. 2020 Jun 10;599(3):819–843. doi: 10.1113/JP278928

Table 2.

Studies of adaptation to ketogenic low‐carbohydrate high‐fat diet (K‐LCHF) on endurance performance or exercise capacity of athletes

Athletes and study design	K‐LCHF adaptation protocol (duration and daily intake)	Performance protocol	Nutritional support for performance	Performance advantage with K‐LCHF	Comments
Trained athletes with verified ketogenic diet
Phinney et al. (1983) Well‐trained cyclists (n = 5 M) Cross‐over design with HCHO first	28 days HCHO (7 d): CHO: 57% E; protein: 1.75 g kg⁻¹ K‐LCHF: CHO < 20 g; protein: 1.75 g kg⁻¹; fat = 85% E Energy‐matched and balanced. Controlled diets consumed with supervision; blood ketones measured to verify ketosis.	Cycling TTE at ∼63% ${\dot{V}}_{O_{2} peak}$	Both trials: Pre‐exercise meal = overnight‐fasted Intake during exercise = water	No NS difference in TTE between trials (151 vs. 147 min for LCHF and HCHO). Group data skewed by 1 participant who increased time to fatigue by 156% on LCHF trial (see Fig. 1)	Well controlled study but involved order effect and failure to provide optimal conditions for HCHO trial. K‐LCHF = fasting [β‐HB]: 1.3 mmol l^−1; exercise rates of fat oxidation: 1.5 g min⁻¹.
Burke et al. (2017) Elite (international level) race walkers (n = 19 M: LCHF = 10; HCHO = 9) Parallel group design with non‐randomised treatments (allocation according to preference/belief)	24 days HCHO: 231 kJ kg⁻¹; CHO: 8.6 g kg⁻¹ or 60% E; protein: 2.1 g kg⁻¹ or 16% E K‐LCHF: 223 kJ kg⁻¹; CHO: 0.5 g or 3.5% E; protein: 2.2 g kg⁻¹ or 16% E Energy‐matched but allowing small energy deficit. Controlled diets consumed with supervision; blood ketones measured regularly to verify ketosis. Intensified and supervised training program (endurance + HIT + gym)	Race walking 10,000 m real‐life track race	Pre‐exercise meal at 2 h pre‐race: HCHO = 2 g kg¹ CHO LCHF Race 2 = energy matched high‐fat meal Both races = water station on track; use of performance supplements as in real‐life (e.g. caffeine) as long as use was matched in both races	No In fact, K‐LCHF failed to show the improvement seen in HCHO group HCHO: improved performance by 6.6% [4.1–9.9%, 90% CI] equivalent to 190 s faster K‐LCHF: NS change of −1.6% [−8.5%−5.3%] equivalent to 23 s slower	No improvement in race performance with K‐LCHF, despite equal (∼3–7%) increase in aerobic capacity, greater loss of BM and substantial increase in fat oxidation rates (from ∼0.7 to 1.57 ± 0.32 g min⁻¹) and fasting [β‐HB]: 1.8 mmol l⁻¹. Note that race protocol was reliant on capacity for high‐intensity exercise rather than glycogen depletion. Reduced performance attributed to reduction in race walking economy due to additional oxygen demand of fat oxidation at high exercise intensities.
McSwiney et al. (2018) Trained endurance athletes (runners, cyclists, triathletes) (n = 20: K‐LCHF = 9; HCHO = 11) Parallel group design with non‐randomised treatments (allocation according to preference/belief)	12 weeks HCHO: 147 kJ kg⁻¹; CHO: 5.2 g kg⁻¹ or 61% E; protein: 1.2 g kg⁻¹ or 14% E K‐LCHF: 158 kJ kg⁻¹; CHO: 0.5 g kg⁻¹ or 5% E; protein: 1.6 g kg⁻¹ or 17% E; fat: 77% E Diets consumed in free‐living protocol with education and weekly contact + 3 day diary at 0 and 12 weeks to check compliance. Fasting plasma ketone concentrations checked on test day to verify ketosis. Intensified training programme (endurance + HIT + strength)	Cycling Lab ergometer: 6 s sprint + 100 km TT + critical power test (CPT) undertaken on lab ergometer	HCHO: Pre‐exercise meal at 2 h = CHO‐rich meal (52% E) During exercise: 30–60 g h⁻¹ CHO K‐LCHF Post trial: 2 h post‐fat rich (64% E) Water electrolytes during trial	Perhaps K‐LCHF significantly improved peak but not average power in 6 s and CPT; trend to faster 100 km (166 ± 12.4 vs. 161.5 ± 8.4 min; 2.5%). No differences in HCHO (169.6 ± 8.4 vs. 168.4 ± 9.1). However, 5 additional subjects were unable to adhere to K‐LCHF and 2 failed to complete post‐intervention testing.	Both groups increased aerobic capacity by ∼7%. K‐LCHF group had higher body fat and BM at pre‐trial and although 3 day self‐reported food diaries suggested that energy intake was maintained over 12 weeks, K‐LCHF lost 5.9 kg including 4.6 kg body fat over the 12 weeks with minimal change in HCHO group. K‐LCHF = fasting [β‐HB]: 0.5 mmol l⁻¹; exercise rates of fat oxidation: NA. Large degree of individual variability in response to K‐LCHF; negative experiences were not captured in the performance data. HCHO group may not have achieved optimal nutritional preparation in pre‐trial diet and within‐trial fuelling for 2.5 h protocol
Shaw et al. (2019) Trained endurance runners, triathletes (n = 8 M) Cross‐over counterbalanced design (14–21 days washout)	31 days ‘Habitual’ HCHO diet:178 kJ kg⁻¹; CHO: 4.6 g kg⁻¹; protein: 2.0 g kg⁻¹ K‐LCHF = 191 kJ kg^−1;; CHO: 0.5 g kg⁻¹; protein: 2.0 g kg⁻¹; fat: 78% E Energy‐matched. Diets consumed in free‐living protocol with education and regular monitoring of diet and ketosis (blood/urinary ketones) to check compliance	Running TTE at ∼70% ${\dot{V}}_{O_{2} peak}$ on treadmill	HCHO: Pre‐exercise meal at 2 h = 2 g kg⁻¹ CHO During exercise: 55 g h⁻¹ CHO LCHF: Pre‐exercise meal at 2 h = energy matched fat‐rich foods During exercise = energy matched fat‐rich sources	No NS difference in TTE (∼50 km) from pre‐ to post‐treatment with either diet: HCHO = 237 ± 44 vs. 231 ± 35 min, although post‐treatment with LCHF diet was associated increased variability in results (239 ± 27 vs. 219 ± 53 min, while HCHO treatment showed a reduction in range of post‐treatment results	2 additional subjects failed to complete K‐LCHF treatment due to compliance issues. Other tests showed reduction in efficiency and increased oxygen cost of exercise at intensities >70% ${\dot{V}}_{O_{2} peak}$ with K‐LCHF. K‐LCHF increased rates of max fat oxidation (0.57 ± 0.10 to 1.12 ± 0.10 g min⁻¹ with Fat_max shifting from 43 to 70% ${\dot{V}}_{O_{2} peak}$ . Fasting [β‐HB]: > 0.5 mmol l⁻¹. HCHO may not have achieved optimal nutritional preparation for 4 h run.
Prins et al. (2019) Recreational distance runners (n = 7 M) Cross‐over study (14 days washout)	42 days HCHO diet: 173 kJ kg⁻¹; CHO: 5.8 g kg⁻¹ or 56% E; protein: 1.5 g kg⁻¹ or 15% E K‐LCHF diet:179 kJ kg⁻¹; CHO: 0.6 g kg⁻¹; protein: 2.5 g kg⁻¹ or 25% E; fat: 69% E Energy‐matched. Diets consumed in free‐living protocol with education and regular monitoring of diet and ketosis (blood ketones on race days) to check compliance	Running 5 km treadmill TT (with constant collection of respiratory gases) Undertaken at 4, 14, 28 and 42 days	All trials: Pre‐exercise = overnight fasted During exercise = nil	No Impaired performance of D4 TT in K‐LCHF trial compared with HCHO trial (1231 s vs. 1182 s, p < 0.011), but NS difference between performance on other days. Mean intensity of TT pace = ∼82% ${\dot{V}}_{O_{2} peak}$	K‐LCHF diet was higher in protein and lower in fat than typically observed but participants were in ketosis on TT days. Mean fasting [β‐HB] on TT days = 0.5 mmol l⁻¹. Max rates of exercise fat oxidation significantly increased from 1.01 ± 0.21 to 1.26 ± 0.2 g min⁻¹ over the 6‐w of K‐LCHF. Despite some counter‐balancing of treatment order, it is uncertain if 2 week washout was able to stabilise identical baseline metabolic and fitness conditions since mean fat oxidation peak at start of HCHO treatment was 0.67 ± 0.2 g min⁻¹ and individuals showed substantial increases and decreases in peak fat oxidation over the treatment.
Burke et al. (2020) Elite (international level) race walkers (LCHF = 9 M, 1 F; HCHO = 6 M, 2 F) Parallel group design with non‐randomised treatments (allocation according to preference/belief)	25 days HCHO: 223 kJ kg¹; CHO: 8.6 g kg⁻¹ or 65% E; protein: 2.1 g kg⁻¹ or 15% E K‐LCHF: 234 kJ kg⁻¹; CHO: 0.5 g or 4% E; protein: 2.1 g kg⁻¹ or 16% E Energy‐matched but allowing small energy deficit. Controlled diets consumed with supervision; blood ketones measured regularly to verify ketosis. Intensified and supervised training program (endurance + HIT + gym)	Race walking 10,000 m real‐life track race	Pre‐exercise meal at 2 h pre‐race: HCHO = 2 g kg¹ CHO LCHF Race 2 = energy matched high‐fat meal Both races = water station on track; use of performance supplements as in real‐life (e.g. caffeine) as long as use was matched in both races	No In fact K‐LCHF showed impairment of race performance while improvement seen in HCHO group HCHO: improved performance by 4.8% (134 s faster) but K‐LCHF: slower by 2.3% (86 s) (both P < 0.001)	Study undertaken as replication of Burke et al. (2017) in new cohort. Previous findings were clearly repeated including margin of difference in race improvements between groups. Both groups had small increase in aerobic capacity. K‐LCHF group reduced BM by 2.6 kg, and increased maximal fat oxidation from 0.6 to 1.3 g min⁻¹ with fasting [β‐HB]:0.8 mmol l⁻¹.
Studies of interest but with major limitations in study design or application to young highly trained athletes
Zajak et al. (2014) Moderately trained off‐road cyclists (n = 8 M) Cross‐over design with 1 week of washout	28 d HCHO: 202 kJ kg⁻¹; CHO: 50% E; protein: 15% E K‐LCHF: 202 kJ kg⁻¹; CHO: 15% E; protein: 15% E; fat: 70% E Energy matched to habitual diet (as assessed by 3 day food diaries). Unclear whether diets were controlled or self‐administered. High volume, moderate intensity training load	Cycling 105 min with 90 min at 85% ‘LT’ and 15 min at 115% ‘LT’	Pre‐exercise meal at 3 h according to dietary treatment	No Small increase in ${\dot{V}}_{O_{2} peak}$ (56 vs. 59.2 ml kg⁻¹ min⁻¹ and ${\dot{V}}_{O_{2}}$ at ‘LT’ for HCHO and K‐LCHF, p < 0.01) but reduction in maximum workload (350 vs. 362 W, P = 0.037) and workload at ‘LT’	Study was not truly ketogenic (fasting [β‐HB]: 0.15 mmol l⁻¹) despite description in study title. No real measurement of exercise capacity or performance. Small favourable change in body composition with K‐LCHF (loss of ∼ 1.8 kg with body fat loss from 14.9% to 11.0% BM, p < 0.01). Increase in the oxygen cost of cycling at same workload
Zinn et al. (2014) Case history of 5 moderately trained endurance runners and cyclists (4 F, 1 M)	10 weeks Previous diet: CHO: > 45% E K‐LCHF; CHO: <50 g d⁻¹, protein: 1.5 g kg⁻¹, ad libitum fat Diets consumed in free‐living protocol with education and contact at week 5 and 10. Fasting plasma ketone concentrations checked on test day to verify ketosis Existing training continued ad lib	Cycling ${\dot{V}}_{O_{2} peak}$ on cycling ergometer	NA	No In fact, reduction in TTE, peak power and ${\dot{V}}_{O_{2} peak}$	No control group or real measurement of exercise performance. Loss of BM (∼4 kg) and body fat achieved by all subjects. Ketosis with [β‐HB] >0.5 mmol l⁻¹) maintained. Maximal rate of fat oxidation increased from 0.6 to 0.8 g min⁻¹ with Fat_max shifting from 48 to 62% ${\dot{V}}_{O_{2} peak}$
Heatherly et al. (2018) Cross‐over study of older recreationally competitive runners and triathletes (n = 8 M; 40 ± 10 years). Treatment order: all subjects undertook HCHO first	3 weeks HCHO: 148 kJ kg⁻¹; CHO: 3.9 g kg⁻¹ or 43% E; protein: 1.4 g kg⁻¹ or 17% E K‐LCHF: 99 kJ kg⁻¹; CHO: 0.4 g kg⁻¹ or 7% E; protein: 1.7 g kg⁻¹ or 29% E; fat: 65% E Diets consumed in free‐living protocol with education and daily contact + 3 day diary on two occasions to check compliance. Ketone concentrations checked on test days to verify ketosis.	Running 5 km TT on outside hilly course (and following 5 × 10 min treadmill running and various race speeds from 5 km to marathon pace) in heated environmental chamber	Overnight fast and water only for both conditions	No No significant difference (P = 0.25) in 5 km TT performance (K‐LCHF: 23.45 ± 2.25 min vs. HCHO: 23.92 ± 2.57 min).	Order effect with subjects undertaking 3 days HCHO first, then 3 weeks K‐LCHF. K‐LCHF treatment associated with reduced energy intake and loss of ∼ 2.1 kg BM. Fasting [β‐HB] = 0.7 mmol l⁻¹; Maximum observed rates of fat oxidation during exercise = 0.81 g min⁻¹. Despite a lower BM, the oxygen cost of exercise at 10–42 km race pace was higher than with HCHO treatment. Differences in 5 km TT performance not significant.

Athletes and study design

K‐LCHF adaptation protocol (duration and daily intake)

Performance protocol

Nutritional support for performance

Performance advantage with K‐LCHF

Comments

Trained athletes with verified ketogenic diet

Phinney et al. (1983)

Well‐trained cyclists

(n = 5 M)

Cross‐over design with HCHO first

28 days

HCHO (7 d): CHO: 57% E; protein: 1.75 g kg⁻¹

K‐LCHF: CHO < 20 g; protein: 1.75 g kg⁻¹; fat = 85% E

Energy‐matched and balanced. Controlled diets consumed with supervision; blood ketones measured to verify ketosis.

Cycling

TTE at ∼63% ${\dot{V}}_{O_{2} peak}$

Both trials:

Pre‐exercise meal = overnight‐fasted

Intake during exercise = water

NS difference in TTE between trials (151 vs. 147 min for LCHF and HCHO).

Group data skewed by 1 participant who increased time to fatigue by 156% on LCHF trial (see Fig. 1)

Well controlled study but involved order effect and failure to provide optimal conditions for HCHO trial. K‐LCHF = fasting [β‐HB]: 1.3 mmol l^−1; exercise rates of fat oxidation: 1.5 g min⁻¹.

Burke et al. (2017)

Elite (international level) race walkers

(n = 19 M: LCHF = 10; HCHO = 9)

Parallel group design with non‐randomised treatments (allocation according to preference/belief)

24 days

HCHO: 231 kJ kg⁻¹; CHO: 8.6 g kg⁻¹ or 60% E; protein: 2.1 g kg⁻¹ or 16% E

K‐LCHF: 223 kJ kg⁻¹; CHO: 0.5 g or 3.5% E; protein: 2.2 g kg⁻¹ or 16% E

Energy‐matched but allowing small energy deficit. Controlled diets consumed with supervision; blood ketones measured regularly to verify ketosis. Intensified and supervised training program (endurance + HIT + gym)

Race walking

10,000 m real‐life track race

Pre‐exercise meal at 2 h pre‐race:

HCHO = 2 g kg¹ CHO LCHF Race 2 = energy matched high‐fat meal

Both races = water station on track; use of performance supplements as in real‐life (e.g. caffeine) as long as use was matched in both races

In fact, K‐LCHF failed to show the improvement seen in HCHO group

HCHO: improved performance by 6.6% [4.1–9.9%, 90% CI] equivalent to 190 s faster

K‐LCHF: NS change of −1.6% [−8.5%−5.3%] equivalent to 23 s slower

No improvement in race performance with K‐LCHF, despite equal (∼3–7%) increase in aerobic capacity, greater loss of BM and substantial increase in fat oxidation rates (from ∼0.7 to 1.57 ± 0.32 g min⁻¹) and fasting [β‐HB]: 1.8 mmol l⁻¹. Note that race protocol was reliant on capacity for high‐intensity exercise rather than glycogen depletion. Reduced performance attributed to reduction in race walking economy due to additional oxygen demand of fat oxidation at high exercise intensities.

McSwiney et al. (2018)

Trained endurance athletes (runners, cyclists, triathletes)

(n = 20: K‐LCHF = 9; HCHO = 11)

Parallel group design with non‐randomised treatments (allocation according to preference/belief)

12 weeks

HCHO: 147 kJ kg⁻¹; CHO: 5.2 g kg⁻¹ or 61% E; protein: 1.2 g kg⁻¹ or 14% E

K‐LCHF: 158 kJ kg⁻¹; CHO: 0.5 g kg⁻¹ or 5% E; protein: 1.6 g kg⁻¹ or 17% E; fat: 77% E

Diets consumed in free‐living protocol with education and weekly contact + 3 day diary at 0 and 12 weeks to check compliance. Fasting plasma ketone concentrations checked on test day to verify ketosis. Intensified training programme (endurance + HIT + strength)

Cycling

Lab ergometer:

6 s sprint + 100 km TT + critical power test (CPT)

undertaken on lab ergometer

HCHO:

Pre‐exercise meal at 2 h = CHO‐rich meal (52% E)

During exercise: 30–60 g h⁻¹ CHO

K‐LCHF Post trial: 2 h post‐fat rich (64% E)

Water electrolytes during trial

Perhaps

K‐LCHF significantly improved peak but not average power in 6 s and CPT; trend to faster 100 km (166 ± 12.4 vs. 161.5 ± 8.4 min; 2.5%). No differences in HCHO (169.6 ± 8.4 vs. 168.4 ± 9.1). However, 5 additional subjects were unable to adhere to K‐LCHF and 2 failed to complete post‐intervention testing.

Both groups increased aerobic capacity by ∼7%. K‐LCHF group had higher body fat and BM at pre‐trial and although 3 day self‐reported food diaries suggested that energy intake was maintained over 12 weeks, K‐LCHF lost 5.9 kg including 4.6 kg body fat over the 12 weeks with minimal change in HCHO group. K‐LCHF = fasting [β‐HB]: 0.5 mmol l⁻¹; exercise rates of fat oxidation: NA. Large degree of individual variability in response to K‐LCHF; negative experiences were not captured in the performance data. HCHO group may not have achieved optimal nutritional preparation in pre‐trial diet and within‐trial fuelling for 2.5 h protocol

Shaw et al. (2019)

Trained endurance runners, triathletes

(n = 8 M)

Cross‐over counterbalanced design (14–21 days washout)

31 days

‘Habitual’ HCHO diet:178 kJ kg⁻¹; CHO: 4.6 g kg⁻¹; protein: 2.0 g kg⁻¹

K‐LCHF = 191 kJ kg^−1;; CHO: 0.5 g kg⁻¹; protein: 2.0 g kg⁻¹; fat: 78% E

Energy‐matched. Diets consumed in free‐living protocol with education and regular monitoring of diet and ketosis (blood/urinary ketones) to check compliance

Running

TTE at ∼70% ${\dot{V}}_{O_{2} peak}$ on treadmill

HCHO:

Pre‐exercise meal at 2 h = 2 g kg⁻¹ CHO

During exercise: 55 g h⁻¹ CHO

LCHF:

Pre‐exercise meal at 2 h = energy matched fat‐rich foods

During exercise = energy matched fat‐rich sources

NS difference in TTE (∼50 km) from pre‐ to post‐treatment with either diet: HCHO = 237 ± 44 vs. 231 ± 35 min, although post‐treatment with LCHF diet was associated increased variability in results (239 ± 27 vs. 219 ± 53 min, while HCHO treatment showed a reduction in range of post‐treatment results

2 additional subjects failed to complete K‐LCHF treatment due to compliance issues. Other tests showed reduction in efficiency and increased oxygen cost of exercise at intensities >70%

{\dot{V}}_{O_{2} peak}

with K‐LCHF. K‐LCHF increased rates of max fat oxidation (0.57 ± 0.10 to 1.12 ± 0.10 g min⁻¹ with Fat_max shifting from 43 to 70%

{\dot{V}}_{O_{2} peak}

. Fasting [β‐HB]: > 0.5 mmol l⁻¹. HCHO may not have achieved optimal nutritional preparation for 4 h run.

Prins et al. (2019)

Recreational distance runners (n = 7 M)

Cross‐over study (14 days washout)

42 days

HCHO diet: 173 kJ kg⁻¹; CHO: 5.8 g kg⁻¹ or 56% E; protein: 1.5 g kg⁻¹ or 15% E

K‐LCHF diet:179 kJ kg⁻¹; CHO: 0.6 g kg⁻¹; protein: 2.5 g kg⁻¹ or 25% E; fat: 69% E

Energy‐matched. Diets consumed in free‐living protocol with education and regular monitoring of diet and ketosis (blood ketones on race days) to check compliance

Running

5 km treadmill TT

(with constant collection of respiratory gases)

Undertaken at 4, 14, 28 and 42 days

All trials:

Pre‐exercise = overnight fasted

During exercise = nil

Impaired performance of D4 TT in K‐LCHF trial compared with HCHO trial (1231 s vs. 1182 s, p < 0.011), but NS difference between performance on other days. Mean intensity of TT pace = ∼82% ${\dot{V}}_{O_{2} peak}$

K‐LCHF diet was higher in protein and lower in fat than typically observed but participants were in ketosis on TT days. Mean fasting [β‐HB] on TT days = 0.5 mmol l⁻¹. Max rates of exercise fat oxidation significantly increased from 1.01 ± 0.21 to 1.26 ± 0.2 g min⁻¹ over the 6‐w of K‐LCHF. Despite some counter‐balancing of treatment order, it is uncertain if 2 week washout was able to stabilise identical baseline metabolic and fitness conditions since mean fat oxidation peak at start of HCHO treatment was 0.67 ± 0.2 g min⁻¹ and individuals showed substantial increases and decreases in peak fat oxidation over the treatment.

Burke et al. (2020)

Elite (international level) race walkers

(LCHF = 9 M, 1 F; HCHO = 6 M, 2 F)

Parallel group design with non‐randomised treatments (allocation according to preference/belief)

25 days

HCHO: 223 kJ kg¹; CHO: 8.6 g kg⁻¹ or 65% E; protein: 2.1 g kg⁻¹ or 15% E

K‐LCHF: 234 kJ kg⁻¹; CHO: 0.5 g or 4% E; protein: 2.1 g kg⁻¹ or 16% E

Race walking

10,000 m real‐life track race

Pre‐exercise meal at 2 h pre‐race:

HCHO = 2 g kg¹ CHO LCHF Race 2 = energy matched high‐fat meal

Both races = water station on track; use of performance supplements as in real‐life (e.g. caffeine) as long as use was matched in both races

In fact K‐LCHF showed impairment of race performance while improvement seen in HCHO group

HCHO: improved performance by 4.8% (134 s faster) but K‐LCHF: slower by 2.3% (86 s) (both P < 0.001)

Study undertaken as replication of Burke et al. (2017) in new cohort. Previous findings were clearly repeated including margin of difference in race improvements between groups. Both groups had small increase in aerobic capacity.

K‐LCHF group reduced BM by 2.6 kg, and increased maximal fat oxidation from 0.6 to 1.3 g min⁻¹ with fasting [β‐HB]:0.8 mmol l⁻¹.

Studies of interest but with major limitations in study design or application to young highly trained athletes

Zajak et al. (2014)

Moderately trained off‐road cyclists

(n = 8 M)

Cross‐over design with 1 week of washout

28 d

HCHO: 202 kJ kg⁻¹; CHO: 50% E; protein: 15% E

K‐LCHF: 202 kJ kg⁻¹; CHO: 15% E; protein: 15% E; fat: 70% E

Energy matched to habitual diet (as assessed by 3 day food diaries). Unclear whether diets were controlled or self‐administered.

High volume, moderate intensity training load

Cycling

105 min with 90 min at 85% ‘LT’ and 15 min at 115% ‘LT’

Pre‐exercise meal at 3 h

according to dietary treatment

Small increase in ${\dot{V}}_{O_{2} peak}$ (56 vs. 59.2 ml kg⁻¹ min⁻¹ and ${\dot{V}}_{O_{2}}$ at ‘LT’ for HCHO and K‐LCHF, p < 0.01) but reduction in maximum workload (350 vs. 362 W, P = 0.037) and workload at ‘LT’

Study was not truly ketogenic (fasting [β‐HB]: 0.15 mmol l⁻¹) despite description in study title. No real measurement of exercise capacity or performance. Small favourable change in body composition with K‐LCHF (loss of ∼ 1.8 kg with body fat loss from 14.9% to 11.0% BM, p < 0.01). Increase in the oxygen cost of cycling at same workload

Zinn et al. (2014)

Case history of 5 moderately trained endurance runners and cyclists (4 F, 1 M)

10 weeks

Previous diet: CHO: > 45% E

K‐LCHF; CHO: <50 g d⁻¹, protein: 1.5 g kg⁻¹, ad libitum fat

Diets consumed in free‐living protocol with education and contact at week 5 and 10. Fasting plasma ketone concentrations checked on test day to verify ketosis

Existing training continued ad lib

Cycling

${\dot{V}}_{O_{2} peak}$ on cycling ergometer

In fact, reduction in TTE, peak power and ${\dot{V}}_{O_{2} peak}$

No control group or real measurement of exercise performance. Loss of BM (∼4 kg) and body fat achieved by all subjects. Ketosis with [β‐HB] >0.5 mmol l⁻¹) maintained. Maximal rate of fat oxidation increased from 0.6 to 0.8 g min⁻¹ with Fat_max shifting from 48 to 62%

{\dot{V}}_{O_{2} peak}

Heatherly et al. (2018)

Cross‐over study of older recreationally competitive runners and triathletes (n = 8 M; 40 ± 10 years). Treatment order: all subjects undertook HCHO first

3 weeks

HCHO: 148 kJ kg⁻¹; CHO: 3.9 g kg⁻¹ or 43% E; protein: 1.4 g kg⁻¹ or 17% E

K‐LCHF: 99 kJ kg⁻¹; CHO: 0.4 g kg⁻¹ or 7% E; protein: 1.7 g kg⁻¹ or 29% E; fat: 65% E

Diets consumed in free‐living protocol with education and daily contact + 3 day diary on two occasions to check compliance. Ketone concentrations checked on test days to verify ketosis.

Running

5 km TT on outside hilly course

(and following 5 × 10 min treadmill running and various race speeds from 5 km to marathon pace) in heated environmental chamber

Overnight fast and water only for both conditions

No significant difference (P = 0.25) in 5 km TT performance (K‐LCHF: 23.45 ± 2.25 min vs. HCHO: 23.92 ± 2.57 min).

Order effect with subjects undertaking 3 days HCHO first, then 3 weeks K‐LCHF.

K‐LCHF treatment associated with reduced energy intake and loss of ∼ 2.1 kg BM. Fasting [β‐HB] = 0.7 mmol l⁻¹; Maximum observed rates of fat oxidation during exercise = 0.81 g min⁻¹. Despite a lower BM, the oxygen cost of exercise at 10–42 km race pace was higher than with HCHO treatment. Differences in 5 km TT performance not significant.

NA, not available; M, male; F, female; K‐LCHF, ketogenic low‐carbohydrate high‐fat diet; HCHO, high carbohydrate/high carbohydrate availability diet; CHO, carbohydrate; E, energy; ${\dot{V}}_{O_{2} peak}$ , maximal oxygen capacity; W, watts; BM, body mass; ‘LT’, the so‐called lactate threshold; Fat_max, percentage of maximal aerobic capacity at which maximal rate of fat oxidation occurs; TT, time trial; TTE, time to exhaustion; [β‐HB], plasma concentrations of β‐hydroxybutyrate; NS, not significant.