This study was conducted to evaluate the effectiveness of a commercial, personal ice cooling vest on tolerance for exercise in hot (35°C), wet (65% relative humidity) conditions with a nuclear biological chemical suit (NBC). On three separate occasions, 10 male volunteers walked on a treadmill at 3 miles per hour and 2% incline while (a) seminude (denoted CON), (b) dressed with a nuclear, biological, chemical (NBC) suit with an ice vest (V) worn under the suit (denoted NBCwV); or (c) dressed with an NBC suit but without an ice vest (V) (denoted NBCwoV). Participants exercised for 120 min or until volitional fatigue, or esophageal temperature reached 39.5°C. Esophageal temperature (T(es)), heart rate (HR), thermal sensation, and ratings of perceived exertion were measured. Exercise time was significantly greater in CON compared with both NBCwoV and NBCwV (p < 0.05), whereas T(es), thermal sensation, heart rate, and rate of perceived exertion were lower (p < 0.05). Wearing the ice vest increased exercise time (NBCwoV, 103.6 ± 7.0 min; NBCwV, 115.9 ± 4.1 min) and reduced the level of thermal strain, as evidenced by a lower T(es) at end-exercise (NBCwoV, 39.03 ± 0.13°C; NBCwV, 38.74 ± 0.13°C) and reduced thermal sensation (NBCwoV, 6.4 ± 0.4; NBCwV, 4.8 ± 0.6). This was paralleled by a decrease in rate of perceived exertion (NBCwoV, 14.7 ± 1.6; NBCwV, 12.4 ± 1.6) (p < 0.05) and heat rate (NBCwoV, 169 ± 6; NBCwV, 159 ± 7) (p < 0.05). We show that a commercially available cooling vest can significantly reduce the level of thermal strain during work performed in hot environments.

Plasma hyperosmolality and baroreceptor unloading have been shown to independently influence the heat loss responses of sweating and cutaneous vasodilation. However, their combined effects remain unresolved. On four separate occasions, eight males were passively heated with a liquid-conditioned suit to 1.0°C above baseline core temperature during a resting isosmotic state (infusion of 0.9% NaCl saline) with (LBNP) and without (CON) application of lower-body negative pressure (-40 cmH2O) and during a hyperosmotic state (infusion of 3.0% NaCl saline) with (LBNP + HYP) and without (HYP) application of lower-body negative pressure. Forearm sweat rate (ventilated capsule) and skin blood flow (laser-Doppler), as well as core (esophageal) and mean skin temperatures, were measured continuously. Plasma osmolality increased by ∼10 mosmol/kgH2O during HYP and HYP + LBNP conditions, whereas it remained unchanged during CON and LBNP (P ≤ 0.05). The change in mean body temperature (0.8 × core temperature + 0.2 × mean skin temperature) at the onset threshold for increases in cutaneous vascular conductance (CVC) was significantly greater during LBNP (0.56 ± 0.24°C) and HYP (0.69 ± 0.36°C) conditions compared with CON (0.28 ± 0.23°C, P ≤ 0.05). Additionally, the onset threshold for CVC during LBNP + HYP (0.88 ± 0.33°C) was significantly greater than CON and LBNP conditions (P ≤ 0.05). In contrast, onset thresholds for sweating were not different during LBNP (0.50 ± 0.18°C) compared with CON (0.46 ± 0.26°C, P = 0.950) but were elevated (P ≤ 0.05) similarly during HYP (0.91 ± 0.37°C) and LBNP + HYP (0.94 ± 0.40°C). Our findings show an additive effect of hyperosmolality and baroreceptor unloading on the onset threshold for increases in CVC during whole body heat stress. In contrast, the onset threshold for sweating during heat stress was only elevated by hyperosmolality with no effect of the baroreflex.

The relative influence of muscle metabo-and baroreflex activity on heat loss responses during post-isometric handgrip (IHG) exercise ischemia remains unknown, particularly under heat stress. Therefore, we examined the separate and integrated influences of metabo-and baroreceptormediated reflex activity on sweat rate and cutaneous vascular conductance (CVC) under increasing levels of hyperthermia. Twelve men performed 1 min of IHG exercise at 60% of maximal voluntary contraction followed by 2 min of ischemia with simultaneous application of lower body positive pressure (LBPP, ϩ40 mmHg), lower body negative pressure (LBNP, Ϫ20 mmHg), or no pressure (control) under no heat stress. On separate days, trials were repeated under heat stress conditions of 0.6°C (moderate heat stress) and 1.4°C (high heat stress) increase in esophageal temperature. For all conditions, mean arterial pressure was greater with LBPP and lower with LBNP than control during ischemia (all P Յ 0.05). No differences in sweat rate were observed between pressure conditions, regardless of the level of hyperthermia (P Ͼ 0.05). Under moderate heat stress, no differences in CVC were observed between pressure conditions. However, under high heat stress, LBNP significantly reduced CVC by 21 Ϯ 4% (P Յ 0.05) and LBPP significantly elevated CVC by 14 Ϯ 5% (P Յ 0.05) relative to control. These results show that sweating during post-IHG exercise ischemia is activated by metaboreflex stimulation, and not by baroreflexes. In contrast, our results suggest that baroreflexes can influence the metaboreflex modulation of CVC, but only at greater levels of hyperthermia. heat stress; thermoregulation; isometric handgrip exercise; postexercise ischemia EXTENSIVE STUDIES HAVE SHOWN that mechano-and baroreceptors (cardiopulmonary and arterial) modulate the heat loss responses of cutaneous vasodilation and sweating during passive heating, exercise, and postexercise recovery, while central command can influence sweating and cutaneous vasodilation during exercise (12,13,23,24,31,34). In contrast, information regarding the influence of metaboreceptors on thermoeffector activity during and following exercise remains limited, largely because of the difficulties associated with isolating the muscle metaboreflex.Much of our understanding of the influence of metaboreceptor activity on heat loss responses has been limited to findings obtained using an isometric handgrip (IHG) exercise model (18,20,30). After an IHG exercise bout at a given percentage of maximal voluntary contraction (MVC), a 2-min period of ischemia is induced by occlusion of all limb blood flow to the exercising arm, which is thought to trigger group III and IV chemosensitive afferents (26). The activation of the metaboreflex results in an enhanced sweating response (18) while attenuating cutaneous vascular conductance (3).A potential caveat to these findings, however, is the fact that activation of the metaboreflex also results in a reflex increase in arterial blood pressure (26), thereby inducing a concomitant ...

This cross-sectional study documented very low serum calcidiol and calcitriol concentrations and high urinary N-telopeptide excretion in institutionalized elderly people. There was no difference in serum iPTH concentrations between institutionalized and ambulatory elderly. This finding could not be explained by the differences in calcidiol and calcitriol concentration, nor urinary NTX excretion. These results suggest that other factors than vitamin D deficiency, such as lower mobility status and sedentary life style, might have an important role in the regulation of iPTH and mechanisms of bone loss in the elderly.

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