I believe in serendipity. The process of stumbling across a significant finding purely by chance, totally unaware of its potential application. Many great discoveries have been made this way (Viagra, Penicillin and even the microwave oven), as opposed to systematically being teased out, fabricated and ultimately commercialised, with many not standing the true test of time. In fact, the more often you look for a result to be different between two products or interventions, the greater the chance that you will find a statistically significant difference due to random variation in those results alone, with certain assumptions. Smaller trials can result in spuriously large differences between intervention and control groups, eg when comparing an ergogenic aid in performance cycling. This is the problem with small samples of trial participants, not uniformly matched for baseline characteristics and other study criteria. This also leads to bias and study protocols which are not generalisable due to timeframes or highly variable performance metric endpoints, such as time to exhaustion or changes in power outputs.
Larger prospective trials with greater validity should be conducted, and frequently more and more are. Meta-analysis of weighted studies attempt to define any statistical trend. That’s all well and good, but even sometimes the original question is flawed…asking to see a difference in observations with a poorly designed protocol can naturally lead to erroneous conclusions. So I’m over the moon to have come across a product that was found through an alternative application, and has little need to ‘prove’ itself with statistical evidence due to its biological plausibility. This means, just the magnitude of the differences within an individual suggests a practical benefit when compared to the effects of normal practice. Bucking the trends that we have been conditioned by is difficult, but sometimes is just a matter of common sense. Correct pre-/ in-ride fueling is an important part of training and racing, so no wonder conflict and confusion exists in this arena as it does in general nutrition. How have I stumbled across Superstarch? In 2011 I was invited to help organise and support a charity cycling event from Portsmouth, UK to Pompeii, Italia in aid of fundraising for the Association of Glycogen Storage Disease. At that time Generation UCAN had been growing at a fast rate in the US. Since keeping in touch with the director of the AGSD, Generation UCAN has landed on British shores and have created worthwhile alliances to spread the word of this superior nutrition……
Superstarch (Generation UCAN) is a hydrothermally modified cornstarch which was originally designed to treat rare genetic disorders of metabolism, termed glycogen storage disease (GSD). The collection of different types of storage disease (Von Gierkes, Mc Ardles, Pompes, Cori etc) are characterised by an impaired ability to convert glycogen to glucose in the liver. Newborns with glycogen storage disease need to be fed a frequent source of carbohydrate to maintain blood glucose levels or else they risk experiencing severe hypoglycemia and ultimately death. The development of Superstarch evolved from an innovative product discovery for a food that could provide up to ten hours release of energy (as glucose) for children with Glycogen Storage Disease, and for Diabetics who frequently experience episodes of low blood sugar during the night. Recent research has indicated that ingesting a formula containing slow-digesting carbohydrates can lower postprandial (after a meal) glucose responses, attenuate insulin changes, and promote higher levels of Glucagon-like peptide-1, whereas daily ingestion over a 6 month period of high sucrose (high-glycemic) diet can impair glucose uptake and increase enzymes related to lipogenesis (fat synthesis).
Two peer-reviewed scientific studies have confirmed that ingestion of a novel heat-moisture processed cornstarch is superior to conventional treatments in preventing hypoglycemia over extended periods of time in subjects with Glycogen Storage Disease. The patent pending proprietary method for making the starch involves a hydrothermal (heat-moisture) treatment process to the native starch which significantly alters the metabolism of the carbohydrate in the body. The UCAN Company holds the worldwide rights to create a product derived from cornstarch for consumer nutritional purposes.
It hasn’t taken a genius to realise the implications of Superstarch on endurance performance. All athletes share a similar problem to GSD patients, in that chronic exercise requires well controlled levels of energy substrates (carbohydrate and fat) from both endogenously (internally stored) and exogenously (externally ingested) sources. Not that I want to enter into a lengthy explanation of the science behind Superstarch, Jeff Volek, PhD, is a principal nutritionist and UCAN representative who has produced a couple of comprehensive whitepapers, which cover the details very well indeed. Don’t be afraid to read up, the first two aren’t heavily technical and demonstrate the benefits of Superstarch over normal dietary, sucrose, fructose and maltodextrin based products which are commonly used today. These mainstream products are known to cause erratic performances.
The key points are that Superstarch, a hydro-thermally modified complex amlyose pectin corn starch (HMS), is highly absorbed and digested with little impact on gastointestinal disturbance or distress due to its low osmolarity. Superstarch provides as sustained-release of glucose and therefore lower insulin secretion response i.e. it has a low acute glycemic index. This results in stable muscle carbohydrate oxidation for a longer duration and also allows for a speedier recovery (although not totally understood what percentages are from either endogenous or exogenous sources). Further, and importantly, an enhancement of fat oxidation at work rates equivalent to 66% VO2 peak, was seen when compared to isocalorific amounts of maltodextrin.
It seems obvious to me, that avoiding an insulin spike is very desirable when put into context with the biochemistry of metabolism and endocrinology, see my post on Whole Body Metabolism. Insulin promotes anabolic storage of food substrates, reducing the availability of non-essential fatty acid (NEFAs) which are known to be beneficial at lower intensity rates of aerobic exercise, ie below lactate threshold.
I decided to test the hypothesis for myself. Not on myself, but on my AGSD Portsmouth-to-Pompeii finisher/bike buddy/happy guinea pig who happens to be in training for his first and probably only 24hr event (Le Mans), so a fitting case study. I designed a protocol that controlled for practical conditions as much as possible to make as good a comparison as possible, but clearly there are limitations. I know it’s not bullet proof, but it is a pragmatic case study, which may be generalisable under similar situations, and even possibly extrapolated to longer endurance trials.
Please realise that we were not looking for a change in performance metrics as most trials do, but a change in lactate kinetics as a physiological marker which is very difficult to influence through study design alone. Controlling the conditions to be the same on both days as much as possible should only allow natural variation (inter-individual) in lactate levels or a change in diet to effect the results from the investigation. So this is what I believe is the main limitation from the study design. However, based on previous lactate threshold profiling in this volunteer, the changes in blood lactate concentrations were no more than 0.2 mmol/L at sub-threshold intensities and 0.4 mmol/L at the new threshold level, measured two months apart. The typical measurement accuracy is +/- 0.2 mmol/L much less than those changes shown in the results below.
To compare the effect of dietary changes on blood lactate concentrations and differences in maximal lactate steady state levels after a substantial volume of endurance work. Isocalorific (similar energy content) amounts of HMS (Superstarch, UCAN Generation) vs normal diet was given before sub-maximal exercise, and supplemented during exercise (200W target, 70% VO2max), immediately followed by a 10 minute threshold pace effort (250W, 90% VO2max).
The UCAN researchers have concluded from their findings that Superstarch would significantly alter metabolic responses to exercise and promote a more efficient utilisation of fat while controlling release of insulin and maintaining blood glucose levels. Superstarch has been proposed to provide highly absorbed slow-release glucose from its complex chain of amylose:amylopectin (70:30)% of a more favourable glycemic index which avoids undesirable stimulation of insulin release leading to a rebound hypoglycaemia during exercise. This has been implicated as detrimental to performance caused by elevated rates of muscle glycogenolysis (breakdown of glycogen to glucose) and marked reductions in hepatic glucose output and free fatty acid availability, when compared to high GI carbohydrate sources such as Maltodextrin.
Superstarch has a low osmolaric pressure in the gastrointestinal tract and is rapidly emptied from the stomach to the intestines allow use of greater amounts with less GI distress to the athlete.
Conversely, sugar based sports nutrition products encourage the body to rely on carbohydrates for energy while suppressing the use of fat (inhibited by higher levels of insulin) which is related to its glycemic index and rate of absorption. Therefore a more optimal carbohydrate would provide a slower release and use of carbohydrate as fuel while simultaneously permitting increased breakdown and utilisation of fat.
A key study; Effect of pre-exercise Ingestion of Modified Cornstarch on Substrate Oxidation During Endurance Exercise Int J of Sport Nutrition and Exercise Metabolism, 2007, 17, 232-243, looking at the effects of MAMS (acid/alcohol modified starch) vs Dextrose on substrate oxidation during endurance exercise hypothesised that pre-exercise MAMS ingestion would provide additional exogenous glucose during exercise, resulting in carbohydrate oxidation rates similar to those with Dextrose ingestion; increased carbohydrate oxidation late in exercise, and preserve plasma glucose late in exercise. MAMS provided a more stable and slightly elevated plasma glucose level when compared to Dextrose and other controls.
Through carefully controlled isotopic (13C:12C) analysis of substrate oxidation, results showed high initial glucose and insulin concentration in the dextrose group, together with muscle contractions at the onset of exercise, also led to high rates of carbohydrate oxidation. In contrast, a similar calorific amount of MAMS before exercise prevented large disturbances in glucose and insulin homeostasis, at the same time increased increased carbohydrate oxidation. Further to this MAMS ingestion elicited a sustained increase in carbohydrate oxidation which showed no rate of decline towards the end of the exercise duration (120 min) even though the Dextrose group had already returned to baseline. The source of carbohydrate oxidation was determined to be from both endogenous and exogenous supplies during the last 30 minutes.
The authors suggest further studies using glycogen-depletion prior to testing and longer time between ingestion of MAMS and exercise, also the potential of glycogen sparing effects or incorporation of exogenous glucose into the muscles after MAMS.
The relationship between blood lactate concentrations and endurance exercise are now well established. Blood lactate kinetics during endurance exercise are directly associated with cycling performance. Lactate threshold power and heart rate are well correlated with MLSS power and heart rate depending on the method of estimation and protocol used. Production, accumulation and clearance of lactate throughout the spectrum of exercise intensity are independent determinants of maximum aerobic capacity, cycling efficiency and anaerobic tolerance. Consumption of low glycemic foods before sub-maximal endurance exercise maybe beneficial to performance. It has been suggested that a high glycemic index meal ingested 65min prior to incremental exercise has no effect on maximal exercise performance. Such a meal however significantly decreases plasma glucose and increases plasma lactate levels during exercise when compared to a non-carbohydrate placebo.
Calorific expenditure above threshold intensities relies predominantly on glycogen reserves, while a variable ratio of fat and carbohydrate are used at intensities below this threshold. Almost 70% of calorific expenditure at rest comes from fat. Modulating this ratio at higher intensities up to threshold is considered ideal as fat stores are accessed, so that glycogen is preserved. Approaching threshold, lactate starts to be produced by anaerobic metabolism when glycogen is available or by glucose produced from alanine from muscle.
The proposal from the HMS cornstarch research suggests that more fat is utilised by the muscle and the liver, while glucose is produced for export to the brain and blood by the liver. This would preserve glycogen levels, and lactate may well be unaffected until these reserves are relied upon for anaerobic activity by sub-maximally contracting muscle. At this point less available glycogen/ glucose would put a strain on metabolism at threshold as the lactate pool might be depleted and energy must be derived inefficiently from fatty acid, although liberating more energy. Lactate kinetics are affected in different ways by diet and the availability of carbohydrate and glycogen.
The simple intervention test week was non-randomised, although it was investigator blinded as it would be difficult to mask ingestion of each meal and supplement. A well-trained (10 years) 42 year-old male cyclist ingested a Normal diet or Superstarch meal prior to a 4.25hr 200W (70% VO2max) target work-rate ride, supplemented by respective isocalorific amounts of either nutritional option, followed by a 10 minute, 250W constant power (90% VO2max) trial, on two individual occasions separated by two weeks of low volume training. The trial schedule and blood lactate sampling itinerary was as shown in the table. Work rate was measured by a mobile ergometer (Power-2-max, precision +/- 2%) and finger capillary blood lactate was determined using an EKF Lactate Scout (Enzymatic amperometric determination of lactate using lactate oxidase; +/- 0.2 mmol/L precision, range 0.5 – 25.0 mmol/L). The distribution of intensities between the 200W target trials for both weeks was very similar with only a discrepancy of 1% from the total proportion of zones 2 – 4, and 2% difference in Z4. The post load threshold trial of 10 minutes was not performed at a constant power (hyperbolic mode) although the data suggests that both trials (average recorded power) were consistent between weeks. Both test periods were preceded by low volumes of training and normal dietary intake.
The distribution of times between each physiological zone between ND and SS weeks were similar. Resting blood lactate concentrations were higher in the Normal diet, Week 1 (ND) compared to Superstarch, Week 2 (SS), 2.6 vs 1.7 mmol/L and was slightly elevated at the end of the target load trial 200W (actual 137W for week 1 vs 139W for week 2) within each week, 2.8 vs 2.1 mmol/L, a change of 0.2 and 0.4 mmol/L for ND and SS, respectively.
Lactate concentrations after the 10 minute threshold effort (250W target average) following the trial were markedly different at 4.6 vs 6.4 mmol/L, and a change in baseline from resting values of 2.0 and 4.7 mmol/L, respectively for each week. The recovery values after 15 minutes of similarily performed warm down were 3.7 and 3.8 mmol/L, representing a faster overall lactate clearance of 0.17 and 0.06 mmol/L/min for SS vs ND.
From the results it can be observed that the greatest differences between the trials for each week, were seen in the resting and end of trial lactate concentrations (1st & 2nd sample), as well as between resting and the threshold trial lactate levels (1st and 3rd sample). Comparing the differences within each trial, ie resting to threshold (1st & 2nd sample), ingestion of Superstarch trial resulted in almost a 2.5 fold increase in blood lactate concentration compared to the normal diet trial. Lactate clearance was also faster in the Superstarch trial, again demonstrating over 2.5 fold increase in the clearance rate.
Resting lactate levels are a function of anaerobic production and aerobic oxidation in the brain, blood, muscles and heart which are reduced by aerobic oxidation and glycogen depletion and therefore carbohydrate levels in the muscles and liver. Temporal changes occur in both lactate and glucose concentrations following ingestion of a carbohydrate meal over 0-2hrs, fatty acids and lactate are often the preferred fuel as to preserve glucose for essential functions in the brain.
However the relationship between glucose and lactate at different intensities is not so straight forward. Diet affects lactate kinetics during incremental exercise protocols, primarily through the amount of muscle glycogen available. Therefore diet can change plasma lactate concentration at the lactate threshold (MLSS). Even though changes in diet, glycemic index and hence levels of insulin affect lactate levels, the accompanying acidosis is buffered by changes in bicarbonate, but may inhibit the gradient of muscle to plasma lactate.
Sub-threshold intensity levels however may indicate a different phenomenon in a glycogen depleted state (e.g. following a target work-rate trial (70% VO2max 4.25hr), as lactate concentrations were lower after Superstarch when compared to the normal diet. This may reflect the overall rate of carbohydrate oxidation influenced by a greater release of insulin after the higher glycemic carbohydrate initial meal and supplementation.
The observations above may be simply explained by the fact that lower lactate levels at intensities under threshold are due to a greater availability of glucose or fatty acids for aerobic metabolism, while at threshold intensities and above, the ability to produce sufficient amounts of lactate is desirable to sustain greater work-rates in glycogen depleted muscles unable to use aerobic metabolism of fats or glucose.
This fits well with desirable improvements in lactate profiling for well-trained road endurance cyclists; lower aerobic lactate levels as fatty acids are predominantly used for fuel and preserve precious muscle glycogen, and sufficient lactate production at higher anaerobic intensities.
Two fixed work-rate trials (200W target, 70% VO2max, 4.25hr) followed by a 10 minute threshold intensity (250W, 90% VO2max) were performed by a well-trained 42 year-old male cyclist on separate occasions, two weeks apart. Similar calorific amounts of normal diet (Oatmeal, unmodified high amlyose starch content with a glycemic index of 48% compared to pure glucose) versus UCAN Generation Superstarch (a hydrothermally modified cornstarch, HMS), ingested as a meal 60 minutes prior to the trial and evenly throughout with supplementation. Ingestion of the low glycemic modified cornstarch resulted in modified lactate kinetics below and at predetermined lactate threshold intensities (90% VO2max), when compared with normal diet.
This suggests that Superstarch does provide a superior slow-release glucose profile for a longer duration, without stimulating the release of large amounts of insulin. This may allow for a greater percentage use of fatty acids at predominantly aerobic sub-threshold intensities while preserving muscle and liver glycogen for more intense anaerobic efforts as seen by elevated lactate levels at the end of the threshold intensity trial. This ultimately would allow the endurance athlete, in the same way as Glycogen Storage Disease patients to avoid undesirable insulin spikes and hypoglycemic episodes which result from supplementation with higher glycemic products currently on the market.
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