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The small intestine acts as interface and regulator between the gut lumen and the rest of the body and controls the degree and rate of transport of amino acids coming from dietary protein via the portal vein to the liver and the systemic circulation. To measure protein absorption, kinetics multicatheter animal (pig) models in combination with amino acid tracer technology are available. Dietary factors infuence the absorption rates from the lumen to the gut, metabolism of dietary component in the gut, and the release of amino acids to the portal circulation from digested protein. In a balanced-protein meal, the gut dietary amino acid utilization (30–50%) for gut protein synthesis will result in a labile protein pool in the gut that can be benefcial during the postabsorptive state. To enhance gut retention, amount and quality of protein and the presence of carbohydrate are major factors. Besides this the use of a slowly digestible protein or the presence of fber in the meal can increase retention further. During the absorption of low-quality protein meals, fewer amino acids are utilized by the gut, resulting in higher amounts of amino acid release to the portal circulation. Malnutrition or starvation, protein depletion, defciencies of specifc nutrients, or illness such as sepsis all inhibit the growth and change protein turnover of the intestinal mucosa and therefore affect absorption kinetics. Therefore, the kind of protein meal that has the most optimal absorption kinetics (the most benefcial) for gut and for the rest of the body depends on these (patho)physiological circumstances. Despite the absence of different absorption kinetics between protein, peptides, and amino acids, they could be benefcial in specifc circumstances.

This study determined the effect of nutritional supplementation throughout endurance exercise on whole-body leucine kinetics (leucine rate of appearance [Ra], oxidation [Ox], and nonoxidative leucine disposal [NOLD]) during recovery. Five trained men underwent a 2-h run at 65% VO_2max, during which a carbohydrate (CHO), mixed protein-carbohydrate (milk), or placebo (PLA) drink was consumed. Leucine kinetics were assessed during recovery using a primed, continuous infusion of 1-¹³C leucine. Leucine Ra and NOLD were lower for milk than for PLA. Ox was higher after milk-supplemented exercise than after CHO or PLA. Although consuming milk during the run affected whole-body leucine kinetics, the benefits of such a practice for athletes remain unclear. Additional studies are needed to determine whether protein supplementation during exercise can optimize protein utilization during recovery.

The purpose of this study was to profile the effect of active versus passive recovery on acid-base kinetics during multiple bouts of intense exercise. Ten males completed two exercise trials. The trials consisted of three exercise bouts to exhaustion with either a 12 min active (20% workload max) or passive recovery between bouts. Blood pH was lower in the passive (p) recovery compared to active (a) throughout the second and third recovery periods [second recovery: 7.18 ± 0.08 to 7.24 ± 0.09 (p), 7.23 ± 0.07 to 7.32 ± 0.07 (a), P < 0.05; third recovery: 7.17 ± 0.08 to 7.22 ± 0.09 (p), 7.23 ± 0.08 to 7.32 ± 0.08 (a), P < 0.05]. Exercise performance times did not differ between recovery conditions (P = 0.28). No difference was found between conditions for recovery kinetics (slope and half-time to recovery). Subsequent performance during multiple bouts of intense exercise to exhaustion may not be influenced by blood acidosis or mode of recovery.

The purpose of this study was to measure the recovery kinetics of pH and lactate for the conditions of pre-exercise acidosis, alkalosis, and placebo states. Twelve trained male cyclists completed 3 exercise trials (110% workload at VO_2max), ingesting either 0.3 g/kg of NH₄Cl (ACD), 0.2 g/kg of Na⁺HCO₃ ^- and 0.2 g/kg of sodium citrate (ALK), or a placebo (calcium carbonate) (PLAC). Blood samples (heated dorsal hand vein) were drawn before, during, and after exercise. Exercise-induced acidosis was more severe in the ACD and PLAC trials (7.15 ± 0.06, 7.21 ± 0.07, 7.16 ± 0.06, P < 0.05, for ACD, ALK, PLAC, respectively). Recovery kinetics for blood pH and lactate, as assessed by the monoexponential slope constant, were not different between trials (0.057 ± 0.01, 0.050 ± 0.01, 0.080 ± 0.02, for ACD, ALK, PLAC, respectively). Complete recovery of blood pH from metabolic acidosis can take longer than 45 min. Such a recovery profile is nonlinear, with 50% recovery occurring in approximately 12 min. Complete recovery of blood lactate can take longer than 60 min, with 50% recovery occurring in approximately 30 min. Induced alkalosis decreases metabolic acidosis and improves pH recovery compared to acidodic and placebo conditions. Although blood pH and lactate are highly correlated during recovery from acidosis, they recover at significantly different rates.

We hypothesized that when plasma glucose availability is maintained by carbohydrate (CHO) ingestion, trained cyclists can utilize plasma glucose at very high rates during the later stages of prolonged exercise (10). To test this hypothesis, a well-trained male cyclist was studied during exercise to fatigue at 70% ${\text{VO}}_2\max$ when ingesting glucose throughout exercise. A primed continuous infusion of [U-¹³C]glucose was begun after 60 min of exercise to measure rates of plasma glucose appearance ( ${\text{R}}^{\text{a}}$ ), disappearance ( ${\text{R}}^{\text{d}}$ ), and oxidation ( ${\text{R}}^{\text{ox}}$ ). ${\text{R}}_{\mathrm{a}}$ and ${\text{R}}_{\mathrm{d}}$ rose progressively throughout exercise, peaking at 6.85 and 6.99 mmollmin, respectively, at fatigue (i.e., 133 min). Most (93%) of this glucose was oxidized; during the final 30 min of exercise, ${\text{R}}_{\mathrm{ox}}$ , averaged 6.10 mmollmin and accounted for approximately half of total CHO oxidation. These results support the hypothesis that trained cyclists can oxidize plasma glucose at very high rates during the later stages of prolonged exercise when fed CHO.

Postexercise fat oxidation may be important for exercise prescription aimed at optimizing fat loss. The authors examined the effects of exercise intensity, duration, and modality on postexercise oxygen consumption (VO₂) and substrate selection/respiratory-exchange ratio (RER) in healthy individuals. Three experiments (n = 7 for each) compared (a) short- (SD) vs. long-duration (LD) ergometer cycling exercise (30 min vs. 90 min) matched for intensity, (b) low- (LI) vs. high-intensity (HI) cycling (50% vs. 85% of VO_2max) matched for energy expenditure, and (c) continuous (CON) vs. interval (INT) cycling matched for energy expenditure and mean intensity. All experiments were administered by crossover design. Altering exercise duration did not affect postexercise VO₂ or RER kinetics (p > .05). However, RER was lower and fat oxidation was higher during the postexercise period in LD vs. SD (p < .05). HI vs. LI resulted in a significant increase in total postexercise energy expenditure and fat oxidation (p < .01). Altering exercise modality (CON vs. INT) did not affect postexercise VO₂, RER, or fat oxidation (p > .05). These results demonstrate that postexercise energy expenditure and fat oxidation can be augmented by increasing exercise intensity, but these benefits cannot be exploited by undertaking interval exercise (1:2-min work:recovery ratio) when total energy expenditure, duration, and mean intensity remain unchanged. In spite of the apparent benefit of these strategies, the amount of fat oxidized after exercise may be inconsequential compared with that oxidized during the exercise bout.