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.

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.

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.

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.

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 combined histamine H1 and H2 receptor blockade on hemodynamic responses to dynamic exercise in males with high-normal blood pressure.

While postexercise hypotension is associated with histamine H1 and H2 receptor-mediated postexercise vasodilation, effects of histaminergic vasodilation on blood pressure (BP) in response to dynamic exercise are not known. Thus, in 20 recreationally active male participants (10 normotensive and 10 with high-normal BP) we examined the effects of histamine H1 and H2 receptor blockade on cardiac output (CO), mean atrial pressure (MAP), aortic stiffness (AoStiff), and total vascular conductance (TVC) at rest and during progressive cycling exercise. Compared with the normotensive group, MAP, CO, and AoStiff were higher in the high-normal group before and after the blockade at rest, while TVC was similar. At the 40% workload, the blockade significantly increased MAP in both groups, while no difference was found in the TVC. CO was higher in the high-normal group than the normotensive group in both conditions. At the 60% workload, the blockade substantially increased MAP and decreased TVC in the normotensive group, while there were no changes in the high-normal group. A similar CO response pattern was observed at the 60% workload. These findings suggest that the mechanism eliciting an exaggerated BP response to exercise in the high-normal group may be partially due to the inability of histamine receptors. Novelty Males with high-normal BP had an exaggerated BP response to exercise. The overactive BP response is known due to an increase in peripheral vasoconstriction. Increase in peripheral vasoconstriction is partially due to inability of histamine receptors.

Prolonged treadmill running in normobaric hypoxia causes gastrointestinal barrier permeability and elevates circulating levels of pro- and anti-inflammatory cytokines.

This study examined the impact of treadmill running in normobaric hypoxia on gastrointestinal barrier permeability and the systemic inflammatory response. Ten recreationally active participants completed two 1-h bouts of matched-workload treadmill exercise (65% normoxic maximal oxygen consumption) in counterbalanced order. One bout was performed in normoxia (NORM: fraction of inspired oxygen (FIO2) = 20.9%) and the other in normobaric hypoxia (HYP: FIO2 = 13.5%). Minute ventilation, respiratory rate (RR), tidal volume (VT), oxygen consumption, carbon dioxide production, respiratory exchange ratio (RER), and heart rate (HR) were measured with a metabolic cart. Peripheral oxygen saturation (SpO2) was measured with pulse oximetry. Absolute tissue saturation (StO2) was measured with near-infrared spectroscopy. Fatty acid-binding protein (I-FABP) and circulating cytokine concentrations (interleukin (IL)-1Ra, IL-6, IL-10) were assayed from plasma samples that were collected pre-exercise, postexercise, 1 h-postexercise, and 4 h-postexercise. Data were analyzed with 2-way (condition × time) repeated-measures ANOVAs. Newman-Keuls post hoc tests were run where appropriate (p < 0.05). As compared with NORM, 1 h of treadmill exercise in HYP caused greater (p < 0.05) changes in minute ventilation (+30%), RR (+16%), VT (+10%), carbon dioxide production (+18%), RER (+16%), HR (+4%), SpO2 (-16%), and StO2 (-10%). Gut barrier permeability and circulating cytokine concentrations were also greater (p < 0.05) following HYP exercise, where I-FABP was shown increased at postexercise (+68%) and IL-1Ra at 1 h-postexercise (+266%). I-FABP and IL-1Ra did not change (p > 0.05) following NORM exercise. IL-6 and IL-10 increased with exercise in both study conditions but were increased more (p < 0.05) following HYP at postexercise (+705% and +127%, respectively) and 1 h-postexercise (+400% and +128%, respectively). Novelty Normobaric hypoxia caused significant desaturation and increased most cardiopulmonary responses by 10%-30%. Significant gut barrier permeability and increased pro- and anti-inflammatory cytokine concentrations could promote an "open window" in the hours following HYP exercise.

Reduced inflammatory and phagocytotic responses following normobaric hypoxia exercise despite evidence supporting greater immune challenge.

This study examined changes in immune markers following sustained treadmill exercise in normobaric hypoxia. Ten subjects performed 1 h of treadmill exercise (65% maximal oxygen uptake) under normoxic (NORM: fraction of inspired oxygen (FIO2) = 20.9%) and normobaric hypoxic (HYP: FIO2 = 13.5%) conditions. Blood samples, collected before, after (Post), 1 h after (1-Post), and 4 h after (4-Post) exercise, were assayed for plasma cytokines (interleukin (IL)-1RA/IL-1ß/IL-8/tumor necrosis factor alpha (TNF-α)) and markers of leukocyte activation (macrophage inflammatory protein-1ß (MIP-1ß)/myeloperoxidase (MPO)/soluble intercellular adhesion molecule-1 (sICAM-1)) using ELISA. Pro- to anti-inflammatory cytokine ratios (TNF-α/IL-1RA; IL-1ß/IL-1RA) were calculated. Peripheral blood mononuclear cells (PBMC) were analyzed for changes in inflammatory status (phosphorylated nuclear factor kappa B/nuclear factor kappa B) using Western Blot. Data were analyzed with 2-way (condition × time) repeated-measure ANOVAs with Newman-Keuls post hoc tests. MIP-1ß was elevated at 1-Post HYP exercise (+11%; p < 0.01) but did not increase following exercise in NORM. TNF-α/IL-1RA and IL-1ß/IL-1RA ratios were both reduced (p < 0.05) following HYP exercise (-16% and -52%, respectively, at 1-Post and -7% and -32%, respectively, at 4-Post). IL-8 increased (p < 0.05) at Post and 1-Post NORM (+33% and +57%, respectively) and HYP (+60% and +83%, respectively) exercise, but was not different between conditions (p > 0.05). Interestingly, plasma sICAM-1 did not increase (p > 0.05) following NORM exercise but was increased (p < 0.05) at Post (+17%), 1-Post (+16%), and 4-Post (+14%) HYP exercise. There was also a delayed peak in plasma MPO concentrations following HYP exercise and PBMC exhibited a reduced (p < 0.05) inflammatory capacity at Post (-38%) and 1-Post (-49%). Novelty Following HYP exercise, participants exhibited (i) circulatory bias towards anti-inflammation; (ii) elevated sICAM; (iii) delayed peak in plasma MPO; and (iv) diminished inflammatory response in PBMC. Collectively, these data suggest immunosuppression. This is undesirable, given that elevated MIP-1ß (reported here) and elevated intestinal fatty acid binding protein (reported previously) both suggest higher lipopolysaccharide concentrations following HYP exercise.

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.

Heat acclimation increases inflammatory and apoptotic responses to subsequent LPS challenge in C2C12 myotubes.

This work investigated the ability of a 6-day heat acclimation protocol to impart heat acclimation-mediated cross-tolerance (HACT) in C2C12 myotubes, as indicated by changes in inflammatory and apoptotic responses to subsequent lipopolysaccharide (LPS) challenge. Myotubes were incubated at 40 °C for 2 h/day over 6 days (HA) or maintained for 6 days at 37 °C (C). Following 24 h recovery, myotubes from each group received either no stimulation or 500 ng/ml LPS for 2 h (HA + LPS and C + LPS, respectively). Cell lysates were collected and analyzed for protein markers of the heat shock response, inflammation, and apoptosis. As compared to C, HA exhibited an elevated heat shock response [HSP70 (+ 99%); HSP60 (+ 216%); HSP32 (+ 40%); all p < 0.01] and reduced inflammatory and apoptotic signaling [p-NF-ĸB:NF-ĸB (- 99%%); p-JNK (- 49%); all p < 0.01]. When compared to C + LPS, HA + LPS also exhibited an elevated heat shock response [HSP70 (+ 68%); HSP60 (+ 32%); HSP32 (+ 38%); all p < 0.01]. However, inflammatory and apoptotic responses in HA + LPS were increased [p-IKBa:IKBa (+ 432%); p-NF-ĸB:NF-ĸB (+ 283%); caspase-8p18 (+ 53%); p-JNK (+ 41%); all p < 0.05]. This unanticipated finding may be due to increased TLR4-mediated signaling capacity in HA + LPS, as indicated by upregulation of TLR4 [(+ 24%); MyD88 (+ 308%); p-NIK (+ 199%); and p-IKKα/b (+ 81%); all p < 0.05]. Data suggest HA reduces inflammatory and apoptotic signaling in skeletal muscle cells that are maintained under basal conditions. However, HACT is selective and does not apply to TLR4 signaling in the present model.

Heat acclimation increases mitochondrial respiration capacity of C2C12 myotubes and protects against LPS-mediated energy deficit.

This work investigated the effect of a 6-day heat acclimation (HA) protocol on myotube metabolic responses at baseline and in response to a subsequent lipopolysaccharide (LPS) challenge. C2C12 myotubes were incubated for 2 h/day at 40 °C for 6 days (HA) or maintained at 37 °C (C). Following 24-h recovery, myotubes were challenged with 500 ng/ml LPS for 2 h, then collected for analysis of protein markers of mitochondrial biogenesis and macronutrient storage. Functional significance of these changes was confirmed with mitochondrial respiration and glycolytic measurements on a Seahorse XF-96 analyzer. HA stimulated mitochondrial biogenesis and increased indicators of mitochondrial content [SIRT1 (+ 62%); PGC-1α (+ 57%); NRF-1 (+ 40%); TFAM (+ 141%); CS (+ 25%); CytC (+ 38%); all p < 0.05]. Altered lipid biosynthesis enzymes [p-ACCa:ACC (+ 59%; p = 0.04) and FAS (- 86%; p < 0.01)] suggest fatty acid generation may have been downregulated, whereas increased GLUT4 (+ 69%; p < 0.01) and LDH-B (+ 366%; p < 0.01) suggest aerobic glycolytic capacity may have been improved. Mitochondrial biogenesis signaling in HA myotubes was suppressed by 500 ng/ml LPS (PGC-1α, NRF-1, TFAM; all p > 0.05) but increased LDH-B (+ 30%; p = 0.02) and CPT-1 (+ 55%; p < 0.01) suggesting improved catabolic function. Basal respiration was increased in HA myotubes (+ 8%; p < 0.01) and HA myotubes maintained elevated basal respiration during LPS challenge (+ 8%; p < 0.01). LPS reduced peak respiration in C myotubes (- 6%; p < 0.01) but did not impair peak respiration in HA myotubes (p > 0.05). Oxidative reliance was elevated in HA over that in control (+ 25%; p < 0.01) and in HA + LPS over C + LPS (+ 30%; p < 0.01). In summary, HA stimulated mitochondrial biogenesis in C2C12 myotubes. HA myotubes exhibited (1) elevated basal/peak mitochondrial respiration capacities; (2) greater oxidative reliance; and (3) protection against LPS-mediated respiration impairment. Collectively, these data suggest HA may improve aerobic metabolism in skeletal muscle and protect against LPS-mediated energy deficit.

Short-term dietary curcumin supplementation reduces gastrointestinal barrier damage and physiological strain responses during exertional heat stress.

Szymanski MC, Gillum TL, Gould LM, Morin DS, Kuennen MR. Short-term dietary curcumin supplementation reduces gastrointestinal barrier damage and physiological strain responses during exertional heat stress. J Appl Physiol 124: 330-340, 2018. First published September 21, 2017; doi: 10.1152/japplphysiol.00515.2017 .-This work investigated the effect of 3 days of 500 mg/day dietary curcumin supplementation on gastrointestinal barrier damage and systems-physiology responses to exertional heat stress in non-heat-acclimated humans. Eight participants ran (65% V̇o2max) for 60 min in a Darwin chamber (37°C/25% relative humidity) two times (Curcumin/Placebo). Intestinal fatty acid-binding protein (I-FABP) and associated proinflammatory [monocyte chemoattractant protein-1, tumor necrosis factor-α (TNF-α), interleukin-6] and anti-inflammatory [interleukin-1 receptor antagonist (IL-1RA), interleukin-10 (IL-10)] cytokines were assayed from plasma collected before (Pre), after (Post) and 1 (1-Post) and 4 (4-Post) h after exercise. Core temperature and HR were measured throughout exercise; the physiological strain index (PSI) was calculated from these variables. Condition differences were determined with 2-way (condition × time) repeated-measures ANOVAs. The interaction of condition × time was significant ( P = 0.05) for I-FABP and IL-1RA. Post hoc analysis indicated I-FABP increased more from Pre to Post (87%) and 1-Post (33%) in Placebo than in Curcumin (58 and 18%, respectively). IL-1RA increased more from Pre to 1-Post in Placebo (153%) than in Curcumin (77%). TNF-α increased ( P = 0.01) from Pre to Post (19%) and 1-Post (24%) in Placebo but not in Curcumin ( P > 0.05). IL-10 increased ( P < 0.01) from Pre to Post (61%) and 1-Post (42%) in Placebo not in Curcumin ( P > 0.05). The PSI, which indicates exertional heatstroke risk, was also lower ( P < 0.01) in Curcumin than Placebo from 40 to 60 min of exercise. These data suggest 3 days curcumin supplementation may improve gastrointestinal function, associated cytokines, and systems-level physiology responses during exertional heat stress. This could help reduce exertional heatstroke risk in non-heat-acclimated individuals. NEW & NOTEWORTHY Exercise-heat stress increases gastrointestinal barrier damage and risk of exertional heatstroke. Over the past decade at least eight different dietary supplements have been tested for potential improvements in gastrointestinal barrier function and systems-level physiology responses during exercise-heat stress. None have been shown to protect against both insults simultaneously. In this report 3 days of 500 mg/day dietary curcumin supplementation are shown to improve gastrointestinal barrier function, associated cytokine responses, and systems-level physiology parameters. Further research is warranted.

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.

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.

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.

Prohormone supplement 3ß-hydroxy-5α-androst-1-en-17-one enhances resistance training gains but impairs user health.

Prohormone supplements (PS) are recognized not to impart anabolic or ergogenic effects in men, but the research supporting these conclusions is dated. The Anabolic Steroid Control Act was amended in 2004 to classify androstenedione and 17 additional anabolic compounds as controlled substances. The viability of PS that entered the market after that time have not been evaluated. Seventeen resistance-trained men (23 ± 1 yr; 13.1 ± 1.5% body fat) were randomly assigned to receive either 330 mg/day of 3ß-hydroxy-5α-androst-1-en-17-one (Prohormone; n = 9) or sugar (Placebo; n = 8) per os and complete a 4-wk (16 session) structured resistance-training program. Body composition, muscular strength, circulating lipids, and markers of liver and kidney dysfunction were assessed at study onset and termination. Prohormone increased lean body mass by 6.3 ± 1.2%, decreased fat body mass by 24.6 ± 7.1%, and increased their back squat one repetition maximum and competition total by 14.3 ± 1.5 and 12.8 ± 1.1%, respectively. These improvements exceeded (P < 0.05) Placebo, which increased lean body mass by 0.5 ± 0.8%, reduced fat body mass by 9.5 ± 3.6%, and increased back squat one repetition maximum and competition total by 5.7 ± 1.7 and 5.9 ± 1.7%, respectively. Prohormone also experienced multiple adverse effects. These included a 38.7 ± 4.0% reduction in HDL (P < 0.01), a 32.8 ± 15.05% elevation in LDL (P < 0.01), and elevations of 120.0 ± 22.6 and 77.4 ± 12.0% in LDL-to-HDL and cholesterol-to-HDL ratios, respectively (both P < 0.01). Prohormone also exhibited elevations in serum creatinine (19.6 ± 4.3%; P < 0.01) and aspartate transaminase (113.8 ± 61.1%; P = 0.05), as well as reductions in serum albumin (5.1 ± 1.9%; P = 0.04), alkaline phosphatase (16.4 ± 4.7%; P = 0.04), and glomerular filtration rate (18.0 ± 3.3%; P = 0.04). None of these values changed (all P > 0.05) in Placebo. The oral PS 3ß-hydroxy-5α-androst-1-en-17-one improves body composition and muscular strength. However, these changes come at a significant cost. Cardiovascular health and liver function are particularly compromised. Given these findings, we feel the harm associated with this particular PS outweighs any potential benefit.

A review of sex differences in immune function after aerobic exercise.

When menstrual phase and oral contraceptives are controlled for, males and females display marked differences in immune response to an exercise stress. In highly controlled research studies, sex differences in immune cell changes, cytokine alterations, along with morbidity and mortality after inoculation are apparent. Exercise has been hypothesized to serve as a model of various clinical stresses by inducing similar hormonal and immunological alterations. Thus, a greater understanding of sex differences in post exercise non-specific immune function may provide insight into more effective clinical approaches and treatments. This paper reviews the recent evidence supporting sex differences in post exercise immune response and highlights the need for greater control when comparing the post exercise immune response between sexes.

Palm cooling to reduce heat strain in subjects during simulated armoured vehicle transport.

This study examined whether palm cooling (PC) could reduce heat strain, measured through changes in core, mean skin, mean body temperatures, and thermal sensation in resting hyperthermic subjects wearing chemical protective garments. Ten male subjects performed three exercise bouts (6.1 km h(-1), 2-4% grade) in a hot, dry environment [mean (SD) air temperature 42.2 (0.5 degrees C), relative humidity 36.5 (1%)] until core temperature reached 38.8 degrees C. Subjects then simulated transport in an armoured vehicle by resting in a seated position for 50 min with either no cooling (NC), (PC at 10 degrees C) or palm cooling with vacuum application around the hand (PCVAC, 10 degrees C, 7.47 kPa negative pressure). Core, skin, and mean body temperatures with PC and PCVAC were lower (P < 0.05) than NC from 15 to 50 min of cooling, and thermal sensation was lower (P < 0.05) from 30 to 50 min, with no differences in any variables between PC and PCVAC. Maximal heat extraction averaged 42 (12 W), and core temperature was reduced by 0.38 (0.21 degrees C) after 50 min of PC. Heat extraction with PC was modest compared to other cooling approaches in the literature.