The effect of medium-term heat acclimation on endurance performance in a temperate environment.

We investigated whether an 11-day heat acclimation programme (HA) enhanced endurance performance in a temperate environment, and the mechanisms underpinning any ergogenic effect. Twenty-four males (V̇O2max: 56.7 ± 7.5 mL·kg-1·min-1) completed either: (i) HA consisting of 11 consecutive daily exercise sessions (60-90 min·day-1; n = 16) in a hot environment (40°C, 50% RH) or; (ii) duration and exertion matched exercise in cool conditions (CON; n = 8 [11°C, 60% RH]). Before and after each programme power at lactate threshold, mechanical efficiency, VO2max, peak power output (PPO) and work done during a 30-minute cycle trial (T30) were determined under temperate conditions (22°C, 50% RH). HA reduced resting (-0.34 ± 0.30°C) and exercising (-0.43 ± 0.30°C) rectal temperature, and increased whole-body sweating (+0.37 ± 0.31 L·hr-1) (all P≤0.001), with no change in CON. Plasma volume increased in HA (10.1 ± 7.2%, P < 0.001) and CON (7.2 ± 6.3%, P = 0.015) with no between-groups difference, whereas exercise heart rate reduced in both groups, but to a greater extent in HA (-20 ± 11 b·min-1) than CON (-6 ± 4 b·min-1). VO2max, lactate threshold and mechanical efficiency were unaffected by HA. PPO increased in both groups (+14 ± 18W), but this was not related to alterations in any of the performance or thermal variables, and T30 performance was unchanged in either group (HA: Pre = 417 ± 90 vs. Post = 427 ± 83 kJ; CON: Pre = 418 ± 63 vs. Post = 423 ± 56 kJ). In conclusion, 11-days HA induces thermophysiological adaptations, but does not alter the key determinants of endurance performance. In trained males, the effect of HA on endurance performance in temperate conditions is no greater than that elicited by exertion and duration matched exercise training in cool conditions.

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.

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.

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.

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.

Inspiratory Muscle Training Effects on Cycling During Acute Hypoxic Exposure.

INTRODUCTION: Hypoxic environments increase the physiological demands of exercise. Inspiratory muscle training can reduce the demands of exhaustive exercise in this environment. This study examined the impact of inspiratory muscle training on moderate intensity hypoxic cycling exercise. METHODS: There were 17 healthy adult men who undertook 4 wk of inspiratory muscle training (N = 8) or 4 wk of sham inspiratory muscle training (N = 9). Subjects completed four fixed intensity (100 W) and duration (10 min) cycle ergometry tests. Two were undertaken breathing normoxic ambient air and two breathing a hypoxic gas mixture (14.6% oxygen, balance nitrogen). One normoxic and hypoxic test occurred before, and one after, inspiratory muscle training. RESULTS: Inspiratory muscle training increased maximal inspiratory mouth pressure by 21 ± 16 cmH2O. Arterial oxygen saturation and its ratio to minute ventilation also increased after inspiratory muscle training during hypoxic exercise from 83 ± 4% to 86 ± 3% (approximately 3%) and 2.95 ± 0.48 to 3.52 ± 0.54% · L · min-1(approximately 21%), respectively. In addition, minute ventilation and carbon dioxide output fell by 12-13% after inspiratory muscle training during hypoxic exercise. DISCUSSION: Inspiratory muscle training reduced the physiological demand of moderate intensity exercise during acute hypoxic, but not normoxic, exercise. It may therefore be of benefit in adults exercising in a hypoxic environment.Lomax M, Massey HC, House JR. Inspiratory muscle training effects on cycling during acute hypoxic exposure. Aerosp Med Hum Perform. 2017; 88(6):544-549.

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.