Performance and Health Implications of High Fat Diets on Endurance Performance.
Athletes experiment with nutritional and training strategies to give themselves a competitive edge over rivals. Although high carbohydrate (H-CHO) diets are typically recommended for endurance athletes, some athletes have ignored this advice, consumed high fat (H-FAT) diets and have competed successful. Mark Allen and Jonas Colting are examples of two tri-athletes who have successfully followed H-FAT diets and won Iron Man and Ultra Man World Championships. Sparing limited glycogen reserves and increasing fat oxidation may be a viable strategy for improved endurance performance.
One of the first studies examining the effect of a high fat (H-FAT) diet on performance was undertaken by Phinney, Bistrian, Evans, Gervino & Blackburn (1983). Five endurance trained athletes consumed either a H-FAT (85% energy) or high carbohydrate (H-CHO) (66% energy) diet for four weeks. During a performance test after dieting, there was a decrease in the Respiratory Exchange Ratio (RER), a three-fold drop in glucose oxidation and a four-fold reduction in muscle glycogen use on the H-FAT diet, indicative of an increased rate of fat oxidation. Similar results were reported by other investigators (Goedecke, Christie, Wilson, Dennis, Noakes, Hopkins & Lambert, 1999; Helge, Watt, Richter, Rennie & Kiens, 2001).
Although H-FAT diets promote fat metabolism and glycogen sparing, one of the problems encountered by early investigators was that muscle glycogen was substantially reduced after a high fat diet due to low carbohydrate intake (Lambert, Speechly, Dennis & Noakes, 1994), which may negatively affect endurance performance (Bergström, Hermansen, Hultman, & Saltin, 1967). Therefore, later research utilised a dietary periodisation strategy, whereby glycogen loading would be undertaken after a period of H-FAT consumption, to replenish glycogen stores. Burke, Angus, Cox, Cummings, Febbraio, Gawthorn, Hawley, Minehan, Hargreaves & Hawley (2000) reported the effects a shorter adaptation period (5 days) with CHO restoration, comparing H-FAT (4g/kg/day) and H-CHO (9.6g/kg/day). During 2 hours steady state exercise at 70% VO2 max, RER was reduced, fat oxidation increased and CHO oxidation decreased. Thus, even with CHO restoration and availability, exercising muscle preferentially oxidised fat as a fuel substrate.
Therefore, H-FAT diets promote fat oxidation and glycogen sparing during exercise. How might this work? Many of the cellular adaptations associated with H-FAT diets include increased enzymes involved in beta oxidation (Helge & Kiens, 1997), increased fatty acid transporters (Glatz, Luiken & Bonen, 2010) and increased mRNA concentrations of proteins involved in fatty acid transport and metabolism (Cameron-Smith, Burke, Angus, Tunstall, Cox, Bonen, Hawley & Hargreaves, 2003). Therefore, H-FAT diets up-regulate the metabolic machinery for the transport and oxidation of fats into the muscle cell and mitochondria.
How might H-FAT diets affect performance? Helge, Richter & Kiens (1996) divided subjects into H-CHO (65% energy) or H-FAT (62% energy) group for seven weeks followed by carbohydrate restoration in week 8. Subjects trained 3-4 times per week during the study period. After 7 weeks, time trial to exhaustion (TTE) at 81% of pre-training VO2 max increased from a mean of 35 mins to 102 mins in the H-CHO and 65 mins in H-FAT, with the improvement in performance significantly greater in the H-CHO group versus the H-FAT group. Even with a CHO restoration protocol in week 8, TTE improved slightly in the H-FAT group (77 mins) but was still significantly less than H-CHO TTE.
Other studies have demonstrated improvements in performance on H-FAT diets. Phinney et al. (1983) demonstrated that although there was no difference in time to exhaustion (TTE – cycle ergometer test at 62-64% of VO2 max) between the H-FAT and L-FAT diets, TTE increased by four minutes in H-FAT compared to baseline. However, closer inspection of the results revealed that one athlete had an abnormally large increase in TTE in week five while the other subjects either had no change or a decrease in performance.
Lambert et al. (1994) demonstrated an improvement in a cycle to exhaustion at 50% Peak Power Output (PPO) after a two week H-FAT (70% total energy) compared to H-CHO (74% total energy). There was no difference in cycle to exhaustion at 85% PPO. Carey, Staudacher, Cummings, Stepto, Nikolopoulos, Burke & Hawley (2001) examined the effects of H-CHO (11 g/kg/day CHO, 1 g/kg/day FAT) or an isoenergetic high-fat diet (2.6 g/kg/day CHO, 4.6 g/kg/day FAT) diet for 6 days followed by CHO restoration on time trial performance. After cycling for 4 hours at 65% peak VO2 uptake, subjects on the H-FAT diet maintained an 11% non-significant (P=0.11) higher power output in a 1 hour time-trial task compared to H-CHO.
Therefore, the results from the effects of H-FAT diets on performance are equivocal. However, one observation is that performance in low and medium intensity exercise is enhanced. This might be expected, as substrate oxidation at these intensities is predominately fat (Van Loon, Greenhaff, Constantin-Teodosiu, Saris & Wagenmakers, 2001). If we look at exercising at higher intensities, a different picture emerges.
Stepto, Carey, Staudacher, Cummings, Burke & Hawley (2002) compared a three day H-FAT (4.6g/kg/day) or H-CHO (11g/kg/day) diet on high intensity interval exercise (8×5 min bouts at 86% VO2 peak) and reported higher Rate of Perceived Exertion (RPE) in the H-FAT versus H-CHO. Havemann, West, Goedecke, Macdonald, St Clair Gibson, Noakes & Lambert (2006) examined the effects of a six day H-FAT (68% energy) or H-CHO (68% energy) diet followed by carbohydrate restoration on a 100km TT interspersed with one kilometre sprints. This may be a more realistic scenario for elite performance compared to constant lower intensity performance trials. The one kilometre sprint power output was significantly lower in the H-FAT diet compared with the H-CHO diet.
Stellingwerff, Spriet, Watt, Kimber, Hargreaves, Hawley & Burke (2006) measured the effects of either a five day H-FAT (4.6g/kg/day) or H-CHO (10.3g/kg/day) diet, followed by carbohydrate restoration on 1 min sprint performance. Pyruvate Dehydrogenase activity was significantly reduced at rest and during low and high intensity exercise and estimated rates of glycogenolysis were reduced in H-FAT condition. This suggests that H-FAT diets work not through glycogen sparing but through glycogen impairment.
Intramuscular Triglycerides (IMTG) have been identified as an important fuel substrate during exercise, even at power outputs approaching 85% VO2 max in trained athletes. If undertaking high training volumes on consecutive days, athletes may need to consume higher than normal fat intakes (35-57% of energy) in order to replenish IMTG (Spriet & Gibala, 2004). Decombraz (2003) has suggested consuming a H-CHO diet in the initial 6-8 hours of recovery, with fat content increasing thereafter.
The World Health Organisation (2003) has recommended fat intakes of 15-35% of total energy intake for optimal health. Long-term H-FAT diets are associated with development of obesity, coronary heart disease and certain cancers (Manore, Meyer, & Thompson, 2009) and thus would not be recommended as a lifestyle choice. Acute fat intake results in transient suppression of muscle glucose uptake and muscle glycogen synthesis (Boden, 1997) and in the long-term may lead to insulin resistance, although this may be attenuated in endurance trained athletes (Goodpaster, He, Watkins & Kelley, 2001). However, training while fasting, during periods of hyper-caloric H-FAT intake, can improve whole body glucose tolerance and markers of insulin sensitivity (Van Proeyen, Szlufcik, Nielens, Pelgrim, Deldicque, Hesselink, Veldhoven, & Hespel, 2010). Training 3-4 times per week over seven weeks on a H-FAT (62% E) diet compared to a H-CHO (65% E) has been shown to reduce Natural Killer cell activity (Pedersen, Helge, Richter, Rohde & Kiens, 2000). This may compromise innate immunity and increase the risk of athlete infection. Therefore, there may be several adverse health consequences with consuming H-FAT diets.
From the research reviewed, it would be prudent to form the opinion that H-FAT diets, while increasing the ability to oxidise fat and spare glycogen at lower exercise intensities, reduces the ability to oxidise glucose at high intensities. Given that the outcome of all Olympic endurance events are decided at exercise intensities above 85% VO2 max (Joyner & Coyle, 2008), a compromised ability to oxidise glucose at high intensities would have negative consequences on elite performance. Long term H-FAT intake may compromise adaptations to training and may negatively affect health, although some of these ill effects may be attenuated by training. Reviews of the relevant literature do not recommend high fat diets to enhance performance (Hargreaves, Hawley & Jeukendrup, 2004) or training (Burke, Kiens & Ivy, 2004).
Using different nutrition practices (e.g. carbohydrate restriction before/during/after training – Hawley & Burke, 2010; Van Proyen, Szlufcik, Nielens, Ramaekers, & Hespel, 2011) or performing high-intensity interval training (Burgomaster, Howarth, Phillips, Rakobowchuk, MacDonald, McGee, & Gibala, 2008) may replicate many of the cellular and metabolic adaptations associated with H-FAT diets. High rates (1.75g/min) of exogenous carbohydrate oxidation can be achieved during exercise using multiple transportable carbohydrates (Jeukendrup, 2010), negating the need to protect glycogen stores. Short-term carbohydrate loading can increase muscle glycogen stores two-fold (Fairchild, Fletcher, Steele, Goodman, Dawson & Fournier, 2002). Strategies other than H-FAT diets are available to athletes to promote fat oxidation and boost glycogen stores without the need to compromise high intensity performance or health.
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