CJC4ME
02-03-2017, 11:05 AM
Glycogen is the main storage form of carbohydrates and in humans it is mainly stored in the muscles (around 350-700g) and in the liver (around 100g) (Reference 1). Glycogen is the preferential fuel used for higher intensity physical activity, at above a level of around 65-70% VO2max (Reference 1,2,7), although highly trained athletes have a greater capacity for fat oxidation even at higher exercise intensities (Reference 3). Below this threshold the main fuel used are liberated fatty acids deriving from body fat stores. Glycogen is an important source of fuel for the body for the so-called fight-or-flight response (Reference 7), when there is a need for an immediate source of energy and high levels of glycogen are needed for optimal performance for events such as running or cycling. In the past the advice was to consume large amounts of carbohydrates post-activity in order to rapidly replenish glycogen. When the body runs out of glycogen the feeling of intense fatigue is known as “hitting the wall”.
When glycogen is depleted a protein called GLUT-4 is activated and acts to increase glucose transport into muscle. Glycogen synthase acts to trigger the production of glycogen and as glycogen is replenished the activity of glycogen synthase goes down as does GLUT-4. The replenishment of glycogen has a high metabolic priority for the body and the main dietary substrate used for producing glycogen is carbohydrate. In the complete absence of food, glycogen replenishment still takes place (Reference 9), albeit at a much slower rate because the body is forced to provide other substrates for glycogen replenishment. These substrates are known to be lactate produced during exercise, amino acids deriving from skeletal muscle and glycerol from body fat stores.
It is well known that high-intensity (at/above 70% VO2 max) training with low starting glycogen results in greater oxidation of fatty acids and a greater training adaptation (Reference 8, 10, 36, 43) by enhancing mitochondrial biogenesis. Following glycogen depletion exercise, there is increased fat oxidation even when high carbohydrates are being consumed. This is because the ingested carbohydrates are preferentially channeled for glycogen repletion and liberated free fatty acids and possibly muscle trialglycerols are utilized instead for energy (Reference 34, 35). However in this post-exercise recovery period, for two isoenergetic diets the one providing lower carbohydrates will result in greatly increased fatty acid oxidation (Reference 45), furthermore not as a result of energy deficit.
The first two hours of post-exercise recovery are particularly critical, because a deprivation of dietary carbohydrates in this period will sharply limit glycogen replenishment. In an experiment in which the test subjects performed 75 minutes at 75% VOx max (Reference 46) two hours post-exercise they had a glycogen depletion of approximately 40%. It is likely that immediately post-exercise it would have been greater, but these results weren’t published. There were two groups for the recovery diet – one a high-carbohydrate group (5g carbohydrate/kg body-weight every 8 hours) and the other low-carbohydrate (0,5g carbohydrate/kg body-weight every 8 hours). I will say that I would have expected a far higher depletion of muscle glycogen for this level of activity, but in any case even 24 hours post-exercise the low-carbohydrate group still had a roughly 37% depletion of muscle glycogen, and it had barely risen from the 8 hour mark. The low carbohydrate group had high levels of key genes involved in fat metabolism such as PDK4, UCP3, LPL, CPT I, CD36, FOXO1. Note also in this study that carbohydrates were not totally avoided, but rather sharply limited. In other words consuming a limited amount of carbohydrates from vegetables or from a protein shake will not cause the beneficial effects on fat metabolism to be suddenly lost.
It has been long known that a short term high fat diet up-regulates key fat loss genes (Reference 55) involved in fatty acid transportation and oxidation such as FAT/CD36, UCP-3 and beta-HAD. The reference study had two groups of highly trained cyclists – one on a high-carbohydrate diet and the other on an isocaloric high-fat diet, both for 5 days. At the start and end of the dietary intervention all subjects did 20 minutes of cycling at 70% VO2max and the high-fat group displayed significantly enhanced fat oxidation in the end test as compared to the high-carbohydrate group, or baseline. This study employed a 5-day period for the two studied diets, another study (Reference 37) had test subjects do high-intensity interval training in the morning and then 60 minutes of steady-state running at 70% VO2max. One group consumed high-carbohydrates after the morning exercise session and the other was matched for calories but consumed high-fat. Both groups continued with their diets over the following 15 hours after the second exercise session. The high-fat group displayed a far greater capacity to oxidize fat in the afternoon training session, together with greater expression of fat loss genes such as FAT/CD36 and CPT1. Moreover the enhanced fat-burning in the high-fat group continued well past the second training session. The only fly in the ointment was a diminished MPS response as measured by suppression of p70S6K1 activity. What was notable in this more recent study is that even one high-fat meal was able to elicit enhanced fat burning in the afternoon training session. Going back to the study from Reference 46, we should note that the recovery diet had a 71% contribution from dietary fats, thus the fat burning would have been than it would have been if the diet had been more protein-based. The logical inference is that if engaging in resistance training it may be wise to avoid an excessively high intake of fats in the recovery period if muscle accrual is a priority, as it should normally be even in fat loss phases. However increasing dietary fats post-workout could be a useful strategy if performing high-intensity aerobic activity, especially if another such session is planned soon after.
If we’re going to divide training into two broad categories – resistance training and endurance training, whilst further breaking down endurance training into high-intensity and low-intensity, then I would see the most benefit of adopting a low/no-carbs post-workout period for resistance training and – if included in ones’ personal training protocol – high-intensity endurance training. However there are a number of provisos in order to make the system work properly.
It has been suggested (Reference 29) that significant glycogen depletion must occur to activate AMPK, the latter being a key nutrient sensor which regulates metabolism based on intake and expenditure. AMPK activation triggers a cascade of key genes involved in fat metabolism – the study discussed above no doubt significantly activated AMPK and thus the above-mentioned genes (Reference 4, 5). Post-workout protein ingestion does not impair AMPK activation (Reference 50), whereas carbohydrate ingestion will (Reference 51). However AMPK also suppresses protein synthesis by deactivating mTOR activity (Reference 30), which on the face of it does not sound conducive to accruing muscle. Resistance training – and indeed aerobic activity – do activate AMPK, and in the case of the former, temporarily suppress muscle protein synthesis (Reference 31). However 1-2 hrs post-workout AMPK activity diminishes and protein synthesis rises. AMPK activation though is far less pronounced after resistance training as compared to high-intensity cycling. In one study (Reference 6) they compared two groups – one performed 60 minutes of cycling at 70% VO2max and the other did 8 sets of leg extension at 80% 1RM. A resistance workout of this type doesn’t really correspond to what most trainees would really do in the gym, however it’s also worth bearing in mind that the workout was done after an overnight fast, and thus likely not full levels of muscle glycogen. In any case the finding of the study is that – at least in these conditions – AMPK was only activated significantly after cycling. The activation reached a peak 30 mins after the end of the cycling, at 195% of baseline.
It also appears that there is a critical defended minimum level of muscle glycogen, and if commencing and finishing a workout (whether resistance or endurance) without going below this threshold then there will be little or no glycogen replenishment (nor AMPK activation). In other words there will be none of the magic discussed above of significant and extended post-exercise fat burning, even whilst maintaining a positive calorie balance. This is a very significant point not to be glossed over. Reference 56 details a study in which two groups of test subjects performed a glycogen depletion protocol consisting of warm-up then 180seconds of cycling at 130% VO2max, followed by a 30-second all-out sprint. They then followed either a high-carbohydrate (10g/kg BW/day) or else normal-carbohydrate (4.5g/kg BW/day) for 48 hours. In the next phase they did 60 minutes of cycling at 70% VO2max, a level which was determined to not raise lactate levels too much. The subjects were then followed for the next 300 minutes with blood assays and muscle biopsies to assess the variables. The high-carbohydrate group – in stark contrast to the normal-carbohydrate group – had no muscle glycogen replenishment. The researchers equated this result to the low lactate produced in the exercise protocol and the glycogen level post-exercise in the high-carbohydrate group being above a defended level which appears to be around 200mmol/kg dry muscle weight. It was noted however that some glycogen replenishment occurs even with post-exercise glycogen above the minimum defended level if sufficient lactate is produced.
If we remember that body fat stores will be used for energy in the absence of dietary carbohydrates when muscle glycogen is depleted, then it stands to reason that it would make sense for the purposes of maximizing fat oxidation to continue well beyond the 24-hour point with the avoidance of carbohydrates. There is evidence from some older studies that muscle glycogen will remain depressed even for several days after depletion activity (Reference 52), despite an adequate intake of calories albeit deriving from fat and protein. One study (Reference 53) had two isocaloric groups of high-carb and low-carb subjects do 2hrs of cycling at 65% VO2max with subsequent massive depletion of muscle glycogen. 52hrs into the recovery period, the low-carb group still had a 35% depletion of glycogen. This was despite low-carb still being 2,9g/kg/day, i.e. not that low. The greater point here is that the longer carbohydrates can be avoided, the slower the replenishment of muscle glycogen and the longer the period of increased fat oxidation for the same amount of calories in the recovery period.
However the rate of glycogen repletion in the face of reduced carbohydrates in the recovery period depends on the type of activity which created the depletion. In the case of high-intensity activity which produces high levels of glucose and lactate, then the replenishment is more rapid since the lactate produced is then used as substrate for post-exercise synthesis of glycogen, whilst if it is lower-intensity and thus associated with diminished levels of lactate then the replenishment is slower. Lactate production is closely related to glycogen breakdown in exercise (Reference 12, 13) and indeed resistance training is generally associated with moderate lactate production (Reference 11) and a low contribution of lactate to subsequent production of glycogen. However in the previous study despite the high-intensity activity which produced undoubtedly high levels of lactate, the replenishment of glycogen was still very slow. In one study (Reference 39) the test subjects did an average of 8,8 sets of 6 reps of one-legged knee extension at 70% 1RM, thus depleting muscle glycogen by 30%. The researchers felt that lactate didn’t contribute much to glycogen resynthesis, suggesting that glycogen synthase was not activated much due to only modest glycogen depletion. There was nearly full glycogen repletion after 6 hrs in the group who consumed two meals at 0hrs and 1hrs of 1,5g carbohydrate/kg bodyweight, and almost no repletion in the group who consumed only water.
There are several ways of increasing glycogen resynthesis in the recovery period, namely by decreasing utilization of carbohydrates and increasing fat oxidation. Following an exercise protocol of 60 minutes of cycling at 75% VO2max, 500mg of oral hydroxicitrate (i.e. Garcinia cambogia) (Reference 14) appears to have this effect. Furthermore the environmental temperature post-exercise also influences glycogen resynthesis – a warmer environment slows it down whilst a cooler environment increases repletion (Reference 15) by decreasing utilization of carbohydrates. Although not specifically tested it is likely that fat oxidation was increased by the cooler conditions, with the dietary carbohydrate diverted for glycogen repletion.
Taurine ingestion in the recovery period appears to increase glycogen repletion whilst simultaneously increasing fat oxidation (Reference 16). It appears to do this by sparing exogenous carbohydrates for utilization as fuel. Taurine is known to increase the activity of an enzyme called cAMP-activated Kinase A which increases lipolysis in adipocytes (Reference 17), and thus would be compatible with the results of this study.
In a comparison between whey and casein ingestion post-exercise, it was found that whey significantly accelerates glycogen synthesis (Reference 40) as compared to casein. Whey increases GLUT-4 activity in muscle (Reference 41) and indeed stimulates fatty acid synthesis in muscle (Reference 42).
Caffeine ingestion whilst exercising and initially in the recovery period appears to accelerate fat burning in the first 5 hours, especially so in the first two hours (Reference 28). The dose given in this study was 6mg/kg BW.
It is furthermore beneficial to time the first post-workout meal immediately after training (Reference 44) since eating straight after resistance exercise increases muscle mass and reduces fat, as compared to the same meal several hours later. This phenomenon is linked to the increased muscle LPL when consuming a meal immediately post-exercise.
For the purposes of comparison with the above cited studies done when depleting glycogen with cycling, resistance training will typically generate a 20-40% depletion in the worked muscle. In Reference 18 they found that 6 sets of 70% 1RM or else 6 sets of 35% 1RM (both groups trained to muscular failure) of one-legged leg extension elicited virtually the same amount of glycogen depletion, i.e. around 39%. After 3 sets the glycogen depletion was around 20,5% for the 70% 1RM group and 25,6% for the 35% 1RM group. This study is also interesting because it shows that glycogen depletion is not greater when performing higher reps, as is commonly believed. Resistance training is not the most efficient means of depleting muscle glycogen – indeed it is thought that intramuscular lipoloysis contributes to production of force in resistance training (Reference 54).
The science showing increased fat oxidation in the post-exercise recovery period for the same amount of calories but with zero/low carbohydrate dietary intake following glycogen deplenishment exercise is very solid. A contention of many attempting to accrue muscle is that more carbohydrates are needed, also post-workout. However the science does not back this belief in consumption of carbohydrates in the post-workout period for the purposes of muscle accrual (Reference 38, 47, 48). A failure to replete glycogen post resistance training is not linked to a diminished anabolic response (Reference 19) however sufficient calories DO need to be provided (Reference 20, 25, 49) as well as the requisite essential amino acids, either in the free form or else as protein (Reference 21). In Reference 19, the test subjects did a glycogen depletion protocol of one leg, whilst resting the other leg. The next morning following an overnight fast, they then did 8 sets of 5 reps of single-leg leg press at 80% 1RM. 2 hours later they either took a supplement with 20g whey + 40g maltodextrin or else a zero-calorie placebo. There was no difference in MPS between the low-glycogen and normal glycogen leg in the nutrient-supplement group. MPS was higher in the nutrient-supplemented group for both the low and normal glycogen legs. Thus the conclusion is that in the early post-exercise recovery period (4 hours) low muscle glycogen does not compromise the anabolic signal and subsequent rates of MPS. Worth noting in this study is how the low-glycogen leg was weaker in the execution of the resistance training.
It is only in the case of inadequate post-exercise protein intake that carbohydrate ingestion can be of any benefit for normalizing protein synthesis, by reducing muscle protein breakdown (Reference 22).
Reading a bit between the lines however, there was a greater post-workout increase in Atrogin-1 in the low-glycogen leg in both placebo and nutrient groups, as well as a greater increase in Myostatin. Atrogin-1 is a muscle catabolic gene and Myostatin is a negative regulator of muscle growth.
mTOR activation was higher post-workout in the normal-glycogen leg in both groups.
However – and as noted in the previous study – commencing resistance exercise with depleted muscle glycogen is detrimental for strength training (Reference 23), but curiously could be beneficial for increased hypertrophy (Reference 24). So if we need complete repletion of muscle glycogen for strength training, how long is enough to achieve full repletion? What is known is that the first two hours immediately into the recovery period are most critical for rapid replenishment of muscle glycogen (Reference 32). However trained athletes can still replenish glycogen somewhere within 20 hours even if missing the first four hours post-workout, following a massive (68%) depletion of muscle glycogen after 4 hrs of cycling at 56% VO2max, and whilst consuming 10g carbohydrate/kg bodyweight (Reference 33).
Several strategies can be adopted to increase the rate of glycogen replenishment, such as the following:
- Caffeine ingestion together with carbohydrates (Reference 27). A Dose of 8mg/kg BW over the course of 4 hrs was used in this study.
- Preference for high GI carbohydrates (Reference 26).
The quicker one can replenish glycogen, the longer can be the low/no-carbohydrate period, and thus prolonging the window of fat burning.
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Key bulletpoints
- Glycogen needs to be significantly depleted in order to significantly activate fat burning effect and make the low/no-carb post-workout period effective.
- The commonly cited period of 5 hours carbless post-workout is not nearly enough for maximizing fat oxidation. This time period should be increased as much as possible – even well over 24 hours – whilst allowing adequate time for replenishing muscle glycogen in time for the next workout.
- Adequate protein and calories need to be consumed after resistance training for maximizing MPS whilst burning fat.
- Need for immediate meal post-exercise.
- High post-workout fat intake will maximize fat oxidation, but at the expense of MPS.
- Give priority to post-workout protein derived from whey.
- No need to be completely carb-free to still reap benefits from the protocol, however probably best to sharply limit carbohydrates in the first two hours of the recovery period (I think that trace carbs are still fine).
- Full starting muscle glycogen is important for strength training, but not necessary for hypertrophy training.
- Taurine, caffeine and hydroxicitrate ingestion after workouts (resistance training/cardio) could be good strategy for increasing fat burning.
- In the carbing-up period prior to resistance training, caffeine ingestion together with carbohydrate ingestion (incorporating also high GI carbs) will enable quicker glycogen replenishment and thus longer carbless periods after workouts.
- Try to avoid warm environments post-workout.
Reference 1: “Glycogen availability and skeletal muscle adaptations with endurance and resistance exercise”
Glycogen availability and skeletal muscle adaptations with endurance and resistance exercise | Nutrition & Metabolism | Full Text (https://nutritionandmetabolism.biomedcentral.com/articles/10.1186/s12986-015-0055-9)
Reference 2: “The effects of increasing exercise intensity on muscle fuel utilisation in humans”
The effects of increasing exercise intensity on muscle fuel utilisation in humans (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2278845/)
Reference 3: “The regulation of carbohydrate and fat metabolism during and after exercise”
The regulation of carbohydrate and fat metabolism during and after exercise. - PubMed - NCBI (https://www.ncbi.nlm.nih.gov/pubmed/9740552)
Reference 4: “AMP-activated protein kinase (AMPK) action in skeletal muscle via direct phosphorylation of PGC-1α”
AMP-activated protein kinase (AMPK) action in skeletal muscle via direct phosphorylation of PGC-1α (http://www.pnas.org/content/104/29/12017.full)
Reference 5: “Role of AMPK and PPARγ1 in exercise-induced lipoprotein lipase in skeletal muscle”
Role of AMPK and PPARγ1 in exercise-induced lipoprotein lipase in skeletal muscle. - PubMed - NCBI (https://www.ncbi.nlm.nih.gov/pubmed/24644240)
Reference 6: “Early time course of Akt phosphorylation after endurance and resistance exercise”
http://journals.lww.com/acsm-msse/Fulltext/2010/10000/Early_Time_Course_of_Akt_Phosphorylation_after.7.a spx
Reference 7: “The role of skeletal muscle glycogen breakdown for regulation of insulin sensitivity by exercise”
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3248697/
Reference 8: “Influence of muscle glycogen content on metabolic regulation”
https://www.ncbi.nlm.nih.gov/pubmed/9458750
Reference 9: “Post-exercise muscle glycogen repletion in the extreme: effect of food absence and active recovery”
https://www.ncbi.nlm.nih.gov/pubmed/24482591
Reference 10: “Metabolic characteristics of keto-adapted ultra-endurance runners”
https://www.ncbi.nlm.nih.gov/pubmed/?term=Metabolic+characteristics+of+keto-adapted+ultra-endurance+runners
Reference 11: “Muscle Substrate Utilization and Lactate Production During Weightlifting”
https://www.researchgate.net/publication/239999181_Muscle_Substrate_Utilization_and_Lactate _Production_During_Weightlifting
Reference 12: “Lactate production and clearance in exercise. Effects of training. A mini-review”
https://www.ncbi.nlm.nih.gov/pubmed/9659671
Reference 13: “Glycogen breakdown and lactate accumulation during high-intensity cycling”
https://www.ncbi.nlm.nih.gov/pubmed/8237426
Reference 14: ““Oral hydroxycitrate supplementation enhances glycogen synthesis in exercised human skeletal muscle”
https://www.ncbi.nlm.nih.gov/pubmed/21824444
Reference 15: “Environmental temperature and glycogen resynthesis”
https://www.ncbi.nlm.nih.gov/pubmed/20464645
Reference 16: “Post-exercise taurine administration enhances glycogen repletion in tibialis anteriori muscle
https://www.jstage.jst.go.jp/article/jpfsm/3/5/3_531/_pdf
Reference 17: “Taurine in adipocytes prevents insulin-mediated H2O2 generation and activates Pka and lipolysis”
https://www.ncbi.nlm.nih.gov/pubmed/?term=taurine+in+adipocytes+prevents+insulin-mediated
Reference 18: ““Muscle glycogenolysis during differing intensities of weight-resistance exercise”
https://www.researchgate.net/publication/21099878_Muscle_glycogenolysis_during_differing_in tensities_of_weight-resistance_exercise
Reference 19: “Low muscle glycogen concentration does not suppress the anabolic response to resistance exercise
https://www.ncbi.nlm.nih.gov/pubmed/22628371
Reference 20: “Acute Energy Deprivation Affects Skeletal Muscle Protein Synthesis and Associated Intracellular Signaling Proteins in Physically Active Adults”
http://jn.nutrition.org/content/140/4/745.long
Reference 21: “Postexercise nutrient intake timing in humans is critical to recovery of leg glucose and protein homeostasis”
http://ajpendo.physiology.org/content/280/6/E982
Reference 22: “The role of post-exercise nutrient administration on muscle protein synthesis and glycogen synthesis”
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3761704/
Reference 23: “Effects of Carbohydrate Restriction on Strength Performance”
https://www.researchgate.net/publication/43490306_Effects_of_Carbohydrate_Restriction_on_St rength_Performance
Reference 24: “Exercise-induced AMPK activation does not interfere with muscle hypertrophy in response to resistance training in men
https://www.ncbi.nlm.nih.gov/pubmed/24408998
Reference 25: “Energy balance changes the anabolic effect of postexercise feeding in older individuals”
https://www.ncbi.nlm.nih.gov/pubmed/22459620
Reference 26: “Muscle glycogen storage after prolonged exercise: effect of the glycemic index of carbohydrate feedings”
https://www.ncbi.nlm.nih.gov/pubmed/8226443
Reference 27: “High rates of muscle glycogen resynthesis after exhaustive exercise when carbohydrate is coingested with caffeine”
https://www.ncbi.nlm.nih.gov/pubmed/18467543
Reference 28: “Caffeine ingestion does not impede the resynthesis of proglycogen and macroglycogen after prolonged exercise and carbohydrate supplementation in humans”
http://jap.physiology.org/content/96/3/943?ijkey=c0de530ccb41f23d2db13844eed0c61a4f92d622&keytype2=tf_ipsecsha
Reference 29: “More than a store: regulatory roles for glycogen in skeletal muscle adaptation to exercise”
http://ajpendo.physiology.org/content/302/11/E1343.long
Reference 30: ““AMP-activated protein kinase suppresses protein synthesis in rat skeletal muscle through down-regulated mammalian target of rapamycin (mTOR) signaling”
https://www.ncbi.nlm.nih.gov/pubmed/?term=AMP-activated+protein+kinase+suppresses+protein+synthe sis+in+rat+skeletal+muscle+through+down-regulated+mammalian+target+of+rapamycin+(mTOR)+sig naling
Reference 31: “Resistance exercise increases AMPK activity and reduces 4E-BP1 phosphorylation and protein synthesis in human skeletal muscle”
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1890364/
Reference 32: “Muscle glycogen synthesis after exercise: effect of time of carbohydrate ingestion
https://www.ncbi.nlm.nih.gov/pubmed/3132449/
Reference 33: “Carbohydrate restricted recovery from long term endurance exercise does not affect gene responses involved in mitochondrial biogenesis in highly trained athletes”
https://www.ncbi.nlm.nih.gov/pubmed/25677542
Reference 34: “Skeletal muscle fat and carbohydrate metabolism during recovery from glycogen-depleting exercise in humans
http://onlinelibrary.wiley.com/doi/10.1111/j.1469-7793.2003.00919.x/full
Reference 35: “Utilization of skeletal muscle triacylglycerol during postexercise recovery in humans”
https://www.ncbi.nlm.nih.gov/pubmed/9688636
Reference 36: “Glycogen availability and skeletal muscle adaptations with endurance and resistance exercise”
https://www.ncbi.nlm.nih.gov/pubmed/26697098
Reference 37: ““Postexercise High-Fat Feeding Suppresses p70S6K1 Activity in Human Skeletal Muscle”
https://www.ncbi.nlm.nih.gov/pubmed/27327024
Reference 38: “Carbohydrate does not augment exercise-induced protein accretion versus protein alone”
https://www.ncbi.nlm.nih.gov/pubmed/21131864
Reference 39: “Glycogen resynthesis in skeletal muscle following resistive exercise”
https://www.ncbi.nlm.nih.gov/pubmed/?term=Glycogen+resynthesis+in+skeletal+muscle+foll owing+resistive+exercise
Reference 40: “Dietary whey protein increases liver and skeletal muscle glycogen levels in exercise-trained rats”
https://www.ncbi.nlm.nih.gov/pubmed/15946405
Reference 41: “Whey protein hydrolysate increases translocation of GLUT-4 to the plasma membrane independent of insulin in wistar rats”
https://www.ncbi.nlm.nih.gov/pubmed/24023607
Reference 42: “Dietary whey protein downregulates fatty acid synthesis in the liver, but upregulates it in skeletal muscle of exercise-trained rats”
https://www.ncbi.nlm.nih.gov/pubmed/16157243
Reference 43: “Training with low muscle glycogen enhances fat metabolism in well-trained cyclists”
https://www.ncbi.nlm.nih.gov/pubmed/20351596
Reference 44: “Effect of meal timing after resistance exercise on hindlimb muscle mass and fat accumulation in trained rats”
https://www.jstage.jst.go.jp/article/jnsv1973/45/4/45_4_401/_pdf
Reference 45: “Postexercise macronutrient intake and subsequent postprandial triglyceride metabolism”
https://www.ncbi.nlm.nih.gov/pubmed/24621959
Reference 46: “Substrate availability and transcriptional regulation of metabolic genes in human skeletal muscle during recovery from exercise”
http://www.metabolismjournal.com/article/S0026-0495(05)00131-9/abstract
Reference 47: “Coingestion of carbohydrate with protein does not further augment postexercise muscle protein synthesis”
http://ajpendo.physiology.org/content/293/3/E833.long
Reference 48: “Muscle protein breakdown has a minor role in the protein anabolic response to essential amino acid and carbohydrate intake following resistance exercise”
https://www.ncbi.nlm.nih.gov/pubmed/20519362
Reference 49: “Fuel for the work required: a practical approach to amalgamating train-low paradigms for endurance athletes”
https://www.ncbi.nlm.nih.gov/pubmed/27225627
Reference 50: “Protein ingestion does not impair exercise-induced AMPK signalling when in a glycogen-depleted state: implications for train-low compete-high”
https://www.ncbi.nlm.nih.gov/pubmed/23263742
Reference 51: “Optimizing Intramuscular Adaptations to Aerobic Exercise: Effects of Carbohydrate Restriction and Protein Supplementation on Mitochondrial Biogenesis”
https://www.ncbi.nlm.nih.gov/pubmed/24228194
Reference 52: “Muscle glycogen synthesis in relation to diet studied in normal subjects”
https://www.ncbi.nlm.nih.gov/pubmed/6028947
Reference 53: “Rapid exercise-induced changes in PGC-1α mRNA and protein in human skeletal muscle”
https://www.ncbi.nlm.nih.gov/pubmed/18653753
Reference 54: “Glycogen and triglyceride utilization in relation to muscle metabolic characteristics in men performing heavy-resistance exercise”
https://www.ncbi.nlm.nih.gov/pubmed/2289498/
Reference 55: “A short-term, high-fat diet up-regulates lipid metabolism and gene expression in human skeletal muscle”
https://www.ncbi.nlm.nih.gov/pubmed/12540388
Reference 56: “Muscle glycogen repletion without food intake during recovery from exercise in humans”
http://research-repository.uwa.edu.au/files/3244582/Low_Chee_Yong_2010.pdf
When glycogen is depleted a protein called GLUT-4 is activated and acts to increase glucose transport into muscle. Glycogen synthase acts to trigger the production of glycogen and as glycogen is replenished the activity of glycogen synthase goes down as does GLUT-4. The replenishment of glycogen has a high metabolic priority for the body and the main dietary substrate used for producing glycogen is carbohydrate. In the complete absence of food, glycogen replenishment still takes place (Reference 9), albeit at a much slower rate because the body is forced to provide other substrates for glycogen replenishment. These substrates are known to be lactate produced during exercise, amino acids deriving from skeletal muscle and glycerol from body fat stores.
It is well known that high-intensity (at/above 70% VO2 max) training with low starting glycogen results in greater oxidation of fatty acids and a greater training adaptation (Reference 8, 10, 36, 43) by enhancing mitochondrial biogenesis. Following glycogen depletion exercise, there is increased fat oxidation even when high carbohydrates are being consumed. This is because the ingested carbohydrates are preferentially channeled for glycogen repletion and liberated free fatty acids and possibly muscle trialglycerols are utilized instead for energy (Reference 34, 35). However in this post-exercise recovery period, for two isoenergetic diets the one providing lower carbohydrates will result in greatly increased fatty acid oxidation (Reference 45), furthermore not as a result of energy deficit.
The first two hours of post-exercise recovery are particularly critical, because a deprivation of dietary carbohydrates in this period will sharply limit glycogen replenishment. In an experiment in which the test subjects performed 75 minutes at 75% VOx max (Reference 46) two hours post-exercise they had a glycogen depletion of approximately 40%. It is likely that immediately post-exercise it would have been greater, but these results weren’t published. There were two groups for the recovery diet – one a high-carbohydrate group (5g carbohydrate/kg body-weight every 8 hours) and the other low-carbohydrate (0,5g carbohydrate/kg body-weight every 8 hours). I will say that I would have expected a far higher depletion of muscle glycogen for this level of activity, but in any case even 24 hours post-exercise the low-carbohydrate group still had a roughly 37% depletion of muscle glycogen, and it had barely risen from the 8 hour mark. The low carbohydrate group had high levels of key genes involved in fat metabolism such as PDK4, UCP3, LPL, CPT I, CD36, FOXO1. Note also in this study that carbohydrates were not totally avoided, but rather sharply limited. In other words consuming a limited amount of carbohydrates from vegetables or from a protein shake will not cause the beneficial effects on fat metabolism to be suddenly lost.
It has been long known that a short term high fat diet up-regulates key fat loss genes (Reference 55) involved in fatty acid transportation and oxidation such as FAT/CD36, UCP-3 and beta-HAD. The reference study had two groups of highly trained cyclists – one on a high-carbohydrate diet and the other on an isocaloric high-fat diet, both for 5 days. At the start and end of the dietary intervention all subjects did 20 minutes of cycling at 70% VO2max and the high-fat group displayed significantly enhanced fat oxidation in the end test as compared to the high-carbohydrate group, or baseline. This study employed a 5-day period for the two studied diets, another study (Reference 37) had test subjects do high-intensity interval training in the morning and then 60 minutes of steady-state running at 70% VO2max. One group consumed high-carbohydrates after the morning exercise session and the other was matched for calories but consumed high-fat. Both groups continued with their diets over the following 15 hours after the second exercise session. The high-fat group displayed a far greater capacity to oxidize fat in the afternoon training session, together with greater expression of fat loss genes such as FAT/CD36 and CPT1. Moreover the enhanced fat-burning in the high-fat group continued well past the second training session. The only fly in the ointment was a diminished MPS response as measured by suppression of p70S6K1 activity. What was notable in this more recent study is that even one high-fat meal was able to elicit enhanced fat burning in the afternoon training session. Going back to the study from Reference 46, we should note that the recovery diet had a 71% contribution from dietary fats, thus the fat burning would have been than it would have been if the diet had been more protein-based. The logical inference is that if engaging in resistance training it may be wise to avoid an excessively high intake of fats in the recovery period if muscle accrual is a priority, as it should normally be even in fat loss phases. However increasing dietary fats post-workout could be a useful strategy if performing high-intensity aerobic activity, especially if another such session is planned soon after.
If we’re going to divide training into two broad categories – resistance training and endurance training, whilst further breaking down endurance training into high-intensity and low-intensity, then I would see the most benefit of adopting a low/no-carbs post-workout period for resistance training and – if included in ones’ personal training protocol – high-intensity endurance training. However there are a number of provisos in order to make the system work properly.
It has been suggested (Reference 29) that significant glycogen depletion must occur to activate AMPK, the latter being a key nutrient sensor which regulates metabolism based on intake and expenditure. AMPK activation triggers a cascade of key genes involved in fat metabolism – the study discussed above no doubt significantly activated AMPK and thus the above-mentioned genes (Reference 4, 5). Post-workout protein ingestion does not impair AMPK activation (Reference 50), whereas carbohydrate ingestion will (Reference 51). However AMPK also suppresses protein synthesis by deactivating mTOR activity (Reference 30), which on the face of it does not sound conducive to accruing muscle. Resistance training – and indeed aerobic activity – do activate AMPK, and in the case of the former, temporarily suppress muscle protein synthesis (Reference 31). However 1-2 hrs post-workout AMPK activity diminishes and protein synthesis rises. AMPK activation though is far less pronounced after resistance training as compared to high-intensity cycling. In one study (Reference 6) they compared two groups – one performed 60 minutes of cycling at 70% VO2max and the other did 8 sets of leg extension at 80% 1RM. A resistance workout of this type doesn’t really correspond to what most trainees would really do in the gym, however it’s also worth bearing in mind that the workout was done after an overnight fast, and thus likely not full levels of muscle glycogen. In any case the finding of the study is that – at least in these conditions – AMPK was only activated significantly after cycling. The activation reached a peak 30 mins after the end of the cycling, at 195% of baseline.
It also appears that there is a critical defended minimum level of muscle glycogen, and if commencing and finishing a workout (whether resistance or endurance) without going below this threshold then there will be little or no glycogen replenishment (nor AMPK activation). In other words there will be none of the magic discussed above of significant and extended post-exercise fat burning, even whilst maintaining a positive calorie balance. This is a very significant point not to be glossed over. Reference 56 details a study in which two groups of test subjects performed a glycogen depletion protocol consisting of warm-up then 180seconds of cycling at 130% VO2max, followed by a 30-second all-out sprint. They then followed either a high-carbohydrate (10g/kg BW/day) or else normal-carbohydrate (4.5g/kg BW/day) for 48 hours. In the next phase they did 60 minutes of cycling at 70% VO2max, a level which was determined to not raise lactate levels too much. The subjects were then followed for the next 300 minutes with blood assays and muscle biopsies to assess the variables. The high-carbohydrate group – in stark contrast to the normal-carbohydrate group – had no muscle glycogen replenishment. The researchers equated this result to the low lactate produced in the exercise protocol and the glycogen level post-exercise in the high-carbohydrate group being above a defended level which appears to be around 200mmol/kg dry muscle weight. It was noted however that some glycogen replenishment occurs even with post-exercise glycogen above the minimum defended level if sufficient lactate is produced.
If we remember that body fat stores will be used for energy in the absence of dietary carbohydrates when muscle glycogen is depleted, then it stands to reason that it would make sense for the purposes of maximizing fat oxidation to continue well beyond the 24-hour point with the avoidance of carbohydrates. There is evidence from some older studies that muscle glycogen will remain depressed even for several days after depletion activity (Reference 52), despite an adequate intake of calories albeit deriving from fat and protein. One study (Reference 53) had two isocaloric groups of high-carb and low-carb subjects do 2hrs of cycling at 65% VO2max with subsequent massive depletion of muscle glycogen. 52hrs into the recovery period, the low-carb group still had a 35% depletion of glycogen. This was despite low-carb still being 2,9g/kg/day, i.e. not that low. The greater point here is that the longer carbohydrates can be avoided, the slower the replenishment of muscle glycogen and the longer the period of increased fat oxidation for the same amount of calories in the recovery period.
However the rate of glycogen repletion in the face of reduced carbohydrates in the recovery period depends on the type of activity which created the depletion. In the case of high-intensity activity which produces high levels of glucose and lactate, then the replenishment is more rapid since the lactate produced is then used as substrate for post-exercise synthesis of glycogen, whilst if it is lower-intensity and thus associated with diminished levels of lactate then the replenishment is slower. Lactate production is closely related to glycogen breakdown in exercise (Reference 12, 13) and indeed resistance training is generally associated with moderate lactate production (Reference 11) and a low contribution of lactate to subsequent production of glycogen. However in the previous study despite the high-intensity activity which produced undoubtedly high levels of lactate, the replenishment of glycogen was still very slow. In one study (Reference 39) the test subjects did an average of 8,8 sets of 6 reps of one-legged knee extension at 70% 1RM, thus depleting muscle glycogen by 30%. The researchers felt that lactate didn’t contribute much to glycogen resynthesis, suggesting that glycogen synthase was not activated much due to only modest glycogen depletion. There was nearly full glycogen repletion after 6 hrs in the group who consumed two meals at 0hrs and 1hrs of 1,5g carbohydrate/kg bodyweight, and almost no repletion in the group who consumed only water.
There are several ways of increasing glycogen resynthesis in the recovery period, namely by decreasing utilization of carbohydrates and increasing fat oxidation. Following an exercise protocol of 60 minutes of cycling at 75% VO2max, 500mg of oral hydroxicitrate (i.e. Garcinia cambogia) (Reference 14) appears to have this effect. Furthermore the environmental temperature post-exercise also influences glycogen resynthesis – a warmer environment slows it down whilst a cooler environment increases repletion (Reference 15) by decreasing utilization of carbohydrates. Although not specifically tested it is likely that fat oxidation was increased by the cooler conditions, with the dietary carbohydrate diverted for glycogen repletion.
Taurine ingestion in the recovery period appears to increase glycogen repletion whilst simultaneously increasing fat oxidation (Reference 16). It appears to do this by sparing exogenous carbohydrates for utilization as fuel. Taurine is known to increase the activity of an enzyme called cAMP-activated Kinase A which increases lipolysis in adipocytes (Reference 17), and thus would be compatible with the results of this study.
In a comparison between whey and casein ingestion post-exercise, it was found that whey significantly accelerates glycogen synthesis (Reference 40) as compared to casein. Whey increases GLUT-4 activity in muscle (Reference 41) and indeed stimulates fatty acid synthesis in muscle (Reference 42).
Caffeine ingestion whilst exercising and initially in the recovery period appears to accelerate fat burning in the first 5 hours, especially so in the first two hours (Reference 28). The dose given in this study was 6mg/kg BW.
It is furthermore beneficial to time the first post-workout meal immediately after training (Reference 44) since eating straight after resistance exercise increases muscle mass and reduces fat, as compared to the same meal several hours later. This phenomenon is linked to the increased muscle LPL when consuming a meal immediately post-exercise.
For the purposes of comparison with the above cited studies done when depleting glycogen with cycling, resistance training will typically generate a 20-40% depletion in the worked muscle. In Reference 18 they found that 6 sets of 70% 1RM or else 6 sets of 35% 1RM (both groups trained to muscular failure) of one-legged leg extension elicited virtually the same amount of glycogen depletion, i.e. around 39%. After 3 sets the glycogen depletion was around 20,5% for the 70% 1RM group and 25,6% for the 35% 1RM group. This study is also interesting because it shows that glycogen depletion is not greater when performing higher reps, as is commonly believed. Resistance training is not the most efficient means of depleting muscle glycogen – indeed it is thought that intramuscular lipoloysis contributes to production of force in resistance training (Reference 54).
The science showing increased fat oxidation in the post-exercise recovery period for the same amount of calories but with zero/low carbohydrate dietary intake following glycogen deplenishment exercise is very solid. A contention of many attempting to accrue muscle is that more carbohydrates are needed, also post-workout. However the science does not back this belief in consumption of carbohydrates in the post-workout period for the purposes of muscle accrual (Reference 38, 47, 48). A failure to replete glycogen post resistance training is not linked to a diminished anabolic response (Reference 19) however sufficient calories DO need to be provided (Reference 20, 25, 49) as well as the requisite essential amino acids, either in the free form or else as protein (Reference 21). In Reference 19, the test subjects did a glycogen depletion protocol of one leg, whilst resting the other leg. The next morning following an overnight fast, they then did 8 sets of 5 reps of single-leg leg press at 80% 1RM. 2 hours later they either took a supplement with 20g whey + 40g maltodextrin or else a zero-calorie placebo. There was no difference in MPS between the low-glycogen and normal glycogen leg in the nutrient-supplement group. MPS was higher in the nutrient-supplemented group for both the low and normal glycogen legs. Thus the conclusion is that in the early post-exercise recovery period (4 hours) low muscle glycogen does not compromise the anabolic signal and subsequent rates of MPS. Worth noting in this study is how the low-glycogen leg was weaker in the execution of the resistance training.
It is only in the case of inadequate post-exercise protein intake that carbohydrate ingestion can be of any benefit for normalizing protein synthesis, by reducing muscle protein breakdown (Reference 22).
Reading a bit between the lines however, there was a greater post-workout increase in Atrogin-1 in the low-glycogen leg in both placebo and nutrient groups, as well as a greater increase in Myostatin. Atrogin-1 is a muscle catabolic gene and Myostatin is a negative regulator of muscle growth.
mTOR activation was higher post-workout in the normal-glycogen leg in both groups.
However – and as noted in the previous study – commencing resistance exercise with depleted muscle glycogen is detrimental for strength training (Reference 23), but curiously could be beneficial for increased hypertrophy (Reference 24). So if we need complete repletion of muscle glycogen for strength training, how long is enough to achieve full repletion? What is known is that the first two hours immediately into the recovery period are most critical for rapid replenishment of muscle glycogen (Reference 32). However trained athletes can still replenish glycogen somewhere within 20 hours even if missing the first four hours post-workout, following a massive (68%) depletion of muscle glycogen after 4 hrs of cycling at 56% VO2max, and whilst consuming 10g carbohydrate/kg bodyweight (Reference 33).
Several strategies can be adopted to increase the rate of glycogen replenishment, such as the following:
- Caffeine ingestion together with carbohydrates (Reference 27). A Dose of 8mg/kg BW over the course of 4 hrs was used in this study.
- Preference for high GI carbohydrates (Reference 26).
The quicker one can replenish glycogen, the longer can be the low/no-carbohydrate period, and thus prolonging the window of fat burning.
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Key bulletpoints
- Glycogen needs to be significantly depleted in order to significantly activate fat burning effect and make the low/no-carb post-workout period effective.
- The commonly cited period of 5 hours carbless post-workout is not nearly enough for maximizing fat oxidation. This time period should be increased as much as possible – even well over 24 hours – whilst allowing adequate time for replenishing muscle glycogen in time for the next workout.
- Adequate protein and calories need to be consumed after resistance training for maximizing MPS whilst burning fat.
- Need for immediate meal post-exercise.
- High post-workout fat intake will maximize fat oxidation, but at the expense of MPS.
- Give priority to post-workout protein derived from whey.
- No need to be completely carb-free to still reap benefits from the protocol, however probably best to sharply limit carbohydrates in the first two hours of the recovery period (I think that trace carbs are still fine).
- Full starting muscle glycogen is important for strength training, but not necessary for hypertrophy training.
- Taurine, caffeine and hydroxicitrate ingestion after workouts (resistance training/cardio) could be good strategy for increasing fat burning.
- In the carbing-up period prior to resistance training, caffeine ingestion together with carbohydrate ingestion (incorporating also high GI carbs) will enable quicker glycogen replenishment and thus longer carbless periods after workouts.
- Try to avoid warm environments post-workout.
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Glycogen availability and skeletal muscle adaptations with endurance and resistance exercise | Nutrition & Metabolism | Full Text (https://nutritionandmetabolism.biomedcentral.com/articles/10.1186/s12986-015-0055-9)
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The effects of increasing exercise intensity on muscle fuel utilisation in humans (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2278845/)
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The regulation of carbohydrate and fat metabolism during and after exercise. - PubMed - NCBI (https://www.ncbi.nlm.nih.gov/pubmed/9740552)
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https://www.ncbi.nlm.nih.gov/pubmed/20464645
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http://jap.physiology.org/content/96/3/943?ijkey=c0de530ccb41f23d2db13844eed0c61a4f92d622&keytype2=tf_ipsecsha
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https://www.ncbi.nlm.nih.gov/pubmed/?term=AMP-activated+protein+kinase+suppresses+protein+synthe sis+in+rat+skeletal+muscle+through+down-regulated+mammalian+target+of+rapamycin+(mTOR)+sig naling
Reference 31: “Resistance exercise increases AMPK activity and reduces 4E-BP1 phosphorylation and protein synthesis in human skeletal muscle”
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