New Zealand blackcurrant extract modulates the heat shock response in men during exercise in hot ambient conditions.

PURPOSE: To determine if 7d of New Zealand blackcurrant (NZBC) extract alters the heat shock, inflammatory and apoptotic response during prolonged exertional-heat stress. METHODS: Ten men (Age: 29 ± 2 years, Stature: 1.82 ± 0.02 m, Mass: 80.3 ± 2.7 kg, V̇O2max: 56 ± 2 mL·kg-1·min-1) ingested two capsules of CurraNZ™ (NZBC extract: 210 mg anthocyanins·day-1) or PLACEBO for 7d prior to 1 h treadmill run (65% V̇O2max) in hot ambient conditions (34 °C/40% RH). Blood samples were collected before (Pre), immediately after (Post), 1 h after (1-Post), and 4 h after (4-Post) exercise. Heat shock proteins (HSP90, HSP70, HSP32) were measured in plasma. HSP and protein markers of inflammatory capacity (TLR4, NF-κB) and apoptosis (BAX/BCL-2, Caspase 9) were measured in peripheral blood mononuclear cells (PBMC). RESULTS: eHSP32 was elevated at baseline in NZBC(+ 31%; p < 0.001). In PLACEBO HSP32 content in PBMC was elevated at 4-Post(+ 98%; p = 0.002), whereas in NZBC it fell at Post(- 45%; p = 0.030) and 1-Post(- 48%; p = 0.026). eHSP70 was increased at Post in PLACEBO(+ 55.6%, p = 0.001) and NZBC (+ 50.7%, p = 0.010). eHSP90 was increased at Post(+ 77.9%, p < 0.001) and 1-Post(+ 73.2%, p < 0.001) in PLACEBO, with similar increases being shown in NZBC (+ 49.0%, p = 0.006 and + 66.2%, p = 0.001; respectively). TLR4 and NF-κB were both elevated in NZBC at PRE(+ 54%, p = 0.003 and + 57%, p = 0.004; respectively). Main effects of study condition were also shown for BAX/BCL-2(p = 0.025) and Caspase 9 (p = 0.043); both were higher in NZBC. CONCLUSION: 7d of NZBC extract supplementation increased eHSP32 and PBMC HSP32 content. It also increased inflammatory and apoptotic markers in PBMC, suggesting that NZBC supports the putative inflammatory response that accompanies exertional-heat stress.

High-altitude exposures and intestinal barrier dysfunction.

Gastrointestinal complaints are often reported during ascents to high altitude (>2,500 m), though their etiology is not known. One potential explanation is injury to the intestinal barrier which has been implicated in the pathophysiology of several diseases. High-altitude exposures can reduce splanchnic perfusion and blood oxygen levels causing hypoxic and oxidative stress. These stressors might injure the intestinal barrier leading to consequences such as bacterial translocation and local/systemic inflammatory responses. The purpose of this mini-review is to 1) discuss the impact of high-altitude exposures on intestinal barrier dysfunction and 2) present medications and dietary supplements which may have relevant impacts on the intestinal barrier during high-altitude exposures. There is a small but growing body of evidence which shows that acute exposures to high altitudes can damage the intestinal barrier. Initial data also suggest that prolonged hypoxic exposures can compromise the intestinal barrier through alterations in immunological function, microbiota, or mucosal layers. Exertion may worsen high-altitude-related intestinal injury via additional reductions in splanchnic circulation and greater hypoxemia. Collectively these responses can result in increased intestinal permeability and bacterial translocation causing local and systemic inflammation. More research is needed to determine the impact of various medications and dietary supplements on the intestinal barrier during high-altitude exposures.

Short-term hot water immersion results in substantial thermal strain and partial heat acclimation; comparisons with heat-exercise exposures.

OBJECTIVE: To examine the effectiveness of hot water immersion (HWI) as a heat acclimation strategy in comparison to time and temperature matched, exercise-heat acclimation (EHA). METHODS: 8 males performed heat stress tests (HST) (45 min of cycling at 50% of VO2max in 40 °C, 40% RH) before and after heat acclimation sessions. Acclimation sessions were either three consecutive bouts of HWI (40 min of submersion at 40 °C) or EHA (40 min of cycling at 50% VO2max in 40 °C, 40% RH). RESULTS: Average change in tympanic temperature (TTympanic) was significantly higher following HWI (2.1 °C ± 0.4) compared to EHA (1.5 °C ± 0.4) (P < 0.05). Decreases in peak heart rate (HR) (HWI: -10 bpm ± 8; EHA: -6 ± 7), average HR (-7 bpm ± 6; -3 ± 4), and average core temperature (-0.4 °C ± 0.3; -0.2 ± 0.4) were evident following acclimation (P < 0.05), but not different between interventions (P > 0.05). Peak rate of perceived exertion (RPEPeak) decreased for HWI and EHA (P < 0.05). Peak thermal sensation (TSPeak) decreased following HWI (P < 0.05) but was not different between interventions (P > 0.05). Plasma volume increased in both intervention groups (HWI: 5.9% ± 5.1; EHA: 5.4% ± 3.7) but was not statistically different (P > 0.05). CONCLUSION: HWI induced significantly greater thermal strain compared to EHA at equivalent temperatures during time-matched exposures. However, the greater degree of thermal strain did not result in between intervention differences for cardiovascular, thermoregulatory, or perceptual variables. Findings suggest three HWI sessions may be a potential means to lower HR, TCore, and perceptual strain during exercise in the heat.

Effects of exercise in hot and humid conditions and bovine colostrum on salivary immune markers.

The purpose of this study was to examine the effects of exercise in a hot and humid environment on salivary lactoferrin and lysozyme. A secondary aim was to quantify the effects of 14-day bovine colostrum (BC) supplementation on salivary lactoferrin and lysozyme at rest and following exercise in hot and humid conditions. Using a randomized, double-blind, and counterbalanced design, ten males (20 ± 2 years, VO2max 55.8 ± 3.7 mL kg-1 min-1, 11.8 ± 2.7% body fat) ran for 46 ± 7.7 min at 95% of ventilatory threshold in a 40 °C and 50% RH environment after 14-days of supplementation with either BC or placebo. Saliva was collected pre, post, 1-h, and 4-h post exercise, and was analyzed for lactoferrin and lysozyme using ELISA. There was an immediate increase in the concentration and secretion rate of lactoferrin and lysozyme (p < 0.05) with exercise, but BC had no effect (p > 0.05). Saliva flow rate was not different between conditions [(PLA: pre: 0.54 ± 0.3, post: 0.44 ± 0.3, 1-h: 0.67 ± 0.3, 4-h: 1.0 ± 0.4 mL min-1); (BC: pre: 0.58 ± 0.2, post: 0.37 ± 0.1, 1-h: 0.63 ± 0.2, 4-h: 0.83 ± 0.4 mL min-1)]. There were no differences in thermoregulatory markers (core temperature or physiological strain index) between BC and placebo trials. Interestingly, exercise-induced heat stress did not impair mucosal immune parameters, instead participants showed a transient increase in salivary lactoferrin and lysozyme. Further, 14-day BC supplementation had no effect on mucosal immunity at any time point.

Dietary curcumin supplementation does not alter peripheral blood mononuclear cell responses to exertional heat stress.

INTRODUCTION: Curcumin reduces gut barrier damage and plasma cytokine responses to exertional heat stress. However, the role of peripheral blood mononuclear cell (PBMC) in this response remains unclear. PURPOSE: This work investigated the effect of 3 days of 500 mg/day dietary curcumin supplementation on PBMC responses to exertional heat stress in non-heat acclimated humans. METHODS: Eight participants ran (65% VO2max) for 60 min in an environmental chamber (37 °C/25% RH) two times (curcumin/placebo). Blood samples were collected pre, post, 1 h post, and 4 h post-exercise. PBMC were isolated from blood samples and the protein content of markers along the TLR4 signaling pathway (TLR4, MyD88, pNF-κB, NF-κB), indicators of cellular energy status (SIRT1 and p-AMPK), and mediators of cellular heat shock response (pHSF-1 and HSP70) were examined with Western blot. Data were analyzed with two-way (condition × time) RM-ANOVAs with Newman-Keuls post hocs. RESULTS: As compared to placebo, curcumin did not alter protein expression in PBMC (p > 0.05). However, in both study conditions at 1 h post-reductions were noted in TLR 4 (- 21.5%; p = 0.03), HSP70 (- 11.0%; p = 0.04), pAMPK (- 48.5%; p < 0.01), and SIRT1 (- 47.8%; p < 0.01). Remarkably, the ratio of pNF-κB to NF-κB was elevated in both conditions at this same timepoint (+ 75.4%; p = 0.02). CONCLUSIONS: Inflammatory protein expression in PBMC did not differ between curcumin and placebo conditions. Downregulation of pAMPK/SIRT1 and release of HSP70 to the bloodstream may compensate for reduced TLR4, allowing PBMC to maintain inflammatory capacity and preventing an "open window" during the hours following hyperthermic exercise.

Exercise increases lactoferrin, but decreases lysozyme in salivary granulocytes.

INTRODUCTION: Intracellular lactoferrin (Lac) and lysozyme (Lys) content play an important role in regulating inflammation and promoting host protection. While exercise has demonstrated an increase in Lac and Lys concentration in exocrine solutions, little is known regarding intracellular concentration changes in response to exercise. PURPOSE: To quantify intracellular Lac and Lys concentration before and after exercise in salivary CD45+CD15+ cells. METHODS: 11 males (20.3 ± 0.8 years, 57.2 ± 7.6 mL/kg/min V̇O2pk, 11.1 ± 3.9% body fat) ran for 45 min at 75% of VO2pk. 12 mL of stimulated saliva were collected pre and immediately post exercise. Saliva was filtered through a 30-µm filter before analysis of leukocytes (CD45+) and granulocytes (CD45+CD15+) using flow cytometry. RESULTS: Median fluorescent intensity (MFI) of Lac increased from pre (64,268 ± 46,036 MFI) to post (117,134 ± 88,115 MFI) exercise (p <0.05). Lys MFI decreased with exercise (pre: 16,933 ± 8249; post: 11,616 ± 6875) (p <0.05). CONCLUSION: Acute running resulted in an increased Lac concentration which could lead to a decrease in inflammation, adding further evidence of the anti-inflammatory effects of exercise. Conversely, the exercise-associated decrease of intracellular Lys content could be the cause of increased Lys in exocrine solutions.

Bovine colostrum supplementation does not affect plasma I-FABP concentrations following exercise in a hot and humid environment.

PURPOSE: To quantify the impact of a 14-day bovine colostrum (BC) supplementation on intestinal cell damage following exercise in a hot and humid environment. METHODS: Ten male participants (20 ± 2 years, VO2max 55.80 ± 3.79 mL kg-1 min-1, 11.81 ± 2.71% body fat) ran for 46 ± 7.75 min at 95% of ventiliatory threshold in 40 °C and 50% RH following a 14-day double-blinded supplementation with either BC or placebo (Plac). Core temperature, skin temperature, heart rate, and rating of perceived exertion were recorded every 5 min during exercise. Blood was taken pre, post, 1 h, and 4 h post exercise. Intestinal cell damage was assessed via intestinal fatty acid binding protein (I-FABP). RESULTS: I-FABP concentrations were similar between conditions at all time points [pre 989.39 ± 490.88 pg ml-1 (BC) 851.35 ± 450.71 pg ml-1 (Plac) post 1505.10 ± 788.63 pg ml-1 (BC) 1267.12 ± 521.51 pg ml-1 (Plac) 1-h, 1087.77 ± 397.06 pg ml-1 (BC) 997.25 ± 524.74 pg ml-1 (Plac) 4-h, 511.35 ± 243.10 pg ml-1 (BC) 501.46 ± 222.54 pg ml-1 (Plac)]. I-FABP was elevated pre to post exercise for both BC (162 ± 50%) and Plac (162 ± 56%) (p < 0.05). BC had no effect on mean body temperature [beginning 36.11 ± 0.30 °C, ending: 39.52 ± 0.28 °C (BC); beginning:35.96 ± 0.43 °C, ending:39.42 ± 0.38 °C (Plac)]. CONCLUSIONS: While BC supplementation may protect against enterocyte damage during exercise in thermonuetral environments, our data suggest that BC supplementation may not be an effective technique for preventing enterocyte damage during exercise when core temperature exceeds 39 °C.

Exercise does not increase salivary lymphocytes, monocytes, or granulocytes, but does increase salivary lysozyme.

An increase in salivary leukocytes may contribute to the exercise-induced increase in salivary antimicrobial proteins (AMPs). However, exercise-induced changes in salivary leukocytes have not been studied. The purpose of the study was to describe salivary leukocyte changes with exercise. Participants (n = 11, 20.3 ± 0.8 years, 57.2 ± 7.6 ml kg-1 min-1 peak oxygen uptake ((VO) ̇2peak), 11.1 ± 3.9% body fat) ran for 45 min at 75% of VO2peak. Stimulated saliva (12 mL) was collected pre- and immediately post exercise. Saliva was filtered through a 30 µm filter before analysis of leukocytes (CD45+), granulocytes (CD45+CD15+), monocytes (CD45+CD14+), T-cells (CD45+CD3+), and B-cells (CD45+CD20+) using flow cytometry. Saliva was analysed for Lysozyme (Lys) using ELISA. Exercise did not alter any leukocyte subset. The major constituent of leukocytes pre-exercise were granulocytes (57.9 ± 30.3% compared with monocytes: 5.1 ± 2.7%, T-cells: 17.1 ± 8.9%, B-cells: 12.1 ± 10.2%) (P < 0.05). In a subset of n = 6, Lys secretion rate increased after exercise (pre: 5,170 ± 5,215 ng/min; post: 7,639 ± 4,140 ng/min) (P < 0.05). Exercise does not result in increased granulocytes, but does increase Lys. Further, these data suggest that an increase in salivary leukocytes is not needed to increase Lys.

Effects of Exercise Induced Dehydration and Glycerol Rehydration on Anaerobic Power in Male Collegiate Wrestlers.

McKenna, ZJ and Gillum, TL. Effects of exercise induced dehydration and glycerol rehydration on anaerobic power in male collegiate wrestlers. J Strength Cond Res 31(11): 2965-2968, 2017-Wrestlers attempting to reach a specific weight class often use rapid weight loss (RWL). Rapid weight loss is associated with high levels of dehydration, which may hinder athletic performance. Thus, there is a need for wrestlers to optimize rehydration after achieving a specific weight. We sought to observe the effects of RWL on anaerobic power and the impact of glycerol on rehydration and power in male collegiate wrestlers (n = 7, 19.75 ± 1.67 years, 76.8 ± 4.32 kg, 11.6 ± 4.32% body fat, 59.9 ± 6.42 ml·kg·min). Subjects were assessed for body mass (BM), hydration, and mean power output (Wmean) before exercise (pre), immediately after exercise (3% dehydrated), and 60 minutes after exercise (rehydrated). Participants ran at 70% of V[Combining Dot Above]O2max in a heated room (30° C) until 3% BM loss (BML). Subjects rehydrated drinking either 26 ml·kg of water (control) or a 3% glycerol (treatment) solution containing 26 ml·kg of water and 1 g·kg of glycerol. Participants lost 3.00 ± 0.31% (control) and 2.89 ± 0.26% (treatment) of their BM from the pre- to dehydrated conditions. Wmean (control: 659.29 ± 79.12, 651.43 ± 70.71, 659.71 ± 82.78; treatment: 647.71 ± 110.64, 644.57 ± 118.15, 638.14 ± 100.71) did not differ across time (p = 0.87) nor condition (p = 0.80). In addition, glycerol had no significant impact on acute hydration (control: urine-specific gravity [SG] = 1.019 ± 0.010; treatment: SG = 1.017 ± 0.017). These data show that 3% BML did not impair anaerobic performance, and furthermore that glycerol proved ineffective for rehydration in a match like scenario for the competing wrestler.

"Functional" Respiratory Muscle Training During Endurance Exercise Causes Modest Hypoxemia but Overall is Well Tolerated.

A novel commercial training mask purportedly allows for combined respiratory muscle training and altitude exposure during exercise. We examined the mask's ability to deliver on this claim. Ten men completed three bouts of treadmill exercise at a matched workload (60%VO2peak) in a controlled laboratory environment. During exercise, the mask was worn in 2 manufacturer-defined settings (9,000 ft [9K] and 15,000 ft [15K]) and a Sham configuration (∼3,500 ft). Ventilation (V(E)), tidal volume (V(T)), respiratory rate (R(R)), expired oxygen (F(E)O2) and carbon dioxide (F(E)CO2), peripheral oxygen saturation (S(P)O2), heart rate, and RPE were measured each minute during exercise, and subjects completed the Beck Anxiety Inventory (BAI) immediately after. The mask caused a reduction in V(E) of ∼20 L/min in both the 9K and 15K configurations (p < 0.001). This was due to a reduction in R(R) of ∼10 b·min, but not V(T), which was elevated by ∼250 ml (p < 0.001). F(E)O2 was reduced and F(E)CO2 was elevated above Sham in both 9K and 15K (p < 0.001). VO2 was not different across conditions (p = 0.210), but VCO2 trended lower at 9K (p = 0.093) and was reduced at 15K (p = 0.016). V(E)/VO2 was 18.3% lower than Sham at 9K and 19.2% lower at 15K. V(E)/VCO2 was 16.2% lower than Sham at 9K and 18.8% lower at 15K (all p < 0.001). Heart rate increased with exercise (p < 0.001) but was not different among conditions (p = 0.285). S(P)O2 averaged 94% in Sham, 91% at 9K, and 89% at 15K (p < 0.001). RPE and BAI were also higher in 9K and 15K (p < 0.010), but there was no difference among mask conditions. The training mask caused inadequate hyperventilation that led to arterial hypoxemia and psychological discomfort, but the magnitude of these responses were small and they did not vary across mask configurations.

Dietary nitrate reduces the O2 cost of desert marching but elevates the rise in core temperature.

PURPOSE: Dietary nitrate (NO3 (-)) supplementation reduces the O2 cost of fixed-workload tasks performed in temperate environments but has not been examined in the heat. If this effect were retained it could reduce heatstroke risk in military personnel that are deployed for desert combat. METHODS: Nine men completed three 45 min loaded battle marches at a standard cadence (4.83 km h(-1)/1.5 % grade) while wearing full combat gear [BDU, boots, body armor (8 kg), NBC suit] and carrying a loaded rucksack (16 kg). The 1st March (FAM) commenced in a temperate environment. The 2nd and 3rd commenced in simulated dry desert conditions (41 °C/20 % RH) and required subjects to ingest the beetroot juice equivalent of 8.4 mmol NO3 (-) (BRJ) or a NO3 (-) depleted placebo (PLA) for 6 days prior. VO2, VCO2, V E, core (T re), skin (T sk), and mean body (T b) temperatures, HR, and physiological strain index (PSI) were measured continuously. Thermal sensation, generalized discomfort, and perceived exertion (RPE) were measured at 5 min intervals. Heat storage (HS) was calculated. Blood markers of gastrointestinal permeability (TNF, Il-6, HO-1) were measured before and after exercise. RESULTS: VO2 in BRJ was lower than PLA from 1 to 12; 16 to 26; and 29 to 45 min of exercise (p < 0.05). VCO2 in BRJ was lower than PLA from 1 to 12 min (p < 0.05). V E in BRJ was lower than PLA from 1 to 20 min of exercise (p < 0.05). T re and T b in BRJ exceeded PLA from 16 to 45 min (p < 0.05). TNF, Il-6, and HO-1 were reduced in BRJ (p < 0.05) while HR, PSI, Tsk, and HS were not altered (p > 0.05). Thermal sensation, generalized discomfort, and RPE were elevated in BRJ from 40 to 45, 25 to 45, and 10 to 45 min, respectively (p < 0.01). CONCLUSION: Metabolic efficiency was improved in BRJ. Paradoxically, body temperatures rose more. This was not due to gut permeability. Therefore, we speculate that based on elimination of other possibilities, blood redistribution from skin to skeletal muscle may have contributed to impaired heat exchange.

Manipulation of step height and its effect on lactate metabolism during a one-minute anaerobic step test.

The purpose of this study was to observe the effects of the 1-minute anaerobic step test on lactate production. In addition, a comparison of postexercise lactate levels between the traditional 40-cm step height and a modified 20-cm step height was tested along with multiple biomechanical components such as torque, knee angle, and power. A convenience sample of 9 healthy moderately trained individuals were recruited for this experiment. Each subject performed the 1-minute anaerobic step test in a counterbalanced, crossover, and repeated-measures design. They performed 2 trials, 1 with a 40-cm step height and another with a 20-cm step height. Results showed statistical significance in terms of the postexercise lactate concentration (40 cm: 8.04 ± 2.13 mmol·L(-1); 20 cm: 6.18 ± 2.62 mmol·L(-1)) and lactate production (40 cm: 5.36 ± 2.73 mmol·L(-1); 20 cm: 3.06 ± 2.96 mmol·L(-1)) between the 2 step heights (p ≤ 0.05). With a lowered step height, the moment arm decreased significantly, which lowered the torque placed on the knee joint. Knee angle and power both decreased with a lowered step height of 20 cm. These results suggest that the 1-minute anaerobic step test is effective at eliciting lactate and can be used as an anaerobic exercise modality to train the anaerobic energy system. Furthermore, a step height of 40 cm seemed to be more effective at taxing the anaerobic energy system and eliciting lactate compared with a step height of 20 cm.

Exercise, but not acute sleep loss, increases salivary antimicrobial protein secretion.

Sleep deficiencies may play a role in depressing immune parameters. Little is known about the impact of exercise after sleep deprivation on mucosal immunity. The purpose of this study was to quantify salivary antimicrobial proteins (AMPs) in response to sleep loss before and after exercise. Four men and 4 women (age: 22.8 ± 2; : 49.1 ± 7.1 ml · kg(-1) · min(-1)) completed 2 exercise trials consisting of 45 minutes of running at 75% VO2peak after a normal night of sleep (CON) and after a night without sleep (WS). Exercise trials were separated by 10 ± 3 days. Saliva was collected before, immediately after, and 1 hour after exercise. LL-37, HNP1-3, Lactoferrin (Lac), and Lysozyme (Lys) were measured. Sleep loss did not affect the concentration or secretion rate of AMPs before or in response to exercise. However, exercise increased the concentration from pre- to post-exercise of LL-37 (pre: 15.5 ± 8.7; post: 22.3 ± 16.2 ng · ml(-1)), HNP1-3 (pre: 2.2 ± 2.3; post: 3.3 ± 2.5 µg · ml(-1)), Lac (pre: 5,234 ± 4,202; post: 12,283 ± 10,995 ng · ml(-1)), and Lys (pre: 5,831 ± 4,465; post: 12,542 ± 10,755 ng · ml(-1)), p <= 0.05. The secretion rates were higher immediately after and 1 hour after exercise compared with before exercise for LL-37 (pre: 3.1 ± 2.1; post: 5.1 ± 3.7; +1: 6.9 ± 8.4 ng · min(-1)), HNP1-3 (pre: 0.38 ± 0.38; post: 0.80 ± 0.75; +1: 0.84 ± 0.67 µg · min(-1)), Lac (pre: 1,096 ± 829; post: 2,948 ± 2,923; +1: 2,464 ± 3,785 ng · min(-1)), and Lys (pre: 1,534 ± 1,790; post: 3,042 ± 2,773; +1: 1,916 ± 1,682 ng · min-(1)), p <= 0.05. These data suggest that the major constituents of the mucosal immune system are unaffected by acute sleep loss and by exercise after acute sleep loss. Exercise increased the concentration and secretion rate of each AMP suggesting enhanced immunity and control of inflammation, despite limited sleep.

The effects of exercise, sex, and menstrual phase on salivary antimicrobial proteins.

Salivary antimicrobial protein (AMP) expression is a primary determinant of mucosal immunity. This expression can be altered by exercise. While salivary IgA has been extensively studied, less is known about Lysozyme (Lys) and Lactoferrin (Lac). Knowledge on how sex and menstrual phase affect mucosal immunity is also limited. The purpose of this study was to examine how sex, menstrual phase, and exercise impact IgA, Lys, and Lac expression. Men (n = 9) and women (n = 9) ran for 45 min at 75% VO2(peak). Women were tested in the follicular and luteal phase. Saliva was collected pre-exercise, immediately post-exercise and 1 h postexercise. Pre-exercise, women had higher secretion rates of IgA compared to men (154 +/- 106 vs 85 +/- 44 microg/min) (p < 0.05). Lac secretion rate increased with exercise in both sexes and remained above baseline 1 h after exercise in men (7460 +/- 4839 ng/min), but had returned to pre-exercise levels at 1 h post-exercise in women (5720 +/- 4661 ng/min) (time * sex interaction, p < 0.05). Men had higher secretion rates of Lys (p < 0.05) at each time point compared to women (Men pre-exercise: 31042 +/- 23132, post-exercise: 29521 +/- 13205, 1 h post-exercise: 41229 +/- 31270 ng/min vs Women pre-exercise: 11585 +/- 10367, post-exercise: 22719 +/- 19452, 1 h post-exercise: 17303 +/- 11419 ng/min). Both sexes increased the secretion rate of Lys and Lac with exercise, whereas IgA was unchanged. Menstrual phase did not affect IgA, Lys, or Lac and men and women did not differ in saliva flow rates. In conclusion, regularly menstruating women who are not taking hormonal contraceptives differently express AMPs compared to men.

Exercise induced plasma volume expansion lowers cardiovascular strain during 15-km cycling time-trial in acute normobaric hypoxia.

The purpose of our study was to assess the influence of a single high-intensity interval exercise (HIIE) bout in normoxia on plasma volume (PV) and consequent cycling performance in normobaric hypoxia (0.15 FiO2, simulating ~2,500 m). Eight males (VO2peak: 48.8 ± 3.4 mL/kg/min, 24.0 ± 1.6 years) completed a hypoxic 15 km cycling time trial (TT), followed by a crossover intervention of either HIIE (8x4 min cycling bouts at 85% of VO2peak) or CON (matched kJ production from HIIE at 50% of VO2peak). 48 hours post intervention, an identical TT was performed. Cardiovascular parameters were measured via impedance cardiography during each TT. Changes in PV was measured 24 and 48 hours post HIIE and CON. HIIE increased PV at 24 (4.1 ± 3.9%, P = 0.031) and 48 (6.7 ± 1.7, P = 0.006) hours post, while no difference was observed following the CON (1.3 ± 1.1% and 0.3 ± 2.8%). The higher PV led to an increased stroke volume (P = 0.03) and cardiac output (P = 0.02) during the hypoxic TT, while heart rate was not changed (P = 0.49). We observed no changes in time to completion (-0.63 ± 0.57 min, P = 0.054) and power output (7.37 ± 7.98 W, P = 0.078) between TTs. In the absence of environmental stress, a single bout of HIIE was an effective strategy to increase PV and reduce the cardiovascular strain during a cycling TT at moderate simulated altitude but did not impact hypoxic exercise performance. Trial registration: Clinical Trials ID: NCT05800808.

Repeated short cold-water immersions are sufficient to habituate to the cold, but do not lead to adaptations during exercise in normobaric hypoxia.

We sought to assess the effects of repeated cold-water immersions (CWI) on respiratory, metabolic, and sympathoadrenal responses to graded exercise in hypoxia. Sixteen (2 female) participants (age: 21.2 ± 1.3 years; body fat: 12.3 ± 7.7%; body surface area 1.87 ± 0.16 m2, VO2peak: 48.7 ± 7.9 mL/kg/min) underwent 6 CWI in 12.0 ± 1.2 °C. Each CWI was 5 min, twice daily, separated by ≥4 h, for three consecutive days, during which metabolic data were collected. The day before and after the repeated CWI intervention, participants ran in normobaric hypoxia (FIO2 = 0.135) for 4 min at 25%, 40%, 60%, and 75% of their sea level peak oxygen consumption (VO2peak). CWI had no effect on VO2 (p > 0.05), but reduced the VE (CWI #1: 27.1 ± 17.8 versus CWI #6: 19.9 ± 12.1 L/min) (p < 0.01), VT (CWI #1: 1.3 ± 0.4 vs CWI #6: 1.1 ± 0.4 L) (p < 0.01), and VE:VO2 (CWI #1: 53.5 ± 24.1 vs CWI #6: 41.6 ± 20.5) (p < 0.01) during subsequent CWI. Further, post exercise plasma epinephrine was lower after CWI compared to before (103.3 ± 43.1; 73.4 ± 34.6 pg/mL) (p = 0.03), with no change in pre-exercising values (75.4 ± 30.7; 72.5 ± 25.9 pg/mL). While these changes were noteworthy, it is important to acknowledge there were no changes in pulmonary (VE, VT, and VE:VO2) or metabolic (VO2, SmO2, and SpO2) variables across multiple hypoxic exercise workloads following repeated CWI. CWI habituated participants to cold water, but this did not lead to adaptations during exercise in normobaric hypoxia.

Caffeine has no effect on submaximal running in hypoxia in low caffeine consuming males and females.

BACKGROUND: Exposure to hypoxia immediately challenges a variety of physiologic systems that limit exercise capacity. Under normoxia, caffeine (CAFF) increases ventilation and subsequent oxygenation of hemoglobin (SpO2) and skeletal muscle (SmO2). CAFF improves exercise performance at altitude. However, little attention has been given to submaximal exercise in hypoxia, particularly regarding low CAFF consumers and female participants. The aim of this study was to determine the effect of CAFF on pulmonary, metabolic, and perceptual variables in response to submaximal running in hypoxia in low CAFF consuming males and females. METHODS: In a double blinded, counterbalanced design, 14 (6 females) individuals (24.1±5.1 years; VO2max: 40.6±5.6 mL × kg-1 × min-1; 20.8±8.0% body fat), who habitually consumed ≤150 mg/day of CAFF performed treadmill running at workloads of 25%, 40%, 60%, and 75% of sea level VO2max in normobaric hypoxia (FIO2=0.15) on two separate occasions: 1) 60 minutes after 6 mg/kg of CAFF; or 2) placebo. RESULTS: CAFF had no effect on any variable measured. Specifically, VE (condition: P=0.12; interaction: P=0.19), VT (condition: P=0.16; interaction: P=0.57), and Ve:VO2 (condition: P=0.07; interaction: P=0.69) were similar between groups. Further, CAFF had no effect on relative VO2 (condition: P=0.84; interaction: P=0.95), HR (condition: P=0.28; interaction: P=0.35), SmO2 (condition: P=0.66; interaction: P=0.82), or SpO2 (condition: P=0.16; interaction: P=0.97). Finally, rating of perceived exertion (RPE; P=0.92) and acute mountain sickness scores (P=0.29) were similar across conditions. CONCLUSIONS: These data demonstrate that CAFF provides no physiologic advantage to submaximal exercise in acute, normobaric hypoxia with low CAFF consuming males and females.

Effect of Combined Grape Seed Extract and L-Citrulline Supplementation on Hemodynamic Responses to Exercise in Young Males.

Grape seed extract (GSE) or L-citrulline supplement has been known to increase nitric oxide (NO) bioavailability and enhance endothelial-mediated vasodilation. Accordingly, to examine the additive benefits of combination of the two supplementations on hemodynamic responses to dynamic exercise, young, healthy males were recruited for this study. Effects of 7 days of 1) GSE + L-citrulline, 2) GSE, 3) L-citrulline, and 4) placebo supplementation on systolic blood pressure (SBP), diastolic blood pressure (DBP), mean arterial blood pressure (MAP), cardiac output, total vascular conductance (TVC), and oxygen (O2) consumption were examined at rest and during cycling exercise. Compared with placebo, GSE, L-citrulline, and combined supplementations did not reduce SBP, DBP, and MAP, while cardiac output (placebo; 23.6 ± 1.3 L/min, GSE; 25.7 ± 1.1 L/min; L-citrulline, 25.2 ± 1.2 L/min; GSE + L-citrulline; 25.3 ± 0.9 L/min) and TVC (placebo; 234.7 ± 11.3 ml/min/mmHg, GSE; 258.3 ± 10.6 ml/min/mmHg; L-citrulline, 255.2 ± 10.6 ml/min/mmHg; GSE + L-citrulline; 260.4 ± 8.9 ml/min/mmHg) were increased at only the 80% workload (p < 0.05). Compared with placebo and L-citrulline, GSE and combined supplementations had a reduction in VO2 across workloads (p < 0.05). However, there was no additive benefits on these variables. We conclude that supplementation with GSE, L-citrulline, and combined supplementations increased cardiac output due partially to decreased vascular resistance. Our findings suggest that GSE may act as an ergogenic aid that can improve O2 delivery to exercising muscles.

Ibuprofen Increases Markers of Intestinal Barrier Injury But Suppresses Inflammation at Rest and After Exercise in Hypoxia.

PURPOSE: The purpose of this study was to evaluate the effects of acute ibuprofen consumption (2 × 600-mg doses) on markers of enterocyte injury, intestinal barrier dysfunction, inflammation, and symptoms of gastrointestinal (GI) distress at rest and after exercise in hypobaric hypoxia. METHODS: Using a randomized double-blind placebo-controlled crossover design, nine men (age, 28 ± 3 yr; weight, 75.4 ± 10.5 kg; height, 175 ± 7 cm; body fat, 12.9% ± 5%; V̇O 2 peak at 440 torr, 3.11 ± 0.65 L·min -1 ) completed a total of three visits including baseline testing and two experimental trials (placebo and ibuprofen) in a hypobaric chamber simulating an altitude of 4300 m. Preexercise and postexercise blood samples were assayed for intestinal fatty acid binding protein (I-FABP), ileal bile acid binding protein, soluble cluster of differentiation 14, lipopolysaccharide binding protein, monocyte chemoattractant protein-1, tumor necrosis factor α (TNF-α), interleukin-1ß, and interleukin-10. Intestinal permeability was assessed using a dual sugar absorption test (urine lactulose-to-rhamnose ratio). RESULTS: Resting I-FABP (906 ± 395 vs 1168 ± 581 pg·mL -1 ; P = 0.008) and soluble cluster of differentiation 14 (1512 ± 297 vs 1642 ± 313 ng·mL -1 ; P = 0.014) were elevated in the ibuprofen trial. Likewise, the urine lactulose-to-rhamnose ratio (0.217 vs 0.295; P = 0.047) and the preexercise to postexercise change in I-FABP (277 ± 308 vs 498 ± 479 pg·mL -1 ; P = 0.021) were greater in the ibuprofen trial. Participants also reported greater upper GI symptoms in the ibuprofen trial ( P = 0.031). However, monocyte chemoattractant protein-1 ( P = 0.007) and TNF-α ( P = 0.047) were lower throughout the ibuprofen trial compared with placebo (main effect of condition). CONCLUSIONS: These data demonstrate that acute ibuprofen ingestion aggravates markers of enterocyte injury and intestinal barrier dysfunction at rest and after exercise in hypoxia. However, ibuprofen seems to suppress circulating markers of inflammation.