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The contribution of amino acid oxidation to total energy expenditure is negligible during short-term intense exercise and accounts for 3–6% of the total adenosine triphosphate supplied during prolonged exercise in humans. While not quantitatively important in terms of energy supply, the intermediary metabolism of several amino acids—notably glutamate, alanine, and the branched-chain amino acids—afreets other metabolites .including the intermediates within the tricarboxylic acid (TCA) cycle. Glutamate appears to be a key substrate for the rapid increase in muscle TCA cycle intermediates (TCAI) that occurs at the onset of moderate to intense exercise, due to a rightward shift of the reaction catalyzed by alanine aminotransferase (glutamate + pyruvate <-> alanine + 2-oxoglutarate). The pool of muscle TCAI declines during prolonged exercise, and this has been attributed to an increase in leucine oxidation that relies on one of the TCAI. However, this mechanism does not appear to be quantitatively important due of the relatively low maximal activity of branched-chain oxoacid dehydrogenase, the key enzyme involved. It has been suggested that an increase in TCAI is necessary to attain high rates of aerobic energy production and that a decline in TCAI may be a causative factor in local muscle fatigue. These topics remain controversial, but recent evidence suggests that changes in TCAI during exercise are unrelated to oxidative energy provision in skeletal muscle.

Supplementation with green tea extract (GTE) in animals has been reported to induce numerous metabolic adaptations including increased fat oxidation during exercise and improved performance. However, data regarding the metabolic and physiological effects of GTE during exercise in humans are limited and equivocal.

During postexercise recovery, optimal nutritional intake is important to replenish endogenous substrate stores and to facilitate muscle-damage repair and reconditioning. After exhaustive endurance-type exercise, muscle glycogen repletion forms the most important factor determining the time needed to recover. Postexercise carbohydrate (CHO) ingestion has been well established as the most important determinant of muscle glycogen synthesis. Coingestion of protein and/or amino acids does not seem to further increase muscle glycogensynthesis rates when CHO intake exceeds 1.2 g · kg⁻¹ · hr⁻¹. However, from a practical point of view it is not always feasible to ingest such large amounts of CHO. The combined ingestion of a small amount of protein (0.2–0.4 g · (0.2−0.4 g · kg⁻¹ · hr⁻¹) with less CHO (0.8 g · kg⁻¹ · hr⁻¹) stimulates endogenous insulin release and results in similar muscle glycogen-repletion rates as the ingestion of 1.2 g · kg⁻¹ · hr⁻¹ CHO. Furthermore, postexercise protein and/or amino acid administration is warranted to stimulate muscle protein synthesis, inhibit protein breakdown, and allow net muscle protein accretion. The consumption of ~20 g intact protein, or an equivalent of ~9 g essential amino acids, has been reported to maximize muscle protein-synthesis rates during the first hours of postexercise recovery. Ingestion of such small amounts of dietary protein 5 or 6 times daily might support maximal muscle protein-synthesis rates throughout the day. Consuming CHO and protein during the early phases of recovery has been shown to positively affect subsequent exercise performance and could be of specific benefit for athletes involved in multiple training or competition sessions on the same or consecutive days.

Six days of dietary nitrate supplementation in the form of beetroot juice (~0.5 L/d) has been reported to reduce pulmonary oxygen uptake (VO₂) during submaximal exercise and increase tolerance of high-intensity work rates, suggesting that nitrate can be a potent ergogenic aid. Limited data are available regarding the effect of nitrate ingestion on athletic performance, and no study has investigated the potential ergogenic effects of a small-volume, concentrated dose of beetroot juice. The authors tested the hypothesis that 6 d of nitrate ingestion would improve time-trial performance in trained cyclists. Using a double-blind, repeated-measures crossover design, 12 male cyclists (31 ± 3 yr, VO_2peak = 58 ± 2 ml · kg⁻¹ · min⁻¹, maximal power [W_max] = 342 ± 10 W) ingested 140 ml/d of concentrated beetroot (~8 mmol/d nitrate) juice (BEET) or a placebo (nitrate-depleted beetroot juice; PLAC) for 6 d, separated by a 14-d washout. After supplementation on Day 6, subjects performed 60 min of submaximal cycling (2 × 30 min at 45% and 65% W_max, respectively), followed by a 10-km time trial. Time-trial performance (953 ± 18 vs. 965 ± 18 s, p < .005) and power output (294 ± 12 vs. 288 ± 12 W, p < .05) improved after BEET compared with PLAC supplementation. Submaximal VO₂ was lower after BEET (45% W_max = 1.92 ± 0.06 vs. 2.02 ± 0.09 L/min, 65% W_max 2.94 ± 0.12 vs. 3.11 ± 0.12 L/min) than with PLAC (main effect, p < .05). Wholebody fuel selection and plasma lactate, glucose, and insulin concentrations did not differ between treatments. Six days of nitrate supplementation reduced VO₂ during submaximal exercise and improved time-trial performance in trained cyclists.

Commencing some training sessions with reduced carbohydrate (CHO) availability has been shown to enhance skeletal muscle adaptations, but the effect on exercise performance is less clear. We examined whether restricting CHO intake between twice daily sessions of high-intensity interval training (HIIT) augments improvements in exercise performance and mitochondrial content. Eighteen active but not highly trained subjects (peak oxygen uptake [VO_2peak] = 44 ± 9 ml/kg/min), matched for age, sex, and fitness, were randomly allocated to two groups. On each of 6 days over 2 weeks, subjects completed two training sessions, each consisting of 5 × 4-min cycling intervals (60% of peak power), interspersed by 2 min of recovery. Subjects ingested either 195 g of CHO (HI-HI group: ~2.3 g/kg) or 17 g of CHO (HI-LO group: ~0.3 g/kg) during the 3-hr period between sessions. The training-induced improvement in 250-kJ time trial performance was greater (p = .02) in the HI-LO group (211 ± 66 W to 244 ± 75 W) compared with the HI-HI group (203 ± 53 W to 219 ± 60 W); however, the increases in mitochondrial content was similar between groups, as reflected by similar increases in citrate synthase maximal activity, citrate synthase protein content and cytochrome c oxidase subunit IV protein content (p > .05 for interaction terms). This is the first study to show that a short-term “train low, compete high” intervention can improve whole-body exercise capacity. Further research is needed to determine whether this type of manipulation can also enhance performance in highly-trained subjects.

Sprint interval training (SIT), repeated bouts of high-intensity exercise, improves skeletal muscle oxidative capacity and exercise performance. β-alanine (β-ALA) supplementation has been shown to enhance exercise performance, which led us to hypothesize that chronic β-ALA supplementation would augment work capacity during SIT and augment training-induced adaptations in skeletal muscle and performance. Twenty-four active but untrained men (23 ± 2 yr; VO_2peak = 50 ± 6 mL·kg⁻¹·min⁻¹) ingested 3.2 g/day of β-ALA or a placebo (PLA) for a total of 10 weeks (n = 12 per group). Following 4 weeks of baseline supplementation, participants completed a 6-week SIT intervention. Each of 3 weekly sessions consisted of 4–6 Wingate tests, i.e., 30-s bouts of maximal cycling, interspersed with 4 min of recovery. Before and after the 6-week SIT program, participants completed a 250-kJ time trial and a repeated sprint test. Biopsies (v. lateralis) revealed that skeletal muscle carnosine content increased by 33% and 52%, respectively, after 4 and 10 weeks of β-ALA supplementation, but was unchanged in PLA. Total work performed during each training session was similar across treatments. SIT increased markers of mitochondrial content, including cytochome c oxidase (40%) and β-hydroxyacyl-CoA dehydrogenase maximal activities (19%), as well as VO_2peak (9%), repeated-sprint capacity (5%), and 250-kJ time trial performance (13%), but there were no differences between treatments for any measure (p < .01, main effects for time; p > .05, interaction effects). The training stimulus may have overwhelmed any potential influence of β-ALA, or the supplementation protocol was insufficient to alter the variables to a detectable extent.

Carbohydrate mouth rinsing during exercise has been suggested to enhance performance of short (45–60 min) bouts of high-intensity (>75% VO_2peak) exercise. Recent studies indicate that this performance enhancing effect may be dependent on the prandial state of the athlete. The purpose of this study was to define the impact of a carbohydrate mouth rinse on ~1-hr time trial performance in both the fasted and fed states. Using a double-blind, crossover design, 14 trained male cyclists (27 ± 6 years; 5.0 ± 0.5 W·kg⁻¹) were selected to perform 4 time trials of ~1 hr (1,032 ± 127 kJ) on a cycle ergometer while rinsing their mouths with a 6.4% sucrose solution (SUC) or a noncaloric sweetened placebo (PLA) for 5 s at the start and at every 12.5% of their set amount of work completed. Two trials were performed in an overnight fasted state and two trials were performed 2 h after consuming a standardized breakfast. Performance time did not differ between any of the trials (fasted-PLA: 68.6 ± 7.2; fasted-SUC: 69.6 ± 7.5; fed-PLA: 67.6 ± 6.6; and fed-SUC: 69.0 ± 6.3 min; Prandial State × Mouth Rinse Solution p = .839; main effect prandial state p = .095; main effect mouth rinse solution p = .277). In line, mean power output and heart rate during exercise did not differ between trials. In conclusion, a sucrose mouth rinse does not improve ~1-hr time trial performance in well-trained cyclists when performed in either the fasted or the fed state.