Andy King

A really interesting approach to conditioning from @HongKongRugby 7s’ rehab group here. You’ll notice the players are doing track based conditioning with their mouths taped - meaning the running is completed using nasal breathing only. As intensity & physical strain increases, athletes naturally want to switch towards mouth breathing to increase ventilation. Restricting them to nasal breathing adds another constraint to the session, encouraging more controlled breathing. The players are also wearing our conductive heart rate vests, allowing GPS and HR to be monitored together throughout the session, giving staff a view of the external running load as well as the internal physiological response to the session. When rehabbing, that relationship can be particularly useful when the goal is to create a conditioning stimulus without unnecessarily increasing running exposure. The tape essentially adds another layer to that stimulus, without asking the player to run further or faster. A pretty unique way of adding another constraint to a conditioning session, depending on the adaptation you’re after. 7s rugby is already well known as one of the most physically demanding sports around, but this is something else.

Fructose does not need insulin to enter the cell. Every other sugar triggers an insulin response. Fructose bypasses that mechanism entirely and goes straight to the liver. The liver is the only organ that can process it in significant amounts. When fructose arrives at the liver in large quantities, the liver has no way to pace the intake. It converts it rapidly into fat through a process called de novo lipogenesis. That fat either gets packaged into VLDL particles and sent into the bloodstream as triglycerides, or it stays in the liver and starts accumulating there. This is how a low fat diet causes fatty liver. Not dietary fat. Fructose from foods marketed as healthy because they contain no added fat. The food industry removed fat and replaced it with sugar, often in the form of high fructose corn syrup, because fat carries flavour and removing it makes food taste like cardboard. That swap has been driving fatty liver, high triglycerides and insulin resistance for forty years. Dietary fat does not cause fatty liver. Fructose does. The two have been consistently confused and the confusion has been enormously profitable for the people selling low fat products. What does your liver look like after decades of low fat eating?

An interesting case study on Kristian Blummenfelt: "The findings question the validity of the 2.5× basal metabolic rate ceiling, suggesting world-class athletes may sustain energy expenditure well beyond previously accepted physiological limits." journals.physiology.org/doi/…

Major respect @mackinprof! Thank you for this response. Much more agreement than disagreement! 1) This is a very well-founded point. Agree, it is only a hypothesis that requires testing. The primary reason that a 4-week analysis MAY change (of course, not proven) is that, as observed here in ironman competitors, we see the physiology adaptation window of glucose and ketones (brain energy metabolites) does not normalize in these athletes until 4 weeks on the diet. Unique in this study is that this timeline was verified when activity, calories, macronutrients, genetic and environmental factors were controlled. Since these metabolites are attached to performance, it is logical that when glucose has not normalized, nor has ketone peaked (and then normalized), we would expect these to impact performance as glycopenia has been demonstrated to negatively impact performance since 1920s. See thread here: xitter.gq/AKoutnik/status/201651… 2) Good point. We did test at 86% VO2Max on athletes adapted to 4 weeks on ketgoenic diet, and they didnt see a difference in performance, but fat made up the majority of fuel. We observe some incredibly high fat oxidation levels despite such a high VO2Max as well since it was unique: frontiersin.org/journals/nut… The main limitation some may cite is the duration of exercise. If they went for longer, would the results differ? Maybe, but this work does provide evidence that fat can infact make up the majority of fuel substrate at 80-90% VO2max and sustain performance (despite ATP advantage). This suggests other variables beyond ATP advantage are at work so solely focusing on ATP advantage makes it hard to explain work much of the KD work and the study above at 86% VO2Max. 3) Yes! Very familiar with Jamie's work (well done)! We have done a few performance analyses with exogenous ketones and performance, and the results are often all over the map, likely explained by variable methodology, exogenous ketone type, etc. Discussed herein in 2022 (but requires an update): pmc.ncbi.nlm.nih.gov/article…. We often see some cognitive improvements, but many of these studies are compared directly with carbohydrates, and many see little or no difference on physical performance. This is often framed as "they don't work" for physical performance, but ironically, this is against carbohydrate control, so maybe they are just equivalent? Alot to unpack here. We have work coming soon on this exact question, so I'll share when ready. What is interesting is that in our work looking at ketogenic diet vs high carb diets (+/- 10g CHO/hr), there was a greater incidence of hypoglycemia in the ketogenic diet group...yet they didnt performance worse on ketogenic diet arm? How was this? journals.physiology.org/doi/… After a debate on twitter, I went and calculated the total kcal in energy from circulating metabolites (glucose+ketone+lactate) in our study, the total kcal in circulating brain energy metabolites was equivalent across both groups at baseline and post-exercise despite lower glucose in KD arm (yet they had higher ketones). This supports the hypothesis that other brain energy metabolites may support brain needs during exercise. Obviously something that requires more testing. 4) Thank you for sharing! I had not seen this and just took a look. I need to dissect this further, but see that there is a noted drop in performance including trails from 2-12weeks. If we consider the key variable of time (atleast I am arguing time above point #1), we do see consistent drops in performance in studies <4 weeks in duration. See the graph in this thread highlighting red versus non-red. xitter.gq/AKoutnik/status/201651… Note that the figure show timeline differences on performance does not include multiple studies that were published after the figure came out including two studies that show no difference in performance. journals.physiology.org/doi/… pubmed.ncbi.nlm.nih.gov/4162… Again, this doesn't prove the point one way or the other, but simply demonstrates that the thesis around carbs being essential or critical isn't consistent with alot of work, particularly when you consider (imo) the key criteria of time on diet (4 weeks being one we point out for reasons noted above). 5) Thank you for clarifying that. In this context of dose-response, but pivoting back to carbohydrates, many have argued to push for up to 120grams per hour based on the hypothesis of a dose-dependent response. As you know, there is a whole sports nutrition marketing pushing higher and fasting carbohydrates (gatorade is a great example). However, we outlined all these studies up to the time of publication to the review in Table 9 (academic.oup.com/edrv/articl…). I will admit it was quite surprising to see the lack of consistent dose-responses across all these studies. In fact, some show that pushing up to what some athletes consume >80g/hour can lead to drops in performance. Two subsequent studies have since come out after our review: 1) Dose-Response up to 120grams (@JamesyMorton group): journals.physiology.org/doi/…. 2) 40 v 90 grams: onlinelibrary.wiley.com/doi/… These studies suggest to me that the weight of 12 studies in total, the clear effect that is: 1) Some carbohydrates can be beneficial. 2) More =/= better. 6) Debate/Discussion: I hear you on this and I know what you are getting at. I may be incorrect, but I suspect that may not be of interest to some? Maybe one day what you are saying will happen, maybe at a conference at ACSM or otherwise, but we both know that is contingent on organizational bodies and the selected chair's interest. While some may disagree (and that is ok), overall, I think this discussion is very important. It isn’t pro-low carb or pro-high carb. Instead, I hope it is an open discussion on the emergent data and the options athletes may have. Hopefully, athletes, practitioners, and coaches are more aware of these discussions and can make a call for themselves on what to do. Personally, I have changed my mind multiple times since some of our work was published, based on the feedback and discussions I observed. I hope it continues to be that way as time goes on! Cheers and thank you @mackinprof

I'm guessing no one will question the role of a particular diet favoured by Tour de France cyclists in producing these negative consequences.

The other striking thing is that one of the explanations offered for why high CHO would be 'bad' is that the more you ingest, the more glycogen you use. That's true. But it's also the whole point - that's the mechanism for the benefit - you get more energy per L O2 that way, and