Heather Massey

Effect of short-term heat acclimation with permissive dehydration on thermoregulation and temperate exercise performance

We examined the effect of short‐term heat acclimation with permissive dehydration (STHADe) on heat acclimation (HA) and cycling performance in a temperate environment. Ten trained male cyclists [mean (SD) maximal oxygen uptake: 63.3(4.0) mL/kg/min; peak power output (PPO): 385(40) W; training: 10 (3) h/week] underwent a STHADe program consisting of 5 days of exercise (maximum 90 min/day) in a hot environment (40 °C, 50% RH) to elicit isothermic heat strain [rectal temperature 38.64(0.27) °C]. Participants abstained from fluids during, and 30 min after, HA sessions. Pre‐ and post‐STHADe HA was evaluated during euhydrated fixed‐intensity exercise (60 min) in hot conditions; the effect of STHADe on thermoregulation was also examined under temperate conditions (20 min fixed‐intensity exercise; 22 °C, 60% RH). Temperate cycling performance was assessed by a graded exercise test (GXT) and 20‐km time trial (TT). STHADe reduced thermal and cardiovascular strain in hot and temperate environments. Lactate threshold [Δ = 16 (17) W] and GXT PPO [Δ = 6 (7) W] were improved following STHADe (P < 0.05), but TT performance was not affected (P > 0.05), although there was a trend for a higher mean power (P = 0.06). In conclusion, STHADE can reduce thermal and cardiovascular strain under hot and temperate conditions and there is some evidence of ergogenic potential for temperate exercise, but longer HA regimens may be necessary for this to meaningfully influence performance.

Cold water immersion: kill or cure?

What is the topic of this review? This is the first review to look across the broad field of ‘cold water immersion’ and to determine the threats and benefits associated with it as both a hazard and a treatment. What advances does it highlight? The level of evidence supporting each of the areas reviewed is assessed.

Effect of Permissive Dehydration on Induction and Decay of Heat Acclimation, and Temperate Exercise Performance

Purpose: It has been suggested that dehydration is an independent stimulus for heat acclimation (HA), possibly through influencing fluid-regulation mechanisms and increasing plasma volume (PV) expansion. There is also some evidence that HA may be ergogenic in temperate conditions and that this may be linked to PV expansion. We investigated: (i) the influence of dehydration on the time-course of acquisition and decay of HA; (ii) whether dehydration augmented any ergogenic benefits in temperate conditions, particularly those related to PV expansion. Methods: Eight males [VO2max: 56.9(7.2) mL·kg−1·min−1] undertook two HA programmes (balanced cross-over design), once drinking to maintain euhydration (HAEu) and once with restricted fluid-intake (HADe). Days 1, 6, 11, and 18 were 60 min exercise-heat stress tests [HST (40°C; 50% RH)], days 2–5 and 7–10 were 90 min, isothermal-strain (Tre ~ 38.5°C), exercise-heat sessions. Performance parameters [VO2max, lactate threshold, efficiency, peak power output (PPO)] were determined pre and post HA by graded exercise test (22°C; 55%RH). Results: During isothermal-strain sessions hypohydration was achieved in HADe and euhydration maintained in HAEu [average body mass loss −2.71(0.82)% vs. −0.56(0.73)%, P < 0.001], but aldosterone concentration, power output, and cardiovascular strain were unaffected by dehydration. HA was evident on day 6 {reduced end-exercise Tre [−0.30(0.27)°C] and exercise heart rate [−12(15) beats.min−1], increased PV [+7.2(6.4)%] and sweat-loss [+0.25(0.22) L.h−1], P < 0.05} with some further adaptations on day 11 {further reduced end-exercise Tre [−0.25(0.19)°C] and exercise heart rate [−3(9) beats.min−1], P < 0.05}. These adaptations were not notably affected by dehydration and were generally maintained 7-days post HA. Performance parameters were unchanged, apart from increased PPO (+16(20) W, irrespective of condition). Conclusions: When thermal-strain is matched, permissive dehydration which induces a mild, transient, hypohydration does not affect the acquisition and decay of HA, or endurance performance parameters. Irrespective of hydration, trained individuals require >5 days to optimize HA.

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.

Habituation of the cold shock response is inhibited by repeated anxiety: Implications for safety behaviour on accidental cold water immersions

INTRODUCTION Accidental cold-water immersion (CWI) triggers the life-threatening cold shock response (CSR) which is a precursor to sudden death on immersion. One practical means of reducing the CSR is to induce an habituation by undergoing repeated short CWIs. Habituation of the CSR is known to be partially reversed by the concomitant experience of acute anxiety, raising the possibility that repeated anxiety could prevent CSR habituation; we tested this hypothesis. METHOD Sixteen participants (12 male, 4 female) completed seven, seven-minute immersions in to cold water (15°C). Immersion one acted as a control (CON1). During immersions two to five, which would ordinarily induce an habituation, anxiety levels were repeatedly increased (CWI-ANXrep) by deception and a demanding mathematical task. Immersions six and seven were counter-balanced with another high anxiety condition (CWI-ANXrep) or a further control (CON2). Anxiety (20cm visual analogue scale) and cardiorespiratory responses (cardiac frequency [fc], respiratory frequency [fR], tidal volume [VT], minute ventilation [V̇E]) were measured. Comparisons were made between experimental immersions (CON1, final CWI-ANXrep, CON2), across habituation immersions and with data from a previous study. RESULTS Anxiety levels were sustained at a similar level throughout the experimental and habituation immersions (mean [SD] CON1: 7.0 [4.0] cm; CON2: 5.8 [5.2] cm cf CWI-ANXrep: 7.3 [5.5] cm; p>0.05). This culminated in failure of the CSR to habituate even when anxiety levels were not manipulated (i.e. CON2). These data were different (p<0.05) to previous studies where anxiety levels were allowed to fall across habituation immersions and the CSR consequently habituated. DISCUSSION Repeated anxiety prevented CSR habituation. A protective strategy that includes inducing habituation for those at risk should include techniques to lower anxiety associated with the immersion event or habituation may not be beneficial in the emergency scenario.

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

HighlightsAcute exercise in the heat increases IL‐6 regardless of hydration status.Acute exercise in the heat increases cortisol only when fluid‐intake is restricted.This cortisol response was strongly correlated with whole body sweat loss.Cortisol, IL‐6 and CRP were not augmented after heat acclimation. &NA; 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; VO2max: 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 &Dgr;cortisol (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.

Cold water swimming and upper respiratory tract infections

It is often suggested that habitual cold water swimming (HCS) may improve resistance to infection [1], yet research into effects of HCS on the immune system has produced inconclusive results. This may be due to the wide range of protocols, from brief ice-cold dips [2] to long cold water swims [3]. Many studies measured blood and saliva markers rather than actual illness, and the clinical significance of these markers is not well established [4]. Incidence of upper respiratory tract infection (URTI), i.e. the common cold, is a useful indication of in vivo immune system function [5,6]. This study compared URTI susceptibility in those practising HCS with that in their non-swimming co-habiting partners. To control for any effect of swimming, those who swim in indoor heated pools and their partners were also investigated. The null hypothesis (H0) was that there would be no difference between swimming groups.

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.

Acute Anxiety Predicts Components of the Cold Shock Response on Cold Water Immersion: Toward an Integrated Psychophysiological Model of Acute Cold Water Survival

Introduction: Drowning is a leading cause of accidental death. In cold-water, sudden skin cooling triggers the life-threatening cold shock response (CSR). The CSR comprises tachycardia, peripheral vasoconstriction, hypertension, inspiratory gasp, and hyperventilation with the hyperventilatory component inducing hypocapnia and increasing risk of aspirating water to the lungs. Some CSR components can be reduced by habituation (i.e., reduced response to stimulus of same magnitude) induced by 3–5 short cold-water immersions (CWI). However, high levels of acute anxiety, a plausible emotion on CWI: magnifies the CSR in unhabituated participants, reverses habituated components of the CSR and prevents/delays habituation when high levels of anxiety are experienced concurrent to immersions suggesting anxiety is integral to the CSR. Purpose: To examine the predictive relationship that prior ratings of acute anxiety have with the CSR. Secondly, to examine whether anxiety ratings correlated with components of the CSR during immersion before and after induction of habituation. Methods: Forty-eight unhabituated participants completed one (CON1) 7-min immersion in to cold water (15°C). Of that cohort, twenty-five completed four further CWIs that would ordinarily induce CSR habituation. They then completed two counter-balanced immersions where anxiety levels were increased (CWI-ANX) or were not manipulated (CON2). Acute anxiety and the cardiorespiratory responses (cardiac frequency [fc], respiratory frequency [fR], tidal volume [VT], minute ventilation [E]) were measured. Multiple regression was used to identify components of the CSR from the most life-threatening period of immersion (1st minute) predicted by the anxiety rating prior to immersion. Relationships between anxiety rating and CSR components during immersion were assessed by correlation. Results: Anxiety rating predicted the fc component of the CSR in unhabituated participants (CON1; p < 0.05, r = 0.536, r2= 0.190). After habituation immersions (i.e., cohort 2), anxiety rating predicted the fR component of the CSR when anxiety levels were lowered (CON2; p < 0.05, r = 0.566, r2= 0.320) but predicted the fc component of the CSR (p < 0.05, r = 0.518, r2= 0.197) when anxiety was increased suggesting different drivers of the CSR when anxiety levels were manipulated; correlation data supported these relationships. Discussion: Acute anxiety is integral to the CSR before and after habituation. We offer a new integrated model including neuroanatomical, perceptual and attentional components of the CSR to explain these data.

Open water swimming as a treatment for major depressive disorder

A 24-year-old woman with symptoms of major depressive disorder and anxiety had been treated for the condition since the age of 17. Symptoms were resistant to fluoxetine and then citalopram. Following the birth of her daughter, she wanted to be medication-free and symptom-free. A programme of weekly open (cold) water swimming was trialled. This led to an immediate improvement in mood following each swim and a sustained and gradual reduction in symptoms of depression, and consequently a reduction in, and then cessation of, medication. On follow-up a year later, she remains medication-free.