPO treatment enhanced the peak but did not influence kinetic$

*extrapolation using a surrogate for performace
$ kinetics ? I R Not an exercise physiologist – what id the implication of this being unaltered ?

We conclude that a reduction in blood O2-carrying capacity, achieved through the withdrawal of approximately 450 ml blood, results in a significant reduction in VO2peak and exercise tolerance but has no effect on the fundamental phase of the VO2 on-kinetics during severe-intensity exercise

I’m back on kinetics and its meaning (rather the significance of “no effect”). Besides, removing blood cells and seeing a reduction does not allow the assumption that supraphysiological levels are better, does it ?

(or, to put it another way, what would TJ say if you were milkman and posted all that up, but swapped “colostrum” for “epo” ?)

Scardypants:

Paper 1:

Four weeks of RhEPO treatment resulted in a 7% increase both in [Hb] (from 15.8 +/- 1.0 to 16.9 +/- 0.7 g dl(-1); P < 0.01) and (from 47.5 +/- 4.2 to 50.8 +/- 10.7 ml kg(-1).min(-1); P < 0.05), with no significant change in CON

Paper 2:

The blood withdrawal resulted in a significant reduction in haemoglobin concentration (pre: 15.4 +/- 0.9 versus post: 14.7 +/- 1.3 g dl(-1); 95% confidence limits (CL): -0.04, -1.38) and haematocrit (pre: 44 +/- 2 versus post: 41 +/- 3%; 95% CL: -1.3, -5.1). Compared to the control condition

Are we agreed that these two interventions have opposite effects here?

Paper 1:

RhEPO treatment enhanced the peak but did not influence kinetics

(The ‘peak’ refers to VO2peak and simply, the kinetics are how quick you get to VO2peak)

Paper 2:

blood withdrawal resulted in significant reductions in VO2peak

Again, are we agreed with opposing effects here?

Paper 2:

and time to exhaustion (pre: 375 +/- 129 versus post: 321 +/- 99 s; 95% CL: -24, -85)

We conclude that a reduction in blood O2-carrying capacity, achieved through the withdrawal of approximately 450 ml blood, results in a significant reduction in VO2peak and exercise tolerance

Paper 1:

So, as EPO has the opposing effect on the physiology, it is ‘likely’ that exercise tolerance would be enhanced, no?

Jon

Scardypants:

Also sorry, I forget to answer your first question

Not athletes? Were they even used to regular exercise, I wonder

I personally know a good number of the authors on these papers and I was a participant in paper 2 – all of the people used in these studies were used to regular exercise, a good proportion would be described as athletes, and some were ‘well trained’. At the time, my first year as an undergraduate, I held a BCF elite XC racing licence.

I am an exercise physiologist, I am not endorsing any product and my PhD involves these VO2 kinetics, VO2max/peak/ and exercise tolerance. I have no external agenda, and I believe that EPO does work as it appears to enhance haemoglobin concentration, and VO2peak, by ~7% in almost everybody tested.

Jon

p.s. I hope I make a better argument than our Milkman, these questions are good as will be asked similar questions in my PhD viva examination in a few months.

could someone sum this thread up? getting a bit wordy..

rootes1;

Wierd cows milk based drink.

You may or may not die of heatstroke if you exercise without drinking it first.

In a nutshell – milkman makes wonder milk, foxyrider and TJ are organising the STW group-buy.

right….. should i can the daily pint of Sterilized Milk then? It makes nice tea you see… (though not as good as condensed milk)

Colostrum ‘may’ enhance recovery and immune function… which in turn might allow an athlete to train harder/longer/more often without illness… thereby by proxy may also lead to enhanced performance (although data to support these suggestions is limited at best).

labmonkey – why did they bugger about with loads of “measures” in the epo study while failing to address or report the key issue, ie performance ?

it’s obvious to me that the more RBC/Hb in the blood, the greater the O2 carrying capacity of said blood but I need to see that this translates into performance

(I notice incidentally, we’re only on epo – presumably no, or far far softer, data for the other banned substances then ? As acknowledged on p1 of this lot, case for epo is probably clear and has a convincing rationale – though not proven imo, at least on this thread)

Don’t get me wrong, I don’t use or want to use any of this shite and I’ve no interest in seeing no-hopers like me wasting money on colostrum or anything else. I am a bit perplexed by the lambasting of milkman & his product and calls for utterly unimpeachable evidence (blinded controlled trials with big numbers of athletes) in support, when I don’t believe this can be achieved for dozens of drugs that wada and uci would have us believe are “cheat” drugs.
I’d also be surprised if loads of top athletes aren’t using the stuff, with or without evidence. If the purported mechanism (reduction in minor infection rates and their subsequent effect on training as I understand the stuff above) is correct then it’ll be virtually impossible to demonstrate, ever.

I can only speak for myself but milkman was making claims that clearly cannot be supported by the research he produced and he used loads of anecdote and endorsements as “proof” which it is not. He also made some ludicrous claims about heatstroke.

Scaredypants:

As acknowledged on p1 of this lot, case for epo is probably clear and has a convincing rationale – though not proven imo, at least on this thread

Taking a step back from Sport and Performance for a second;

EPO was developed as a drug to combat severe clinical anemia (and other red blood cell related ‘issues/diseases’ etc). The vast majority of the research into this drug was undertaken to determine whether it would increase red blood cell mass, haemoglobin concentration, haematocrit etc -this research is a resounding YES and so the drug is widely used within the medical world to treat such conditions.

‘Cheats’ in sport got hold of this evidence and decided to take it to enhance performance, as the evidence for its effecton the blood would suggest a likely ergogenic effect. The number of ‘very good’ (and maybe artificially enhanced) athletes (mainly cyclists) that have been caught for using EPO and its derivatives (NESP and CERA) suggest that it may well work pretty well.

As exercise physiologists, we are not too concerned as to whether EPO actually enhances performance per se (I am not aware of a single paper that has tested that hypothesis) but we are interested into the mechanisms that determine exercise tolerance (in health and also in disease).

The research group that I work within (including the authors of these two papers) strongly believe that the interaction between the VO2 kinetics, VO2max and the ‘anaerobic capacity’ play a central role in determining exercise tolerance/performance.

The purpose of these two papers was to investigate the effects of altering haemoglobin of these measures, rather than performance itself.

Jon

Furthermore, it is unlikley that any real ‘athletes’ would agree to take EPO as part of a study, as a positive test would result in a two year ban.

Jon / (LM)

As exercise physiologists, we are not too concerned as to whether EPO actually enhances performance per se (I am not aware of a single paper that has tested that hypothesis) ….. Furthermore, it is unlikley that any real ‘athletes’ would agree to take EPO as part of a study, as a positive test would result in a two year ban.

Aye, that’s my point really – people asking for scientifically rigorous testing of a “new” fad product is ludicrous and UNFAIR

Out of interest, in your 2nd study, were you blinded as to whether blood was actually taken from you (ie control grp cannulated but minimal blood removal)?
I’d guess (from the almost nothing I know) that VO2peak might be more dependent on psychology than VO2max is and I might not try as hard if I’d had blood removed. Intuitively I’d expect a fall, but always nice to see controls all the same …

Aye, that’s my point really – people asking for scientifically rigorous testing of a “new” fad product is ludicrous and UNFAIR

Hay – wait up – this was in response to the wildish claims made by Milkman. My OP indicated I did not believe the hype concerning how beneficial Bovine Colostrum is with intensive training NOT how it hasn’t been researched enough yet. Then it has gone on to how Milkman is suggesting its a wonder supplement and spouting rubbish he did obviously not understand. If you make claims you should back it up not spouting stupid pseudo-science!

If you notice it seems his claims have been edited by EU directives!

http://www.neovite.com/benefits/Default.asp

This was my point – you cannot make claims if you can’t prove them. We would have been happy if he suggested the potential benefits and they are researching them as we speak!!! And yes some of us have a biomedical research background too!

Oh god I said I wasn’t going to get sucked in again 😯 🙁

just when i thought i was out…they pull me back in

Scaredypants:

I am quite enjoying this debate, thanks for the questions!

Aye, that’s my point really – people asking for scientifically rigorous testing of a “new” fad product is ludicrous

People need to understand the EPO was not developed for sport, it was developed to treat a disease – therefore the evidence does not exist.

Milkmans marketing of his colostrum product suggests that it will be of use in sport and they appear to be selling it on that premise – therefore he needs to get research to directly support such claims.

Out of interest, in your 2nd study, were you blinded as to whether blood was actually taken from you (ie control grp cannulated but minimal blood removal)?

Nope, we all went down to the NHS blood donation service and did our bit for society… we knew that blood was being withdrawn, you could see it if you looked around a bit on the bed.

It would have been nice to have a control group that did not have blood withdrawn, but whether there was a (negative) placebo effect was not the focus of this work.

We have to trust our participants to go ‘as hard as possible, for as long as possible’ – we verbally encourage (shout at) then to give a maximal effort!

I’d guess (from the almost nothing I know) that VO2peak might be more dependent on psychology than VO2max is and I might not try as hard if I’d had blood removed.

VO2max and VO2peak are essentially the same thing, its the highest amount of oxygen consumed by the muscle in one minute. Differing methods of determination of this measure has given rise to the two names. I won’t go into the detail here unless really prompted – or put Day et al 2003 into pubmed.com and you might find it yourselves.

Psychology is a factor in performance, there is no denying that, and as a physiologist, it pains me to accept that. Someone could intentially ‘fake’ exhaustion early and we would then get a lower VO2peak, yeah sure, we have to trust them not to do that. But, no will in the world can make you get a higher VO2max either, your body can only use so much oxygen – end of story.

Jon

foxy – my point is, what’s your take on the claims that THG, testosterone etc help with intensive training ?

Foxyrider:

Oh god I said I wasn’t going to get sucked in again

Sorry, I am avoiding the colostrum debate as much as possible.

Just answeing some questions on EPO / blood donation etc as someone appears interested in our work – this is rare in Science!

@ jon – VO2max is sort of incontrovertible, I thought (where the line forms a plateau). I thought VO2peak was the point at which subjects (most of us) don’t reach plateau but it hurts too much to go on, hence more susceptible to psychology ?

foxy – my point is, what’s your take on the claims that THG, testosterone etc help with intensive training ?

I don’t care as its off my topic list!

Scaredypants:

my point is, what’s your take on the claims that THG, testosterone etc help with intensive training?

This is my last post (hopefully) before I vanish (not literally) for the day…

For ‘endurance exercise’ i.e. that lasting more than about 2 mins, the most effective ergogenic aids/drugs are the ones that enhance either O2 delivery to the muscle or those that facilitate O2 utilization within the muscle – as oxygen and carbohydrate (and fats) are the principle providers of energy to the muscle to support exercise.

Jon

Scaredypants:

OK, one more… Day and collegues can explain this one!

VO2max is sort of incontrovertible, I thought (where the line forms a plateau). I thought VO2peak was the point at which subjects (most of us) don’t reach plateau but it hurts too much to go on, hence more susceptible to psychology ?

J Appl Physiol. 2003 Nov;95(5):1901-7. Epub 2003 Jul 11.

The maximally attainable VO2 during exercise in humans: the peak vs. maximum issue.

Day JR, Rossiter HB, Coats EM, Skasick A, Whipp BJ.

Abstract

The quantification of maximum oxygen uptake (V(O2 max)), a parameter characterizing the effective integration of the neural, cardiopulmonary, and metabolic systems, requires oxygen uptake (VO2) to attain a plateau. We were interested in whether a VO2 plateau was consistently manifest during maximal incremental ramp cycle ergometry and also in ascertaining the relationship between this peak VO2 (V(O2 peak)) and that determined from one, or several, maximal constant-load tests. Ventilatory and pulmonary gas-exchange variables were measured breath by breath with a turbine and mass spectrometer. On average, V(O2 peak) [3.51 +/- 0.8 (SD) l/min] for the ramp test did not differ from that extrapolated from the linear phase of the response in 71 subjects. In 12 of these subjects, the V(O2 peak) was less than the extrapolated value by 0.1-0.4 l/min (i.e., a “plateau”), and in 19 subjects, V(O2 peak) was higher by 0.05-0.4 l/min. In the remaining 40 subjects, we could not discriminate a difference. The V(O2 peak) from the incremental test also did not differ from that of a single maximum constant-load test in 38 subjects or from the V(O2 max) in 6 subjects who undertook a range of progressively greater discontinuous constant-load tests. A plateau in the actual VO2 response is therefore not an obligatory consequence of incremental exercise. Because the peak value attained was not different from the plateau in the plot of VO2 vs. work rate (for the constant-load tests), the V(O2 peak) attained on a maximum-effort incremental test is likely to be a valid index of V(O2 max), despite no evidence of a plateau in the data themselves. However, without additional tests, one cannot be certain.

once you’re back from work then 😉 :

For ‘endurance exercise’ i.e. that lasting more than about 2 mins, the most effective ergogenic aids/drugs are the ones that enhance either O2 delivery to the muscle or those that facilitate O2 utilization within the muscle – as oxygen and carbohydrate (and fats) are the principle providers of energy to the muscle to support exercise.

so which are they ?
any drugs to increase lactate tolerance in the shorter term (eg “sprinting” the last mile of a stage or a short TT) ?
and why did landis do that stoopid thing with testosterone ? (or did he re-dope with contaminated blood?)

Your milkman is back from the dairy
On Tuesday I posted literature showing the effect of heat stress on the performance of your gut barrier function. I have also illustrated that endoxemia can be measured by bacterial fragments from the gut, found in the bloodstream (LPS). Foxyrider claims he has an alternative theory of endotoxemia, but has yet to produce it. Please do.

Heat stress can be induced both exothermically, as in the laboratory study, or by intense exercise as illustrated in the Ashton study. Remember that the return blood-flow from the legs, where the heat is being generated, flows along the posterior vena cava right next to your small intestine, so it’s no surprise that this is the hottest part.

Let me now introduce a further example of heat stress and the response on the mammalian gut, the design of which goes back to our common mammal ancestor. The only mammal capable of enduring high core temperatures is the camel. The pathway utilised by this species is to enhance the repair capacity of the gut in the form of increased IGF-1 production and a higher number if IGF-1 receptors in the surface tissue of the gut. Please consider the following study

Growth Factors. 2003 Sep-Dec;21(3-4):131-7.

Distribution of insulin like growth factor-1 (IGF-1) and its receptor in the intestines of the one-humped camel (Camelus dromedarius).
Al Haj Ali M, Mensah-Brown E, Chandranath SI, Adeghate E, Adem A.

Department of Pharmacology, UAE University, United Arab Emirates.

Abstract
The distribution of insulin-like growth factor-1 (IGF-1) and its receptor in the gut of the one-humped camel (Camelus dromedarius) were studied by immunohistochemistry and quantitative receptor autoradiography. IGF-1-IR cells occurred mainly in the lamina propria and epithelium of the small intestine, while in the large intestine positive cells were seen in the columnar cells of the epithelial layer of colonic glands. IGF-I was also discernible in the muscularis externa of the intestines. Autoradiography revealed a higher concentration of receptors in the mucosa compared to the muscular layer. With regard to the mucosa, the highest density of receptors was discernible in the duodenum. Immunohistochemistry revealed the main sites of the receptors to be the lamina propria, epithelia of the crypts and the villi of intestines. Double immunofluorescence studies with combined antisera to IGF-I and its receptor showed that the ligand and its receptor usually occurred within the same cell in the mucosa. A few cells with varied profiles immunoreacted to either the ligand or the receptor but not to both. Cells with varied profiles immunoreacted to antiserum of the receptors but not to the ligand in the muscle layer. Thus IGF-1 might be acting on its receptor via both an autocrine and paracrine modes in the camel mucosa. In the muscularis layer, IGF-1 may be acting by different mechanisms. Our data demonstrate that unlike all other mammals studied, the camel contains a high concentration of IGF-1 receptors in the duodenal mucosa compared to other parts of the camel gut. It also possesses a higher concentration of the receptor in its mucosa compared to the muscle layer. We speculate that this might be a significant feature necessary for the regenerative ability of the duodenal mucosa in the one-humped camel.

PMID: 14708941 [PubMed – indexed for MEDLINE]

So, for readers that have a science based education, the idea that a source of repair trigger proteins (IGF-1, EGF) other than from your own saliva can effect an improvement in the performance of your gut under conditions of heat stress must surely be getting clearer even to the most stubborn resisters and ranters. For those of you unfortunate not to have had the education of Foxyrider or Tandemjeremy I have shown a practical example of heat stress resilience in the Attenborough video showing human performance where humans are specifically adapted do dissipate our excess heat by being bare skinned, sweating over the whole area of the skin, reduced sun exposed surface area by standing vertically with an insulating heat protecting hair cover for the top of the head, with low energy two leg locomotion, compared with that of the much stronger faster Kudu which isn’t.

Let’s look at some the consequences of the rants that started this thread. Kimber has stopped eating black pudding now that he knows it’s made from ox-blood. Clubber is planning to make a fortune by harvesting the saliva that Kimber has become reluctant to swallow now that he’s learned it’s full of growth factors, and at a cheaper price than goat’s milk, camel’s milk or cow’s colostrum too. Seriously Kimber, you will have to swallow your saliva. If you don’t your small intestine may ulcerate leading to toxic shock and organ failure, not unlike heatstroke. There is plenty of research into this gut state where it has been induced by the tube feeding of comatose patients in intensive care but you’ll have to look this bit up for yourself.

There are studies showing a number of other ways of combating the problem but you’ll all have to be very good and apologise nicely before I’ll tell you. One thing for free however, be careful if you use the Tony Ashton vitamin C method. A national Olympic road race squad used added vitamin C in their drinks to guard against heat stress permeability at the Beijing games. Unfortunately the coaches underestimated their actual hydration needs. They ended up with too much retained ascorbate, had a lot of excess fluid in their muscles to buffer it and suffered from a lot of cramps and had lousy results, or at least so I am informed by a reliable source. Call me if you want to know which country

Labrat may be pleased to know that his trip to hospital may have been one of the number leading to our first NHS trial planned with his local hospital for that very thing, post operative recovery.

Your claims to have a bullshit detector really do seem pretty thin. When was it last calibrated? Rather than my 40-year professional career, try initialising it with the credentials of our principle gastroenterology researcher – he is a Fellow of the Royal College of Physicians, the Royal College of Pathologists and the Academy of Medical Scientists and probably UK’s most published author in this field. It’s a comfort to me to know that an eminent researcher is prepared to include a humble chap like your milkman as a co-author in spite of Foxyrider’s reservations. Here’s a look at one of his studies where he uses colostrum to prevent permeability inducing gut damage caused by using non-steroidal anti-inflammatory drugs.

Clin Sci (Lond). 2001 Jun;100(6):627-33.

Co-administration of the health food supplement, bovine colostrum, reduces the acute non-steroidal anti-inflammatory drug-induced increase in intestinal permeability.
Playford RJ, MacDonald CE, Calnan DP, Floyd DN, Podas T, Johnson W, Wicks AC, Bashir O, Marchbank T.

Department of Gastroenterology, Imperial College School of Medicine, Hammersmith Hospital, Du Cane Road, London W120NN, UK. r.playford@ic.ac.uk

Abstract
Non-steroidal anti-inflammatory drugs (NSAIDs) are effective analgesics but cause gastrointestinal injury. Present prophylactic measures are suboptimal and novel therapies are required. Bovine colostrum is a cheap, readily available source of growth factors, which reduces gastrointestinal injury in rats and mice. We therefore examined whether spray-dried, defatted colostrum could reduce the rise in gut permeability (a non-invasive marker of intestinal injury) caused by NSAIDs in volunteers and patients taking NSAIDs for clinical reasons. Healthy male volunteers (n=7) participated in a randomized crossover trial comparing changes in gut permeability (lactulose/rhamnose ratios) before and after 5 days of 50 mg of indomethacin three times daily (tds) per oral with colostrum (125 ml, tds) or whey protein (control) co-administration. A second study examined the effect of colostral and control solutions (125 ml, tds for 7 days) on gut permeability in patients (n=15) taking a substantial, regular dose of an NSAID for clinical reasons. For both studies, there was a 2 week washout period between treatment arms. In volunteers, indomethacin caused a 3-fold increase in gut permeability in the control arm (lactulose/rhamnose ratio 0.36+/-0.07 prior to indomethacin and 1.17+/-0.25 on day 5, P<0.01), whereas no significant increase in permeability was seen when colostrum was co-administered. In patients taking long-term NSAID treatment, initial permeability ratios were low (0.13+/-0.02), despite continuing on the drug, and permeability was not influenced by co-administration of test solutions. These studies provide preliminary evidence that bovine colostrum, which is already currently available as an over-the-counter preparation, may provide a novel approach to the prevention of NSAID-induced gastrointestinal damage in humans.

PMID: 11352778 [PubMed – indexed for MEDLINE]

I really must thank the contribution of Rocky Robin, he really made my day –
“what a load of old b****x, in my time I’ve worked and trained with some world class athletes (not cycling) and none of them would attribute their success to cow colostrum- genetics first and foremost, training second, vision and mental attributes next. All a bit of snake oil peddling if you ask me- Steve Peat’s favourite supplements are Stella Artois and curry (info courtesy of his blog).Says it all in my book! “
The very essence of rant. A perfect 10. “It can’t possibly be true because he hasn’t heard of it.” He may not have had the education of Tandemjeremy or Foxyrider but he’s certainly made of the same stuff.

A point where Robin and I will certainly agree is that you will need to train harder or smarter to become faster. We don’t sell colostrum on the basis that if you take it you don’t need to train. But if you increase your training load to the point where the physiology of your gut or immune system is challenged then you really should consider using it.

I would like to thank the more open minded members who have offered me their sympathy. I am not defensive however, I am indignant. The only consolation I can draw from these exchanges is that not one of the scientists here have picked up the phone to engage in a real world debate rather than posting snide remarks and anonymous sniping. Whatever happened to scientific curiosity.

Whatever happened to scientific curiosity.

It was killed in the stw ‘cut and paste’ war of October 2010…

I think the problem is Milkman that no one is going to get you to change your mind – you have a business to run, even if someone on here said ‘hang on mate what about ….’ and it shot all your ‘evidence’ down in flames you’d still carry on because you have to.

It would be like trying to convionce a Jehovas witness on the doorstep that God doesn’t exist – fun for a bit but ultimately pointless.

It may be that your product is suitable for use by certain elite athletes but for the average mtber the advantages (if there are any) are likely to be vanishingly small.

all in my opinion of course.

Milkman, you are Kasae and i claim my £10, paypal gift is fine !!

Oh god make it stop. 😯

I feel someone is keen for their product’s name to be on the internet no matter what the reason….!

Apologies LabMonkey, labrat an unintended error, no slight intended.

GO AWAY – YOUR JUST ANNOYING NOW!!!!!

[video]http://www.youtube.com/watch?v=oXQkMGffOBo[/video]

YOUR

*ahem* YOU’RE *ahem*

I’m not sure telling him to shut up is the best solution – he’s digging quite a big hole and it woudl be a shame to stop now.

are there other forums where the same conversation is going on or are the doubters limited to stw?

Foxyrider

Is this your last contribution on endotoxemia? do you really have nothing to contribute, having convinced us all that you could back up your rant with a superior theory?

Apologies LabMonkey, labrat an unintended error, no slight intended.

No offence taken.

One question for you…

Q: What is the principal mechanism that regulates time to exhaustion, or more importantly… performance in the heat in humans?

Clue: It’s not the Gut

Big Clue: Is it the brain, and central fatigue?

The brain will stop a human exercising long before the gut becomes damaged.

The end, thank you and goodnight.

Labmonkey

You can confirm with your researchers at Aberystwyth that without any colostrum we have measured an average 240% increase in intestinal permeability after a 20 minute run at 80% VO2max and consistent with a rise in core temperature, and this at normal ambient temperatures not in the environment chamber to simulate hot conditions. What happens when you use colostrum will have to await publication rather than me reveal it here but I’m sure your colleagues will give you a confidential briefing. Perhaps you can report it here in a manner that will not compromise publication, as I’ve already gone as far as I dare.

Milkman

What ‘conditions’ (i.e. temperature and humidity) and type of exercise (i.e. duration and intensity) are you suggesting that colostrum will elicit an improvement in exercise performance?

Perhaps you can report it here in a manner that will not compromise publication

I am not privy to this work, and so I am in no position to comment on unpublished reserach.

Milkman – so what? Your nostrumn is possibly ( but unporoven) treating one symptom of hyperpyrexia. It is not a cure for heatstroke.

You need to stop quoting research you don’t understand. Most of what you posted does not show what you claim and when your claims are true they are irrelevant.

Saved by the bell. Presented in the proceedings of the Annual Conference of the British Society of Gastroenterology. I should have looked here earlier I suppose. Aplologies for keeping you all waiting so long. Peer reviewed publication anticipated soon.

Gut 2010;59:A34-A35; doi:10.1136/gut.2009.208991e
Copyright © 2010 BMJ Publishing Group Ltd & British Society of Gastroenterology.

Small bowel & nutrition free papers

OC-083 Clinical trial: influence of bovine colostrum on intestinal permeability in healthy athletes after heavy exercise
T Marchbank1, G Davison2, J R Oakes2, M Ghatei3, M Patterson3, J Rolfs4, R J Playford1

1 Department of Digestive Diseases, Barts and the London School of Medicine, London, UK
2 Department of Sport and Exercise Science, Aberystwyth University, Aberystwyth, UK
3 Department of Metabolic Medicine, Hammersmith Hospital, Imperial College, London, UK
4 Department of Sport and Exercise Science, Colostrum UK, London, UK

Introduction: Heavy exercise results in gut symptoms and in extreme cases “heat stroke” due, in part, to increased intestinal permeability of luminal toxins. We examined if bovine colostrum a rich source of growth factors and immune modulators could prevent these permeability changes.

Methods: Twelve healthy volunteers completed a double-blind, placebo-controlled, crossover protocol (14 days colostrum or placebo) prior to standardised exercise. Gut permeability utilised 5 h urinary lactulose: rhamnose ratios. In vitro studies (T84 cells) examined effects of colostrum on temperature-induced apoptosis (active caspase-3) and epithelial resistance.

Results: For both arms of study, exercise increased the blood lactate, heart rate, core temperature (mean 2°C rise) and plasma VIP by similar amounts. However, GLP-1 plasma levels results were discordant; rising by 88.7 pmol/l in placebo arm but falling by 4.2 pmol/l in colostrum arm (p=0.026). Intestinal permeability in placebo arm increased 2.5-fold following exercise (0.38±0.012 baseline value, to 0.92±0.014, p<0.01), whereas colostrum truncated this rise by 80% (only rising from 0.38±0.012, initial baseline value, to 0.49±0.017) following exercise. In vitro apoptosis increased by 63% in response to increasing temperature by 2°C whereas this effect was truncated by 66% if colostrum was co-present (all p<0.01). Similar results were obtained when changes in epithelial resistance were assessed (colostrum truncating the fall in resistance by 64%, p<0.01).

Conclusion: Bovine colostrum reduced exercise-induced increase in gut permeability, possibly through mechanisms including reducing temperature-induced apoptosis. This may have value in enhancing athletic performance and preventing heat stroke.

Sorry WW – you are quite right – I was just enraged 😳 My spelling/grammar failed me 🙁

@Milkman – my god you are delusional if you think you understand the complex subject of ENDOTOXEMIA.

Endotoxemia is bacterial toxins, digestive enzymes and part digested food fragments entering the portal circulation, overloading the capacity of the mesentreic lymphatic system and the liver to filter out the toxins and their entry into the systemic circulation where thay can induce organ failure.

It is NOT as you quoted due to absorption of digestive enzymes and part digested food particles. You are WRONG, WRONG, WRONG – I have not replied to this thus far as its like talking to a child in Kindergarten. As for OVERLOADING the lymphatic system, rubbish – toxins are generally conveyed to the liver by venous return via the portal vein into the liver where is it modified by the hepatocytes lining the sinusoids. NOT VIA LYMPHATICS – god damn it. You know nothing of what you are spouting. Bloomin people like you give science a bad name!!!!

I didn’t mean to propose that the mesenteric lymphatic system was the conduit for the portal flow. The lymphatic system is involved in the production of antibodies to effect the abstraction of toxins and this was the purpose of including it, in an attempt to present a simple understanding to others. I don’t intend to contradict your clarification, but I think you’re still missing the bigger picture

BTW- The lymphoid follicles are the source of antibodies in lymph nodes which is part of the lymphatic system. Antibodies are produced but as a result of endotoxaemia not the other way around and also Ab’s are not the only method or main method of neutralising circulating endotoxins!

Edit: I was not interested in adding anymore to this thread but you keep goading people on here so you can seemingly advertise your product. I have no major interest in sport physiology really and I still remain sceptical of the benefits of colostrum and will remain so until good hard evidence is available (In my view not yours). We all have line over which we become irritated. If you want to talk medically with me please use correct terminology otherwise I will make my own assumtions. I think it is time you let this subject die a natural death?

I’m only trying to keep it simple so others can follow the thread. Luminal toxins should not be entering the bloodstream, portal or otherwise. They can challenge the immune system systemically. You’re welcome to elaborate on the particulars.