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The study aimed to determine the impact of a dairy milk recovery beverage immediately after endurance exercise on leukocyte trafficking, neutrophil function, and gastrointestinal tolerance markers during recovery. Male runners (N = 11) completed two feeding trials in randomized order, after 2 hr of running at 70% $\dot{\mathrm{V}}{\mathrm{O}}_2\text{max}$ , fluid restricted, in temperate conditions (25 °C, 43% relative humidity). Immediately postexercise, the participants received a chocolate-flavored dairy milk beverage equating to 1.2 g/kg body mass carbohydrate and 0.4 g/kg body mass protein in one trial, and water volume equivalent in another trial. Venous blood and breath samples were collected preexercise, postexercise, and during recovery to determine the leukocyte counts, plasma intestinal fatty acid binding protein, and cortisol concentrations, as well as breath H₂. In addition, 1,000 µl of whole blood was incubated with 1 μg/ml Escherichia coli lipopolysaccharide for 1 hr at 37 °C to determine the stimulated plasma elastase concentration. Gastrointestinal symptoms and feeding tolerance markers were measured preexercise, every 15 min during exercise, and hourly postexercise for 3 hr. The postexercise leukocyte (mean [95% confidence interval]: 12.7 [11.6, 14.0] × 10⁹/L [main effect of time, MEOT]; p < .001) and neutrophil (10.2 [9.1, 11.5] × 10⁹/L; p < .001) counts, as well as the plasma intestinal fatty acid binding protein (470 pg/ml; +120%; p = .012) and cortisol (236 nMol/L; +71%; p = .006) concentrations, were similar throughout recovery for both trials. No significant difference in breath H₂ and gastrointestinal symptoms was observed between trials. The total (Trial × Time, p = .025) and per cell (Trial × Time, p = .001) bacterially stimulated neutrophil elastase release was greater for the chocolate-flavored dairy milk recovery beverage (+360% and +28%, respectively) in recovery, compared with the water trial (+85% and −38%, respectively). Chocolate-flavored dairy milk recovery beverage consumption immediately after exercise prevents the decrease in neutrophil function during the recovery period, and it does not account for substantial malabsorption or gastrointestinal symptoms over a water volume equivalent.

We sought to assess the accuracy of current or developing new prediction equations for resting metabolic rate (RMR) in adolescent athletes. RMR was assessed via indirect calorimetry, alongside known predictors (body composition via dual-energy X-ray absorptiometry, height, age, and sex) and hypothesized predictors (race and maturation status assessed via years to peak height velocity), in a diverse cohort of adolescent athletes (n = 126, 77% male, body mass = 72.8 ± 16.6 kg, height = 176.2 ± 10.5 cm, age = 16.5 ± 1.4 years). Predictive equations were produced and cross-validated using repeated k-fold cross-validation by stepwise multiple linear regression (10 folds, 100 repeats). Performance of the developed equations was compared with several published equations. Seven of the eight published equations examined performed poorly, underestimating RMR in >75% to >90% of cases. Root mean square error of the six equations ranged from 176 to 373, mean absolute error ranged from 115 to 373 kcal, and mean absolute error SD ranged from 103 to 185 kcal. Only the Schofield equation performed reasonably well, underestimating RMR in 51% of cases. A one- and two-compartment model were developed, both r ² of .83, root mean square error of 147, and mean absolute error of 114 ± 26 and 117 ± 25 kcal for the one- and two-compartment model, respectively. Based on the models’ performance, as well as visual inspection of residual plots, the following model predicts RMR in adolescent athletes with better precision than previous models; RMR = 11.1 × body mass (kg) + 8.4 × height (cm) − (340 male or 537 female).

The delivery to and utilization of oxygenated hemoglobin to the forearm muscles are key determinants of rock-climbing performance. Anthocyanin-rich New Zealand blackcurrant (NZBC) has been suggested to improve blood flow and may enhance forearm endurance performance. As such, a double-blind, randomized crossover design study with 12 participants performed submaximal intermittent contractions (at 40% maximal voluntary contraction) to failure after a 7-day intake of 600 mg/day NZBC extract or placebo. Minimum tissue saturation index (TSI%) was assessed during the contractions. During recovery, time to half recovery of TSI% and brachial artery blood flow were assessed. There was no difference in time to exhaustion between NZBC and placebo. Minimum TSI% was lower with NZBC extract (43 ± 8 vs. 50 ± 11 TSI%; p = .007; Cohen’s d = 1.01). During recovery, there was no effect on brachial artery blood flow. However, time to half recovery was faster with NZBC (26 ± 17 vs. 42 ± 26 s; p = .001; Cohen’s d = 1.3) following exhaustive contractions. Seven days of NZBC extract appears to improve muscle oxygenation during and following contractions with no change in either arterial blood flow or forearm endurance performance.

Insulin resistance is associated with cardiometabolic risk factors, and exercise training can improve insulin-mediated glucose uptake. However, few studies have demonstrated the reversibility of exercise-induced benefits. Thus, the authors examine the time–response effects of exercise training and detraining on glucose transporter 4 (GLUT4) content, insulin-dependent and insulin-independent pathways in cardiac and gastrocnemius muscle tissues of spontaneously hypertensive rats. Thirty-two male spontaneously hypertensive rats, 4 months old, were assigned to (n = 8/group): T (exercise training: 10-week treadmill exercise, 50–70% maximum effort capacity, 1 hr/day, 5 days/week); D2 (exercise training + 2-day detraining), D4 (exercise training + 4-day detraining); and S (no exercise). The authors evaluated insulin resistance, maximum effort capacity, GLUT4 content, p-IRS-1^Tyr1179, p-AS160^Ser588, p-AMPKα1^Thr172, and p-CaMKII^Thr286 in cardiac and gastrocnemius muscle tissues (Western blot). In response to exercise training, there were improvements in insulin resistance (15.4%; p = .010), increased GLUT4 content (microsomal, 29.4%; p = .012; plasma membrane, 27.1%; p < .001), p-IRS-1 (42.2%; p < .001), p-AS160 (60.0%; p < .001) in cardiac tissue, and increased GLUT4 content (microsomal, 29.4%; p = .009; plasma membrane, 55.5%; p < .001), p-IRS-1 (28.1%; p = .018), p-AS160 (76.0%; p < .001), p-AMPK-α1 (37.5%; p = .026), and p-CaMKII (30.0%; p = .040) in the gastrocnemius tissue. In D4 group, the exercise-induced increase in GLUT4 was reversed (plasma membrane, −21.3%; p = .027), p-IRS1 (−37.1%; p = .008), and p-AS160 (−82.6%; p < .001) in the cardiac tissue; p-AS160 expression (−35.7%; p = .034) was reduced in the gastrocnemius. In conclusion, the cardiac tissue is more susceptible to exercise adaptations in the GLUT4 content and signaling pathways than the gastrocnemius muscle. This finding may be explained by particular characteristics of insulin-dependent and insulin-independent pathways in the muscle tissues studied.

This study determined normative data for sweat rate (SR) and whole-body (WB) sweat sodium concentration [Na⁺] in athletes indigenous to a tropical climate, categorized by age, gender, and sport classification. We analyzed data from 556 athletes (386 adult and 170 young) in endurance (END), team/ball (TBA), and combat (COM) sports exercising in tropical environments (wet bulb globe temperature = 29.4 ± 2.1 °C). SR was calculated from change in body weight corrected for urine output and fluid/food intake. Sweat was collected using absorbent patches, and regional [Na⁺] was determined using an ion selective analyzer and normalized to WB sweat [Na⁺]. Data are expressed as mean ± SD. SR was higher in males compared with females in both young (24.2 ± 7.7 ml·kg⁻¹·hr⁻¹ vs. 16.7 ± 5.7 ml·kg⁻¹·hr⁻¹) and adult (22.8 ± 7.4 ml·kg⁻¹·hr⁻¹ vs. 18.6 ± 7.0 ml·kg⁻¹·hr⁻¹) athletes, in END sports in girls (END = 19.1 ± 6.0 ml·kg⁻¹·hr⁻¹; TBA = 14.6 ± 4.5 ml·kg⁻¹·hr⁻¹), and in adult males (END = 25.2 ± 6.3 ml·kg⁻¹·hr⁻¹; TBA = 19.1 ± 7.2 ml·kg⁻¹·hr⁻¹; COM = 18.4 ± 8.5 ml·kg⁻¹·hr⁻¹) and females (END = 23.5 ± 5.6 ml·kg⁻¹·hr⁻¹; TBA = 14.2 ± 5.2 ml·kg⁻¹·hr⁻¹; COM = 15.3 ± 5.2 ml·kg⁻¹·hr⁻¹); p < .05. WB sweat [Na⁺] was higher in adult athletes than in young athletes (43 ± 10 mmol/L vs. 40 ± 9 mmol/L, p < .05). These norms provide a reference range for low, low average, average high, and high SR and WB sweat [Na⁺], which serve as a guide for fluid replacement for athletes who live and train in the tropics.

Exercise-associated muscle cramps (EAMCs) are thought to be caused by dehydration and/or electrolyte losses. In this multicenter, cross-sectional study, the authors determined whether sweat rates (SRs), sweat electrolyte concentrations, or sweat electrolyte content differed in athletes with (i.e., crampers) and without (i.e., noncrampers) a history of EAMCs and whether these variables could predict EAMC-prone athletes. Male and female collegiate athletes (N = 350) from 11 sports with (n = 245) and without (n = 105) a self-reported history of EAMCs completed a typical exercise or conditioning session. SRs, calculated from body mass, and posterior forearm sweat were analyzed for sweat sodium concentration ([Na⁺]_sw), sweat potassium concentration ([K⁺]_sw), and sweat chloride concentration ([Cl⁻]_sw). The authors used SRs and sweat electrolyte concentrations to calculate sweat electrolyte content lost. Within each gender, no differences in SRs (204 males, p = .92; 146 females, p = .24); [Na⁺]_sw (191 males, p = .55; 126 females, p = .55); Na⁺ _sw content (191 males, p = .59; 126 females, p = .20); [K⁺]_sw (192 males, p = .57; 126 females, p = .87); K⁺ _sw content (192 males, p = .49; 126 females, p = .03); [Cl⁻]_sw (192 males, p = .94; 77 females, p = .57); and Cl⁻ _sw content (192 males, p = .55; 77 females, p = .34) occurred between crampers and noncrampers. Receiver operating characteristic curve analysis revealed that sweat electrolyte content and SRs were predictive of EAMC-prone athletes in American football (area under curve = 0.65–0.72, p ≤ .005), but not in any other sport. EAMCs may not be solely caused by fluid or electrolyte losses in most athletes. Fluid and electrolyte replacement may help American footballers. Clinicians should individualize fluid and electrolyte replacement and understand different etiologies for EAMCs.

We tested the hypothesis that presleep consumption of α-lactalbumin (LA), a fraction of whey with a high abundance of tryptophan, would improve indices of sleep quality and time-trial (TT) performance in cyclists relative to an isonitrogenous collagen peptide (CP) supplement lacking tryptophan. Using randomized, double-blind, crossover designs, cyclists consumed either 40 g of LA or CP 2 hr prior to sleep. In Study 1, six elite male endurance track cyclists (age 23 ± 6 years, $\dot{\mathrm{V}}{\mathrm{O}}_2\text{peak}$ 70.2 ± 4.4 ml·kg⁻¹·min⁻¹) consumed a supplement for three consecutive evenings before each 4-km TT on a velodrome track, whereas in Study 2, six well-trained cyclists (one female; age 24 ± 5 years, $\dot{\mathrm{V}}{\mathrm{O}}_2\text{peak}$ 66.9 ± 8.3 ml·kg⁻¹·min⁻¹) consumed a supplement the evening before each 4-km TT on a stationary cycle ergometer. Indices of sleep quality were assessed with wrist-based actigraphy. There were no differences between the CP and LA supplements in terms of total time in bed, total sleep time, or sleep efficiency in Study 1 (LA: 568 ± 71 min, 503 ± 67 min, 88.3% ± 3.4%; CP: 546 ± 30 min, 479 ± 35 min, 87.8% ± 3.1%; p = .41, p = .32, p = .74, respectively) or Study 2 (LA: 519 ± 90 min, 450 ± 78 min, 87.2% ± 7.6%; CP: 536 ± 62 min, 467 ± 57 min, 87.3% ± 6.4%; p = .43, p = .44, p = .97, respectively). Similarly, time to complete the 4-km TT was unaffected by supplementation in Study 1 (LA: 274.9 ± 7.6 s; CP: 275.5 ± 7.2 s; p = .62) and Study 2 (LA: 344.3 ± 22.3 s; CP: 343.3 ± 23.0 s; p = .50). Thus, relative to CP, consuming LA 2 hr prior to sleep over 1–3 days did not improve actigraphy-based indices of sleep quality or 4-km TT performance in cyclists.

The authors compared the effectiveness of daily (DAY) versus alternate day (ALT) oral iron supplementation in athletes with suboptimal iron. Endurance-trained runners (nine males and 22 females), with serum ferritin (sFer) concentrations <50 μg/L, supplemented with oral iron either DAY or ALT for 8 weeks. Serum ferritin was measured at baseline and at fortnightly intervals. Hemoglobin mass (Hb_mass) was measured pre- and postintervention in a participant subset (n = 10). Linear mixed-effects models were used to assess the effectiveness of the two strategies on sFer and Hb_mass. There were no sFer treatment (p = .928) or interaction (p = .877) effects; however, sFer did increase (19.7 μg/L; p < .001) over the 8-week intervention in both groups. In addition, sFer was 21.2 μg/L higher (p < .001) in males than females. No Hb_mass treatment (p = .146) or interaction (p = .249) effects existed; however, a significant effect for sex indicated that Hb_mass was 140.85 g higher (p = .004) in males compared with females. Training load (p = .001) and dietary iron intake (p = .015) also affected Hb_mass. Finally, there were six complaints of severe gastrointestinal side effects in DAY, but only one in ALT. In summary, both supplement strategies increased sFer in athletes with suboptimal iron status; however, the ALT approach was associated with lower incidence of gastrointestinal upset.