Impact of nocturnal hypoxia on glycaemic control, appetite, gut microbiota and inflammation in adults with type 2 diabetes mellitus: A single-blind cross-over trial.

High altitude residents have a lower incidence of type 2 diabetes mellitus (T2DM). Therefore, we examined the effect of repeated overnight normobaric hypoxic exposure on glycaemic control, appetite, gut microbiota and inflammation in adults with T2DM. Thirteen adults with T2DM [glycated haemoglobin (HbA1c): 61.1 ± 14.1 mmol mol-1; aged 64.2 ± 9.4 years; four female] completed a single-blind, randomised, sham-controlled, cross-over study for 10 nights, sleeping when exposed to hypoxia (fractional inspired O2 [ F I O 2 ${{F}_{{\mathrm{I}}{{{\mathrm{O}}}_{\mathrm{2}}}}}$ ] = 0.155; ∼2500 m simulated altitude) or normoxic conditions ( F I O 2 ${{F}_{{\mathrm{I}}{{{\mathrm{O}}}_{\mathrm{2}}}}}$  = 0.209) in a randomised order. Outcome measures included: fasted plasma [glucose]; [hypoxia inducible factor-1α]; [interleukin-6]; [tumour necrosis factor-α]; [interleukin-10]; [heat shock protein 70]; [butyric acid]; peak plasma [glucose] and insulin sensitivity following a 2 h oral glucose tolerance test; body composition; appetite indices ([leptin], [acyl ghrelin], [peptide YY], [glucagon-like peptide-1]); and gut microbiota diversity and abundance [16S rRNA amplicon sequencing]. During intervention periods, accelerometers measured physical activity, sleep duration and efficiency, whereas continuous glucose monitors were used to assess estimated HbA1c and glucose management indicator and time in target range. Overnight hypoxia was not associated with changes in any outcome measure (P > 0.05 with small effect sizes) except fasting insulin sensitivity and gut microbiota alpha diversity, which exhibited trends (P = 0.10; P = 0.08 respectively) for a medium beneficial effect (d = 0.49; d = 0.59 respectively). Ten nights of overnight moderate hypoxic exposure did not significantly affect glycaemic control, gut microbiome, appetite, or inflammation in adults with T2DM. However, the intervention was well tolerated and a medium effect-size for improved insulin sensitivity and reduced alpha diversity warrants further investigation. KEY POINTS: Living at altitude lowers the incidence of type 2 diabetes mellitus (T2DM). Animal studies suggest that exposure to hypoxia may lead to weight loss and suppressed appetite. In a single-blind, randomised sham-controlled, cross-over trial, we assessed the effects of 10 nights of hypoxia (fractional inspired O2 ∼0.155) on glucose homeostasis, appetite, gut microbiota, inflammatory stress ([interleukin-6]; [tumour necrosis factor-α]; [interleukin-10]) and hypoxic stress ([hypoxia inducible factor 1α]; heat shock protein 70]) in 13 adults with T2DM. Appetite and inflammatory markers were unchanged following hypoxic exposure, but an increased insulin sensitivity and reduced gut microbiota alpha diversity were associated with a medium effect-size and statistical trends, which warrant further investigation using a definitive large randomised controlled trial. Hypoxic exposure may represent a viable therapeutic intervention in people with T2DM and particularly those unable or unwilling to exercise because barriers to uptake and adherence may be lower than for other lifestyle interventions (e.g. diet and exercise).

Inexperienced water users can "Float to Live" in realistic open water conditions.

BACKGROUND: The RNLI "Float to Live" campaign is based on research conducted in indoor pools with experienced open water swimmers. Study 1 investigated whether the RNLI "Float to Live" guidance would enable less experienced individuals to float in realistic open water conditions. Study 2 examined the separate effects of practice and coaching on floating competence. METHODS: Study 1: Inexperienced water users conducted floats in either still, open fresh (n = 22) or open sea water (n = 13), followed by moving sea (n = 6) or fresh water (n = 5). Participants undertook three 2-min floats in still water wearing swimwear and one clothed float: 1) naïve; 2) following RNLI "Float to live" messaging; 3) individual float coaching; 4) simulated fall wearing summer clothing. In moving sea water, participants undertook two floats equivalent to Floats 3 and 4. In moving fresh water, participants undertook 3 floats: 1) naïve; 2) following "defensive floating" coaching; 3) simulated fall wearing summer clothing. Study 2: Two groups matched for skinfold thickness undertook three 2-min floats in a flume wearing swimwear. PRAC group (n = 12): 1) naïve; 2) following float practice; 3) float coaching; COACH group (n = 11) coaching followed by practice. Floating difficulty, confidence, competence, "efficiency" and perceived exertion were analysed using either a Friedman test or mixed model ANOVA. RESULTS: In both fresh water and sea water, participants' floating competence and confidence increased after viewing the RNLI messaging, it was further improved with individualised float coaching. The additional helpful instructions included: 1) "head back with ears submerged"; 2) "relax"; 3) "breathe normally"; 4) "it is OK if your legs sink"; 5) an accurate description of sculling for "active" floaters that needed it; 6) spread arms and legs for stability. The simulated fall with clothing did not impair floating competence. No difference in floating competence was seen between PRAC and COACH, though confidence may be increased sooner in COACH. CONCLUSIONS: The RNLI float advice can be applied in realistic open water settings by less experienced water users. Additional content could be included to make the messaging even more effective.

Habituation of the cold shock response: A systematic review and meta-analysis.

Cold water immersion (CWI) evokes the life-threatening reflex cold shock response (CSR), inducing hyperventilation, increasing cardiac arrhythmias, and increasing drowning risk by impairing safety behaviour. Repeated CWI induces CSR habituation (i.e., diminishing response with same stimulus magnitude) after ∼4 immersions, with variation between studies. We quantified the magnitude and coefficient of variation (CoV) in the CSR in a systematic review and meta-analysis with search terms entered to Medline, SportDiscus, PsychINFO, Pubmed, and Cochrane Central Register. Random effects meta-analyses, including effect sizes (Cohen's d) from 17 eligible groups (k), were conducted for heart rate (HR, n = 145, k = 17), respiratory frequency (fR, n = 73, k = 12), minute ventilation (Ve, n = 106, k = 10) and tidal volume (Vt, n = 46, k=6). All CSR variables habituated (p < 0.001) with large or moderate pooled effect sizes: ΔHR -14 (10) bt. min-1 (d: -1.19); ΔfR -8 (7) br. min-1 (d: -0.78); ΔVe, -21.3 (9.8) L. min-1 (d: -1.64); ΔVt -0.4 (0.3) L -1. Variation was greatest in Ve (control vs comparator immersion: 32.5&24.7%) compared to Vt (11.8&12.1%). Repeated CWI induces CSR habituation potentially reducing drowning risk. We consider the neurophysiological and behavioural consequences.

The peripheral vascular responses in non-freezing cold injury and matched controls.

NEW FINDINGS: What is the central question of this study? Does non-freezing cold injury (NFCI) alter normal peripheral vascular function? What is the main finding and its importance? Individuals with NFCI were more cold sensitive (rewarmed more slowly and felt more discomfort) than controls. Vascular tests indicated that extremity endothelial function was preserved with NFCI and that sympathetic vasoconstrictor response might be reduced. The pathophysiology underpinning the cold sensitivity associated with NFCI thus remains to be identified. ABSTRACT: The impact of non-freezing cold injury (NFCI) on peripheral vascular function was investigated. Individuals with NFCI (NFCI group) and closely matched controls with either similar (COLD group) or limited (CON group) previous cold exposure were compared (n = 16). Peripheral cutaneous vascular responses to deep inspiration (DI), occlusion (PORH), local cutaneous heating (LH) and iontophoresis of acetylcholine and sodium nitroprusside were investigated. The responses to a cold sensitivity test (CST) involving immersion of a foot in 15°C water for 2 min followed by spontaneous rewarming, and a foot cooling protocol (footplate cooled from 34°C to 15°C), were also examined. The vasoconstrictor response to DI was lower in NFCI compared to CON (toe: 73 (28)% vs. 91 (17)%; P = 0.003). The responses to PORH, LH and iontophoresis were not reduced compared to either COLD or CON. During the CST, toe skin temperature rewarmed more slowly in NFCI than COLD or CON (10 min: 27.4 (2.3)°C vs. 30.7 (3.7)°C and 31.7 (3.9)°C, P < 0.05, respectively); however, no differences were observed during the footplate cooling. NFCI were more cold-intolerant (P < 0.0001) and reported colder and more uncomfortable feet during the CST and footplate cooling than COLD and CON (P < 0.05). NFCI showed a decreased sensitivity to sympathetic vasoconstrictor activation than CON and greater cold sensitivity (CST) compared to COLD and CON. None of the other vascular function tests indicated endothelial dysfunction. However, NFCI perceived their extremities to be colder and more uncomfortable/painful than the controls.

Peripheral sensory function in non-freezing cold injury patients and matched controls.

NEW FINDINGS: What is the central question of this study? Is peripheral sensory function impaired in the chronic phase of non-freezing cold injury (NFCI)? What is the main finding and its importance? Warm and mechanical detection thresholds are elevated and intraepidermal nerve fibre density is reduced in individuals with NFCI in their feet when compared to matched controls. This indicates impaired sensory function in individuals with NFCI. Interindividual variation was observed in all groups, and therefore a diagnostic cut-off for NFCI has yet to be established. Longitudinal studies are required to follow NFCI progression from formation to resolution ABSTRACT: The aim of this study was to compare peripheral sensory neural function of individuals with non-freezing cold injury (NFCI) with matched controls (without NFCI) with either similar (COLD) or minimal previous cold exposure (CON). Thirteen individuals with chronic NFCI in their feet were matched with the control groups for sex, age, race, fitness, body mass index and foot volume. All undertook quantitative sensory testing (QST) on the foot. Intraepidermal nerve fibre density (IENFD) was assessed 10 cm above the lateral malleolus in nine NFCI and 12 COLD participants. Warm detection threshold was higher at the great toe in NFCI than COLD (NFCI 45.93 (4.71)°C vs. COLD 43.44 (2.72)°C, P = 0.046), but was non-significantly different from CON (CON 43.92 (5.01)°C, P = 0.295). Mechanical detection threshold on the dorsum of the foot was higher in NFCI (23.61 (33.59) mN) than in CON (3.83 (3.69) mN, P = 0.003), but was non-significantly different from COLD (10.49 (5.76) mN, P > 0.999). Remaining QST measures did not differ significantly between groups. IENFD was lower in NFCI than COLD (NFCI 8.47 (2.36) fibre/mm2 vs. COLD 11.93 (4.04) fibre/mm2 , P = 0.020). Elevated warm and mechanical detection thresholds may indicate hyposensitivity to sensory stimuli in the injured foot for individuals with NFCI and may be due to reduced innervation given the reduction in IENFD. Longitudinal studies are required to identify the progression of sensory neuropathy from the formation of injury to its resolution, with appropriate control groups employed.

Plasma biomarkers of endothelial function, inflammation and oxidative stress in individuals with non-freezing cold injury.

NEW FINDINGS: What is the central question of this study? Are biomarkers of endothelial function, oxidative stress and inflammation altered by non-freezing cold injury (NFCI)? What is the main finding and its importance? Baseline plasma [interleukin-10] and [syndecan-1] were elevated in individuals with NFCI and cold-exposed control participants. Increased [endothelin-1] following thermal challenges might explain, in part, the increased pain/discomfort experienced with NFCI. Mild to moderate chronic NFCI does not appear to be associated with either oxidative stress or a pro-inflammatory state. Baseline [interleukin-10] and [syndecan-1] and post-heating [endothelin-1] are the most promising candidates for diagnosis of NFCI. ABSTRACT: Plasma biomarkers of inflammation, oxidative stress, endothelial function and damage were examined in 16 individuals with chronic NFCI (NFCI) and matched control participants with (COLD, n = 17) or without (CON, n = 14) previous cold exposure. Venous blood samples were collected at baseline to assess plasma biomarkers of endothelial function (nitrate, nitrite and endothelin-1), inflammation [interleukin-6 (IL-6), interleukin-10 (IL-10), tumour necrosis factor alpha and E-selectin], oxidative stress [protein carbonyl, 4-hydroxy-2-nonenal (4-HNE), superoxide dismutase and nitrotyrosine) and endothelial damage [von Willebrand factor, syndecan-1 and tissue type plasminogen activator (TTPA)]. Immediately after whole-body heating and separately, foot cooling, blood samples were taken for measurement of plasma [nitrate], [nitrite], [endothelin-1], [IL-6], [4-HNE] and [TTPA]. At baseline, [IL-10] and [syndecan-1] were increased in NFCI (P < 0.001 and P = 0.015, respectively) and COLD (P = 0.033 and P = 0.030, respectively) compared with CON participants. The [4-HNE] was elevated in CON compared with both NFCI (P = 0.002) and COLD (P < 0.001). [Endothelin-1] was elevated in NFCI compared with COLD (P < 0.001) post-heating. The [4-HNE] was lower in NFCI compared with CON post-heating (P = 0.032) and lower than both COLD (P = 0.02) and CON (P = 0.015) post-cooling. No between-group differences were seen for the other biomarkers. Mild to moderate chronic NFCI does not appear to be associated with a pro-inflammatory state or oxidative stress. Baseline [IL-10] and [syndecan-1] and post-heating [endothelin-1] are the most promising candidates for diagnosing NFCI, but it is likely that a combination of tests will be required.

Quantifying Risk in Air Sports: Flying Activity and Incident Rates in Paragliding.

INTRODUCTION: The volume, nature, and risks of paragliding are poorly quantified. More comprehensive understanding, including incident rates allowing comparison to similar disciplines, will help direct and appraise safety interventions. METHODS: Paraglider pilots were surveyed regarding experience, incidents, recordkeeping, and risk perception. The survey could not capture those who had left the sport or died, so a subset of responses from UK pilots was compared to records from an incident database. RESULTS: There were 1788 (25%) responses from 7262 surveyed. Respondents flew a total of 87,909 h in 96,042 flights during 2019. Local flying was most frequent (n=37,680 flights, 39%) but a higher proportion of hours were spent flying cross-country (n=33,933 h, 39%). The remainder were spent in competition, hike and fly, tandem, aerobatic, or instructional flight. Flying incidents led to 103 (6%) respondents seeking medical attention, attending hospital, or missing a day of work in 2019. Near misses were reported by 423 (26%) pilots. Asymmetry and rotational forces typically led to incidents, and limb and back injuries resulted. Pilots frequently failed to throw their reserve parachutes. Only 3 (0.6%) incidents involved equipment failure, with the remainder attributed to control or decision errors. Incident rates of paragliding were estimated as 1.4 (1.1-1.9) deaths and 20 (18-27) serious injuries per 100,000 flights, approximately twice as risky as general aviation and skydiving. CONCLUSIONS: Incidents usually resulted from pilot error (control and decision), rather than equipment failure. Future safety interventions should focus on improving glider control skills and encouraging reserve parachute deployment.

Previous recreational cold exposure does not alter endothelial function or sensory thermal thresholds in the hands or feet.

NEW FINDINGS: What is the central question of this study? Does recreational cold exposure result in cold sensitivity and is this associated with endothelial dysfunction and impaired sensory thermal thresholds? What is the main finding and its importance? Previous cold exposure was correlated with cold sensitivity of the foot, which might indicate the development of a subclinical non-freezing cold injury. Endothelial function and thermal detection were not impaired in cold-sensitive individuals; therefore, further research is required to understand the pathophysiology of subclinical and clinical forms of non-freezing cold injury. ABSTRACT: In this study, we investigated whether cold-sensitive (CS) individuals, who rewarm more slowly after a mild cold challenge, have impaired endothelial function and sensory thermal thresholds (STTs) and whether this is related to reported cold exposure. Twenty-seven participants with varying previous cold exposure undertook three tests: an STT test, i.e. determination of warm and cold STTs of the fingers and dorsal foot; an endothelial function test, i.e. measurement of cutaneous vascular conductance (CVC) during iontophoresis of ACh on the forearm, finger and foot; and a CS test, involving immersion of a foot for 2 min in water at 15°C followed by 10 min of rewarming in air at 30°C. Toe skin temperature (Tsk ) measured during the CS test was used to form a CS group (<32°C before and 5 min after immersion) and an otherwise closely matched control group [Tsk >32°C; n = 9 (four women) for both groups]. A moderate relationship was found between cold exposure ranking and Tsk rewarming (r = 0.408, P = 0.035, n = 27) but not STT or endothelial function. The Tsk and blood flow were lower in CS compared with control subjects before and after foot immersion [Tsk , mean (SD): 30.3 (0.9) versus 34.8 (0.8) and 27.9 (0.8) versus 34.3 (0.8)°C, P < 0.001; and CVC: 1.08 (0.79) versus 3.82 (1.21) and 0.79 (0.52) versus 3.45 (1.07) flux mmHg-1 , n = 9, P < 0.001, respectively]. However, no physiologically significant differences were observed between groups for endothelial function or STT. A moderate correlation between previous cold exposure and toe Tsk rewarming after foot immersion was observed; however, CS was not associated with impaired endothelial function or reduced thermal detection.

How cold is too cold? Establishing the minimum water temperature limits for marathon swim racing.

OBJECTIVES: To provide a rationale for minimum water temperature rules for elite and subelite marathon swim racing and highlight factors that make individuals vulnerable to excessive cooling during open water swimming. METHODS: 12 lean competitive swimmers swam for up to 2 hours, three times in different water temperatures between 14°C and 20°C, wearing standard swimming costumes and hats. Rectal temperature (Tre), oxygen consumption, perception of cold and performance were measured. RESULTS: In 16°C, half the swimmers did not complete a 2-hour swim; four became (or were predicted to become) hypothermic within 2 hours. In 18°C, three-quarters completed the swim; three became (or were predicted to become) hypothermic. In 20°C, one swimmer was predicted to become hypothermic in under 2 hours. The mean linear rate of fall of Tre was greater in 16°C (-1.57°C/hour) than 18°C (-1.07°C/hour) (p=0.03). There was no change in swimming performance during the swims or between conditions. Most of the cooling rate could be explained by metabolic heat production and morphology for both 16°C (R2=0.94, p<0.01) and 18°C (R2=0.82, p<0.01) conditions. No relationship was observed between Tre and perception of thermal sensation (r=0.25, p=0.13), and there was a weak correlation between Tre and thermal comfort (r=0.32, p=0.04). CONCLUSION: We recommend that 16°C and 18°C water are too cold for elite marathon swim racing. FédérationInternationale de Natation rules were changed in 2017 to make wetsuits compulsory below 18°C and optional below 20°C.

Practical Considerations for Assessing Pulmonary Gas Exchange and Ventilation During Flume Swimming Using the MetaSwim Metabolic Cart.

Lomax, M, Mayger, B, Saynor, ZL, Vine, C, and Massey, HC. Practical considerations for assessing pulmonary gas exchange and ventilation during flume swimming using the MetaSwim metabolic cart. J Strength Cond Res 33(7): 1941-1953, 2019-The MetaSwim (MS) metabolic cart can assess pulmonary gas exchange and ventilation in aquatic environments. The aims of this study were: (a) to determine the agreement between minute ventilation (VE), pulmonary oxygen uptake (VO2), and carbon dioxide output (VCO2) using the MS and Douglas bag (DB) methods during flume swimming; and (b) to assess the repeatability of these and other MS-derived parameters. Sixteen trained swimmers completed a combined incremental and supramaximal verification cardiopulmonary swimming test to determine maximal VO2, 2 progressive intensity swimming tests during which MS and DB measurements were made (agreement protocol), and 3-4 constant-velocity submaximal swimming tests during which only the MS was used (repeatability protocol). Agreement was determined using limits of agreement (LoA), bias, random error, and 95% confidence intervals with systematic bias assessed using paired samples t-tests. Within-trial and between-trial repeatability were determined using the coefficient of variation (CV) and the repeatability coefficient (CR). Where data were heteroscedastic, LoA and CR were log-transformed, antilogged, and displayed as ratios. MetaSwim underestimated peak VO2 and VCO2 (≤0.39 L·min) and VE (9.08 L·min), whereas submaximal values varied between 2 and 5% for CV and ±1.09-1.22 for ratio CR. The test-retest CV during constant-velocity swimming for VE, tidal volume, breathing frequency, VO2, VCO2, and end-tidal pressures of O2 and CO2 was <9% (ratio CR of ±1.09-1.34). Thus, the MS and DB cannot be used interchangeably. Whether the MS is suitable for evaluating ventilatory and pulmonary responses in swimming will depend on the size of effect required.

Effects of acute or chronic heat exposure, exercise and dehydration on plasma cortisol, IL-6 and CRP levels in trained males.

This study examined the acute and chronic effects of euhydrated and hypohydrated heat exposure, on biomarkers of stress and inflammation. Eight trained males [mean (SD) age: 21 (3) y; mass: 77.30 (4.88) kg; V̇O2max: 56.9 (7.2) mL kg-1 min-1] undertook two heat acclimation programmes (balanced cross-over design), once drinking to maintain euhydration and once with restricted fluid-intake (permissive dehydration). Days 1, 6, and 11 were 60 min euhydrated exercise-heat stress tests (40 °C; 50% RH, 35% peak power output), days 2-5 and 7-10 were 90 min, isothermal-strain (target rectal temperature: 38.5 °C) exercise-heat sessions. Plasma was obtained pre- and post- exercise on day 1, 2, and 11 and analysed for cortisol, interleukin-6 (IL-6), and C-reactive protein (CRP). Cortisol and CRP were also assessed on day 6. IL-6 was elevated following the initial (acute) 90 min isothermal heat strain exercise-heat exposure (day 2) with permissive dehydration ((pre exercise: 1.0 pg mL-1 [0.9], post-exercise: 1.8 pg mL-1 [1.0], P = .032) and when euhydrated (pre-exercise: 1.0 pg mL-1 [1.4], post-exercise: 1.6 pg mL-1 [2.1], P = .048). Plasma cortisol levels were also elevated but only during permissive dehydration (P = .032). Body mass loss was strongly correlated with Δcortisol (r = -0.688, P = .003). Although there was a trend for post-exercise cortisol to be decreased following both heat acclimation programmes (chronic effects), there were no within or between intervention differences in IL-6 or CRP. In conclusion, acute exercise in the heat increased IL-6 and cortisol only when fluid-intake is restricted. There were no chronic effects of either intervention on biomarkers of inflammation as evidenced by IL-6 and CRP returning to basal level at the end of heat acclimation.

Scientific rationale for changing lower water temperature limits for triathlon racing to 12°C with wetsuits and 16°C without wetsuits.

OBJECTIVES: To provide a scientific rationale for lower water temperature and wetsuit rules for elite and subelite triathletes. METHODS: 11 lean, competitive triathletes completed a 20 min flume swim, technical transition including bike control and psychomotor testing and a cycle across five different wetsuit and water temperature conditions: with wetsuit: 10°C, 12°C and 14°C; without wetsuit (skins): 14°C and 16°C. Deep body (rectal) temperature (Tre), psychomotor performance and the ability to complete a technical bike course after the swim were measured, as well as swimming and cycling performance. RESULTS: In skins conditions, only 4 out of 11 athletes could complete the condition in 14°C water, with two becoming hypothermic (Tre<35°C) after a 20 min swim. All 11 athletes completed the condition in 16°C. Tre fell further following 14°C (mean 1.12°C) than 16°C (mean 0.59°C) skins swim (p=0.01). In wetsuit conditions, cold shock prevented most athletes (4 out of 7) from completing the swim in 10°C. In 12°C and 14°C almost all athletes completed the condition (17 out of 18). There was no difference in temperature or performance variables between conditions following wetsuit swims at 12°C and 14°C. CONCLUSION: The minimum recommended water temperature for racing is 12°C in wetsuits and 16°C without wetsuits. International Triathlon Union rules for racing were changed accordingly (January 2017).

Inter-individual variation in the adaptive response to heat acclimation.

AIM: To investigate inter-individual variance in adaptive responses to heat acclimation (HA). METHODS: 17 males (VO2max=58.8(8.4) mL·kg-1·min-1) undertook 10-days (exercise + heat-stress [40 °C, 50%RH]) HA. Adaptation was assessed by heat stress tests (HST; 60-minutes cycling, 35% peak power output) pre- and post-HA. RESULTS: Inter-individual variability was evident in adaptive responses e.g. mean(range) reduction in end-exercise Tre= -0.70(-0.20 to -1.32)°C, but, in the main, the variance in adaptation was unrelated across indices (thermal, sudomotor, cardiovascular, haematological), indicating independence between adaptation indices. Variance in adaptive responses was not correlated with aerobic capacity, history of previous HA, or the accrued thermal-dose. Some responses to the initial HST were related to the subsequent adaptations e.g. ∆T̅sk during the initial HST and the reduction in the within HST ΔTre after HA (r = -0.676), but responses to the initial HST may also have been influenced by HST design e.g. ΔTre correlated with metabolic heat production (r = 0.609). Metabolic heat production also correlated with the reduction in the within HST ΔTre after HA (r = -0.514). SUMMARY: HA indices are mainly independent; 'low', or 'high', responders on one index do not necessarily demonstrate similar response across other indices. Variance in HA responses was not related to aerobic capacity, previous HA, or thermal-dose. Thermo-physiological responses to a HST might identify individuals who will benefit from HA. However, some initial responses are influenced by HST design, which may also affect the scope for demonstrating adaption. CONCLUSION: Variance in the HA response remains largely unaccounted for and future studies should identify factors contributing to this variance.

Cutaneous Vascular Responses of the Hands and Feet to Cooling, Rewarming, and Hypoxia in Humans.

INTRODUCTION: This study investigated skin vasomotor responses in the fingers and toes during cooling and rewarming with and without normobaric hypoxia. METHODS: Fourteen volunteers (8 males and 6 females) were exposed to gradual air cooling (mean±SD: -0.4±0.1oC·min-1) followed by rewarming (+0.5±0.1oC·min-1) while breathing normoxic air (FIO2 0.21 at 761±3 mm Hg) or hypoxic gas (FIO2 0.12, at 761±3 mm Hg, equivalent to ~5000 m above sea level). Throughout the gradual cooling and rewarming phases, rectal temperature was measured, and skin temperatures and laser Doppler skin blood flow were measured on the thumb, little finger, and great and little toe pads. RESULTS: During gradual cooling, skin temperature but not deep body temperature decreased. No differences in cutaneous vascular conductance were found for the toes or thumb (P=0.169 great toe; P=0.289 little toe; P=0.422 thumb). Cutaneous vascular conductance was reduced in the little finger to a greater extent at the same mean skin temperatures (34.5-33.5oC) in the hypoxic compared with normoxic conditions (P=0.047). The onset of vasoconstriction and release of vasoconstriction in the thumb and little finger occurred at higher mean skin temperatures in hypoxia compared with normoxia (P<0.05). The onset of vasoconstriction and release of vasoconstriction in the toes occurred at similar skin temperatures (P=0.181 and P=0.132, respectively). CONCLUSION: The earlier vasoconstrictor response and later release of vasoconstriction in the finger during hypoxic conditions may result in a greater dose of cold to that digit, taking longer to rewarm following the release of vasoconstriction.

Effects of 10 days of separate heat and hypoxic exposure on heat acclimation and temperate exercise performance.

Adaptations to heat and hypoxia are typically studied in isolation but are often encountered in combination. Whether the adaptive response to multiple stressors affords the same response as when examined in isolation is unclear. We examined 1) the influence of overnight moderate normobaric hypoxia on the time course and magnitude of adaptation to daily heat exposure and 2) whether heat acclimation (HA) was ergogenic and whether this was influenced by an additional hypoxic stimulus. Eight males [V̇o2max = 58.5 (8.3) ml·kg-1·min-1] undertook two 11-day HA programs (balanced-crossover design), once with overnight normobaric hypoxia (HAHyp): 8 (1) h per night for 10 nights [[Formula: see text] = 0.156; SpO2 = 91 (2)%] and once without (HACon). Days 1, 6, and 11 were exercise-heat stress tests [HST (40°C, 50% relative humidity, RH)]; days 2-5 and 7-10 were isothermal strain [target rectal temperature (Tre) ~38.5°C], exercise-heat sessions. A graded exercise test and 30-min cycle trial were undertaken pre-, post-, and 14 days after HA in temperate normoxia (22°C, 55% RH; FIO2 = 0.209). HA was evident on day 6 (e.g., reduced Tre, mean skin temperature (T̄sk), heart rate, and sweat [Na+], P < 0.05) with additional adaptations on day 11 (further reduced T̄sk and heart rate). HA increased plasma volume [+5.9 (7.3)%] and erythropoietin concentration [+1.8 (2.4) mIU/ml]; total hemoglobin mass was unchanged. Peak power output [+12 (20) W], lactate threshold [+15 (18) W] and work done [+12 (20) kJ] increased following HA. The additional hypoxic stressor did not affect these adaptations. In conclusion, a separate moderate overnight normobaric hypoxic stimulus does not affect the time course or magnitude of HA. Performance may be improved in temperate normoxia following HA, but this is unaffected by an additional hypoxic stressor.

Effects of dietary nitrate supplementation on the response to extremity cooling and endothelial function in individuals with cold sensitivity. A double blind, placebo controlled, crossover, randomised control trial.

Individuals with cold sensitivity have low peripheral skin blood flow and skin temperature possibly due to reduced nitric oxide (NO•) bioavailability. Beetroot has a high concentration of inorganic nitrate and may increase NO-mediated vasodilation. Using a placebo-controlled, double blind, randomised, crossover design, this study tested the hypotheses that acute beetroot supplementation would increase the rate of cutaneous rewarming following a local cold challenge and augment endothelium-dependent vasodilation in cold sensitive individuals. Thirteen cold sensitive participants completed foot and hand cooling (separately, in 15 °C water for 2 min) with spontaneous rewarming in 30 °C air whilst skin temperature and cutaneous vascular conductance (CVC) were measured (Baseline). On two further separate visits, participants consumed 140 ml of either concentrated beetroot juice (nitrate supplementation) or nitrate-depleted beetroot juice (Placebo) 90 min before resting seated blood pressure was measured. Endothelial function was assessed by measuring CVC at the forearm, finger and foot during iontophoresis of 1% w/v acetylcholine followed by foot and hand cooling as for Baseline. Plasma nitrite concentrations significantly increased in nitrate supplementation compared to Placebo and Baseline (502 ± 246 nmol L-1; 73 ± 45 nmol L-1; 74 ± 49 nmol L-1 respectively; n = 11; P < 0.001). Resting blood pressure and the response to foot and hand cooling did not differ between conditions (all P > 0.05). Nitrate supplementation did not alter endothelial function in the forearm, finger or foot (all P > 0.05) compared to Placebo. Despite a physiologically meaningful rise in plasma nitrite concentrations, acute nitrate supplementation does not alter extremity rewarming, endothelial function or blood pressure in individuals with cold sensitivity.

How do women feel cold water swimming affects their menstrual and perimenopausal symptoms?

OBJECTIVE: This study aimed to determine how women felt cold water swimming affected their menstrual and perimenopausal symptoms. STUDY DESIGN: An online survey that asked women who regularly swim in cold water about their experiences. The survey was advertised for 2 months on social media. Questions related to cold water swimming habits and menstrual and perimenopausal symptoms were analysed. MAIN OUTCOME MEASURES: Quantitative and qualitative data including; frequency of menstrual and menopause symptoms, the effect of cold water swimming on these symptoms. RESULTS: 1114 women completed the survey. Women reported that cold water swimming reduced their menstrual symptoms, notably psychological symptoms such as anxiety (46.7%), mood swings (37.7%) and irritability (37.6%). Perimenopausal women reported a significant improvement in anxiety (46.9%), mood swings (34.5%), low mood (31.1%) and hot flushes (30.3%). The majority of women with symptoms swam specifically to reduce these symptoms (56.4% for period and 63.3% for perimenopause symptoms). Women said they felt it was the physical and mental effects of the cold water that helped their symptoms. For the free text question, five themes were identified: the calming and mood-boosting effect of the water, companionship and community, period improvements, an improvement in hot flushes and an overall health improvement. CONCLUSION: Women felt that cold water swimming had a positive overall effect on menstrual and perimenopause symptoms. Studies on other forms of exercise to relieve menstrual and perimenopause symptoms may show similar findings.

Short-Term Head-Out Whole-Body Cold-Water Immersion Facilitates Positive Affect and Increases Interaction between Large-Scale Brain Networks.

An emerging body of evidence indicates that short-term immersion in cold water facilitates positive affect and reduces negative affect. However, the neural mechanisms underlying these effects remain largely unknown. For the first time, we employed functional magnetic resonance imaging (fMRI) to identify topological clusters of networks coupled with behavioural changes in positive and negative affect after a 5 min cold-water immersion. Perceived changes in positive affect were associated with feeling more active, alert, attentive, proud, and inspired, whilst changes in negative affect reflected reductions in distress and nervousness. The increase in positive affect was supported by a unique component of interacting networks, including the medial prefrontal node of the default mode network, a posterior parietal node of the frontoparietal network, and anterior cingulate and rostral prefrontal parts of the salience network and visual lateral network. This component emerged as a result of a focal effect confined to few connections. Changes in negative affect were associated with a distributed component of interacting networks at a reduced threshold. Affective changes after cold-water immersion occurred independently, supporting the bivalence model of affective processing. Interactions between large-scale networks linked to positive affect indicated the integrative effects of cold-water immersion on brain functioning.

The Effects of Whole-body Cold-water Immersion on Brain Connectivity Related to the Affective State in Adults Using fMRI: A Protocol of a Pre-post Experimental Design.

An emerging body of behavioural studies indicates that regular swimming in cold water has positive effects on mental health and wellbeing, such as reducing fatigue, improving mood, and lessening depressive symptoms. Moreover, some studies reported immediate effects of cold-water immersion (CWI) on elevating mood and increasing a positive emotional state. However, the neural mechanisms underlying these effects remain largely unknown. The lack of studies using neuroimaging techniques to investigate how a whole-body CWI affects neural processes has partly resulted from the lack of a tested experimental protocol. Previous protocols administered tonic limb cooling (1-10 °C) while recording functional magnetic resonance (fMRI) signals. However, using very low water temperature constitutes points of contrast to painful experiences that are different from what we experience after a whole-body head-out CWI. In our protocol, healthy adults unhabituated to cold water were scanned twice: immediately before (pre-CWI) and after (post-CWI) immersion in cold water (water temperature 20 °C) for 5 min. We recorded cardiac and ventilatory responses to CWI and assessed self-reported changes in positive and negative affects. Our protocol showed reliable changes in brain connectivity after a short exposure to cold water, thus enabling its use as a tested experimental framework in future studies.