What Is the Evidence That Dietary Macronutrient Composition Influences Exercise Performance? A Narrative Review.

The introduction of the needle muscle biopsy technique in the 1960s allowed muscle tissue to be sampled from exercising humans for the first time. The finding that muscle glycogen content reached low levels at exhaustion suggested that the metabolic cause of fatigue during prolonged exercise had been discovered. A special pre-exercise diet that maximized pre-exercise muscle glycogen storage also increased time to fatigue during prolonged exercise. The logical conclusion was that the athlete's pre-exercise muscle glycogen content is the single most important acutely modifiable determinant of endurance capacity. Muscle biochemists proposed that skeletal muscle has an obligatory dependence on high rates of muscle glycogen/carbohydrate oxidation, especially during high intensity or prolonged exercise. Without this obligatory carbohydrate oxidation from muscle glycogen, optimum muscle metabolism cannot be sustained; fatigue develops and exercise performance is impaired. As plausible as this explanation may appear, it has never been proven. Here, I propose an alternate explanation. All the original studies overlooked one crucial finding, specifically that not only were muscle glycogen concentrations low at exhaustion in all trials, but hypoglycemia was also always present. Here, I provide the historical and modern evidence showing that the blood glucose concentration-reflecting the liver glycogen rather than the muscle glycogen content-is the homeostatically-regulated (protected) variable that drives the metabolic response to prolonged exercise. If this is so, nutritional interventions that enhance exercise performance, especially during prolonged exercise, will be those that assist the body in its efforts to maintain the blood glucose concentration within the normal range.

Hiding unhealthy heart outcomes in a low-fat diet trial: the Women's Health Initiative Randomized Controlled Dietary Modification Trial finds that postmenopausal women with established coronary heart disease were at increased risk of an adverse outcome if they consumed a low-fat 'heart-healthy' diet.

The Women's Health Initiative Randomized Controlled Dietary Modification Trial (WHIRCDMT) was designed to test whether the US Department of Agriculture's 1977 Dietary Guidelines for Americans protects against coronary heart disease (CHD) and other chronic diseases. The only significant finding in the original 2006 WHIRCDMT publication was that postmenopausal women with CHD randomised to a low-fat 'heart-healthy' diet in 1993 were at 26% greater risk of developing additional CHD events compared with women with CHD eating the control diet. A 2017 WHIRCDMT publication includes data for an additional 5 years of follow-up. It finds that CHD risk in this subgroup of postmenopausal women had increased further to 47%-61%. The authors present three post-hoc rationalisations to explain why this finding is 'inadmissible': (1) only women in this subgroup were less likely to adhere to the prescribed dietary intervention; (2) their failure to follow the intervention diet increased their CHD risk; and (3) only these women were more likely to not have received cholesterol-lowering drugs. These rationalisations appear spurious. Rather these findings are better explained as a direct consequence of postmenopausal women with features of insulin resistance (IR) eating a low-fat high-carbohydrate diet for 13 years. All the worst clinical features of IR, including type 2 diabetes mellitus (T2DM) in some, can be 'reversed' by the prescription of a high-fat low-carbohydrate diet. The Women's Health Study has recently reported that T2DM (10.71-fold increased risk) and other markers of IR including metabolic syndrome (6.09-fold increased risk) were the most powerful predictors of future CHD development in women; blood low-density lipoprotein-cholesterol concentration was a poor predictor (1.38-fold increased risk). These studies challenge the prescription of the low-fat high-carbohydrate heart-healthy diet, at least in postmenopausal women with IR, especially T2DM. According to the medical principle of 'first do no harm', this practice is now shown to be not evidence-based, making it scientifically unjustifiable, perhaps unethical.

Evidence that supports the prescription of low-carbohydrate high-fat diets: a narrative review.

Low-carbohydrate high-fat (LCHF) diets are a highly contentious current topic in nutrition. This narrative review aims to provide clinicians with a broad overview of the effects of LCHF diets on body weight, glycaemic control and cardiovascular risk factors while addressing some common concerns and misconceptions. Blood total cholesterol and LDL-cholesterol concentrations show a variable, highly individual response to LCHF diets, and should be monitored in patients adhering to this diet. In contrast, available evidence from clinical and preclinical studies indicates that LCHF diets consistently improve all other markers of cardiovascular risk-lowering elevated blood glucose, insulin, triglyceride, ApoB and saturated fat (especially palmitoleic acid) concentrations, reducing small dense LDL particle numbers, glycated haemoglobin (HbA1c) levels, blood pressure and body weight while increasing low HDL-cholesterol concentrations and reversing non-alcoholic fatty liver disease (NAFLD). This particular combination of favourable modifications to all these risk factors is a benefit unique to LCHF diets. These effects are likely due in part to reduced hunger and decreased ad libitum calorie intake common to low-carbohydrate diets, allied to a reduction in hyperinsulinaemia, and reversal of NAFLD. Although LCHF diets may not be suitable for everyone, available evidence shows this eating plan to be a safe and efficacious dietary option to be considered. LCHF diets may also be particularly beneficial in patients with atherogenic dyslipidaemia, insulin resistance, and the frequently associated NAFLD.

Influence of Affective Stimuli on Leg Power Output and Associated Neuromuscular Parameters during Repeated High Intensity Cycling Exercises.

The aim of this study was to examine the impact of emotional eliciting pictures on neuromuscular performance during repetitive supramaximal cycling exercises (RSE). In a randomized order, twelve male participants were asked to perform five 6-s cycle sprints (interspaced by 24 s of recovery) on a cycle ergometer in front of neutral, pleasant or unpleasant pictures. During each RSE, mean power output (MPO) and electromyographic activity [root mean square (RMS) and median frequency (MF)] of the vastus lateralis and vastus medialis muscles were analyzed. Neuromuscular efficiency (NME) was calculated as the ratio of MPO to RMS. Higher RMS (232.17 ± 1.17 vs. 201.90 ± 0.47 µV) and MF (68.56 ± 1.78 vs. 64.18 ± 2.17 Hz) were obtained in pleasant compared to unpleasant conditions (p < 0.05). This emotional effect persisted from the first to the last sprint. Higher MPO was obtained in pleasant than in unpleasant conditions (690.65 ± 38.23 vs. 656.73 ± 35.95 W, p < 0.05). However, this emotional effect on MPO was observed only for the two first sprints. NME decreased from the third sprint (p < 0.05), which indicated the occurrence of peripheral fatigue after the two first sprints. These results suggested that, compared with unpleasant pictures, pleasant ones increased the neuromuscular performance during RSE. Moreover, the disappearance of the beneficial effect of pleasant emotion on mechanical output from the third sprint appears to be due to peripheral fatigue.

Evidence of cardiac functional reserve upon exhaustion during incremental exercise to determine VO2max.

BACKGROUND: There remains considerable debate regarding the limiting factor(s) for maximal oxygen uptake (VO2max). Previous studies have shown that the central circulation may be the primary limiting factor for VO2max and that cardiac work increases beyond VO2max. AIM: We sought to evaluate whether the work of the heart limits VO2max during upright incremental cycle exercise to exhaustion. METHODS: Eight trained men completed two incremental exercise trials, each terminating with exercise at two different rates of work eliciting VO2max (MAX and SUPRAMAX). During each exercise trial we continuously recorded cardiac output using pulse-contour analysis calibrated with a lithium dilution method. Intra-arterial pressure was recorded from the radial artery while pulmonary gas exchange was measured continuously for an assessment of oxygen uptake. RESULTS: The workload during SUPRAMAX (mean±SD: 346.5±43.2 W) was 10% greater than that achieved during MAX (315±39.3 W). There was no significant difference between MAX and SUPRAMAX for Q (28.7 vs 29.4 L/min) or VO2 (4.3 vs 4.3 L/min). Mean arterial pressure was significantly higher during SUPRAMAX, corresponding to a higher cardiac power output (8.1 vs 8.5 W; p<0.06). CONCLUSIONS: Despite similar VO2 and Q, the greater cardiac work during SUPRAMAX supports the view that the heart is working submaximally at exhaustion during an incremental exercise test (MAX).

Brain stimulation modulates the autonomic nervous system, rating of perceived exertion and performance during maximal exercise.

BACKGROUND: The temporal and insular cortex (TC, IC) have been associated with autonomic nervous system (ANS) control and the awareness of emotional feelings from the body. Evidence shows that the ANS and rating of perceived exertion (RPE) regulate exercise performance. Non-invasive brain stimulation can modulate the cortical area directly beneath the electrode related to ANS and RPE, but it could also affect subcortical areas by connection within the cortico-cortical neural networks. This study evaluated the effects of transcranial direct current stimulation (tDCS) over the TC on the ANS, RPE and performance during a maximal dynamic exercise. METHODS: Ten trained cyclists participated in this study (33±9 years; 171.5±5.8 cm; 72.8±9.5 kg; 10-11 training years). After 20-min of receiving either anodal tDCS applied over the left TC (T3) or sham stimulation, subjects completed a maximal incremental cycling exercise test. RPE, heart rate (HR) and R-R intervals (as a measure of ANS function) were recorded continuously throughout the tests. Peak power output (PPO) was recorded at the end of the tests. RESULTS: With anodal tDCS, PPO improved by ~4% (anodal tDCS: 313.2±29.9 vs 301.0±19.8 watts: sham tDCS; p=0.043), parasympathetic vagal withdrawal was delayed (anodal tDCS: 147.5±53.3 vs 125.0±35.4 watts: sham tDCS; p=0.041) and HR was reduced at submaximal workloads. RPE also increased more slowly during exercise following anodal tDCS application, but maximal RPE and HR values were not affected by cortical stimulation. CONCLUSIONS: The findings suggest that non-invasive brain stimulation over the TC modulates the ANS activity and the sensory perception of effort and exercise performance, indicating that the brain plays a crucial role in the exercise performance regulation.

Potentiation and electrical stimulus frequency during self-paced exercise and recovery.

The aim of this study was to investigate the effect of potentiation on stimulation-induced muscle function during and after an intense bout of self-paced dynamic exercise. Ten active subjects performed a time trial involving repetitive concentric extension-flexion of the right knee using a Biodex dynamometer. Electrical stimulation before and after a 5 s maximal isometric voluntary contraction was performed before the start of the time trial and immediately (< 5 s) after each 20% of the time trial as well as 1, 2, 4 and 8 min after time trial termination. Potentiation was observed before the time trial and as early as 1-2 min after the time trial, but no potentiation was detected during or immediately after the time trial for neither single or paired stimuli. At termination of the time trial, "potentiated" peak torque was significantly more reduced than "unpotentiated" peak torque for single stimulus (-65 ± 10% and -42 ± 18%, respectively) and paired stimuli at 100 Hz (-51 ± 10% and -33 ± 15%, respectively). Faster recovery for "potentiated" compared to "unpotentiated" peak torque indicate that potentiate peak torque measurements or delay the post-exercise measurements more than a few seconds, will underestimate peripheral fatigue. In conclusion, the potentiation after maximal contraction disappears during intense exercise. Whether the muscle is already potentiated during intense contraction or fatiguing mechanisms inhibits potentiation remains to be clarified.

McArdle disease does not affect skeletal muscle fibre type profiles in humans.

Patients suffering from glycogen storage disease V (McArdle disease) were shown to have higher surface electrical activity in their skeletal muscles when exercising at the same intensity as their healthy counterparts, indicating more muscle fibre recruitment. To explain this phenomenon, this study investigated whether muscle fibre type is shifted towards a predominance in type I fibres as a consequence of the disease. Muscle biopsies from the Biceps brachii (BB) (n = 9) or Vastus lateralis (VL) (n = 8) were collected over a 13-year period from male and female patients diagnosed with McArdle disease, analysed for myosin heavy chain (MHC) isoform content using SDS-PAGE, and compared to healthy controls (BB: n = 3; VL: n = 10). All three isoforms were expressed and no difference in isoform expression in VL was found between the McArdle patients and healthy controls (MHC I: 33±19% vs. 43±7%; MHC IIa: 52±9% vs. 40±7%; MHC IIx: 15±18% vs. 17±9%). Similarly, the BB isoform content was also not different between the two groups (MHC I: 33±14% vs. 30±11%; MHC IIa: 46±17% vs. 39±5%; MHC IIx: 21±13% vs. 31±14%). In conclusion, fibre type distribution does not seem to explain the higher surface EMG in McArdle patients. Future studies need to investigate muscle fibre size and contractility of McArdle patients.

Potentiation increases peak twitch torque by enhancing rates of torque development and relaxation.

The aim of this study was to measure the extent to which potentiation changes in response to an isometric maximal voluntary contraction. Eleven physically active subjects participated in two separate studies. Single stimulus of electrical stimulation of the femoral nerve was used to measure torque at rest in unpotentiated quadriceps muscles (study 1 and 2), and potentiated quadriceps muscles torque in a 10 min period after a 5 s isometric maximal voluntary contraction of the quadriceps muscles (study 1). Additionally, potentiated quadriceps muscles torque was measured every min after a further 10 maximal voluntary contractions repeated every min (study 2). Electrical stimulation repeated several times without previous maximal voluntary contraction showed similar peak twitch torque. Peak twitch torque 4 s after a 5 s maximal voluntary contraction increased by 45±13% (study 1) and by 56±10% (study 2), the rate of torque development by 53±13% and 82±29%, and the rate of relaxation by 50±17% and 59±22%, respectively, but potentiation was lost already two min after a 5 s maximal voluntary contraction. There was a tendency for peak twitch torque to increase for the first five repeated maximal voluntary contractions, suggesting increased potentiation with additional maximal voluntary contractions. Correlations for peak twitch torque vs the rate of torque development and for the rate of relaxation were r(2)= 0.94 and r(2)=0.97. The correlation between peak twitch torque, the rate of torque development and the rate of relaxation suggests that potentiation is due to instantaneous changes in skeletal muscle contractility and relaxation.

The Women's Health Initiative Randomized Controlled Dietary Modification Trial: an inconvenient finding and the diet-heart hypothesis.

One goal of the US$700 million Women's Health Initiative Randomized Controlled Dietary Modification Trial was to determine whether post-menopausal women who adopted what was regarded as a 'heart healthy' low-fat diet, high in vegetables, fruits and grains, reduced their risk of developing cardiovascular disease. The trial substantially favoured the outcome in the intervention group, who also received an intensive nutritional and behaviour education programme not offered to the control group. These studies neatly disprove the diet-heart hypothesis since adoption of 'heart healthy' eating not only failed to influence future cardiac events in the healthy but it increased such events in the unhealthy and worsened diabetic control in those with type 2 diabetes mellitus. 

Low-carbohydrate and high-fat intake can manage obesity and associated conditions: occasional survey.

This study analyses 127 communications from individuals self-reporting their weight change following adoption of a low-carbohydrate, high-fat (LCHF) eating plan. Total combined self-reported weight loss was 1 900 kg (range 5 kg gain to 84 kg loss). The mean ± standard deviation weight loss of 15 (±12) kg is among the largest yet described. Sixteen subjects reported the LCHF 'cured' (i.e. medications no longer required) one or more of their medical conditions, most commonly type 2 diabetes mellitus (T2DM) (n=14), hypertension (n=8) and hypercholesterolaemia (n=7). Another 9 subjects with either type 1 diabetes mellitus or T2DM reduced medications as did 7 patients with hypertension; 8 no longer suffered from irritable bowel syndrome. These data show that significant and rapid weight loss is possible on an unsupervised eating plan that severely restricts daily carbohydrate intake to approximately <75 g/day. Better weight loss on a carbohydrate-restricted LCHF eating plan than on an iso-caloric high-carbohydrate, low-fat (HCLF) diet is well described in the literature, probably due to a paradoxical reduction of hunger by carbohydrate restriction. A randomised controlled clinical trial is urgently required to disprove the hypothesis that the LCHF eating plan can reverse cases of T2DM, metabolic syndrome and hypertension without pharmacotherapy. 

High oxidative capacity and type IIx fibre content in springbok and fallow deer skeletal muscle suggest fast sprinters with a resistance to fatigue.

Some wild antelopes are fast sprinters and more resistant to fatigue than others. This study therefore investigated two wild antelope species to better understand their reported performance capability. Muscle samples collected post mortem from the vastus lateralis and longissimus lumborum of fallow deer (Dama dama) and springbok (Antidorcas marsupialis) were analysed for myosin heavy chain isoform content, citrate synthase, 3-hydroxyacyl CoA dehydrogenase, phosphofructokinase, lactate dehydrogenase and creatine kinase activities. Cross-sectional areas, fibre type and oxidative capacities of each fibre type were determined in the vastus lateralis only. The predominant fibre type in both muscle groups and species were type IIX (>50%), with springbok having more type IIX fibres than fallow deer (P<0.05). Overall cross-sectional area was not different between the two species. The metabolic pathway analyses showed high glycolytic and oxidative capacities for both species, but springbok had significantly higher CS activities than fallow deer. Large variation and overlap in oxidative capacities existed within and between the fibre types. Some type IIX fibres presented with oxidative capacities similar to those from type I and IIA fibres. The data suggest that springbok and fallow deer are able sprint at >90 and 46 km h(-1), respectively, partly from having large type IIX fibre contents and high glycolytic capacities. The high oxidative capacities also suggest that these animals may be able to withstand fatigue for long periods of time.