The Effect of a Ketogenic Low-Carbohydrate, High-Fat Diet on Aerobic Capacity and Exercise Performance in Endurance Athletes: A Systematic Review and Meta-Analysis

The low-carbohydrate, high-fat (LCHF) diet has become popular as a treatment for excess weight, epilepsy and type 2 diabetes in recent decades [1,2,3]. The first LCHF diet study to optimize fat oxidation in endurance athletes was conducted in 1983 by Phinney et al. [4]. He spotlighted various mechanisms to boost endurance performance by promoting a shift in substrate utilization to enhance physiological training benefits by adopting the LCHF diet. However, the concept of improving athletic performance by adapting to a high-fat diet was reconsidered after a series of studies failed to prove significant benefits [5]. As a result, the pace of research in this area has slowed significantly. However, with the resurgence in popularity of “Paleolithic” and “ketogenic” diets, there has been renewed interest in the LCHF diet [6].

Limiting carbohydrate (CHO) consumption can reduce the muscle glycogen concentration, resulting in greater fat oxidation [7,8]. After adapting to the LCHF diet, the body uses more fat for energy, and fat stores are far more abundant than CHO, thus theoretically providing energy for a longer period [9]. A ketogenic LCHF (K-LCHF) diet may influence the adaptation of the body through the molecular mechanism of regulating cell signal transduction [10,11,12,13]. In addition, this signaling pathway’s activation may lead to increased physical and motor ability through, for example, mitochondrial biogenesis, capillary thinning and regeneration processes, especially the efficient utilization of fat energy substrates [14,15,16]. Of note, in the study on adopting ketogenic diets in mice, they found that long-term ketogenic diet might decreased mitochondrial biogenesis, impaired cellular respiration and increased myocardial apoptosis and myocardial fibrosis [17]. The energy obtained from fat under aerobic conditions produces acetoacetic acid, β-hydroxybutyric acid (β-HB) and acetone, of which β-HB accounts for about 70% of the ketone body, which serves as a stable energy source for the body and brain [17,18].

The review by Hawley et al. was the first to summarize the effect of the LCHF diet on exercise performance and metabolism. He found that long-term (>7-day) use of the LCHF diet extended endurance for a fixed, sub-maximum workload in well-trained athletes [19]. One study from Burke examined the LCHF diet’s acute effect and found that it took just five days for muscles to adapt [20]. The metabolic adaptations needed for the full benefit produced from adaptation to LCHF diets are suggested by the long time it takes to lower the rate of carbohydrate oxidation and glycogen utilization [21]. However, LCHF diets have been shown to have mixed results [22], with some studies reporting positive effects [23,24], while other studies finding that prolonged adaptation might not change performance [25,26]. A relatively long period on the LCHF diet did not affect performance in endurance exercise and resistance training [27,28]. In addition, individuals might have different adaptation processes to the LCHF diet [29]. Studies have suggested that, beyond diet duration, other variables may influence the effect of the LCHF diet on exercise performance (e.g., training status, performance test type, intensity and sex differences [30]).

The ketogenic diet is a special case of an LCHF diet. Some studies have suggested that LCHF diets with CHOs accounting for less than 5% [31] or between 5% and 10% [32] of total energy intake belong to the ketogenic diet. Furthermore, it is proposed that diets with less than 10% CHOs can induce ketosis [33]. As there is overlap in the definitions of the LCHF and ketogenic diets, most studies use the term “LCHF”, some use the term “keto” and some use “K-LCHF”, even though the content of these diets are similar. In this study, we use K-LCHF [30] to indicate the diet intervention.

Recent studies on the K-LCHF diet have not systematically analyzed the effects of the K-LCHF diet on endurance performance and related indicators. The effects of the K-LCHF diet on athletes during endurance exercise are controversial. Hence, the objective of this systematic review and meta-analysis was to aggregate the results from experimental data to investigate the overall effects of the K-LCHF diet on aerobic capacity and exercise performance in endurance athletes.

After reviewing the limited literature on the K-LCHF diet in endurance athletes, 10 eligible studies were included in the meta-analysis. Based on the outcomes of aerobic capacity, exercise performance and substrate oxidation in endurance athletes, we only found a significant effect of K-LCHF on RER, but not on VO₂max, HRmax, TTE and RPE. This finding aligns with those of previous studies [18,41,43,44,45,46,47,48,49] that found that the K-LCHF diet had little effect on maximal aerobic capacity.

Under normal circumstances, glycogen stores in the liver and muscle cells need to break down to generate energy, and endogenous carbohydrates are stored mainly in the liver and muscle as a primary energy source in distance races [50,51,52,53,54,55]. In a previous study, Heatherly et al. [46] found that adaptation to a high-fat diet had a negative effect on VO₂max owing to body mass reduction in middle-aged male runners. However, Helge et al. [56] found an increased VO₂max after a fat-rich diet in untrained healthy males, and Phinney et al. found no change in endurance-trained athletes [4]. The K-LCHF diet might alter the maximal aerobic capacity through weight loss [45], but might not change VO₂max as weight loss was not the primary objective in those studies, and is not the objective for endurance athletes generally. In another study, the K-LCHF diet was effective in extending some older athletes’ professional life by controlling or losing weight [9]. Another study analyzed gender differences after adopting the K-LCHF diet for four weeks and found a reduction in VO₂max in women after the intervention, which was not observed in men [31]. We found that body mass was significantly decreased after the K-LCHF diet intervention in seven studies, but no significant changes in VO₂max were observed. Of note, most studies have only reported on absolute VO₂max. Absolute values indicate the total quantity of oxygen being used during exercise, while relative values indicate how aerobically fit someone is compared with their peers. In this report, two studies reported both absolute and relative VO₂max, but neither showed a significant change after intervention [45,48]. Therefore, the interpretation of a K-LCHF diet strategy should be cautiously considered for athletic prowess in endurance sports if VO₂max has not changed but body weight has decreased.

Moreover, no significant effect of K-LCHF diet was found on TTE. However, caution should be paid as only three studies with limited available data were used to examine the impact of the K-LCHF diet on the TTE. A reasonable explanation is that, during adaptation to the K-LCHF diet, individuals still had sufficient muscle glucose stores to sustain high-intensity exercise [57]. A high-fat diet significantly enhanced subsequent prolonged exercise at approximately 60% of VO₂max, but, at the beginning of the workout, they only had 50% muscle glycogen content stored compared with the high-CHO-diet group [51]. In contrast, high-level athletes showed higher rates of fat oxidation, and their bodies utilized fat to replace part of the muscle glycogen for energy at a higher intensity [4]. This study also showed that after the body adapted to the K-LCHF diet, glycogen declined dramatically in muscle [4]. It remains to be studied whether long-term K-LCHF adaptation can restore the muscle glycogen to a comparable level [30]. Even though the ability to utilize fat was theoretically increased after the K-LCHF diet, no positive training effect was found on TTE, which may be related to the combination of diet and training.

Furthermore, no overall effect of the K-LCHF diet on HRmax was found. The potential neurological effect of a high-fat diet is that ketone adaptation increases the metabolic stress response during submaximal exercise. HR could be 7–9 bpm higher, potentially because of increased sympathetic nervous system activity [58]. A previous study suggested that the HR increases associated with obesity are caused by cardiac vagus nerve tension reduction [49]. Helge et al. [59] reported that subjects consuming a high-fat diet had significantly higher catecholamine and HR during submaximal exercise. Those changes may be related to changes in the autonomic nervous system activity at rest and in response to exercise after a short-term reduction in CHO intake (increased sympathetic and possibly decreased parasympathetic response) [59,60]. However, in our analysis, we did not find a significant effect of the K-LCHF diet on HRmax, which implies there is no evidence of a significant performance advantage after the K-LCHF diet (ketogenic or not). The ability to exercise at high intensity may be impaired by the K-LCHF diet.

The RER can indirectly indicate the ability of muscle to obtain energy [61]. A high RER indicates that carbohydrates are mainly used, while a low RER indicates that more fat is oxidized [61]. In our study, we found that the RER was significantly reduced after the adoption of the K-LCHF diet, indicating that more fat is involved in energy supply (Figure 6). In a study that simulated mountaineering after 4 h of cycling, eight out of nine participants improved their exercise ability during the climb after switching to a K-LCHF diet [62]. Throughout the study, five of the nine subjects enhanced their exercise ability by switching to the K-LCHF diet. Interestingly, comparing the high-CHO diet with the LCHF diet, RER improved. Exercise performance increased by an average of 375 s when climbing the mountain [62], indicating that a K-LCHF diet may be more advantageous to RER improvement in athletes. In addition, a study by Durkaleck-Michalski et al. [63] found males were more prone to switch macronutrient use from carbohydrate to more fat after the K-LCHF diet, reaching significance at the lower VO₂ max levels. Conversely, females did not significantly decrease carbohydrate oxidation at any volume of VO₂max. Our finding agrees with that of a previous report [62] suggesting that decreased RER after the K-LCHF diet may involve an energy supply drawing more from fat in endurance athletes.

RPE may decrease after a K-LCHF diet. Some studies have shown that ketones provide most of the fuel for the brain when CHO availability is insufficient and circulating β-HB concentrations are in the 1–5 mmol/L range (ketosis) [9,64,65]. However, not all K-LCHF diets may lead to ketosis [66]. Moreover, to a large extent, even minor dietary abnormalities can lead to an increase in the concentration of ketones in the body even though the diet is still LCHO [67]. After K-LCHF adaption, exercise may improve the brain center’s fatigue and cognitive function. This may be caused by the oxidation of β-HB, which provides a continued stable energy supply for the brain, delays the time of fatigue in the central nervous system and improves exercise performance [68,69,70]. However, no significant changes were found in RPE in this meta-analysis.

There was a large variation in the duration of the diet interventions among the included studies. However, when excluding the study by Burke et al. [41], with a five-day intervention, the results remained the same. Of note, the process of metabolic remodeling may initially take two weeks, with further adaptation in the following months to years [30]. In our report, most of the studies used interventions that were longer than two weeks. Even though we do not know the long-term adaptations, the results derived from these moderate lengths of interventions hint at the direction of the effect of K-LCHF on the aerobic capacity and exercise performance in endurance athletes.

In summary, we found no significant overall effect of a ketogenic low-carbohydrate, high-fat diet on VO₂max, HRmax, TTE and RPE, but a significant overall effect on RER. The K-LCHF diet did not lead to a positive change in aerobic capacity, possibly because the expected improvement was not achieved during the training period. Therefore, a K-LCHF diet is unlikely to change the aerobic capacity and exercise performance of endurance athletes, and there is a need to conduct high-quality intervention studies to assess the impact of different diet treatments for enhancing exercise performance in endurance athletes.

We thank Xiao Tan for insightful comments on a previous version of the manuscript.

The following are available online at https://www.mdpi.com/article/10.3390/nu13082896/s1↗, Table S1: AMSTAR checklist items for each systematic review, Table S2: Search strategy used in each database.

J.C. initiated and designed the study, selected studies, extracted data, assessed the quality of included studies, performed the data analysis and drafted the manuscript. S.L. selected studies, extracted data, assessed the quality of included studies, contributed to the interpretation of the results, edited the manuscript and contacted authors for original data. S.C. initiated and designed the study, contributed to the interpretation of the results and edited the manuscript. X.W. contributed to the interpretation of the results and edited the manuscript. All authors have read and agreed to the published version of the manuscript.

This study was funded by the start-up plan for new young teachers grant (Grant AF4150043) and by the 111 Project (B17029↗) at Shanghai Jiao Tong University.

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The data presented in this study are available on request from the corresponding author.

The authors declare no conflict of interest.