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New Findings: What is the central question of this study?Does inhibition of K+ channels modulate the exercise‐training‐induced augmentation in cholinergic and thermal sweating?What is the main finding and its importance?Iontophoretic administration of tetraethylammonium, a K+ channel blocker, blunted sweating induced by a low dose (0.001%) of the cholinergic agent pilocarpine, but not heat‐induced sweating. However, no differences in the cholinergic sweating were observed between young endurance‐trained and untrained men. Thus, while K+ channels play a role in the regulation of eccrine sweating, they do not contribute to the increase in sweating commonly observed in endurance‐trained adults. Our findings provide important new insights into the mechanisms underlying the regulation of sweating by endurance conditioning. We evaluated the hypothesis that the activation of K+ channels mediates the exercise‐training‐induced augmentation of cholinergic and thermal sweating. On separate days, 11 endurance‐trained and 10 untrained men participated in two experimental protocols. Prior to each protocol, we administered 2% tetraethylammonium (TEA, K+ channels blocker) and saline (Control) at forearm skin sites on both arms via transdermal iontophoresis. In protocol 1, low (0.001%) and high (1%) doses of pilocarpine were administered at the TEA‐treated and Control sites over a 60‐min period. In protocol 2, participants were passively heated by immersing their lower limbs in hot water (43°C) until core (rectal) temperature (Tc) increased by 0.8°C above resting levels. Administration of TEA attenuated cholinergic sweating (P = 0.001) during the initial 20 min after the treatment of low dose of pilocarpine only whilst the response was similar between the groups (P = 0.163). Cholinergic and thermal sweating were higher in the trained relative to the untrained men (all P ≤ 0.033). Thermal sweating reached ∼90% of the response at a Tc elevation of 0.8°C during the initial 20 min of passive heating, which corresponds to the period wherein TEA attenuated cholinergic sweating in protocol 1. However, sweating did not differ between the Control and TEA sites in either group (P = 0.704). We showed that activation of K+ channels does not appear to mediate the elevated sweating response induced by a low dose of pilocarpine in trained men. We also demonstrated that K+ channels do not contribute to sweating during heat stress in either group. [ABSTRACT FROM AUTHOR]

We evaluated the effects of the menstrual cycle and physical training on heat loss (sweating and cutaneous vasodilation) responses during moderate exercise in a temperate environment. Ten untrained (group U) and seven endurance-trained (group T) women (maximal [O.sub.2] uptake of 36.7 [+ or -] 1.1 vs. 49.4 [+ or -] 1.7 ml x [kg.sup.-1] x [min.sup.-1], respectively: P < 0.05) performed a cycling exercise at 50% maximal [O.sub.2] uptake for 30 min during both the midfollicular and midluteal menstrual phase in a temperate environment (ambient temperature of 25[degrees]C, relative humidity of 45%). In group U, plasma levels of estrone, estradiol, and progesterone at rest and esophageal temperature ([T.sub.es]) during exercise were significantly higher during the midluteal than during the midfollicular phase (P < 0.05). Sweating rate and cutaneous blood flow (measured via laser-Doppler flowmetry) on the chest, back, forearm, and thigh were lower during the midluteal than during the midfollicular phase during exercise. [T.sub.es] threshold for heat loss responses was significantly higher and sensitivity of the heat loss responses was significantly lower in the midluteal than in the midfollicular phase, regardless of body site. These effects of the menstrual cycle in group U were not observed in group T. The sweating rate and cutaneous blood flow were significantly higher in group T than in group U, regardless of menstrual phase or body site. [T.sub.es] threshold for heat loss responses was significantly lower and sensitivity of heat loss responses was significantly greater in group T than in group U in the midluteal phase: however, sensitivity of the sweating response was significantly greater in the midfollicular phase. These results suggest that heat loss responses in group U were inhibited in the midluteal phase compared with in the midfollicular phase. Menstrual cycle had no remarkable effects in group T. Physical training improved heat loss responses, which was more marked in the midluteal than in the midfollicular phase. thermoregulation; estradiol; progesterone; long-term endurance training; heat acclimatization

To investigate quantitatively how sweating and cutaneous blood flow responses at the onset of dynamic exercise are affected by increasing exercise intensity in mildly heated humans, 18 healthy male subjects performed cycle exercise at 30, 50, and 70% of maximal [O.sub.2] uptake (V[O.sub.2] max) for 60 s in a warm environment. The study was conducted in a climatic chamber with a regulated ambient temperature of 35[degrees]C and relative humidity of 50%. The subjects rested in the semisupine position in the chamber for 60 min, and then sweating rate (SR) and skin blood flow were measured during cycle exercise at three different intensities. Changes in the heart rate, rating of perceived exertion, and mean arterial blood pressure were proportional to increasing exercise intensity, whereas esophageal and mean skin temperatures were essentially constant throughout the experiment. The SR on the chest, forearm, and thigh, but not on the palm, increased significantly with increasing exercise intensity (P < 0.05). The mean SR of the chest, forearm, and thigh increased 0.05 mg*[cm.sup.-2]*[min.sup.-1] with an increase in exercise intensity equivalent to 10% V[O.sub.2] max. On the other hand, the cutaneous vascular conductance (CVC) on the chest, forearm, and palm decreased significantly with increasing exercise intensity (P < 0.05). The mean CVC of the chest and forearm decreased 5.5% and the CVC on the palm decreased 8.0% with an increase in exercise intensity equivalent to 10% V[O.sub.2] max. In addition, the reduction in CVC was greater on the palm than on the chest and forearm at all exercise intensities (P < 0.01). We conclude that nonthermal sweating and cutaneous blood flow responses are exercise intensity dependent but directionally opposite at the onset of dynamic exercise in mildly heated humans. Furthermore, cutaneous blood flow responses to increased exercise intensity are greater in glabrous (palm) than in nonglabrous (chest and forearm) skin. thermal factors; nonthermal factors; glabrous skin; nonglabrous skin; feedforward manner

Objective: Although elderly patients undergoing surgery for acute type A aortic dissection (ATAAD) is increasing, their physical activities are not fully understood. We report the physical activities and surgical outcomes in elderly patients who underwent ATAAD. Methods: From 2009 to 2019, 103 consecutive patients underwent surgery for ATAAD at our institution. Surgical outcomes along with pre‐ and postoperative physical activities in 52 elderly patients (≥70 years old) were compared with those in 51 younger patients (<70 years old). Postoperative walking difficulty was defined as taking ≥30 days to regain the ability to walk 200 m postoperatively or as the inability to walk at discharge. Results: It took longer for elderly patients to regain the ability to walk 100 or 200 m postoperatively. ROC analysis revealed the AUC of the duration for walking 200 m postoperatively as a prognostic indicator for late deaths was 0.878, with the highest accuracy at 30 days (sensitivity = 83.3%, specificity = 91.8%). Hospital mortality within 30 days was 3.8%, and 1‐, 3‐, and 5‐years survival rates were 92%, 84.7%, 84.7%, respectively, for elderly patients, with no significant differences between groups. Cox proportional hazard analysis showed postoperative walking difficulty was an independent risk factor for late mortality in all cohorts (p =.017). Conclusions: Elderly patients undergoing surgical ATAAD repair showed acceptable surgical outcomes. However, they were more likely to decrease their physical activities postoperatively. Postoperative difficulty in walking was an independent risk factor for the late mortality in patients with ATAAD. [ABSTRACT FROM AUTHOR]

New Findings: What is the central question to this study?Do the sweat glands' maximum ion reabsorption rates increase following heat acclimation in healthy older individuals and is this associated with elevated aldosterone concentrations?What is the main finding and its importance?Sweat gland maximum ion reabsorption rates improved heterogeneously across body sites, which occurred without any changes in aldosterone concentration following a controlled hyperthermic heat acclimation protocol in healthy older individuals. We examined whether the eccrine sweat glands' ion reabsorption rates improved following heat acclimation (HA) in older individuals. Ten healthy older adults (>65 years) completed a controlled hyperthermic (+0.9°C rectal temperature, Tre) HA protocol for nine non‐consecutive days. Participants completed a passive heat stress test (lower leg 42°C water submersion) pre‐HA and post‐HA to assess physiological regulation of sweat gland ion reabsorption at the chest, forearm and thigh. The maximum ion reabsorption rate was defined as the inflection point in the slope of the relation between galvanic skin conductance and sweat rate (SR). We explored the responses again after a 7‐day decay. During passive heating, the Tb thresholds for sweat onset on the chest and forearm were lowered after HA (P < 0.05). However, sweat sensitivity (i.e. the slope), the SR at a given Tre and gross sweat loss did not improve after HA (P > 0.05). Any changes observed were lost during the decay. Pilocarpine‐induced sudomotor responses to iontophoresis did not change after HA (P ≥ 0.801). Maximum ion reabsorption rate was only enhanced at the chest (P = 0.001) despite unaltered aldosterone concentration after HA. The data suggest that this adaptation is lost after 7 days' decay. The HA protocol employed in the present study induced partial adaptive sudomotor responses. Eccrine sweat gland ion reabsorption rates improved heterogeneously across the skin sites. It is likely that aldosterone secretion did not alter the chest sweat ion reabsorption rates observed in the older adults. [ABSTRACT FROM AUTHOR]

While human eccrine sweat glands respond to adrenergic agonists, there remains a paucity of information on the factors modulating this response. Thus, we assessed the relative contribution of α‐ and β‐adrenergic sweating during a heat exposure and as a function of individual factors of sex and training status. α‐ and β‐adrenergic sweating was assessed in forty‐eight healthy young men (n = 35) and women (n = 13) including endurance‐trained (n = 12) and untrained men (n = 12) under non–heat exposure (temperate, 25°C; n = 17) and heat exposure (hot, 35°C; n = 48) conditions using transdermal iontophoresis of phenylephrine (α‐adrenergic agonist) and salbutamol (β‐adrenergic agonist) on the ventral forearm, respectively. Adrenergic sweating was also measured after iontophoretic administration of atropine (muscarinic receptor antagonist) or saline (control) to evaluate how changes in muscarinic receptor activity modulate the adrenergic response to a heat exposure (n = 12). α‐ and β‐adrenergic sweating was augmented in hot compared with temperate conditions (both P ≤.014), albeit the relative increase was greater in β (~5.4‐fold)‐ as compared to α (~1.5‐fold)‐adrenergic‐mediated sweating response. However, both α‐ and β‐adrenergic sweating was abolished by atropinization (P =.001). Endurance‐trained men showed an augmentation in α‐ (P =.043) but not β (P =.960)‐adrenergic sweating as compared to untrained men. Finally, a greater α‐ and β‐adrenergic sweating response (both P ≤.001) was measured in habitually active men than in women. We show that heat exposure augments α‐and β‐adrenergic sweating differently via mechanisms associated with altered muscarinic receptor activity. Sex and training status modulate this response. [ABSTRACT FROM AUTHOR]

New Findings: What is the central question of this study?Does the administration of the adrenergic presynaptic release inhibitor bretylium tosylate modulate sweating during exercise in the heat, and does this response differ between habitually trained and untrained men?What is the main finding and its importance?Iontophoretic administration of bretylium tosylate attenuates sweating during exercise in the heat in habitually trained and untrained men. However, a greater reduction occurred in trained men. The findings demonstrate a role for cutaneous adrenergic nerves in the regulation of eccrine sweating during exercise in the heat and highlight a need to advance our understanding of neural control of human eccrine sweat gland activity. We recently reported an influence of cutaneous adrenergic nerves on eccrine sweat production in habitually trained men performing an incremental exercise bout in non‐heat stress conditions. Based on an assumption that increasing heat stress induces cholinergic modulation of sweating, we evaluated the hypothesis that the contribution of cutaneous adrenergic nerves on sweating would be attenuated during exercise in the heat. Twenty young habitually trained and untrained men (n = 10/group) underwent three successive bouts of 15 min of light‐, moderate‐ and vigorous‐intensity cycling (equivalent to 30, 50, and 70% of peak oxygen uptake (V̇O2peak) respectively), each separated by a 15 min recovery while wearing a perfusion suit perfused with warm water (43°C). Sweat rate (ventilated capsule) was measured continuously at two bilateral forearm skin sites treated with 10 mm bretylium tosylate (an inhibitor of neurotransmitter release from adrenergic nerve terminals) and saline (control) via transdermal iontophoresis. A greater sweat rate was measured during vigorous exercise only in trained as compared to untrained men (P = 0.014). In both groups, sweating was reduced at the bretylium tosylate versus control sites, albeit the magnitude of reduction was greater in the trained men (P ≤ 0.024). These results suggest that cutaneous adrenergic nerves modulate sweating during exercise performed under a whole‐body heat stress, albeit a more robust response occurs in trained men. While it is accepted that a cholinergic mechanism plays a primary role in the regulation of sweating during an exercise‐heat stress, our findings highlight the need for additional studies aimed at understanding the neural control of human eccrine sweating. [ABSTRACT FROM AUTHOR]

Purpose: Human eccrine sweat glands respond to α1-adrenergic receptor agonists. We recently reported that adrenergic mechanisms contribute to sweating in endurance-trained men during an incremental exercise to volitional fatigue. However, it remains unclear if this response is mediated by α1-adrenergic receptor activation.Methods: Twelve endurance-trained men performed an incremental cycling bout until exhaustion while wearing a water-perfused suit to clamp skin temperature at ~ 34 °C. Bilateral forearm sweat rates were measured wherein the distal area was treated with either 1% terazosin (α1-adrenergic receptor antagonist) or saline solution on the opposite limb (Control) via transdermal iontophoresis. We also measured proximal bilateral forearm sweat rate in untreated sites to confirm that no between-limb differences in forearm sweat rate occurred. Once sweat rate returned to pre-exercise resting levels at ~ 20 min postexercise, 0.25% phenylephrine (α1-adrenergic receptor agonist) was iontophoretically administered to skin to verify α1-adrenergic receptor blockade.Results: Sweat rates at the proximal untreated right and left forearm sites were similar during exercise (interaction, P = 0.581). Similarly, no effect of terazosin on sweat rate was measured relative to control site (interaction, P = 0.848). Postexercise administration of phenylephrine increased sweat rate at the control site (0.08 ± 0.09 mg cm-2 min-1), which was suppressed by ~ 90% at the terazosin-treated site (0.01 ± 0.02 mg cm-2 min-1) (P = 0.026), confirming that α1-adrenergic receptor blockade was intact.Conclusion: Our findings demonstrate that α1-adrenergic receptors located at eccrine sweat glands do not contribute to eccrine sweating during incremental exercise in young endurance-trained men. [ABSTRACT FROM AUTHOR]

New Findings: What is the central question of this study?What are the effects of isomaltulose, an ingredient in carbohydrate–electrolyte beverages to maintain glycaemia and attenuate the risk of dehydration during exercise heat stress, on postexercise rehydration and physiological heat loss responses?What is the main finding and its importance?Consumption of a 6.5% isomaltulose–electrolyte beverage following exercise heat stress restored hydration following a 2 h recovery as compared to a 2% solution or water only. While the 6.5% isomaltulose–electrolytes increased plasma volume and plasma osmolality, which are known to modulate postexercise heat loss, sweating and cutaneous vascular responses did not differ between conditions. Consequently, ingestion beverages containing 6.5% isomaltulose–electrolytes enhanced postexercise rehydration without affecting heat loss responses. Isomaltulose is a disaccharide carbohydrate widely used during exercise to maintain glycaemia and hydration. We investigated the effects of ingesting a beverage containing isomaltulose and electrolytes on postexercise hydration state and physiological heat loss responses. In a randomized, single‐blind cross‐over design, 10 young healthy men were hypohydrated by performing up to three 30 min successive moderate‐intensity (50% heart rate reserve) bouts of cycling, each separated by 10 min, while wearing a water‐perfusion suit heated to 45°C. The protocol continued until a 2% reduction in body mass was achieved. Thereafter, participants performed a final 15 min moderate‐intensity exercise bout followed by a 2 h recovery. Following cessation of exercise, participants ingested a beverage consisting of (i) water only (Water), (ii) 2% isomaltulose (CHO‐2%), or (iii) 6.5% isomaltulose (CHO‐6.5%) equal to the volume of 2% body mass loss within the first 30 min of the recovery. Changes in plasma volume (ΔPV) after fluid ingestion were greater for CHO‐6.5% compared with CHO‐2% (120 min postexercise) and Water (90 and 120 min) (all P ≤ 0.040). Plasma osmolality remained elevated with CHO‐6.5% compared with consumption of the other beverages at 30 and 90 min postexercise (all P ≤ 0.050). Urine output tended to be reduced with CHO‐6.5% compared to other fluid conditions (main effect, P = 0.069). Rectal and mean skin temperatures, chest sweat rate and cutaneous perfusion did not differ between conditions (all P > 0.05). In conclusion, compared with CHO‐2% and Water, consuming a beverage consisting of CHO‐6.5% and electrolytes during recovery under heat stress enhances PV recovery without modulating physiological heat loss responses. [ABSTRACT FROM AUTHOR]

The sweat glands maximum ion reabsorption rates were investigated (n = 12, 21.7 ± 3.0 years, 59.4 ± 9.8 kg, 166.9 ± 10.4 cm and 47.1 ± 7.5 mL/kg/min) during two separate endogenous protocols; cycling at 30% (LEX) and 60% VO2max (MEX) and one exogenous trial; passive heating (PH) (43°C water lower leg immersion) in 27°C, 50%RH. Oesophageal temperature (Tes), skin temperature (Tsk), and forearm, chest and lower back sweat rate (SR) and galvanic skin conductance (GSC) were measured. Salivary aldosterone was measured pre-and postheating (n = 3). Using the ØSR threshold for an increasing ΔGSC to identify maximum sweat ion reabsorption rate revealed higher reabsorption rates during MEX compared to PH (mean of all regions: 0.63 ± 0.28 vs. 0.44 ± 0.3 mg/cm²/min, P < 0.05). It was not possible to identify the ion reabsorption rate during LEX for some participants. Tes and mean Tsk were different between conditions but mean body temperature (Tb) and local Tsk (forearm, chest and back) were similar (P > 0.05). Aldosterone increased more during MEX (72.8 ± 36.6 pg/mL) compared to PH (39.2 ± 17.5 pg/mL) and LEX (1.8 ± 9.7 pg/mL). The back had a higher threshold than the forearm (P < 0.05) but it was similar to the chest (P > 0.05) (mean of all conditions; 0.64 ± 0.33, 0.42 ± 0.25, 0.54 ± 0.3 mg/cm²/min, respectively). Although the differences between conditions may be influenced by thermal or nonthermal mechanism, our results indicate a possibility that the sweat glands maximum ion reabsorption rates may be different between exercise and passive heating without mediating skin regional differences. [ABSTRACT FROM AUTHOR]

The aim of our study was to determine if habitual endurance training can influence the relative contribution of nitric oxide synthase ( NOS) and cyclooxygenase ( COX) in the regulation of sweating during a passive heat stress in young adults. Ten trained athletes and nine untrained counterparts were passively heated until oral temperature (as estimated by sublingual temperature, Tor) increased by 1.5°C above baseline resting. Forearm sweat rate (ventilated capsule) was measured at three skin sites continuously perfused with either lactated Ringer's solution (Control), 10 mmol/L N G-nitro-L-arginine methyl ester (L- NAME, non-selective NOS inhibitor), or 10 mmol/L ketorolac (Ketorolac, non-selective COX inhibitor) via intradermal microdialysis. Sweat rate was averaged for each 0.3°C increase in Tor. Sweat rate at the L- NAME site was lower than Control following a 0.9 and 1.2°C increase in Tor in both groups (all P ≤ 0.05). Relative to the Control site, NOS-inhibition reduced sweating similarly between the groups ( P = 0.51). Sweat rate at the Ketorolac site was not different from the Control at any levels of Tor in both groups ( P > 0.05). Nevertheless, a greater sweat rate was measured at the end of heating in the trained as compared to the untrained individuals ( P ≤ 0.05). We show that NOS contributes similarly to sweating in both trained and untrained individuals during a passive heat stress. Further, no effect of COX on sweating was measured for either group. The greater sweat production observed in endurance-trained athletes is likely mediated by factors other than NOS- and COX-dependent mechanisms. [ABSTRACT FROM AUTHOR]

Cutaneous thermal sensitivity to a warm and cold stimulus was compared amongst 12 older (OF, 65.2 ± 1.0 year) and 29 younger (YF, 21.6 ± 0.2 years) female participants, and 17 older (OM, 66.2 ± 1.5 years) and 13 younger (YM, 21.2 ± 0.4 years) male participants to examine the effects of ageing and sex. In a neutral condition (27.5 °C, 50% RH) during rest, warm and cold thermal sensitivity was measured on eight body regions (forehead, chest, back, forearm, hand, thigh, calf, and foot). Using the method of limits, a thermal stimulator was applied to the skin at an adapting temperature and either increased or decreased at a constant rate (0.3 °C/s) until the participants detected the temperature with a push button. Thermal sensitivity declined with ageing to both a cold (older: 1468.6 ± 744.7 W/m 2 , younger: 869.8 ± 654.7 W/m 2 , p < 0.001) and warm (older: 2127.0 ± 1208.3 W/m 2 , younger: 1301.7 ± 1055.2 W/m 2 , p < 0.001) innocuous stimulus. YF and OF were more sensitive than YM and OM to both a warm and cold stimulus (p < 0.05). There was no interaction between age and sex suggesting that whilst thermal sensitivity decreases with age the decrease is similar between the sexes (p > 0.05). There was an interaction between temperatures, age and location and it seemed that cold thermal sensitivity was more homogenous for young and older participants however warm thermal sensitivity was more heterogeneous especially in the younger participants (p < 0.05). Although the pattern was not similar between ages or sexes it was evident that the forehead was the most sensitive region to a warm and cold stimulus. Interestingly the decline in sensitivity observed with ageing occurred for all locations but was attenuated at the forehead in both males and females (p > 0.05). [ABSTRACT FROM AUTHOR]

To investigate the effects of different training methods on nonthermal sweating during activation of the muscle metaboreflex, we compared sweating responses during postexercise muscle occlusion in endurance runners, sprinters, and untrained men under mild hyperthermia (ambient temperature, 35°C; relative humidity, 50%). Ten endurance runners, nine sprinters, and ten untrained men (maximal oxygen uptakes: 57.5 ± 1.5, 49.3 ± 1.5, and 36.6 ± 1.6 ml⋅kg-1, respectively; P < 0.05) performed an isometric handgrip exercise at 40% maximal voluntary contraction for 2 min, and then a pressure of 280 mmHg was applied to the forearm to occlude blood circulation for 2 min. The Δ change in mean arterial blood pressure between the resting level and the occlusion was significantly higher in sprinters than in untrained men (32.2 ± 4.4 vs. 17.3 ± 2.6 mmHg, respectively; P < 0.05); however, no difference was observed between distance runners and untrained men. The Δ mean sweating rate (averaged value of the forehead, chest, forearm, and thigh) during the occlusion was significantly higher in distance runners than in sprinters and untrained men (0.38 ± 0.07, 0.19 ± 0.03, and 0.11 ± 0.04 mg-cm-2-min-1, respectively; P < 0.05) and did not differ between sprinters and untrained men. Our results suggest that the specificity of training modalities influences the sweating response during activation of the muscle metaboreflex. In addition, these results imply that a greater activation of the muscle metaboreflex does not cause a greater sweating response in sprinters. [ABSTRACT FROM AUTHOR]

To examine sex- and menstrual cycle-related differences in thermoregulatory responses to heat exposure, ten young women and six young men were heated passively by immersing their legs in water heated to 42 degrees C for 60 min (in ambient conditions of 30 degrees C and 45% relative humidity). The women underwent heat exposure during the mid-follicular (F) and mid-luteal (L) phases of the menstrual cycle, which were confirmed by assaying plasma female reproductive hormones. The rectal and mean body (T(b)) temperatures of women in the L phase were significantly greater than those of women in the F phase and of men during a pre-heating equilibration period (28 degrees C) and during heat exposure. During heat exposure, the local sweat rates (m(sw)) on the forehead, chest, back, and forearm of women in either phase were significantly lower than those of men, but the thigh (m(sw)) was similar to that of men. The m(sw) did not change at any site during the different phases of the menstrual cycle. The cutaneous blood flow (%LDF) was significantly greater on the thigh for women in either phase compared with men, but no difference was found at any other site (forehead, chest, back, and forearm). The %LDF on the back was significantly greater for women in the L phase than in the F phase, but those at other sites were similar in both phases. We conclude that, compared with men, heat loss from women depends more on cutaneous vasodilation (especially on the thigh) than on sweating, irrespective of the phase of the menstrual cycle. This phenomenon was due to peripheral mechanisms, as reflected in the greater slope of the relationship between %LDF and T(b) lower slope of the relationship between m(sw)) and frequency of sweat expulsion, and lower sweat output per gland. The menstrual cycle modified the T(b) threshold for vasodilation and sweat onset in women. Therefore, the sex difference in the T(b) threshold was more marked for women during the L phase than during the F phase. Moreover, the menstrual cycle modified the slope of the relationship between %LDF on the back and T(b). [ABSTRACT FROM AUTHOR]

Eight men aged 60-65 years and six men aged 20-25 years, wearing only swimming trunks, were exposed to an air temperature of 17° C and 45% R.H. in each of the four seasons. The increase in the rate of metabolic heat production $$\left( {\% \Delta \dot M} \right)$$ for the older group in the cold test was significantly higher in summer and autumn than in winter and spring ( P<0.05), but did not differ in the young group between seasons. Compared to the young group the $$\% \Delta \dot M$$ was significantly greater for the older group (due to a marked increase in four individuals) in summer and autumn ( P<0.04). At the end of the period of cold exposure, the decrements of rectal temperature ( ΔT), mean skin temperature ( $$\bar T_{sk} $$ ; due to a marked decrease in four individuals) and foot skin temperature ( T) were significantly greater for the older group compared to the young group at all times of the year ( P<0.003). Seasonal variations in the two groups were similar, e.g., the ΔT gradually became smaller from summer to winter ( P<0.05) and then increased slightly in the spring ( P=0.07). T for both groups decreased from summer to autumn ( P<0.01) and remained unchanged subsequently. No seasonal variations were observed for $$\bar T_{sk} $$ in either group. The increase in diastolic blood pressure (BP) during the test was significantly smaller in winter in both groups ( P<0.05). BP became larger again during spring in the older group ( P<0.01), but remained low in the young group. The BP was significantly greater for the older group than the young group in winter and spring ( P<0.05). Compared to young men these results suggest that older men may lose the tolerance acquired by earlier cold acclimatization as seen by the BP responses, and have a somewhat lower thermoregulatory capability in coping with mild cold air in all seasons. [ABSTRACT FROM AUTHOR]

An abstract of the study "Aging process in heat adaptability and countermeasures for delaying it," by Yoshimitsu Inoue is presented.