Diet For Athletes : High Fat and Low Carb Diet ?

Diet For Athletes :  High Fat and Low Carb Diet ?

Manipulating dietary macronutrient ratios to maximise athletic performance is an evolving topic of research in sports nutrition. One area of increasing interest in recent years is the effect of a low carbohydrate, high fat (LCHF) diet in endurance sports, diverging from the traditional one-size-fits-all high carbohydrate (CHO) recommendations, demonstrating a move towards more individualised nutritional regimens for athletes.[1,2]

The overall aim of the LCHF approach is to promote maximal substrate adaptation of fat rather than CHO oxidation and utilisation during exercise.[2,3-5] But does the research back up the current popularity and anecdotal, general and social media reports of improvements in sports performance with this macronutrient approach?

This article reviews the current evidence on the physiological adaptations that occur and how sports performance is affected following adoption of a LCHF diet in well-trained endurance athletes.

The specifics of these diets that have been the subject of most research in athletes are the LCHF (CHO: <130g/15-26% and fat: 60-65% of daily energy) and the very LCHF or ketogenic diets (CHO: 20-50g/<10% and fat: 80% of daily energy).[1,3,6] The impact of both short- and long-term use of these diets have also been investigated.[1]

HOW DOES THE BODY USE FAT AND CARBOHYDRATES TO PRODUCE ENERGY?

Fat stored in adipose and muscle tissue as triacylglycerols (TAGs) and intramuscular TAGs (IMTGs) are comprised of three fatty acid chains linked to a glycerol molecule and, along with cholesterol and dietary fat, are substrates for fatty acid oxidation.[7]

Following cytoplasmic lipolysis, involving hormone sensitive lipase (HSL) and adipose triglyceride lipase (ATGP), fatty acids can either be stored in adipose tissue or transported to muscle cells. This involves two main transport proteins, CD36 (transports fatty acids across cell membranes) and carnitine palmitoyltransferase-1 [CPT-1] (transfers fatty acids into the mitochondria).

Oxidation of fatty acids results in the formation of acetyl-CoA, which is subsequently converted to ATP via the Krebs cycle, or ketone bodies (b-hydroxybutyrate or acetoacetic acids) via ketogenesis in the liver when there is an excess of acetyl-CoA. The glycerol backbone enters the glycolysis pathway.[7]

Carbohydrate sources used for energy synthesis are blood glucose, liver and muscle glycogen and gluconeogenesis-derived glucose.[8,9] Glycolysis involves the conversion of glucose to pyruvate via glyceraldehyde-3-phosphate, with the subsequent fate of pyruvate dependent on the presence or absence of oxygen in working muscle cells.[9,10] During aerobic metabolism, pyruvate is converted via pyruvate dehydrogenase (PDH) to acetyl CoA via the Krebs cycle and subsequently ATP. Under anaerobic conditions it is converted by lactic acid fermentation to lactate, which can form ATP for a short time period.[7,9-11]

Both CHO and fat oxidation are necessary for ATP synthesis. However, the proportion each substrate contributes to energy production during exercise is influenced by many factors including exercise intensity and duration, an individuals’ training status, short- and long-term diet patterns and gender.[7,11,12]

UNDERSTANDING EXERCISE INTENSITY

The maximum or peak amount of oxygen that the body can use during intense exercise is known as the VO2max measure. Determined by measuring the millilitres of oxygen used per minute per kilogram of body weight, it indicates what an individual’s fitness and endurance levels are i.e. the more oxygen the body has available, the more ATP or energy it can produce. Exercise intensity is classified as low (25% VO2max), submaximal (<65% VO2max) and high (> 75% VO2max). As the intensity of exercise increases, CHO and fat oxidation increase and decrease, respectively.[7]

FACTORS THAT INFLUENCE WHAT FUEL THE BODY USES DURING EXERCISE

At 25% VO2max, plasma free fatty acids (FFA) contribute the most energy, followed by plasma glucose and IMTGs. At 65% VO2max, there is a larger proportion of muscle glycogen used, followed by equal proportions of plasma FFA and IMTGs, and smaller contributions by plasma glucose. While at 85% VO2max, muscle glycogen is the predominant substrate, followed by fairly equal contributions by IMTGs, plasma FFAs and glucose.[13]

The maximal fat oxidation rate (MFO) is when fat oxidation reaches its upper limit, at which stage the crossover point occurs. That is when CHO oxidation exceeds fat oxidation, meaning that the body’s primary energy source shifts from fat to carbohydrate substrates. This can occur at between 47-75% VO2max, with significant inter-individual variability observed.[7,12]

In regards to exercise duration, for the first hour of submaximal exercise, plasma FFA, muscle glycogen and IMTGs are the primary substrates used, with smaller amounts of blood glucose. As exercise duration extends beyond this to 2-4 hours, plasma FFA and blood glucose are the primary energy substrates, with small contributions by muscle glycogen and IMTGs.[1,7,14] Or, put another way, within the first hour of exercise, the body uses a mixture of fat and carbohydrate fuels, but when exercise is performed for longer than 2 hours, plasma glucose and fat are the primary fuels.

Gender also plays a role, with premenopausal women found to have elevated MFO levels at submaximal intensity compared with men.[7,12,15]

Training status is also a significant contributing factor. The primary metabolic substrate adaptations in skeletal muscle following endurance training is slower utilisation of CHO and increased use of fat substrates, while the aim of training is to maximise power output and metabolic flexibility.[5,11]

Metabolic flexibility is defined as ‘…the ability to alter substrate utilisation in response to substrate availability’ and ‘…to efficiently utilise these pathways to maximize ATP regeneration…’.[11,16]

Altering macronutrient ratios can significantly influence metabolic flexibility, with physiological adaptations observed to occur with a LCHF diet.[7] Such adaptations include increased lipolysis, transport and utilisation of fat in muscle tissue both at rest and during exercise and significantly elevated MFO levels. These are attributed to physiological changes including elevated concentrations of IMTGs in type I muscle fibres, increased activity of HSL and fat transport proteins (CD36 and carnitine palmitoyl transferase) and beta-oxidation potential.[1,3,4,7,11,12]

Training-associated adaptations that also increase fat oxidation capacities include higher mitochondrial and capillary density, lactate thresholds, cardiac outputs and cell membrane CD36 levels.[4,7]
Corresponding CHO adaptations associated with LCHF diets include reduced CHO oxidation during exercise and muscle glycogen levels, partly associated with lower concentrations of the active form of (PDHa) and glycogenetic adaptations.[3,5,7,11]

WHAT IS THE EVIDENCE TELLING US?

While there is consensus regarding the metabolic adaptations that occur with a LCHF diet, the specific impact of such adaptations on endurance sports performance is mixed based on current evidence.

Studies assessing the effect of both short- and long-term LCHF diets on sports performance have been conducted. The short-term studies assessed endurance trained athletes that followed a LCHF diet for 2-4 weeks.[1,4,17,18]

In Lambert et al 18 trained cyclists (n=5) had either a LCHF (70% fat, 7% CHO) or high-CHO (74% CHO, 12% fat) diet for 2 weeks, with consecutive sessions of exercise performed at 85% VO2max (high intensity exercise [HIE]) and 60% VO2max (moderate intensity exercise [MIE]) to determine peak power output and maximal oxygen uptake. Exercise time to exhaustion was similar between the groups during HIE, but was significantly longer in the LCHF vs high CHO group during MIE (79.7 (SEM 7.6) vs 42.5 (SEM 6.8) min, p< 0.01). This was attributed to a lower respiratory exchange ratio and decreased CHO oxidation rate. The LCHF group also had lower starting levels of muscle glycogen but similar rates of muscle glycogen use during HIE.

Some slight improvement in sports performance was also observed by Rowlands et al.[17] who looked at the effect of either a high-CHO (70 +/- 9% CHO, 16 +/-5% fat) or LCHF (66 +/- 10% fat, 15 +/- 4% CHO) diet for 2 weeks, or a high fat diet for 11.5 days followed by 2.5 days of CHO loading on trained cyclists (n=7). All subjects performed both a 15-minute incremental exercise test to assess peak fat oxidation, followed by a 100km test, with a sports bar and 5% CHO solution ingested during the trial. The LCHF and the high-fat CHO loading groups had reduced power output declines during the 100km trial (p=0.03 to 0.07), and 1.3-fold higher power outputs during the final 5km of the 100km trial compared with the high-CHO group (1.0 to 1.6, p=0.04), however the improvements in performance time were non-statistically significant (from 3 to 4%).

These results contrasted somewhat in terms of sports performance with the findings from Burke et al.[1] For 3 weeks, male race walkers (n=21) consumed 1 of 3 diets – LCHF (78% fat, <50g/day CHO), high CHO (60-65%CHO, 20% fat consumed before, after and during training) or days of alternating between high and low CHO diets (PCHO). While the LCHF diet resulted in significant increases in whole-body fat oxidation rates (1.5g/minute), only the HCHO and PCHO diets resulted in improved time performances in the 10km race walk (by 6.6 and 5.3% respectively). Similar to the previous studies, the LCHF group had lower levels of muscle glycogen, blood glucose concentrations and CHO oxidation, as well as elevated blood ketone levels (β-hydroxybutyrate).

In a 2014 crossover design study,[4] male cyclists ingested either a LCHF diet (70% fat, 15% CHO) high in polyunsaturated fatty acids or a mixed diet (50% CHO, 30% fat) for 4 weeks, and performed moderate intensity, high volume training loads over 3 days after a 4-week dietary phase. While the LCHF group had significant improvements in relative values of VO2max and lactate threshold VO2, they also experienced reduced power outputs at maximal exercise intensity (350 + 14.6 vs 362 + 16.09), attributed to lower muscle glycogen stores and glycolytic enzyme activity. Other metabolic changes observed included a 4-fold increase in pre-exercise β-hydroxybutyrate levels and free fatty acid concentrations both at rest and the proportion contributing to energy expenditure during exercise.

The impact of chronic LCHF dietary patterns on metabolic and performance parameters has been investigated by a few studies, with further research required.[2,19]

In a small pilot study comparing pre- and post-intervention results, endurance athletes (n=5) followed a ketogenic diet (<50g/day CHO, ad libitum fat) for 10 weeks along with their normal exercise program, a combination of mountain or road biking, running, cycling or kayaking.2 They also completed an incremental performance test to determine VO2 peak rates and gas exchange thresholds.

The main findings were that after the intervention, there was an increased fat utilisation (by 41.3% at 31.2% higher exercise intensity) and decreased CHO oxidation; and maximal aerobic performance declined (time to exhaustion was reduced by 2 minutes [+ 0.7, p=.004]), with the authors attributing this to impaired glycogen metabolism (downregulation of PDH activity). In a subjective sub-analysis, participants did report improved overall wellbeing, recovery and inflammation with the LCHF regime

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