Jump to content
mccoy

Exercise optimization

Recommended Posts

AFAIY, and I might be wrong, the prions causing Creutfield Jacob disesase are transmitted by contamination from CNS (brain) tissue. Do you have any references supporting milk-based contamination? Also, bovine spongiform encephalitis is CJ-disease, which originates from cows and bovines.

Share this post


Link to post
Share on other sites

Pretty intersting article on plant based protein aminoacid profiles and whey and other animal sources

 

Amino Acids

December 2018, Volume 50, Issue 12, pp 1685–1695| Cite as

Protein content and amino acid composition of commercially available plant-based protein isolates

  • Stefan H. M. Gorissen
  • Julie J. R. Crombag
  • Joan M. G. Senden
  • W. A. Huub Waterval
  • Jörgen Bierau
  • Lex B. Verdijk
  • Luc J. C. van LoonEmail author
    •  
    •  
    •  
    •  
    •  
    •  
    •  
  1. 1.
  2. 2.
Open Access
Original Article
First Online: 30 August 2018

Abstract

The postprandial rise in essential amino acid (EAA) concentrations modulates the increase in muscle protein synthesis rates after protein ingestion. The EAA content and AA composition of the dietary protein source contribute to the differential muscle protein synthetic response to the ingestion of different proteins. Lower EAA contents and specific lack of sufficient leucine, lysine, and/or methionine may be responsible for the lower anabolic capacity of plant-based compared with animal-based proteins. We compared EAA contents and AA composition of a large selection of plant-based protein sources with animal-based proteins and human skeletal muscle protein. AA composition of oat, lupin, wheat, hemp, microalgae, soy, brown rice, pea, corn, potato, milk, whey, caseinate, casein, egg, and human skeletal muscle protein were assessed using UPLC–MS/MS. EAA contents of plant-based protein isolates such as oat (21%), lupin (21%), and wheat (22%) were lower than animal-based proteins (whey 43%, milk 39%, casein 34%, and egg 32%) and muscle protein (38%). AA profiles largely differed among plant-based proteins with leucine contents ranging from 5.1% for hemp to 13.5% for corn protein, compared to 9.0% for milk, 7.0% for egg, and 7.6% for muscle protein. Methionine and lysine were typically lower in plant-based proteins (1.0 ± 0.3 and 3.6 ± 0.6%) compared with animal-based proteins (2.5 ± 0.1 and 7.0 ± 0.6%) and muscle protein (2.0 and 7.8%, respectively). In conclusion, there are large differences in EAA contents and AA composition between various plant-based protein isolates. Combinations of various plant-based protein isolates or blends of animal and plant-based proteins can provide protein characteristics that closely reflect the typical characteristics of animal-based proteins.

Share this post


Link to post
Share on other sites

Perhaps a silly question, but why would anyone on a CR forum choose to bulk up on a full daily dose of methionine at one fell swoop?

There is quite a bit of evidence that restricting methionine and some other BCAAs may be an integral part of the process taking place during CR (which seems to be largely due to reduced protein intake). See for example https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5008916/

 

 

Share this post


Link to post
Share on other sites

Ron, I'm just making an experiment in muscle hypertrophy (which is not being too succesfull though)

Large dosages of AAs may be beneficial just after training, and maybe the day after,.

I too believed in the alleged detrimental effects of mTOR upregulation from protein intake.

There are many hints that such a model is too simplistic though. Also, downregulating mTOR too much may definitely be uneahlty and anti-longevity.

And mTOR upregulation in skeletal muscle is arguable healthy., especially so to counteract older-age anabolic resistance  and myiopenia.

Again, methionine moderation = low IGF-1, but a few authoritative sources affirm that too low of an IGF-1 may be detrimental and that there is an optimum value which is not too low , as discussed in another thread.

Probably we'd need to optimize our own protein and methionine intake to our own IGF-1. I've yet to have myself analyzed.

Edited by mccoy

Share this post


Link to post
Share on other sites
26 minutes ago, mccoy said:

Also, downregulating mTOR too much may definitely be uneahlty and anti-longevity.

Mccoy,

To optimize mTOR while practicing CR, you might want to consider adding cold exposure. See this post and the associated links for discussion of how the combination of CR and CE can allow you to have your cake and eat it too, i.e. enjoy the important anabolic benefits of mTOR activity without giving up the benefits of CR to keep insulin and IGF-1 low.

Here is a teaser:

pLdCgcM.jpg

--Dean

Share this post


Link to post
Share on other sites

Thanks Sibiriak,

Somehow I missed that exchange. I agree with McCoy's conclusion that:

Quote

CE probably will not upregulate mTOR in skeletal muscles directly...

and that to significantly boost muscle mass requires mechanical stimulation along with adequate nutrition.

I just wanted to point out that many of other beneficial anabolic effects of mTOR, e.g. boosting the immune system, improving bone health and increasing neurogenesis, which may otherwise be compromised by serious CR (which downregulates mTOR), may be restored by cold exposure, while still keeping (pro-aging) IGF-1 low.

--Dean

Share this post


Link to post
Share on other sites

It is funny that I was about to answer to Dean's post and diagrams without even remembering that I had already commented on them!

Sibiriak definitely wins the attention and memory contest.

Basically, my present comments would remain the same, except the baseline ideas on androgens and sterodis, which are believed to boost muscles by additional mechanisms such as increasing the number of satellite cells, nuclei and so on.

Dean's thought on CE remains definitely and basically valid: bypassing some known drawbacks of CR by activating useful pathways by CE.

My attitude to CR is that, if Michael Rae's definition is accepted (at least minus 15-20% from the ideal weight in one's twenties), it would imply in myself a loss of conspicuos muscle mass and maybe bone mass since I dont' have much adiposity to begin with.

So I'm experimenting whether a reasonable CR-CM (caloric moderation) is possible while keeping a certain amount of muscle mass/bodyweight.

My intended first stage of the experiment was to boost muscular hypertrophy, increase a few kilograms in muscle mass, then optimize glucose-protein consumption to keep that mass while being in a calorically restricted, or caloric-moderated fashion (a strategy outlined by dr. Peter Attia).

This 1st stage is failing, in that I'm not being able to build muscle mass beyond a certain point which would make me comfortable to restrict calories (due to sensitivity of tendons to higher loads or volumes).

Right now I'm experimenting with relatively low calories (for me) cutting fat but increasing animal protein (nonfat dairy) not to loose muscle mass. 

Why all that worry with muscle mass if there are no signs of sarcopenia yet? I don't know, a fixation of mine probably!

 

 

Edited by mccoy

Share this post


Link to post
Share on other sites

Thanks to Al Pater, who posted in his sections a new interesting article on protein optimization, I've printed the paper and i'm going to commented after the reading.

Quote

Dietary Protein Quantity, Quality, and Exercise Are Key to Healthy Living: A Muscle-Centric Perspective Across the Lifespan.
Burd NA, McKenna CF, Salvador AF, Paulussen KJM, Moore DR.
Front Nutr. 2019 Jun 6;6:83. doi: 10.3389/fnut.2019.00083. eCollection 2019. Review.
PMID: 31245378
Abstract
A healthy eating pattern, regardless of age, should consist of ingesting high quality protein preferably in adequate amounts across all meals throughout the day. Of particular relevance to overall health is the growth, development, and maintenance of skeletal muscle tissue. Skeletal muscle not only contributes to physical strength and performance, but also contributes to efficient macronutrient utilization and storage. Achieving an optimal amount of muscle mass begins early in life with transitions to "steady-state" maintenance as an adult, and then safeguarding against ultimate decline of muscle mass with age, all of which are influenced by physical activity and dietary (e.g., protein) factors. Current protein recommendations, as defined by recommended dietary allowances (RDA) for the US population or the population reference intakes (PRI) in Europe, are set to cover basic needs; however, it is thought that a higher protein intake might be necessary for optimizing muscle mass, especially for adults and individuals with an active lifestyle. It is necessary to balance the accurate assessment of protein quality (e.g., digestible indispensable amino acid score; DIAAS) with methods that provide a physiological correlate (e.g., established measures of protein synthesis, substrate oxidation, lean mass retention, or accrual, etc.) in order to accurately define protein requirements for these physiological outcomes. Moreover, current recommendations need to shift from single nutrient guidelines to whole food based guidelines in order to practically acknowledge food matrix interactions and other required nutrients for potentially optimizing the health effects of food. The aim of this paper is to discuss protein quality and amount that should be consumed with consideration to the presence of non-protein constituents within a food matrix and potential interactions with physical activity to maximize muscle mass throughout life.

 

Share this post


Link to post
Share on other sites
On 6/19/2019 at 4:18 PM, Ron Put said:

Perhaps a silly question, but why would anyone on a CR forum choose to bulk up on a full daily dose of methionine at one fell swoop?

I take moderate amounts of leucine, methionine, isoleucine daily with CR or at least under 2000kCal and IF.  Fasting for approximately 14hrs per day with extremely heavy resistance training and cycling the aminos is my personal experiment which at least looks great and feels good.

 I believe that plenty of skeletal muscle mass, zero visceral fat, high strength and avoidance of micronutrient deficiency are what is important for maximum lifespan.

Share this post


Link to post
Share on other sites

My results of CR+high protein, from nonfat dairy products mainly (20% protein-45-50% carbs) plus moderate exercise are not exactly what I wanted. I did not gain muscle mass, although I sure lost adipose tissue. I followed Brad Schonfeld's reccomendations on nutrient ratios plus timing and quality, although I could not rise very much my caloric intake, because of lack of hunger. I followed Israetel's reccomandations on the dose-response of exercise volume.

The final look is something like very defined, I can even see veins on the pecs and a sixpack which I forgot I had, but sure not fully -fledged hypertrophy.

My conclusion is that, at least in my case, when pursuing hypertrophy, calories govern over protein, although the latter are important as well. Exercise volume governs over everything else of course and this may be my limiting factor.

image.png.ba5794387cf6edc8282b9a01e5561dbe.png

 

Edited by mccoy

Share this post


Link to post
Share on other sites

The extension of the above experiments to CR vs prevention of myiopenia/sarcopenia may have some either general and individual connotations. the baltantly obvious conclusion is that some degree of resistance exercise is necessary, whereas the exercise strategy, the energy o fnutrients and nutrient ratios and meal timing schemes are plausibly different among individuals.

My next phase of the experiment will be to apply the threshold-absorption model of protein described in the Gorissen et al. article described above, which is in one way probably more consistent with a longevity scheme (less protein in total, but more often).

I'm going to coment the paper ASAP.

 

 

Share this post


Link to post
Share on other sites
3 hours ago, mccoy said:

My results of CR+high protein, from nonfat dairy products mainly (20% protein-45-50% carbs) plus moderate exercise are not exactly what I wanted. I did not gain muscle mass, although I sure lost adipose tissue.

Might need more cholesterol...

https://academic.oup.com/biomedgerontology/article/62/10/1164/568431

Quote

Results. We observed a dose-response relationship between dietary cholesterol (from food logs) and gains in lean mass that was not affected by variability in protein intake. 

 

Share this post


Link to post
Share on other sites

Todd, thanks for the linked article. I've read the whole article, whose premise is surely interesting, but it contains some contradictory information, like that both dietary and serum cholesterol are positively correlated to hypertrophy, but also the use of statins is positively correlated to exercise.

At this point, since statins are known to lower serum cholesterol content, and lower cholesterol content should be negatively correlated to strenght exercise according to the results, a conceptual pitfall is present.

The authors were amazed themselves and try to explain the phenomenon by a direct mechanistic action of statins:

Quote

We observed greater hypertrophy in participants using certain statins. This result was unexpected considering that several studies have reported adverse effects of statins on skeletal muscle (9,27). However, statins increase the susceptibility of skeletal muscle to membrane injury in response to an acute exercise challenge (28), which may potentiate hypertrophy if the magnitude of this injury and inflammatory response is directly related to the magnitude of hypertrophy through inflammation-related growth factors. Conversely, a decrease in the synthesis of cholesterol intermediates by statins results in a suppression of isoprenoid derivatives essential for prenylation of Ras and Rho GTPases (29). Reduced function of these GTPases has been shown to decrease myocyte proliferation in cell culture, as they are essential for skeletal muscle differentiation and regulate MyoD and myogenin expression (29). The conflicting observations may be explained by differences in in vivo and in vitro experimental protocols and unique complexity of an exercise intervention.

The authors also envisage a direct anabolic signaling of cholesterol.

They are well aware and explicitly discuss the apparent tradeoff between increased hypertrophy and increased CVD hazard provided by cholesterol. They conclude that these amazing results should be evaluated more in depth.

Quote

The direct association between dietary cholesterol and changes in strength further supports the potential anabolic role of cholesterol. Moreover, the significant indirect association of HDL cholesterol with absolute strength both before and after training highlights the potential role of subfractions in the physiology of this response. Whereas the LDL subfraction delivers cholesterol to tissues and is strongly associated with muscle gain, the HDL subfraction delivers cholesterol away from tissues to be metabolized. Previous studies on cholesterol and muscle characteristics are quite limited; however, Kohl and colleagues (34) reported a strong inverse association, consistent with our findings, between HDL and 1 RM strength for chest and leg press (same as in the present report) in 5460 men.

The results of this study suggest that dietary and serum cholesterol contribute to the skeletal muscle response to resistance exercise, conflicting with recommendations to prevent CVD. The evidence that higher serum cholesterol is associated with greater risk for CVD is clear. However, when confounders of dietary assessment were considered, Kritchevsky and Kritchevsky (35) reported that 1 egg per day (210 mg of cholesterol) was not associated with an elevated risk of coronary events whereas only a small 6% increase in risk was associated with a 200 mg/1000 kcal/d difference. The present study demonstrated a significant reduction in systolic and diastolic blood pressure, and there was not a worsening of serum lipid profile with higher dietary cholesterol. However, the trend toward higher hsCRP suggests at least one cardiovascular risk may be elevated.

.....

The current results clearly suggest and are the first to our knowledge to show that higher dietary and serum cholesterol and statin use are independently associated with greater lean mass responses to RET in this group of generally healthy 60- to 69-year-old men and women. Because cholesterol is negatively associated with cardiovascular health, rigorous efforts to confirm these findings are necessary. Even if results are confirmed, it is necessary to examine changes in cardiovascular risk due to dietary cholesterol consumption (within the context of exercise training) so that reduction in sarcopenia and disability is not at the price of elevated CVD.

My bottom lines:

  • Results undoubtedly very interesting, especially the possible anabolic function of cholesterol
  • Results not confirmed by the present authorities on muscle hypertrophy like Brad Schoenfeld (they do not reccomend more cholesterol/fats in an hypertrophic regime, rather they tend to reccomend more carbs and less fat (about 20% fat ratio)).
  • Results to be further investigated according to the authors of the article
  • I agree that more dietary fats/cholesterol may increase hypertrophy by providing more calories, but at the same time they may increase CVD hazard and they will sure increase adiposity. The latter is my personal n=1 observation.
  • The trade off by increasing cholesterol may result advantageous in people with serious problems of sarcopenia. If in such a predicament, I might  try such a scheme.
  • Presently, my scheme would be more in the line of an optimization of hypertrophy and cholesterol lowering strategies. My personal n=1 observation is that my greater bodyweight (but not necessarily lean mass weight) was reached when I was eating 99% vegan, many fats but no cholesterol eaten.
Edited by mccoy

Share this post


Link to post
Share on other sites

I'll start commentig the previously cited article by Burd et al. on dietary protein optimization.

Quote

Dietary Protein Quantity, Quality, and Exercise Are Key to Healthy Living: A Muscle-Centric Perspective Across the Lifespan.
Burd NA, McKenna CF, Salvador AF, Paulussen KJM, Moore DR.
Front Nutr. 2019 Jun 6;6:83. doi: 10.3389/fnut.2019.00083. eCollection 2019. Review.
PMID: 31245378

https://www.frontiersin.org/articles/10.3389/fnut.2019.00083/full

 

First very relevant aspect. There appears to be a threshold to the dose of protein required to maximize MPS (muscle protein synthesis). This threshold is different in a sedentary state and is lower after training. So the anabolic window concept appears to mean that less protein is needed to require the same maximum amount of MPS.

  • Sedentary state: MPS maximizes at about 10 g of EAAs (about 25 g high quality protein)
  • Immediately post-exercise: MPS maximizes at about 8.6 g of EAAs (about 20 g high quality protein).

The above is very relevant in the optimization of hypertrophy versus CR and longevity.

First of all, it's theoretically useless to eat more than 25 g high quality protein at a time. The surplus EAAs increase plasma concentration, suggesting nutrient excess

Quote

...with greater intakes resulting in an expansion of plasma amino acid pool (26), which represents a metabolic profile that could be suggestive of an acute nutrient excess (27).

The individual post exercise optimum appears to be 0.3 g/kg protein. But this appears to be an average, ranging from 0.25 (young people) to 0.4 g/kg (aging adults).

In my case, at 66 kg present weight, I should eat no more than 20 g hi quality protein after a workout (more precisely, no more than 26.5 grams, since I'm an aging adult). More will be useless or worse than useless.

Also, in 'normal', sedentary conditions, a 25% increase seems to be the maximum (20 to 25 g protein).

This would mean 0.375 g/kg protein, or 0.5 g/kg in aging adults (33 grams to me, which starts to be pretty much).

First and foremost takehome lesson appears to be that protein ingestion should not be above those limits in a CR context.

One obvious objection might be that casein requires time to digest, but the time delay in digestion is not a discussed factor in the article.

Another issue is the definition of hi-quality protein, which is disucssed in the article, meaning animal protein or protein anyway high in the PDCASS or teh DIAAS score. So, grain proteins are required in higher amounts for example, whereas soy protein should be similar to animal protein in this context.

Edited by mccoy

Share this post


Link to post
Share on other sites

The difference in absorption during the post-REsistance exercise, so called anabolic window is huge. Not so post-ENDurance exercise.

image.png.c5cb7faa8a620630a387e0412141ac2f.png

Figure 1. Eating an adequate amount of protein at rest (i.e., in absence of a prior exercise stimulus) generally results in a doubling of the myofibrillar (contractile) protein synthetic response from post-absorptive values in healthy young adults (20–35 years). The fundamentally anabolic nature of resistance exercise results in an interaction between feeding and the exercise stimulus during recovery such that the stimulation of postprandial myofibrillar protein synthesis rates is potentiated when compared to the resting value. This interaction on the stimulation of post-exercise myofibrillar protein synthesis rates is not observed during recovery from endurance exercise (treadmill running at 70% of VO2peak for 1 h). Data adapted from Burd et al. (76) and Abou Sawan et al. (77). *different from post-absorptive value at rest. †different from postprandial value at rest.

 

Share this post


Link to post
Share on other sites

The above 0.3 g/kg value seems to be higher in elder people, where the authors suggest up to 0.4 g/kg doses of protein.

Quote

...Despite this established anabolic resistance with age, current protein requirements as established by whole body nitrogen balance methods are similar throughout adult life (Table 2). When using a muscle-centric approach to protein intake, however, we have observed that the relative quantity of protein to maximize the postprandial muscle protein synthetic response is greater in older when compared to younger men. In particular, we established that older men demonstrated an ingested protein-dose response curve of postprandial muscle protein synthesis rates up to ~0.40 g/kg per meal, which was nearly doubled when compared to young adults (~0.24 g/kg per meal) (72). When considering the value of spread distribution pattern of protein intake at each meal time (i.e., breakfast, lunch, dinner, and evening snack) for maximal muscle anabolic potential (45, 96), it seems that protein intakes for older adults is likely higher than the current RDA or PRI of ~0.8 g/kg/d and nearing values closer to ≥1.2 g/kg/d. These recommendations are supported by whole body tracer estimates using the indicator amino acid oxidation technique of a safe intake of ~1.25 g/kg/d in older (i.e., >65 years) adults (46). In addition, lean body mass loss over 3 years is lowest in older adults consuming ≥1.2 g/kg/d (104), collectively supporting dietary protein as a modifiable risk factor for age-related lean (and muscle) loss. However, a prospective multi-site randomized control trial with defined protein intakes spanning sufficient to deficient with consideration for habitual activity and functional endpoints (e.g., muscle strength/mass) is ultimately needed to guide best practices in nutritional advice.

These are the reccomandations which include aging adults:

image.png.912daf322554176345ec885432ce7a8f.png

 

Share this post


Link to post
Share on other sites

BOTTOM LINE FOR AGING ADULTS

The conclusive suggestions of the authors to coutneract anabolic resistance appear to be the following:

  • Eat at least 1.2 g/kg/d protein (current RDA is 0.8 g/kg/d protein)
  • Reach the above quantities in such a way not to go beyond the maximum MPS threshold which in aging adults is 0.4 g/kg

The very bottom line so should logically be for aging adults: eat three meals a day each with 0.4 g/kg of hi quality protein to maximize MPS.

My objection is that the 0.4 g/kg is referred as to be the post-exercise value, so even though it's a maximum, it may be higher in resting situations. Using the +25% rule it would be 0.5 g/kg, which is close to the 30 grams per at least one meal suggested by Valter Longo to boost MPS.

Valter Longo though if I remember well suggests it only during one meal. or at least one meal.

So, supposing we are aging adults in a resting state, to boost our MPS we should need about 0.5 g/kg high quality protein per meal, reaching about 1.5 g/kg/d. 

Of course the authors' propositions rule out IF and would imply at least 3 meals a day, each one pretty rich in protein.

It doesn't agree too much with the usual CR regime. But the above might be construed as maximum threshold. 

Also, Longo's suggested strategy appears to be a trade off: once a day we maximize MPS, whereas in the other meals we favour restriction leaving aside MPS.

Edited by mccoy

Share this post


Link to post
Share on other sites

FWIW McCoy,

I am eating 1+g/lb/d or 2.2g+/kg/d (and sometimes 10-15% more than this).  This may seem like excessive to many people here, however I look at the extra protein as

  • another source of micronutriets (eggs and sardines are pretty nutrient dense, and dairy and whey is loaded with the amino acids I want plus calcium)
  • any additional saturated fat (not excessive) assists in absorption of fat-soluble vitamins like A, E, K from veggies
  • keeps me (at least personally) feeling FULLER, LONGER than carbs -feeling satiated with higher protein resulting in maintaining CR (or at least eating less to loss body fat) easier than with a lower protein ratio imho is worth the trade off (even if extra protein and specific amino acids is undesirable, if it allows me to maintain a state of CR and zero body fat; I will do that_
  • the higher-ratio of protein intake allows extra tissue repair and extra muscle size & strength vs. a lower protein intake ration.  IMHO the end justifies the means since we know that sarcopenia and strength loss are two serious hallmarks of aging. 

Consider this:

From the book "Biomarkers: the 10 keys to prolonging vitality", Evans and Rosenberg rank the top ten modifiable biomarkers associated with biological aging.

The number one biomarker is muscle mass. From age 20 to 80, the average person loses 20 to 30 % of their muscle mass. Loss of muscle mass, also known as Sarcopenia, produces a multitude of negative metabolic changes, which are incompatible with good health.

The number two biomarker is strength. The importance of strength in the elderly is exemplified by simple, yet critical, actions such as being able to arise from a chair or avoid a fall. Inability to carry on activities of daily living due to muscular weakness is a major cause for loss of independence. Additionally, a study of 8,762 men examined the relationship between strength and longevity. The men were assessed for strength at the beginning of the study. Nineteen years later, it was determined that the death rate was highest in the one-third of men who were weakest.

Longo and Greger and many other highly educated, extremely intelligent PhDs or MDs may be pro-vegan and low-protein advocates, but they are not (afaik) studying individuals that actually make USE of additional protein to specifically dramatically delay or REVERSE sarcopenia and strength loss.

For an individual that doesn't do any form of resistance training, or is not making any effort to avoid those two biomarkers, extra protein is likely completely useless.

Edited by Clinton

Share this post


Link to post
Share on other sites
5 hours ago, Clinton said:

I am eating 1+g/lb/d or 2.2g+/kg/d (and sometimes 10-15% more than this).  This may seem like excessive to many people here

Clinton, that's the standard quantity usually suggested for hypertrophy, by Brad Schoenfeld himself.

Of course that's relative to those who complete regular workouts with hi volume. In such conditions, apparently muscle tissue needs continuos replenishment.

From your reports it seems that you belong to this category. I don't know if in your case an optimization may allow lesser protein, but judging on your relatively modest caloric intake, probably not.

Share this post


Link to post
Share on other sites

Back to the article by Buird et al. 2019, reasoning about it one thing seems to be applicable to all aging adults here, with just a few exceptions:

0.5 g/kg/d constitutes the upper bound on protein absorption in a single meal, in the rested state. More than that is at best useless, at worst deleterious.

After a workout, that threshold becomes 0.4 g/kg/d.

Share this post


Link to post
Share on other sites

Create an account or sign in to comment

You need to be a member in order to leave a comment

Create an account

Sign up for a new account in our community. It's easy!

Register a new account

Sign in

Already have an account? Sign in here.

Sign In Now

×