|
Podcast merch!
Listen and subscribe: RSS FEED ITUNES Soundcloud Stitcher Spotify If the episodes below don't load, turn off your ad blocker. |
|
|
After some background information on what redox state means for exercise and your mitochondria, we look at some experiments linking various intensities of exercise to adaptations. Then we look at where these signals overlap with dieting and rest, and tie these into advice and realistic expectations for training, recovery, and nutrition. We also answer your listener questions on RED-S, measuring recovery, exercise intensity, and more.
Show Notes Review papers on fluorescence measurement and redox adaptations Mitochondrial function in vivo evaluated by NADH fluorescence: from animal models to human studies NAD+/NADH and skeletal muscle mitochondrial adaptations to exercise Main podcast study Nuclear SIRT1 activity, but not protein content, regulates mitochondrial biogenesis in rat and human skeletal muscle Frequently referenced study linking SIRT activation to mitochondrial biogenesis (not mentioned in episode) Sirtuin 1 (SIRT1) Deacetylase Activity Is Not Required for Mitochondrial Biogenesis or Peroxisome Proliferator-activated Receptor-γ Coactivator-1α (PGC-1α) Deacetylation following Endurance Exercise*
0 Comments
When it comes to glycogen, does "train low" actually work? Rory joints to co-host as we examine and dissect the existing literature, and explore the limits of knowledge on p38 MAPK signaling as it relates to aerobic performance. We go through Kolie's coaching experience with these protocols, compare to existing recommendations, discuss why you should always check someone's references, and answer your listener questions.
Show Notes Exercise Stimulates Pgc-1α Transcription in Skeletal Muscle through Activation of the p38 MAPK Pathway Acute signalling responses to intense endurance training commenced with low or normal muscle glycogen Skeletal muscle adaptation and performance responses to once a day versus twice every second day endurance training regimens
This episode takes a long look at the mechanisms behind aerobic adaptations from high intensity exercise, starting with an early study showing how AMPK activation leads directly to mitochondrial biogenesis, followed by a recent meta-analysis showing when high intensity exercise does and doesn't lead to adaptation. We provide guidelines in terms of exercise intensity, duration, and how well trained you are. Then we give some practical takeaways, plus debunk all the ways "hacking" this adaptive signal chain don't work. Marinus Petersen of KiloWatt Coaching steps in as a guest co-host for Kyle and provides an additional perspective from his coaching experience, and his formal exercise physiology education.
Show Notes Chronic activation of AMP kinase results in NRF-1 activation and mitochondrial biogenesis Factors Influencing AMPK Activation During Cycling Exercise: A Pooled Analysis and Meta-Regression Skeletal muscle AMPK is not activated during 2 h of moderate intensity exercise at ∼65% ?˙O2peak in endurance trained men Carbohydrate improves exercise capacity but does not affect subcellular lipid droplet morphology, AMPK and p53 signalling in human skeletal muscle Effect of exercise intensity and hypoxia on skeletal muscle AMPK signaling and substrate metabolism in humans Marinus' email KiloWatt Coaching IG
The host of benefits associated with over-under workouts include improved lactate oxidation and clearance capacity, great expression of MCT enzymes, as well as improved tolerance of associated metabolic byproducts over threshold. We look at the established mechanisms behind these phenomena and find that over-unders, as well as lactate presence and oxidation itself, probably don't have a unique adaptation unavailable to other types of training. The follow-up episode, Ten Minute Tips #27, will discuss how Kolie views and programs over-under workouts, as well as alternative workouts to achieve the same ultimate effects.
Show Notes Running intensity and lactate clearance rate study Association of MCT1 and CS activity study (figure 4, below) Paper on training volume and mitochondrial mass (CS activity vs volume, below) Lactate oxidation in trained vs untrained men (Berkeley cyclists) Tabata study on anaerobic capacity 
This episode answers the question: is there something unique about endurance riding that is unavailable at other intensities? After discussing "zone 2" definitions, we look at adaptations and dose relative to other training intensities, fatigue, and volume. We look at the relative necessity of endurance riding in both very low and high volume training, and answer listener questions, including if there's a lower limit for endurance pace.
This episode breaks down the origins of endurance performance and how cells control substrate oxidation. We review a paper looking at the difference in adaptive aerobic signals when participants used significantly different amounts of fat and carbs at the same intensity. We then look at the role of mitochondria in cellular energetics, the pivotal role they play in aerobic endurance adaptations, and finally what the training implications are. Plus we answer your listener questions submitted to Kolie's Instagram.
Show Notes Carbohydrate improves exercise capacity but does not affect subcellular lipid droplet morphology, AMPK and p53 signalling in human skeletal muscle Regulation of skeletal muscle mitochondrial fatty acid metabolism in lean and obese individuals Metabolic adaptations to short-term training are expressed early in submaximal exercise Biochemical adaptations in muscle
While the phosphocreatine energy system is well known for sprinting, it also has another crucial role as part of the aerobic energy system. We delve into creatine's part in not only temporal energy buffering, but spatial too, and how cells are organized to support this and how badly organisms suffer without it. Then we look at more research showing that the aerobic recovery of phosphocreatine is highly correlated with repeated sprint power, and come to some practical conclusions we can make from the research.
Show Notes "Conveyor Belt" paper: Mitochondrial creatine kinase in human health and disease Impaired voluntary running capacity of creatine kinase-deficient mice Relationship between different measures of aerobic fitness and repeated-sprint ability in elite soccer players The Recovery of Repeated-Sprint Exercise Is Associated with PCr Resynthesis, while Muscle pH and EMG Amplitude Remain Depressed You're Training Too Hard For Criteriums -- Here's Why 
The "creatine conveyor belt" main pathway.
The mitochondrial structure of embedded creatine kinase enzymes to aid energy buffering.
In this episode we look at what fatmax is, where the promise lies, and what validity there is. Do you get better at burning fat by burning more fat? Do you lose more weight by burning more fat? How does e=mc^2 relate to the energy stored in food? This episode answers all these questions and more.
Show Notes 2001 Jeukendreup and Achten fatmax paper Elevated calcium and mitochondrial biogenesis in rat muscle (full text) Papers not referenced in main podcast: Exercise: It's the real thing! Maximal fat oxidation during exercise in trained me 
Idealized fatmax curve, from original Jeukendrup and Achten paper
If you've ever thought about using the ketogenic diet for cycling, you may want to listen in. We look at a pair of modern classic studies that compare traditional high carbohydrate diets to periodized low carb and keto. This includes a study with, and a study without a carbohydrate re-adaptation period.
Show Notes Low carbohydrate, high fat diet impairs exercise economy and negates the performance benefit from intensified training in elite race walkers https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5407976 Crisis of confidence averted: Impairment of exercise economy and performance in elite race walkers by ketogenic low carbohydrate, high fat (LCHF) diet is reproducible https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7272074
We look deeper into how the body chooses to use carbohydrates and fats, and specifically when and how carbohydrates inhibit fat oxidation. This serves as a jumping off point to take a critical look at VLamax and how it may, or may not, affect your FTP.
Show Notes Study on increased gene expression following endurance exercise https://pubmed.ncbi.nlm.nih.gov/19705999/ 
Acetyl buffering via carnitine frees CoA for continued pyruvate shuttling into the Krebs cycle.
Malonyl-CoA inhibition of CPT1.
|
Archives
June 2025
Categories
All
|
RSS Feed