Dynamics of sweating in men and women during passive heating

Summary The dynamics of sweating was investigated at rest in 8 men and 8 women. Electrical skin resistance (ESR), rectal temperature (T_re) and mean skin temperature were measured in subjects exposed to 40‡ C environmental temperature, 30% relative air humidity, and 1 m · s⁻¹ air flow. Sweat rate was computed from continuous measurement of the whole body weight loss. It was found that increases in T_re, and mean body temperature were higher in women than in men by 0.16, 0.38 and 0.21‡ C, but only the difference in δ was significant (p<0.05). The dynamics of sweating in men and women respectively, was as follows: delay (t_d) 7.8 and 18.1 min (p<0.01), time constant (Τ) 7.5 and 8.8 min (N.S.), inertia time (t_i) 15.3 and 26.9 min (p<0.002), and total body weight loss 153 and 111 g · m⁻² · h⁻¹ (p<0.001). Dynamic parameters of ESR did not differ significantly between men and women. Inertia times of ESR and sweat rate correlated in men (r=0.93, p<0.001), and in women (r=0.76, p<0.02). In men, δ T_re correlated with inertia time of sweat rate (r=0.81, p<0.01) as well as with the inertia time of ESR (r=0.83, p<0.001). No relation was found between δ T_re and the dynamics of sweating in women. It is concluded that the dynamics of sweating plays a decisive role in limiting δ T_re in men under dry heat exposure. The later onset of sweating in women does not influence the rectal temperature increase significantly. In women, δ T_re is probably limited by a complex interaction of sweating, skin blood flow increase, and metabolic rate decrease. This work was supported by the Centre National de la Recherche Scientifique and Polish Academy of Siences     

Mean skin temperature in warm humid climates

Summary Mean skin temperature was measured in 24 subjects during experiments in a climatic chamber. Three conditions of ambient temperature (T _a=25.6°, 28.9° and 32.2° C), and three of humidity (relative humidity = 50%, 70% and 90%) were studied. A relationship was established by a linear regression technique. It is valid in the 24°–34° C range, for air velocity =0.2 m·s⁻¹, clothing insulation =0.077° C·m²·w⁻¹ (0.5 clo), metabolic rate =64 w·m⁻² (1.1 met) and radiant temperature = air temperature. In these conditions =28.125+0.021P _w+0.210T _a (P _w: ambient water vapour pressure in mb). It shows a small humidity influence. The influences of sex, transition from one condition to the next, and air velocity were also studied. Measurements in Africa confirmed the small influence of humidity. Ethnic life-style differences indicated that a high precision in determination is difficult to achieve.     

Residual analysis in the determination of factors affecting the estimates of body heat storage in clothed subjects

Body heat storage can be estimated by calorimetry (from heat gains and losses) or by thermometry [from changes (Δ) in mean body temperature (T _b) calculated as a weighted combination of rectal (T _re) and mean skin temperatures (T _sk)]. If an invariant weighting factor ofT _re andT _sk were to be used (for instance, ΔT _b = 0.8 · ΔT _re + 0.2 · ΔT _sk under hot conditions), body heat storage could be over- or underestimated substantially relative to calorimetry, depending on whether the subject was wearing light or protective clothing. This study investigated whether discrepancies between calorimetry and thermometry arise from methodological errors in the calorimetric estimate of heat storage, from inappropriate weightings in the thermometric estimate, or from both. Residuals of calorimetry versus thermometric estimates were plotted against individual variables in the standard heat balance equation, applying various weighting factors toT _re andT _sk. Whether light or protective clothing was worn, the calorimetric approach generally gave appropriate estimates of heat exchange components and thus heat storage. One exception was in estimating latent heat loss from sweat evaporation. If sweat evaporation exceeded 650 g·h⁻¹ when wearing normal clothing, evaporative heat loss was overestimated and thus body heat storage was underestimated. Nevertheless, if data beyond this ceiling were excluded from the analyses, the standard 4:1 weighting matched calorimetric heat storage estimates quite well. When wearing protective clothing, the same 4:1 weighting approximated calorimetric heat storage with errors of less than approximately 10%, but only if environmental conditions allowed a subject to exercise for more than 90 min. The best thermometric estimates of heat storage were provided by using two sets of relative weightings, based upon the individual's metabolic heat production ( in kilojoules per metre squared per hour): {4 − [( )· ] 2}:1 for an initial, thermoneutral environment and {4 + [( ) · ] · 5}: 1 for a final, hot environment; the optimal value of lay between 450 and 500 kJ m⁻² · h⁻¹. We concluded that the accuracy of thermometric estimates of heat storage can be improved by modifying weighting factors ofT _re andT _sk according to the environment, type of clothing, and metabolic rate.     

Hyperpnoea and CO2 sensitivity of the respiratory centres during exercise

Summary The aim of this study was to specify whether exercise hyperpnoea was related to the CO₂ sensitivity of the respiratory centres measured during steady-state exercise of mild intensity. Thus, ventilation , breathing pattern [tidal volume (V _T), respiratory frequency (f), inspiratory time (T _I), total time of the respiratory cycle (T _TOT),V _T/T _I,T _I/T _TOT] and CO₂ sensitivity of the respiratory centres determined by the rebreathing method were measured at rest (SCO_{2 re}) and during steady-state exercise (SCO_{2 ex}) of mild intensity [CO₂ output =20 ml·kg⁻¹·min⁻¹] in 11 sedentary male subjects (aged 20–34 years). The results showed that SCO_{2 re} and SCO_{2 ex} were not significantly different. During exercise, there was no correlation between and SCO_{2 ex} and, for the same , all subjects had very close values normalized for body mass (bm), regardless of their SCO_{2 ex} ( =1.44 l·min⁻¹·kg⁻¹ SD 0.10). A highly significant positive correlation between SCO_{2 ex} andV _T (normalised for bm) (r=0.80,P<0.01),T _I (r=0.77,P<0.01) andT _TOT (r=0.77,P<0.01) existed, as well as a highly significant negative correlation between SCO_{2 ex} and (normalised for bm^−0.25) (r=−0.73,P<0.01). We conclude that the hyperpnoea during steady-state exercise of mild intensity is not related to the SCO_{2 ex}. The relationship between breathing pattern and SCO_{2 ex} suggests that the breathing pattern could influence the determination of the SCO_{2 ex}. This finding needs further investigation.     

Influence of the menstrual cycle and oral contraceptives on thermoregulatory responses to exercise in young women

Summary Thermoregulatory responses to exercise in relation to the phase of the menstrual cycle were studied in ten women taking oral contraceptives (P) and in ten women not taking oral contraceptives (NP). Each subject was tested for maximal aerobic capacity ( ) and for 50% exercise in the follicular (F) and luteal (L) phases of the menstrual cycle. Since the oral contraceptives would have prevented ovulation a quasi-follicular phase (q-F) and a quasi-luteal phase (q-L) of the menstrual cycle were assumed for P subjects. Exercise was performed on a cycle ergometer at an ambient temperature of 24° C and relative air humidity of 50%. Rectal (T _re), mean skin ( ), mean body ( ) temperatures and heart rate (f _c) were measured. Sweat rate was estimated by the continuous measurement of relative humidity of air in a ventilated capsule placed on the chest, converted to absolute pressure (PH₂O_chest). Gain for sweating was calculated as a ratio of increase inPH₂O_chest to the appropriate increase inT _re for the whole period of sweating (G) and for unsteady-state (G_u) separately. The did not differ either between the groups of subjects or between the phases of the menstrual cycle. In P, rectal temperature threshold for sweating (T _{re, td}) was 37.85° C in q-L and 37.60° C in q-F (P < 0.01) and corresponded to a significant difference fromT _re at rest. TheT _re, andf _c increased similarly during exercise in q-F and q-L. No menstrual phase-related differences were observed either in the dynamics of sweating or in G. In NP,T _{re, td} was shorter in L than in F (37.70 vs 37.47° C,P<0.02) with a significantly greater value fromT _re at rest. The dynamics and G for sweating were also greater in L than in F. The G_u was 36.8 versus 16.6 kPa · ° C^–1 (P<0.01) while G was 6.4 versus 3.8 kPa · ° C^–1 (P<0.05), respectively. TheT _re, andf _c increased significantly more in phase F than in phase L. It was concluded that in these women performing moderate exercise, there was a greater temperature threshold and larger gains for sweating in phase L than in phase F. Intake of oral contraceptives reduced the differences in the gains for sweating making the thermoregulatory responses to exercise more uniform.     

The thermogenic effect of a carbohydrate feeding during exposure to 8,12 and 27° C

The increased metabolic heat production in humans exposed to cold stress results from an increased oxidation of both carbohydrate and fat to provide energy to sustain temperature homeostasis. Research suggests that dietary manipulations may enhance metabolic heat production, thereby delaying hypothermia. Therefore, the present investigation examined the thermogenic effect of a sequential timed feeding regime of either a carbohydrate (CHO) or a placebo beverage (PL) before and again midway through 120 min of exposure to 8, 12 and 27° C in well-nourished men. The following were examined: tissue insulation (I), rectal temperature (T _re), mean skin temperature , metabolism (M), time-weighted heat production and respiratory exchange ratio (R).T _re, T _re, M, M,I and time-weighted heat production revealed no significant differences between treatment (PL vs CHO) at any temperature (8, 12 and 27° C). However,T _re decreased (P < 0.05) as time increased at 8, 12 and 27° C while M increased (P < 0.05) andI decreased (P < 0.05) at 8 and 12° C. At 8 and 27° C,R differed (P < 0.05) between the PL and CHO treatments. In addition, at 8 and 12° C,R increased (P < 0.05) across time reflecting the feeding. From these data it appears that while substrate utilization differed between dietary treatment (8 and 27° C) and across time, this feeding regime did not differentially affectT,T _re, andI during 120 min of exposure to 8, 12 and 27° C.     

Control of sweating during the human menstrual cycle

Summary Thermoregulatory responses were studied in seven women during two separate experimental protocols in the follicular (F, days 4–7) phase and during the luteal (L, days 19–22) phase of the menstrual cycle. Continuous measurements of esophageal temperature (T _es), mean skin temperature ( ), oxygen uptake and forearm sweating ( ) were made during all experiments. Protocol I involved both passive heat exposure (3 h) and cycle exercise at ∼80% peak during which the environmental chamber was controlled atT _a=50.0° C, rh=14% (P _w=1.7 kPa). In protocol II subjects were tested during thirty-five minutes of exercise at ∼85% peak atT _a=35° C and rh=25% (P _w=1.4 kPa). The normal L increase in restingT _es (≈0.3° C) occurred in all seven subjects. was higher during L than F in all experiments conducted at 50° C. During exercise and passive heat exposure, theT _es threshold for sweating was higher in L, with no change in the thermosensitivity (slope) of toT _es between menstrual cycle phases. This rightward or upward shift inT _es threshold for initiation of sweating averaged 0.5° C for all experiments. The data indicate the luteal phase modulation in the control of sweating in healthy women is also apparent during severe exercise and/or heat stress.     

Exercise thermoregulation after 6 h of chair rest, 6° head-down bed-rest,and water immersion deconditioning in men

The purpose was to investigate the mechanism for the excessive exercise hyperthermia following deconditioning (reduction of physical fitness). Rectal (T _re) and mean skin ( ) temperatures and thermoregulatory responses were measured in six men [mean (SD) age, 32 (6) years; mass, 78.26 (5.80) kg; surface area, 1.95 (0.11)m²; maximum oxygen uptake ( ), 48 (6) ml·min^–1·kg^–1; whilst supine in air at dry bulb temperature 23.2 (0.6)°C, relative humidity 31.1 (11.1)% and air speed 5.6 (0.1) m·min^–1] during 70 min of leg cycle exercise [51 (4)% ] in ambulatory control (AC), or following 6 h of chair rest (CR), 6° head-down bed rest (BR), and 20° (WI20) and 80° (WI80) foot-down water immersion [water temperature, 35.0 (0.1)°C]. Compared with the AC exercise T _re [mean (SD) 0.77 (0.13)°C], T _re after CR was 0.83 (0.08)°C (NS), after BR 0.92 (0.13)°C (^*P<0.05), after WI80 0.96 (0.13)°C^*, and after WI20 1.03 (0.09)°C^*. All responded similarly to exercise: they decreased (NS) by 0.5–0.7°C in minutes 4–8 and equilibrated at +0.1 to +0.5°C at 60–70. Skin heat conductance was not different among the five conditions (range = 147–159 kJ·m^–2·h^–1·°C^–1). Results from an intercorrelation matrix suggested that total body sweat rate was more closely related toT _re at 70 min (T _re70) than limb sweat rate or blood flow. Only 36% of the variability inT _re70 could be accounted for by total sweating, and less than 10% from total body dehydration. It would appear that multiple factors are involved which may include change in sensitivity of thermo- and osmoreceptors.     

Passive temperature lability in the elderly

Thermoregulatory responses of nine healthy elderly [seven men and two women; mean age (SD) 73.9 (4.8) years] were compared to those of nine young adult men [26.6 (5.2) years]. They exercised on a cycle ergometer for 20 min at an intensity inducing a heart rate equivalent to 65% of their predicted maximum, and were thereafter immersed in 28°C water. The exercise was conducted to elevate tympanic temperature (T _ty) and initiate a steady rate of sweating. The post-exercise immersion period induced gradual cooling ofT _ty, and changes inT _ty relative to resting levels (ΔT _ty) at which sweating abated and shivering commenced were defined as the ΔT _ty thresholds for the cessation of sweating (T _sw) and onset of shivering (T _sh), respectively. In addition toT _ty, oxygen uptake ( ; 1 · min⁻¹), sweating rate (g · m⁻² · min⁻¹), and forehead skin blood perfusion were also measured during the trials. The mean (SD)T _sw occurred at a significantly (P <0.005) higher ΔT _ty [0.48 (0.18)°C] in the elderly than in the young adults [0.21(0.06)°C], while the Tsh occurred at significantly (P < 0.005) lower ΔT _ty in the elderly [ −0.64 (0.34)°C] than in young adults [−0.22 (0.10)°C]. Decreases in ΔT _ty below the shivering threshold were met with a significantly (P <0.01) reduced . The range of temperature lability between Ts, andT _sh, defined as the null-zone, was significantly greater in the elderly [1.12 (0.39)°C] than in the young adults [0.43 (0.12)°C], and the slope of the vasoconstrictor response in the null-zone was significantly (P <0.001) lower in the elderly subjects. The present study demonstrates a greater passive core temperature lability in older individuals, since the effector responses of sweating and shivering were initiated at higher and lower levels ofT _ty, respectively. The magnitudes of the effector responses beyond the thresholds were also significantly reduced, suggesting that the elderly may be more susceptible to hypo-/hyperthermia during periods of endogenous and/or exogenous thermal stress.     

Effects of metabolic rate and ambient vapour pressure on heat strain in protective clothing

Studies have shown that variations in ambient water vapour pressure from 1.7 to 3.7 kPa have little effect on heat tolerance time at a metabolic rate above 450 W while wearing protective clothing. With lighter exercise, where tolerance times exceed 60 min, variations in vapour pressure have a significant impact on evaporative heat loss and, therefore, heat tolerance. The present study has examined whether these findings extend to conditions with more extreme variations in vapour pressure. Twelve males performed light (L, 350 W) and heavy (H, 500 W) exercise at 40°C in a dry (D, 1.1 kPa) and humid (H, 4.8 kPa) environment while wearing a semi-permeable nuclear, biological and chemical protective clothing ensemble (0.29 m²×°C⁻¹·W⁻¹ or 1.88 clo; Woodcock vapour permeability coefficient,i _m=0.33). Partitional calorimetry was used to determine the rate of heat storage ( ) with evaporative heat loss from the skin ( ) calculated from changes in dressed mass or the physical properties of the clothing and the vapour pressure gradient between the skin and the environment. Skin vapour pressure was predicted from measurements of water vapour pressure above the skin surface and in the clothing with humidity sensors coupled with thermistors. Final mean skin temperature ( _sk) was higher for the humid trials and averaged 37.4 (0.3)°C, 38.9 (0.4)°C, 37.6 (0.5)°C and 38.5 (0.4)°C for LD, LH, HD and HH, respectively. Final rectal temperature (T _re ) was higher for D with respective values for LD, LH, HD and HH of 39.0 (0.4)°C, 38.7 (0.4)°C, 38.8 (0.4)°C and 38.5 (0.4)°C. Tolerance time was significantly different among the trials and averaged 120.3 (19.3) min, 54.8 (7.3) min, 63.5 (6.9) min and 36.8 (3.1) min for LD, LH, HD and HH, respectively. was overestimated and, therefore, was underestimated when the changes in dressed mass were used to determine evaporative heat loss. When skin vapour pressure determined from the humidity sensor data was used to calculate , heat storage was significantly different among the trials and averaged 15.0 (3.0), 13.0 (1.8), 14.2 (2.6) and 12.2 (1.9) kJ·kg⁻¹ for LD, LH, HD and HH, respectively. It was concluded that while wearing the protective clothing all indices of heat strain, including tolerance time, were significantly affected by the change in ambient water vapour pressure from 1.1 to 4.8 kPa during both light and heavy exercise.     

The effect of acute metabolic alkalosis on bicarbonate transport along the loop of Henle. The role of active transport processes and passive paracellular backflux

The loop of Henle (LOH) reabsorbs approximately 15% of filtered HCO ₃ ⁻ via a luminal Na⁺-H⁺ exchanger and H⁺ATPase. During acute metabolic alkalosis (AMA) induced by i.v. HCO ₃ ⁻ infusion, we have observed previously inhibition of LOH net HCO ₃ ⁻ reabsorption , which contributes to urinary elimination of the HCO ₃ ⁻ load and correction of the systemic alkalosis. To determine whether the activities of the Na⁺-H⁺ exchanger and/or H⁺-ATPase are reduced during AMA, two inhibitors believed to be sufficiently specific for each transporter were delivered by in vivo LOH microperfusion during AMA. AMA reduced LOH from 205.0±0.8 to 96.2±11.8 pmol · min⁻¹ (P<0.001). Luminal perfusion with bafilomycin A₁ (10⁻⁴ mol · l⁻¹) caused a further reduction in by 83% and ethylisopropylamiloride (EIPA; 5.10⁻⁴ mol · l⁻¹) completely abolished net HCO ₃ ⁻ reabsorption. The combination of bafilomycin A₁ and EIPA in the luminal perfusate was additive, resulting in net HCO ₃ ⁻ secretion (−66.6±20.8 pmol · min⁻¹;P<0.001) and abolished net fluid reabsorption (from 5.0±0.6 during AMA to 0.2±1.1 nl · min⁻¹;P<0.001). To establish whether HCO ₃ ⁻ secretion via luminal stilbenesensitive transport mechanism participates in LOH adaptation to AMA, we added diisothiocyanato-2,2′-stilbenedisulphonate (DIDS; 10⁻⁴ mol · l⁻¹) to the perfusate. No effect was found. However, when the same LOH were exposed to luminal DIDS for more than 10 min, the direction of net HCO ₃ ⁻ movement was reversed and net HCO ₃ ⁻ secretion occurred: changed from 90.6±8.8 to −91.9±34.1 pmol · min⁻¹;P<0.01, an effect that was not observed in the control state (undisturbed acid-base balance). Thus, during AMA, neither the luminal Na⁺-H⁺ exchanger nor the H⁺-ATPase are noticeably suppressed. However, pharmacological elimination of both transporters, as well as prolonged exposure of the tubular lumen to DIDS, induced net HCO ₃ ⁻ secretion. This secretory flux may reflect paracellular backflux due to the steeper blood to lumen HCO ₃ ⁻ concentration gradient that presumably prevails in AMA.     

Longitudinal associations between anaerobic threshold and distance running performance

Summary Longitudinal alterations in anaerobic threshold (AT) and distance running performance were assessed three times within a 4-month period of intensive training, using 20 male, trained middle-distance runners (19–23 yr). A major effect of the high intensity regular intensive training together with 60- to 90-min AT level running training (2d ·wk ⁻¹) was a significant increase in the amount of O₂ uptake corresponding to AT ( AT; ml O₂ · min⁻¹ · kg⁻¹) and in maximal oxygen uptake ( ; ml O₂ · min⁻¹ · kg⁻¹). Both AT and showed significant correlations (r=−0.69 to −0.92 andr=−0.60 to −0.85, respectively) with the 10,000 m run time in every test. However, further analyses of the data indicate that increasing AT (r=−0.63,P<0.05) rather than (r=−0.15) could result in improving the 10,000 m race performance to a larger extent, and that the absolute amount of change (δ) in the 10,000 m run time is best accounted for by a combination of δ AT and δ5,000 m run time. Our data suggest that, among runners not previously trained over long distances, training-induced alterations in AT in response to regular intensive training together with AT level running training may contribute significantly to the enhancement of AT and endurance running performance, probably together with an increase in muscle respiratory capacity. This study was supported by Grant 59780141 from the Scientific Research Fund of the Ministry of Education, Science, and Culture, Japan     

Hypoxic ventilatory response during rest and exercise after a Himalayan expedition

Hypoxic ventilatory response (HVR) was examined before and after acclimatization to high altitude. Transient hyperoxic switches according to Dejours's technique were used to examine the contribution of HVR to the hyperpnoea of increasing exercise intensities. Ten mountaineers were exposed to hypoxia (oxygen fraction in inspired gas,F ₁O₂ = 0.11, 79 mmHg) before the expedition and after return from altitude (56 days, 30 days at 4900 m or higher). After 25-min breathing hypoxic gas, the subjects performed a maximal cycle ergometer test (increments 50 W per 5 min). Respired gases and ventilation were analysed breath-by-breath, partial pressure of oxygen (PO₂) and oxygen saturation (SO₂) were measured in capillary blood. The HVR was tested by switching two breaths to anF ₁O₂ of 1.0. The nadir of after the switch was measured (decrease in ventilation, D ). The HVR was expressed as the D at a PO₂ of 40 mmHg (D ) and the D versus decrease ofSO₂ (D /[100 −SO₂]). The HVR estimated by D increased from 19.9 to 28.01 · min⁻¹ (median,P = 0.013). The HVR expressed as D /(100 −SO₂) at rest was no different before and after acclimatization (0.89 and 0.86 l · min⁻¹ · %⁻¹, respectively) and during exercise it did not change before the expedition (0.831 · min⁻¹ %⁻¹). However, D /(100 −SO₂) increased significantly with exercise intensity after the expedition (1.61 l · min⁻¹ · %⁻¹ at 200 W). The changes of D versusSO₂ as well as of D versus were steeper after the expedition than before. In summary, after return from 30 day at high altitude, an increased HVR was observed. The augmentation of HVR was evident at higher exercise intensities and we suggest that this reflects a change in sensitivity of the peripheral chemoreflex loop.     

Blood lactate responses in incremental exercise as predictors of constant load performance

Summary Seven trained male cyclists ( =4.42±0.23 l·min⁻¹; weight 71.7±2.7 kg, mean ± SE) completed two incremental cycling tests on the cycle ergometer for the estimation of the “individual anaerobic threshold” (IAT). The cyclists completed three more exercises in which the work rate incremented by the same protocol, but upon reaching selected work rates of approximately 40, 60 and 80% , the subjects cycled for 60 min or until exhaustion. In these constant load studies, blood lactate concentration was determined on arterialized venous ([La⁻]a_v) and deep venous blood ([La⁻]_v) of the resting forearm. The a_v-v lactate gradient across the inactive forearm muscle was −0.08 mmol·l⁻¹ at rest. After 3 min at each of the constant load work rates, the gradients were +0.05, +0.65* and +1.60* mmol·l⁻¹ (*P<0.05). The gradients after 10 min at these same work rates were −0.09, +0.24 and +1.03* mmol·l⁻¹. For the two highest work rates taken together, the lactate gradient was less at 10 min than 3 min constant load exercise (P<0.05). The [La⁻]a_v was consistently higher during prolonged exercise at both 60 and 80% than that observed at the same work rate during progressive exercise. At the highest work rate (at or above the IAT), time to exhaustion ranged from 3 to 36 min in the different subjects. These data showed that [La⁻] uptake across resting muscle continued to increase to work rates above the IAT. Further, the greater a_v-v lactate gradient at 3 min than 10 min constant load exercise supports the concept that inactive muscle might act as a passive sink for lactate in addition to a metabolic site.     

How should body heat storage be determined in humans: by thermometry or calorimetry?

Summary The aim of this study was to determine whether in humans there are differences in the heat storage calculated by partitional calorimetry (S, the balance of heat gains and heat losses) compared to the heat storage obtained by conventional methods (thermometry) via either core temperature or mean body temperatures ( , whereT _c is core temperature and is mean skin temperature) when two different sites are used as an index ofT _c [rectal (T _re) and auditory canal (T _ac) temperatures]. Since women respond to the heat differently than men, both sexes were studied. After a stabilisation period at thermal neutrality, six men and seven women were exposed to a globe temperature of 50°C, relative humidity of 17% and wind speed of 0.8–1.0 m·s^–1 for 90 min semi-nude at rest, whereT _re,T _ac, , metabolic rate, dry (radiant+convective heat exchange) and evaporative heat losses,S, heat storage byT _c ( ) and heat storage by were assessed every minute. In the men,S was equal to 350.8(SEM 49.6) kJ whereas amounted to only 114.6(SEM 16.2) and 196.7(SEM 32.3) kJ forT _re andT _ac, respectively (P<0.05). Final underestimatedS by 49% [177.7(SEM 23.0) kJ;P<0.05] whereas was not significantly different than S [255.7(SEM 37.9) kJ]. In the women,S corresponded to a total of 294.3(SEM 23.2) kJ, a value that was very similar to the 262.6(SEM 31.0) kJ], whereas underpredicted by 35% [190.4(SEM 26.3) kJ;P<0.05]. As in the men,S _{T c} was much lower thanS [116.6(SEM 19.9) and 190.3(SEM 24.2) kJ forT _re andT _ac, respectively;P<0.05]. Using seven other well-known weighting coefficients, could under- and overestimateS by up to 55% and 11%, respectively. In all subjects, a large portion of the variance (68% and 75%) in the difference betweenS and , could be explained primarily by the T _ac. The results demonstrated that although some estimates of thermometric heat storage matched the calorimetricS, other predictions underestimated it by up to 67% during passive heating. It is suggested that these differences can be explained in part by he site chosen to representT _c, the use of eitherT _c or in the heat storage calculation, and the thermoneutral/hot weighting coefficient(s) chosen to determine . Until more representative measurements of body temperatures at different depths (core, shell and intermediate) are possible, the use of and -derived heat storage is difficult to justify.     

The influence of acute and 23 days of intermittent hypoxic exposures on the exercise-induced forehead sweating response

The effect of acute and 23 days of intermittent exposures to normobaric hypoxia on the forehead sweating response during steady-state exercise was investigated. Eight endurance athletes slept in a normobaric hypoxic room for a minimum of 8 h per day at a simulated altitude equivalent to 2,700 m for 23 days (sleep high–train low regimen). Peak oxygen uptake and peak work rate (WR_peak) were determined under normoxic (20.9%O₂) and hypoxic (13.5%O₂) conditions prior to (pre-IHE), and immediately after (post-IHE) the intermittent hypoxic exposures (IHE). Also, each subject performed three 30-min cycle-ergometry bouts: (1) normoxic exercise at 50% WR_peak attained in normoxia (control trial; CT); (2) hypoxic exercise at 50% WR_peak attained in hypoxia (hypoxic relative trial; HRT) and (3) hypoxic exercise at the same absolute work rate as in CT (hypoxic absolute trial; HAT). Exposure to hypoxia induced a 33 and 37% decrease (P < 0.001) in pre-IHE and post-IHE, respectively. Despite similar relative oxygen uptake during HAT pre-IHE and post-IHE, the ratings of perceived whole-body exertion decreased substantially (P < 0.05) post-IHE. Pre-IHE the sweat secretion on the forehead was greater (P < 0.01) in the HAT (2.60 (0.80) mg cm⁻² min⁻¹) compared to the other two trials (CT = 1.87 (1.09) mg cm⁻² min⁻¹; HRT = 1.57 (0.82) mg cm⁻² min⁻¹) despite a similar exercise-induced elevation in body temperatures, resulting in an augmented (P < 0.01) gain of the sweating response The augmented and during the HAT were no longer evident post-IHE. Thus, it appears that exercise sweating on the forehead is potentiated by acute exposure to hypoxia, an effect which can be abolished by 23 days of intermittent hypoxic exposures.     

Cardiac frequency in miners recorded during four to five work shifts

Cardiac frequency (f _c) was recorded in 101 coal-face miners [mean age 32.7 (range 21–49) years, mean height 169.6 (range 150–185) cm, mean body mass 76.9 (range 54–106) kg, mean maximal cardiac frequency (f _cmax) 180.2 (range 154–197) beats min⁻¹, mean maximal oxygen uptake 2.93 (range 1.9–4.0) l · min⁻¹] with a small-size, nonintrusivef _c counter, during the five (n = 76) or at least four (n = 25) work-shifts in a week. Thef _cmax and were determined during a progressive test to exhaustion on a treadmill. Overall (four to five work-shifts) mean work-timef _c (f _c) was 97.7 (range 74.9–122.4) beats · min⁻¹, restingf _c (f _{c rest}) 59.1 (range 50–75) beats · min⁻¹, work-time increase inf _c (f _c —f _{c rest}) 38.5 (range 21.1–55.8) beats · min⁻¹ and percentage off _c reserve used (f _{c reserve} =f _{c max} —f _crest)32.0(range 18.5–50.9). Multiple regression analysis showed thatf _c andf _c —f _{c rest}, as dependent variables, correlated with predicted percentage of CO lung diffusion capacity, (D _LCO_SB%) (r = −0.334 andr = −0.273, respectively) but not with age,f _{c max}, , · kg⁻¹ body mass, effort test Δoxygen uptake/Δf _c or percentage of forced expiratory volume in 1 s as independent variables. The percentage off _{c reserve} used as dependent variable, correlated withD _LCO_SB (r = − 0.265) andf _{c max} (r = − 0.227) but not with any of the other variables listed. Individual differences in worktimef _c are thus large and virtually unpredictable. Other physiological variables not taken in account here (i.e. sense of effort, fatigue perception) as well as psychological ones (work satisfaction, motivation) may have played a role in those differences. At peaks of effort, some subjects reachedf _c values within the range off _{c max}.     

A prediction equation for indirect assessment of anaerobic threshold in male distance runners

Summary The predictability of anaerobic threshold (AT) from maximal aerobic power, distance running performance, chronological age, and total running distance achieved on the treadmill (TRD) was investigated in a sample of 53 male distance runners, 17–23 years of age. The dependent variable was oxygen uptake ( ) at which AT was detected (i. e., @AT). A regression analysis of the data indicated @AT could be predicted from the following four measurements with a multipleR=0.831 and a standard error of the estimate of 2.66 ml · min⁻¹ · kg⁻¹: (67.9±5.7 ml · min⁻¹ · kg⁻¹), 1,500-m running performance (254.5±14.2 s), TRD (6.82±1.13 km), and age (19.4±2.2 years). When independent variables were limited to (X ₁) and 1,500-m running performance (X ₂) for simpler assessment, a multipleR=0.806 and a standard error of the estimate of 2.76 ml · min⁻¹ · kg⁻¹ were computed. A useful prediction equation with this predictive accuracy was considered to be @AT= 0.386X₁−0.128X₂+57.11. To determine if the prediction equation developed for the 53 male distance runners could be generalized to other samples, cross-validation of the equation was tested, using 21 different distance runners, 17–22 years of age. A high correlation (R=0.927) was obtained between @AT predicted from the above equation and directly measured @AT. It is concluded that the generalized equation may be applicable to young distance runners for indirect assessment of @AT. This study was supported by grants from The Descente Foundation for the Promotion of Sports Science, awarded to K. Tanaka     

Three nights of sleep deprivation does not alter thermal strain during exercise in the heat

Purpose

Individuals exposed to total sleep deprivation may experience an increased risk of impaired thermoregulation and physiological strain during prolonged physical activity in the heat. However, little is known of the impact of more relevant partial sleep deprivation (PSD). This randomized counterbalanced study investigated the effect of PSD on thermal strain during an exercise-heat stress.

Methods

Ten healthy individuals performed two stress tests (45 min running, 70 % ${\dot{V}\text{O}}_{2\hbox{max} }$ V · O 2 max 33 °C, 40 % RH). Each trial followed three nights of controlled sleep: normal [479 (SD 2) min sleep night^?1; Norm] and PSD [116 (SD 4) min sleep night^?1]. Energy balance and hydration state were controlled throughout the trials. Rectal temperatures (T _re), mean skin temperature ( $\bar{T}_{\text{sk}}$ T ¯ sk ), heart rate (HR), RPE, and thermal sensations (TS) were measured at regular intervals during each heat stress trial.

Results

There was a significant main effect of time (P < 0.05) for all of these variables. However, no differences (P > 0.05) were observed between PSD and Norm, respectively, for T _re [39.0 (0.5) vs. 39.1 (0.5)  °C], $\bar{T}_{\text{sk}}$ T ¯ sk , [36.1 (0.6) vs. 36.0 (0.7)  °C] and HR [181 (13) vs. 182 (13) beats min^?1)] at the end of exercise-heat stress. There were no differences (P > 0.05) in $\bar{T}_{\text{sk}}$ T ¯ sk , PSI, RPE, TS and whole-body sweat rate between PSD versus Norm.

Conclusion

Since greater physiological strain during exercise-heat stress did not follow three nights of PSD, it appears that sleep loss may have minimal impact upon thermal strain during exercise in the heat, at least as evaluated within this experiment.     

Thermoregulatory responses of circum-pubertal children

Passive temperature lability of nine circumpubertal children [11.4 (1.2) years] was compared to that of nine young adult males [26.6 (5.2) years]. Each subject completed a 20-min period of exercise, followed immediately by post-exercise immersion in water at 28°C. The aim of the exercise protocol was to induce a steady rate of sweating (E _SW) while the postexercise immersion period induced cooling of the core region (tympanic temperature:T _ty). TheT _ty values (relative to rest, ΔT _ty) at which sweating abated and at which shivering commenced were defined as the thresholds for the cessation of sweating and onset of shivering, respectively. While there was no significant difference between the ΔT _ty sweating thresholds, the onset of shivering, as reflected in the oxygen uptake response, occurred at significantly higher (P < 0.05) ΔT _ty values in the children [mean (SD): −0.07 (0.07)°C] than in the adults [−0.22 (0.10)°C]. The slope of theE _SW/ΔT _ty relationship was found to be significantly lower in the children (z = −5.64;P < 0.05), while the slopes of the /ΔT _ty relationship were not significantly different (z = −0.84;P > 0.05). Skin blood perfusion was measured at the forehead (SkBP), and the slope of the SkBP/ΔT _ty relationship across the nullzone was significantly less in the children than in the adults (z = −2.13;P < 0.05) with the greatest reduction in perfusion occurring prior to the offset of sweating in the children. The subjective ratings of thermal comfort indicated that the children were more sensitive to changes in core temperature than the adults. It is concluded that maturation plays an important role in modifying thermoregulatory responses to deviations in core temperature. These results suggest that there may be differences in thermoregulatory “strategies” which are maturationally related.