Search

The aim of the study was to determine the influence of immediate and 1-hr-delayed carbohydrate (CHO) and protein (PRO) feeding after prolonged exercise on leukocyte trafficking, bacterially stimulated neutrophil degranulation, saliva secretory IgA (S-IgA) responses, and circulating stress hormones. In randomized order, separated by 1 wk, 9 male runners completed 3 feeding interventions after 2 hr of running at 75% VO2max. During control (CON), participants received water (12 ml/kg body mass [BM]) immediately and 1 hr postexercise. During immediate feeding (IF), participants received a CHO-PRO solution equal to 1.2 g CHO/kg BM and 0.4 g PRO/kg BM immediately postexercise and water 1 hr postexercise. During delayed feeding (DF), participants received water immediately postexercise and CHO-PRO solution 1 hr postexercise. Unstimulated saliva and venous blood samples were collected preexercise, immediately postexercise, and every 20 min until 140 min postexercise. No significant interactions were observed for circulating leukocytes and T-lymphocyte subset counts, S-IgA secretion rate, or plasma cortisol, epinephrine, or norepinephrine concentration. Bacterially stimulated neutrophil degranulation decreased during recovery on CON and DF (24% and 31%, respectively, at 140 min; p < .01) but not on IF. Compared with CON, neutrophil degranulation was higher on IF at 100 min postexercise and higher on IF than DF at 80 min and 100 min onward postexercise (p < .05). Ingestion of a CHO-PRO solution immediately after, but not 1 hr after, prolonged strenuous exercise prevented the decrease in neutrophil degranulation but did not alter circulating stress hormone, leukocyte trafficking, or S-IgA responses. Further research should identify the independent effect of different quantities of CHO and PRO ingestion during recovery on neutrophil responses and other aspects of immune function.

A one night period without sleep is not uncommon amongst athletes travelling across time zones and military personnel during training and operations. However, the effect of one night without sleep on immune indices in response to strenuous exercise remains unknown. The objective was to determine the effect of one night without sleep on immune indices in response to subsequent strenuous exercise. Using a repeated measures cross-over design, on one occasion eleven male participants slept normally (CON) and on another they were sleep deprived for 30 h (SDEP). After 30 h participants performed 30 min steady state (SS) treadmill exercise at 60% VO2max followed by a 30 min treadmill time trial (TT). Blood and saliva samples were collected at 0 h, 30 h, post-SS, post-TT, 2 h post-TT and 18 h post-TT. Circulating leukocyte and T-lymphocyte subset counts, bacterially-stimulated neutrophil degranulation, saliva secretory immunoglobulin A (S-IgA) and plasma cortisol were determined. No trial x time interactions were observed for immune indices and plasma cortisol. A leukocytosis, neutrophilia, and lymphocytosis was observed post-TT compared with 30 h (P < 0.01). Also, at post-TT compared with 30 h an increase in circulating T-lymphocyte CD3 + (55%) and CD8 + (67%) counts (P < 0.05), a decrease in neutrophil degranulation (20%; P < 0.05) and an increase in S-IgA concentration (83%) was observed (P < 0.01). Plasma cortisol concentration increased post-TT (62%) compared with post-SS (P < 0.01). In conclusion, a 30 h period of sleep deprivation does not alter leukocyte trafficking, neutrophil degranulation or S-IgA responses either at rest or after submaximal and strenuous exercise.

To investigate whether unstimulated whole saliva flow rate (UFR) and osmolality (Sosm) track changes in hydration status during 48h of restricted fluid intake (RF) or combined fluid and energy restriction (RF+RE). Following the 48h periods, UFR and Sosm were assessed after acute exercise dehydration and rehydration.Thirteen healthy males completed three trials in a randomised order: control (CON) where participants received their estimated energy (12,154+/-230kJ/d: mean+/-S.E.M) and fluid (3912+/-140ml/d) requirements, RF trial where participants received their energy requirements and 193+/-19ml/d water to drink (total fluid 960+/-15ml/d) and RF+RE where participants received 1214+/-25kJ/d and 962+/-16ml/d. After 48h, participants completed 30min of maximal exercise followed by rehydration (0-2h) and refeeding (2-6h).At 48h body mass loss exceeded 3% on RF and RF+RE. UFR decreased during 48h on RF (510+/-122 to 169+/-37microl/min) and RF+RE (452+/-92 to 265+/-53microl/min) and was lower than CON at 48h (441+/-90microl/min: P0.05). Sosm increased during 48h on RF (54+/-3 to 73+/-5mOsmol/kg) and RF+RE (52+/-3 to 68+/-5mOsmol/kg) and was greater than CON at 48h (52+/-2mOsmol/kg: P0.05). Unlike UFR, Sosm identified the additional hypohydration associated with exercise (P0.05) and returned to within 0h values with rehydration.Sosm, and to a lesser extent UFR, track hydration status during a 48h period of RF or RF+RE and after subsequent exercise and rehydration.

The aim was to investigate the effects of a 48 h period of fluid, energy or combined fluid and energy restriction on salivary IgA (s-IgA) responses at rest and after exercise. Thirteen healthy males (age 21 (sem1) years) participated in four randomised 48 h trials. In the control trial participants received their estimated energy (12 154 (sem230) kJ/d) and water (3912 (sem140) ml/d) requirements. On fluid restriction (FR) participants received their energy requirements and 193 (sem19) ml water/d to drink and on energy restriction (ER) participants received their water requirements and 1214 (sem25) kJ/d. Fluid and energy restriction (F+ER) was a combination of FR and ER. After 48 h, participants performed a 30 min treadmill time trial (TT) followed by rehydration (0–2 h) and refeeding (2–6 h). Unstimulated saliva was collected at 0, 24 and 48 h, post-TT, and 2 and 6 h post-TT. Saliva flow rate (sflw) and s-IgA (ELISA) remained unchanged in control conditions and on ER. However, 48 h on FR decreased sflw (64 %) which most probably accounted for the increase in s-IgA concentration (P sem2); 24 h: 12 (sem2) μg/min;P

The aim of this study was to determine the effects of prolonged exercise in hot conditions on saliva IgA (s-IgA) responses in trained cyclists. On two occasions, in random order and separated by 1 week, 12 male cyclists cycled for 2 h on a stationary ergometer at 62 (3)% VO2 max [194 (4) W; mean (SEM)], on one occasion (HOT: 30.3°C, 76% RH) and on another occasion (CONTROL: 20.4°C, 60% RH). Water was available ad-libitum. Venous blood samples and 2-min whole unstimulated saliva samples were collected at pre, post and 2 h post-exercise. The s-IgA concentration was determined using a sandwich-type ELISA. Exercising heart rate, rating of perceived exertion, rectal temperature, corrected body mass loss (P

Firstly, to identify whether saliva flow rate, osmolality, and total protein are potential markers of hydration, we compared changes in these parameters with changes in plasma osmolality during progressive dehydration. Secondly, we compared the sensitivity of saliva parameters to track hydration changes with the sensitivity of urine osmolality. Thirdly, to test the hypothesis that dehydration, rather than neuroendocrine regulation, is responsible for the decrease in saliva flow rate during prolonged exercise, we compared flow rate and catecholamine responses to prolonged exercise with and without fluids.colon; Fifteen males (plasma osmolality 289 +/- 4 mOsmol x kg(-1); mean +/- SD) exercised (30 degrees C, 70% RH) with no fluid intake (NFI) until body mass loss (BML) of 1.1, 2.1, and 3.0% and on another occasion with fluid intake (FI) to offset losses.colon; Plasma and urine osmolality increased during NFI (plasma osmolality 3.0% BML: 298 +/- 4 mOsmol x kg(-1); P0.01). Saliva flow rate decreased (P0.01), saliva total protein increased (P0.01), and saliva osmolality increased from preexercise (50 +/- 11 mOsmol x kg(-1)) to 3.0% BML (105 +/- 41 mOsmol x kg(-1)) during NFI (P0.01). Saliva osmolality, urine osmolality, and saliva total protein correlated strongly with plasma osmolality during dehydration (r 0.87, 0.83, and 0.91, respectively; P0.01). During the FI trial, saliva flow rate and osmolality remained unchanged. Plasma catecholamine concentration increased during exercise (P0.01) with no difference between trials.colon; Saliva osmolality and total protein appear to be as sensitive as urine osmolality to track hydration changes during hypertonic-hypovolemia. These results also suggest that dehydration has a greater involvement in the decrease in saliva flow rate during prolonged exercise than neuroendocrine regulation.

PURPOSE: It has been suggested that, because of the low sitting position in short-track speed skating, muscle blood flow is restricted, leading to decreases in tissue oxygenation. Therefore, wearable wireless-enabled near-infrared spectroscopy (NIRS) technology was used to monitor changes in quadriceps muscle blood volume and oxygenation during a 500-m race simulation in short-track speed skaters. METHODS: Six elite skaters, all of Olympic standard (age = 23 ± 1.8 yr, height = 1.8 ± 0.1 m, mass = 80.1 ± 5.7 kg, midthigh skinfold thickness = 7 ± 2 mm), were studied. Subjects completed a 500-m race simulation time trial (TT). Whole-body oxygen consumption was simultaneously measured with muscle oxygenation in right and left vastus lateralis as measured by NIRS. RESULTS: Mean time for race completion was 44.8 ± 0.4 s. VO 2 peaked 20 s into the race. In contrast, muscle tissue oxygen saturation (TSI%) decreased and plateaued after 8 s. Linear regression analysis showed that right leg TSI% remained constant throughout the rest of the TT (slope value = 0.01), whereas left leg TSI% increased steadily (slope value = 0.16), leading to a significant asymmetry (P < 0.05) in the final lap. Total muscle blood volume decreased equally in both legs at the start of the simulation. However, during subsequent laps, there was a strong asymmetry during cornering; when skaters traveled solely on the right leg, there was a decrease in its muscle blood volume, whereas an increase was seen in the left leg. CONCLUSIONS: NIRS was shown to be a viable tool for wireless monitoring of muscle oxygenation. The asymmetry in muscle desaturation observed on the two legs in short-track speed skating has implications for training and performance. © 2012 by the American College of Sports Medicine.

The aim was to investigate the effects of 48 hr of fluid, energy, or combined fluid and energy restriction on circulating leukocyte and lymphocyte subset counts (CD3+, CD4+, and CD8+) and bacterially stimulated neutrophil degranulation at rest and after exercise. Thirteen healthy men (M ± SEM age 21 ± 1 yr) participated in 4 randomized 48-hr trials. During control (CON) participants received their estimated energy (2,903 ± 17 kcal/day) and fluid (3,912 ± 140 ml/day) requirements. During fluid restriction (FR) they received their energy requirements and 193 ± 19 ml/day water to drink. During energy restriction (ER) they received their fluid requirements and 290 ± 6 kcal/day. Fluid and energy restriction (F+ER) was a combination of FR and ER. After 48 hr, participants performed a 30-min treadmill time trial (TT) followed by rehydration (0–2 hr) and refeeding (2–6 hr). Circulating leukocyte and lymphocyte counts remained unchanged for CON and FR. Circulating leukocyte, lymphocyte, CD3+, and CD4+ counts decreased by ~20% in ER and ~30% in F+ER by 48 hr (p < .01), returning to within 0-hr values by 6 hr post-TT. Circulating neutrophil count and degranulation were unaltered by dietary restriction at rest and after TT. In conclusion, a 48-hr period of ER and F+ER, but not FR, decreased circulating leukocyte, lymphocyte, CD3+, and CD4+ counts but not neutrophil count or degranulation. Circulating leukocyte and lymphocyte counts normalized on refeeding. Finally, dietary restriction did not alter circulating leukocyte, lymphocyte, and neutrophil responses to 30 min of maximal exercise.

The purpose of this study was to investigate the effects of prolonged exercise with and without a thermal clamp on neutrophil trafficking, bacterial-stimulated neutrophil degranulation, stress hormones, and cytokine responses. Thirteen healthy male volunteers (means ± SE: age 21 ± 1 yr; mass 74.9 ± 2.1 kg; maximal oxygen uptake 58 ± 1 ml·kg−1·min−1) completed four randomly assigned, 2-h water-immersion trials separated by 7 days. Trials were exercise-induced heating (EX-H: water temperature 36°C), exercise with a thermal clamp (EX-C: 24°C), passive heating (PA-H: 38.5°C), and control (CON: 35°C). EX-H and EX-C was comprised of 2 h of deep water running at 58% maximal oxygen uptake. Blood samples were collected at pre-, post-, and 1 h postimmersion. Core body temperature was unaltered on CON, clamped on EX-C (−0.02°C), and rose by 2.23°C and 2.31°C on EX-H and PA-H, respectively. Exercising with a thermal clamp did not blunt the neutrophilia postexercise (EX-C postexercise: 9.6 ± 1.1 and EX-H postexercise: 9.8 ± 1.0 × 109/liter). Neutrophil degranulation decreased ( P < 0.01) similarly immediately after PA-H (−21%), EX-C, and EX-H (−28%). EX-C blunted the circulating norepinephrine, cortisol, granulocyte-colony stimulating factor, and IL-6 response ( P < 0.01) but not the plasma epinephrine and serum growth hormone response. These results show a similar neutrophilia and decrease in neutrophil degranulation after prolonged exercise with and without a thermal clamp. As such, the rise in core body temperature does not appear to mediate neutrophil trafficking and degranulation responses to prolonged exercise. In addition, these results suggest a limited role for cortisol, granulocyte-colony stimulating factor, and IL-6 in the observed neutrophil responses to prolonged exercise.

The contribution of heat and exercise related stress to the release of heat shock protein 72 (HSP72) is currently unknown. The purpose of the present study was to determine the combined and independent effects of heat and exercise on the extracellular (e)HSP72 response. Eleven moderately trained male volunteers [means ± SD: age 21 ± 4 yr; body mass 75.7 ± 7.7 kg; maximal oxygen uptake (V̇o2 max) 57.8 ± 3.3 ml·kg−1·min−1] completed four 2-h, heat-manipulated, water-immersion trials. Trials were exercise-induced heat (EIH; rectal temperature change +2.2°C), clamped exercise (CEx; 0°C), passive heating (PHT; +2.3°C), and control (Con; 0°C). Exercise trials (EIH and CEx) comprised deep-water running at 58.5 ± 2.4 and 59.1 ± 1.7% v̇o2max. eHSP72 and catecholamine concentrations were determined by ELISA and HPLC, respectively, pre- and postimmersion. All trials induced an eHSP72 response ( P < 0.05) with postimmersion values significantly greater on EIH compared with other trials (6.0 ± 3.4; CEx 3.8 ± 2.6; PHT 2.7 ± 2.1; Con 2.2 ± 1.9 ng/ml). Exercising with a thermal clamp blunted the eHSP72 response, but postimmersion values were also greater than Con. PHT induced a large catecholamine response, but postimmersion eHSP72 values did not reach significance vs. Con. Given that exercising with a thermal clamp evoked a significant increase in plasma eHSP72 concentration, exercise-related stressors other than heat appeared influential in stimulating HSP72 release. Moreover, the catecholamine data from PHT suggest neither epinephrine nor norepinephrine was solely responsible for eHSP72 release.