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This study sought to determine the chronic and postprandial blood lipid alterations in a group of trained competitive cyclists and triathletes following a two-week ad libitum KD when compared to a HCD and HD. Although several studies have examined the changes in blood lipid profiles following a KD in various groups of trained athletes [9, 10, 20,21,22,23,24,25], fewer have evaluated the KD ad libitum [10, 20,21,22, 24], and the majority have compared the KD to a HCD [9, 10, 20,21,22,23,24], or a HD [21, 25], but not both. As such, our approach allowed us to evaluate diet-induced changes in blood lipids (i) under more practical circumstances—demonstrating the responses more likely to be observed outside of a laboratory environment; and (ii) when compared to the HCD recommended by most professional organizations [26] and the athletes’ typical dietary patterns —generally more reflective of a high-fat Western diet [2]. To our knowledge, our study may be the first to examine the postprandial blood lipid responses to a KD test meal during a KD in endurance athletes, as most studies have evaluated blood lipid shifts in response to exercise [22, 24, 25], despite that athletes are in the interprandial state more often than training [2]. Overall, the primary finding of our study was that a two-week KD resulted in higher TC compared to a HCD and the athlete’s HD. While we observed lower postprandial LDL-C and LDL:HDL, postprandial TRG, TRG:HDL, and VLDL-C were higher following the KD test meal compared to the other diet conditions.
In accordance with our findings, prior studies have reported chronic hypercholesterolemia following a KD in trained athletes [9, 10, 22, 23, 25], with some (similar to our study) observing increases in TC after 14-d [23], highlighting the rapid nature of these alterations following this extreme dietary shift. Under normal circumstances, aerobic exercise at higher training intensities alters blood lipids by directly increasing HDL-C and decreasing LDL-C [27]. However, our finding of higher TC following the KD was a product of simultaneous increases (albeit non-significant) in HDL-C and LDL-C as previously reported [9, 23, 25]. This is noteworthy considering that higher HDL-C concentrations would typically stimulate LDL-C removal with additional reductions in LDL-C expected to occur from the training practices of our sample. However, not only did we observe significantly higher TC following the KD without differences in HDL-C or LDL-C between diet conditions, we did not observe lower TRG which has been frequently reported for KD [20, 23, 28]. Our previous work in this line of investigation has shown that fat oxidation is similar between a KD and HD; where athlete’s may demonstrate a degree of “fat adaptation” (or tolerance) as a result of their higher-fat HD. Yet, TC was significantly higher following KD in our study despite continual exposure to the high-fat intakes of their HD patterns. We suggest several potential explanations below.
Our findings conflict with the findings of other studies that report improvements in cardiometabolic profiles following a KD when compared to an HCD. This is likely because the KD is predominately used as a weight-loss intervention for individuals with existing cardiometabolic abnormalities [29, 30], with few studies examining the KD under eucaloric conditions. As such, our eucaloric design, evident by weight maintenance and negligible differences between estimated total daily energy needs and verified energy intake, may explain the differences between our findings and others, given that the greatest changes in TC for both trained and untrained individuals are observed when energy balance during a KD is maintained [31]. Moreover, and given that studies showing improvements in blood lipids following a KD are often conducted at lower absolute energy intakes, the higher maintenance energy needs of endurance athletes are worth noting, as the energy from fat necessary to facilitate weight maintenance during intensive training periods are expected to be considerably higher than the fat intakes of hypocaloric diets. Interestingly, the athletes in our study did experience significantly greater weight loss during KD, and we were able to observe higher TC during the KD despite the well-reported effects of weight loss on circulating blood lipids [32]. However, this could be considered speculative, as weight loss was modest and likely a product of losses in glycogen and total body water [16]. While we did monitor physical activity and training throughout the intervention, it is common for athletes following the KD to experience fatigue and increased perception of effort during training [13, 33]. As such, athletes in our study may have felt they were giving greater training efforts during the KD (i.e., increased perceptual effort), but were undergoing passive declines in objective training intensity (i.e., lower power output). This may have blunted any exercised-induced increases in HDL-C or decreases in LDL-C that they may have experienced under normal circumstances; although it could also be that the two-week intervention was too short in duration to observe these changes.
Although studies have consistently shown increases in HDL-C following a KD, these increases are relatively modest; often showing an inability to overcome the simultaneous increases in LDL-C that occur when large quantities of dietary fat are rapidly introduced. This may be particularly true for endurance athletes who typically demonstrate higher HDL-C from favorable lifestyle behaviors and consistent aerobic training. It is possible that differences in fatty acid composition explains our findings of higher TC, as the KD is inherently higher in saturated fatty acids (SFA) which largely contributes to increases in LDL-C and TC. In fact, Burén and colleagues [34] showed that in a sample of normal-weight young healthy females, a eucaloric KD with ~ 33% energy from SFA resulted in significantly higher TC, LDL-C, and small dense LDL subfractions, and lower LDL particle size; similar to our postprandial results showing significantly higher LDLPpeak and LDLIIIpeak following the KD. Additionally, Creighton et al. [9] also found higher TC, LDL-C, and LDL particle number in a group of keto-adapted endurance athletes consuming ~ 27% of their total energy from SFA when compared to athletes participating in a HCD. Although unsurprising, the findings from the aforementioned studies were observed despite increases in HDL-C; further supporting the inability of HDL-C to facilitate the removal of LDL-C during a KD. While a low-SFA KD could be proposed, this is typically less feasible in practice, as athletes may have difficulty reaching the proposed fat intakes of a KD. Thus, athlete’s may be more likely to resort to more convenient fat sources (which are often higher in both total fat and SFA) to meet the dietary fat demands of a KD.
Coupled with elevated fat intake, the KD is fundamentally lower in fiber. Bile acids, which are important lipid emulsifiers synthesized from cholesterol, undergo elevated synthesis and release in response to higher fat intakes [35]. After facilitating lipid absorption in the small intestine, bile acids are reabsorbed and transported back into hepatic tissue. Fiber, however, prevents bile acid reabsorption, stimulating the removal of cholesterol from the plasma (i.e., lowering cholesterol) to resynthesize bile acids in the liver [36]. Nevertheless, without sufficient fiber intake from severe carbohydrate restriction, bile acid reabsorption suppresses the transportation of cholesterol to liver, particularly LDL-C, potentially contributing to the higher TC observed during a KD.
Although the majority of available literature regarding the relationship between KDs and blood lipids are based on findings in the fasted state [37], humans spend the majority of their waking hours in the interprandial state, where additional food and beverage are consumed before circulating lipids return to pre-prandial levels [38]. Because the postprandial state is more translatable to practice and demonstrates more dynamic shifts in lipid metabolism relative to the fasted state [38], examining postprandial lipid alterations after the consumption of a KD-type meal, whilst in a ketogenic state, may more effectively highlight the changes in circulating lipids expected to occur in practice. To that end, we observed significantly higher postprandial iAUC responses for TRG, TRG:HDL, VLDL-C, in addition to significantly lower postprandial iAUC responses for LDL-C and LDL:HDL following the consumption of a KD meal compared to the other conditions. Is has been postulated that endurance athletes demonstrate greater metabolic flexibility relative to their untrained counterparts, which refers to an individual’s ability to match fat oxidization to fat availability [2, 39]. The increased metabolic flexibility of endurance athletes is supported by studies showing lower fasting TRG during eucaloric KDs. However, our findings are unique, showing that TRGs remain elevated following the consumption of a KD meal under ketogenic conditions compared to the other postprandial conditions. Given our collective postprandial findings, the metabolic flexibility of endurance athletes may be subjected to a potential ceiling effect; where fat oxidation eventually plateaus despite increasing fat availability. It is important to note, however, that LDL-C responses were lower following the consumption of a KD meal. It could be that the higher fat content within the KD meal stimulated bile acid synthesis, requiring LDL-C extraction from the plasma to the liver (leading to lower postprandial plasma concentrations), or that the higher peak HDL-C facilitated LDL-C removal. However, it remains unknown if these dynamic changes manifest in chronic lipid alterations and thus, further research is necessary.
A complete list of the limitations within this line of investigation have been described in detail elsewhere [1, 2, 14] but are briefly described. The primary limitation was that the COVID-19 pandemic resulted in the premature stoppage of our study, leading to a smaller sample size than originally anticipated. However, using the achieved effect size (f = 1.47) for our primary variables of interest (TC) and with a conservative correlation of r = 0.30, our achieved power analysis indicated that six participants would produce 98.6% power at an α = 0.05, and we were able to observe several other significant findings. Nevertheless, large effect sizes produced from a small sample should be interpreted with caution. The length of each intervention may also be considered as a limitation, but several studies have reported that ketosis can be achieved within 5-d of a KD [6] and others have reported blood lipid changes within two-weeks of a KD [23]. The ad libitum nature of the KD in our study also led to higher protein intake than expected. However, given the difficulty in consuming the fat intakes required for the KD, it is likely that this better represents the composition of the KD in practice.
In conclusion, trained competitive cyclists and triathletes may demonstrate increased TC in response to a 14-d KD compared to a HCD or the athletes’ HD. Further, the consumption of a KD test meal during a KD may result in higher postprandial responses for TRG, TRG:HDL, and VLDL-C, and higher postprandial peaks for TC and HDL-C; but may also result in lower postprandial responses for LDL-C and LDL:HDL. Given the ambiguous findings for endurance performance, trained competitive cyclists and triathletes contemplating a KD strategy should consider the potential for these blood lipid alterations. Future research should consider a focus on postprandial blood lipid alterations to determine if this more dynamic measurement manifests in chronic blood lipid changes in this group.
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