Дисертації з теми "Whole body heat"

This thesis examined the effect of differences in body surface area-to-lean body mass ratio (AD/LBM) on core temperature cooling rates during cold water immersion (2°C, CWI) and temperate water immersion (26°C, TWI) following exercise-induced hyperthermia (end-exercise rectal temperature of 40°C). Individuals with a High AD/LBM (315 cm2/kg) had a ~1.7-fold greater overall rectal cooling rate relative to those with Low AD/LBM (275 cm2/kg) during both CWI and TWI. Further, overall rectal cooling rates during CWI were ~2.7-fold greater than during TWI for both the High and Low AD/LBM groups. Study findings show that AD/LBM must be considered when determining the duration of the immersion period. However, CWI provides the most effective cooling treatment for EHS patients irrespective of physical differences between individuals.

Exercise and/or heat-induced dehydration is associated with decreases in plasma volume (hypovolemia) and increases in plasma osmolality (hyperosmolality), which are thought to stimulate peripheral baroreceptors and central osmoreceptors respectively. Independently, plasma hyperosmolality and baroreceptor unloading have been shown to attenuate sweating and cutaneous vasodilation during heat stress, and therefore, negatively impact body temperature regulation. However, to date little is known regarding the combined influence of plasma hyperosmolality and baroreceptor unloading on thermoefferent activity. Therefore, we evaluated the separate and combined effects of baroreceptor unloading (via lower body negative pressure, LBNP) and plasma hyperosmolality (via infusion of 3% NaCl saline) on heat loss responses of sweating and cutaneous vascular conductance (CVC) during progressive whole-body heating. We show that the combined nonthermal influences of plasma hyperosmolality and baroreceptor unloading additively delay the onset threshold for CVC, relative to their independent effects. In contrast, baroreceptor unloading has no influence on the sweating response regardless of osmotic state. These divergent roles of plasma hyperosmolality and the baroreflex on heat loss responses might serve to enhance blood pressure and body core temperature regulation during dehydration and heat stress.

It is well established that older adults display marked impairments in the heat loss responses of sweating and skin blood flow relative to young adults which can exacerbate body heat storage by compromising whole-body heat loss (evaporative + dry heat exchange). Similarly, young women display reductions in whole-body heat loss relative to young men during exercise in dry heat. As such, it is possible that the age-related decline in whole-body heat loss will be greater among women relative to men. To examine whether the age-related decline in whole-body heat loss would be greater in women relative to men during exercise in dry heat, and whether this response would be more pronounced with a greater elevation in the level of heat stress, whole-body heat loss (evaporative ± dry heat exchange) was evaluated in 80 individuals (46 men, 34 women) aged between 18-70 years. Participants completed an incremental exercise model involving three, 30-min bouts of semi-recumbent cycling at fixed rates of metabolic heat production (150, 200, 250 W/m2), each separated by a 15-min recovery period in hot-dry conditions (40˚C, ~15% relative humidity). Whole-body heat loss was measured using direct calorimetry whereas metabolic heat production was measured using indirect calorimetry. Whole-body heat loss declined with age (across men and women) during moderate- and vigorous-intensity exercise by 4.2 and 6.6 W/m2 (both P < 0.050), respectively, however, these relationships were not modified by sex (both P > 0.050). Nonetheless, whole-body heat loss was lower in women relative to men during moderate- and vigorous-intensity exercise by 8.4 and 12.1 W/m2 (both P < 0.05), respectively. Therefore, the results of this thesis demonstrate that the age-related decline in whole-body heat loss is not dependent on sex.

The current thesis examined whether sex-differences in local and whole-body heat loss are evident after accounting for confounding differences in physical characteristics and rate of metabolic heat production. Three experimental studies were performed: the first examined whole-body heat loss in males and females matched for body mass and surface area during exercise at a fixed rate of metabolic heat production; the second examined local and whole-body heat loss responses between sexes during exercise at increasing requirements for heat loss; the third examined sex-differences in local sweating and cutaneous vasodilation to given doses of pharmacological agonists, as well as during passive heating. The first study demonstrates that females exhibit a lower whole-body sudomotor thermosensitivity (553 ± 77 vs. 795 ± 85 W•°C-1, p=0.05) during exercise performed at a fixed rate of metabolic heat production. The second study shows that whole-body sudomotor thermosensitivity is similar between sexes at a requirement for heat loss of 250 W•m-2 (496 ± 139 vs. 483 ± 185 W•m-2•°C-1, p=0.91) and 300 W•m-2 (283 ± 70 vs. 211 ± 66 W•m-2•°C-1, p=0.17), only becoming greater in males at a requirement for heat loss of 350 W•m-2 (197 ± 61 vs. 82 ± 27 W•m-2•°C-1, p=0.007). In the third study, a lower sweat rate to the highest concentration of acetylcholine (0.27 ± 0.08 vs. 0.48 ± 0.13 mg•min-1•cm-2, p=0.02) and methylcholine (0.41 ± 0.09 vs. 0.57 ± 0.11 mg•min-1•cm-2, p=0.04) employed was evidenced in females, with no differences in cholinergic sensitivity. Taken together, the results of the current thesis show that sex itself can modulate sudomotor activity, specifically the thermosensitivity of the response, during both exercise and passive heat stress. Furthermore, the results of the third study point towards a peripheral modulation of the sweat gland as a mechanism responsible for the lower sudomotor thermosensitivity in females.

The human central nervous system (CNS) is capable of significant architectural and physiological reorganization in response to environmental stimuli. Novel sensorimotor experiences stimulate neuronal networks to modify their intrinsic excitability and spatial connectivity within and between CNS structures. Early learning-induced adaptations in the primary motor cortex are thought to serve as a priming stimulus for long term CNS reorganization underlying long-lasting changes in motor skill. Recent animal and human studies suggest that whole body exercise and core temperature elevation as systemic stressors also recruit activity-dependent processes that prime the motor cortex, cerebellum, and hippocampus to process sensorimotor stimuli from the environment, enhancing overall CNS learning and performance. A primary goal of rehabilitation specialists is to evaluate and design activity-based intervention strategies that induce or enhance beneficial neuroplastic processes across the lifespan. As such, an investgation of the influence of physical, non-pharmacological interventions on cortical excitability, motor learning, and cognitive function provide the central theme of this dissertation. The first study investigated the effects of a visually-guided motor learning task on motor cortex excitability at rest and during voluntary activation measured via transcranical magnetic stimulation (TMS). Motor learning significantly increased resting cortical excitability that was not accompanied by changes in excitability as a function of voluntary muscle activation. The cortical silent period, a measure of inhibition, increased after learning and was associated with the magnitude of learning at low activation. These findings suggest that separate excitatory and inhibitory mechanisms may influence motor output as a function of learning success. The following studies investigated the influence of systemic whole-body thermal stress on motor cortex excitability, motor learning and cognitive performance. We established the reliability of a novel TMS cortical mapping procedure to study neurophysiological responses after whole-body heat stress. Heat stress significantly potentiated motor cortex excitability, though acute motor learning and cognitive test performance did not differ between subjects receiving heat stress and control subjects. Future research is needed to delineate the potential of whole body heat stress as a therapeutic modality to influence central nervous system plasticity and performance.

This thesis sought to evaluate whether the increased risk of heat-related illness observed in black-African descendants stems from impairements in local- and whole-body heat loss responses in this ethnic group. To evaluate this, in separate studies local- (study 1) and whole–body (study 2) heat loss responses were compared in young men (18-30 y) of black-African (n=21) and Caucasian (n=21) descent, matched for physical characteristics and fitness and born and raised in the same temperate environment. In study 1, we compared nitric oxide-dependent skin blood flow and sweating responses in young men of black-African (n=10) and Caucasian (n=10) descent during rest, exercise, and recovery in the heat. Both groups rested for 10-min, and then performed 50-min of moderate-intensity exercise at 200 W/m2, followed by 30-min of recovery in hot-dry heat (35°C, 20% RH). Local cutaneous vascular conductance (CVC%max) and sweat rate (SR) were measured at two forearm skin sites treated with a) lactated-Ringer (Control), or b) 10 mM NG-nitro-L-arginine methyl ester (L‐NAME, NO synthase-inhibitor). L-NAME significantly reduced CVC%max throughout rest, exercise, and recovery in both groups (both p<0.001). However, there were no significant main effects for the NO contribution to CVC%max between groups (all p>0.500). L-NAME significantly reduced local SR in both groups (both p<0.050). The NO contribution to SR was similar between groups such that L-NAME reduced SR relative to control at 40 and 50 min into exercise (both p<0.050). In study 2, we assessed whole-body total heat loss (evaporative + dry heat exchange) in black-African (n=11) and Caucasian (n=11) men using direct calorimetry. Participants performed three, 30-min bouts of semi-recumbent cycling at fixed metabolic heat productions (and therefore matched heat loss requirements between groups) of 200 (light), 250 (moderate), and 300 W/m2 (vigorous), each followed by 15-min recovery, in dry heat (40°C, ~13% relative humidity). Across all exercise bouts, dry (p=0.435) and evaporative (p=0.600) heat exchange did not differ significantly between groups. As such, total heat loss during light, moderate and vigorous exercise was similar between groups (p=0.777), averaging ((mean (SD)); 177 (10), 217 (13) and 244 (20) W/m2 in men of black-African descent, and 172 (13), 212 (17) and 244 (17) W/m2 in Caucasian men. Accordingly, body heat storage across all exercise bouts (summation of metabolic heat production and total heat loss) was also similar between the black-African (568 (142) kJ) and Caucasian groups (623 (124) kJ; p=0.356). This thesis demonstrates that ethnicity does not influence NO-dependent cutaneous vasodilation and sweating in healthy, young black-African descent and Caucasian men during exercise in the heat. Furthermore, we extend upon these observations by showing no differences in whole-body dry and evaporative heat exchange and therefore body heat storage.

Abstract The purpose of this study was to examine thermal (body temperature, thermal sensation and comfort ratings), circulatory (blood pressure, heart rate variability) and neuromuscular performance responses to whole-body cryotherapy (WBC, -110 °C). Altogether 66 healthy subjects were exposed to WBC for two minutes. The acute and long-term changes were examined, when the subjects were exposed to WBC three times a week during three months. Skin temperatures decreased very rapidly during WBC, but remained such a high level that there was no risk for frostbites. The effects on rectal temperature were minimal. Repeated exposures to WBC were mostly well tolerated and comfortable and the subjects became habituated at an early stage of trials. WBC increased both systolic (24 mmHg) and diastolic (5 mmHg) blood pressures temporarily. Adaptation of blood pressure was not found during three months. The acute cooling-related increase in high-frequency power of RR-intervals indicated an increase in cardiac parasympathetic modulation, but after repeated WBC the increase was attenuated. The repeated WBC exposure-related increase in resting low frequency power of RR-intervals resembles the response observed related to exercise training. There are signs of neuromuscular adaptation, especially in dynamic performance. A single WBC decreased flight time in drop-jump exercise, but after repeated WBC these changes were almost vanished. This adaptation was confirmed by the change of the activity of the agonist muscle, which increased more and the change of the activity of antagonist muscle, which increased less/did not change after repeated WBC indicating reduced co-contraction and thus, neuromuscular adaptation.

It is well known that sitting posture is associated with discomfort and a number of musculoskeletal disorders. Seat manufacturers have made great strides toward developing seats for equipment which helped in alleviating the vibration transferring to the lower area of the spine; however, increased neck and head motion resulting from these seat designs may have been overlooked. Many cervical spine studies have been developed to estimate the response of the head and neck; however, these current studies do not take head and neck posture into account. The objective of this work was to study and demonstrate the difference in human biomechanical response to WBV when they use different neck postures. Four head and neck postures: up, down, to the side, and normal (straight forward) were investigated. Ten male subjects with ages ranging from 19 to 28 years were used to test each of the four postures, using the discrete sinusoidal frequencies of 2, 3, 4, 5, 6, 7, and 8 Hz at constant amplitudes of 0.8 m/s^2 RMS and 1.15 m/s^2 RMS in the x-direction (fore-and-aft). Subjects were seated in a rigid seat rigidly mounted to a vibration platform and vibration was generated using a six-degree-of-freedom man-rated shaker table. Subjects were tightly coupled to the seat back, using a neoprene vest and 5 straps, in an effort to reduce any relative motion between the seat and the subject. Subjects reported their head and neck discomfort using the Borg CR-10 scale with each of the postures, and then gave a second discomfort rating for the normal posture for each combination. Motion capture and accelerometer data were used to acquire the motion of the seat, C7 vertebrae, and center-of-head motion. The 3D motion of selected points on the heads and necks of the subjects were acquired using a twelve-camera Vicon motion capture system. Accelerometer data at the head, C7, and seat was used to verify the motion capture data. For the head-down posture, the magnitude of the discomfort function was higher than the normal posture. The head-to-side and head-up postures have shown less discomfort have shown less discomfort in the critical resonance area; however, these postures show roughly the same discomfort as the normal posture in other frequency ranges. In these postures, the subjects are using major neck-back muscles which create a stiffer system and may explain why there is a shift in the second peak in the head-to-side and head-up postures. Interestingly, the head-to-side and head-up postures show a similar trend as the normal posture, however, the peak transmissibility is attenuated. In addition, the subject's average discomfort was lower in this range compared to the normal posture. The head-down posture had the highest transmissibility and discomfort overall and suggests that workers in vibration environments should reduce any head-down postures to avoid unwanted head accelerations and discomfort. This work has demonstrated the importance of considering the head-neck posture in future seat-design studies.

Head stabilisation during gait related tasks is thought to be fundamental to whole body stability, but this has received little attention in the older population. There is a need to examine any age related changes in neuromechanical mechanisms underpinning head stabilisation that may challenge the control of head stability, and consequently whole body stability. The present Thesis examined the mechanisms contributing to head stabilisation, and whole body stability during two gait tasks, steady state gait and gait initiation in young and older females, with the overall aim of contributing to negating fall risk. Four studies were designed to examine a) head position and walking speed on gait stability during steady state gait; b) neuromechanical mechanisms underpinning head stabilisation during gait initiation; c) head position on whole body stability during gait initiation; and d) head stabilisation during gait initiation at different speeds. Results showed that a) gait stability, was unaffected by head position and different walking speeds during steady state gait, b) decreased head stability in older individuals during gait initiation can be attributed to a deterioration of the neuromechanical mechanisms relating to head stability, c) free head movement during gait initiation does not affect head stabilisation or whole body stability but it does affect gait parameters, while d) initiating gait at faster than comfortable speeds compromises head stabilisation and reduces whole body stability in older individuals. Collectively, these results demonstrate that older individuals adopt an increased head flexion position when walking, while impaired head stability can be attributed to deterioration of the function of their neuromechanical mechanisms compared to their younger counterparts during gait tasks at comfortable speeds. These findings provide an understanding of the effect head stabilisation can have on older adults’ gait and on their fall risk during gait and gait initiation.

Abstract The aim of the present study was to describe the effects of different types of cold exposures on blood pressure (BP) and heart rate (HR) and to test how these cold-induced effects are modulated by antihypertensive drugs representing different kind of mechanisms of action. The tested drugs represented the following antihypertensive drug subgroups: metoprolol from beta-blocking agents, carvedilol from alfa- and beta-blocking agents, lisinopril from angiotensin converting enzyme inhibitors, eprosartan from angiotensin II antagonists, amlodipine from calcium channel blockers and hydrochlorothiazide from diuretics. The main outcome measures were the levels and changes in systolic (SBP) and diastolic blood pressure (DBP) and HR before, during and after cold exposure. The normotensive and mildly hypertensive subjects were exposed either to –15°C for 15 minutes (with winter clothing), 5°C for 45 minutes (minimal clothing) or to a cold pressor test (CPT). Before measurements at –15°C, metoprolol, carvedilol, lisinopril, eprosartan, hydrochlorothiazide or placebo were given for a week in a double-blind and crossover manner. In one test procedure (5°C and CPT) the test subjects ingested amlodipine for three days or were without drug ingestion before the tests in a crossover manner. Both SBP and DBP were markedly increased by all types of cold exposure. Cold-induced rises of SBP/DBP were higher during the exposure to 5°C and –15°C (19–35/20–24 mmHg) than during CPT (13/16 mmHg). Metoprolol, carvedilol, lisinopril, eprosartan and amlodipine decreased the level of BP during the exposure to 5°C and –15°C compared to placebo or no drug. The antihypertensive drugs, with dosages used in this study, did not affect the cold-induced rise of BP compared to no drug or placebo. HR increased during CPT, but decreased during exposure to 5°C and –15°C. Metoprolol and carvedilol decreased HR during exposure to –15°C compared to placebo. The present study demonstrates for the first time the effects of antihypertensive drugs on BP in hypertensive subjects exposed to cold similar to normal outdoor exposure in winter. Although the magnitude of the cold-induced rise in BP was not affected by the drugs, the drug-induced decrease in the level of BP kept the peak values in the cold closer to the recommended threshold limit values
Tiivistelmä Tutkimuksen tarkoituksena oli selvittää eri mekanismeilla vaikuttavien verenpainelääkkeiden vaikutusta verenpainevasteisiin ja sydämen lyöntitiheyteen kylmässä sekä verrata erilaisten kylmäaltistusten vaikutusta verenpaineeseen ja sydämen lyöntitiheyteen. Tutkitut lääkkeet edustivat seuraavia verenpainelääkeryhmiä: metoprololi beetasalpaajia, karvediloli yhdistettyjä alfa- ja beetasalpaajia, lisinopriili ACE-estäjiä, eprosartaani angiotensiini II antagonisteja, amlodipiini kalsiumestäjiä ja hydroklooritiatsidi diureetteja. Tärkeimmät mitatut vasteet olivat systolisen ja diastolisen verenpaineen ja sydämen lyöntitiheyden tasot ja muutokset ennen kylmäaltistusta, kylmäaltistuksen aikana ja sen jälkeen. Lisäksi mitattiin lämpötilavasteita ja tuntemuksia. Normo- ja hypertensiiviset koehenkilöt altistettiin joko –15°C:seen 15 minuutin ajaksi (talvivaatetuksessa), 5°C:seen 45 minuutin ajaksi (minimaalisella vaatetuksella) tai tehtiin ns. käden kylmävesitesti (CPT). Testisarjoissa (–15°C) metoprololi, karvediloli, lisinopriili, eprosartaani ja hydroklooritiatsidi tai plasebo annettiin viikon ajan kaksoissokko- ja vaihtovuoromenetelmällä. Yhdessä testisarjassa (5°C ja CPT) koehenkilöt ottivat amlodipiinia 3 päivän ajan tai olivat ilman lääkettä ennen testikertoja vaihtovuoroisessa järjestyksessä. Kaikki kylmäaltistustyypit nostivat merkittävästi sekä systolista että diastolista verenpainetta. Systolisen ja diastolisen verenpaineen nousu oli korkeampi koko kehon kylmäaltistuksissa (5°C tai –15°C) (19–35/20–24 mmHg) kuin ns. kylmävesitestissä (13/16 mmHg). Metoprololi, karvediloli, lisinopriili, eprosartaani ja amlodipiini laskivat verenpaineen tasoja koko kehon kylmäaltistuksessa verrattuna plaseboon. Yksikään verenpainelääkkeistä ei vaikuttanut merkittävästi kylmän aiheuttamaan verenpaineen nousuun verrattuna tutkimuskertaan ilman lääkettä tai plaseboon. Sydämen lyöntitiheys nousi ns. kylmävesitestin aikana, mutta laski koko kehon kylmäaltistuksissa (5°C ja –15°C). Metoprololi ja karvediloli laskivat sydämen lyöntiheyttä kylmäaltistuksessa (–15°C) verrattuna plaseboon. Tämä tutkimus kuvaa ensimmäistä kertaa, kuinka verenpainelääkkeet vaikuttavat verenpainetasoihin ja -vasteisiin kylmäaltistuksessa, joka simuloi tyypillisiä ulko-olosuhteita talvella. Vaikka lääkkeet eivät estäneet kylmän aiheuttamaa verenpaineen nousua, ne laskivat verenpaineen tasoa, jolloin verenpaine pysyi kylmässäkin lähempänä suositusrajoja

Exposure to extreme temperature conditions such as occurs in certain occupations is known to induce male infertility. In humans and most of the eutherian mammals, it has been shown that whole body heat stress decreases fertility and produces defective embryos. However, the mechanisms producing fertility defects post exposure to whole body heat are not yet fully determined. Hence, the present study aimed at gaining some insight into the mechanisms producing fertility defects after whole body heat stress. Laboratory mice were exposed to constant temperatures higher than their core body temperature of 37-38°C for 8h on three consecutive days. A decrease in testis weight occurred as early as 7 days post exposure to heat with weights comparable to controls by 21 days post heat exposure. Histology of the testicular tissue showed germ cell apoptosis affecting the pachytene spermatocytes and the spermatids. Germ cell apoptosis was investigated by TUNEL 16h, 7, 14 and 21 days following the heat treatment. Apoptosis was found to be stage-specific affecting early and late stages of the seminiferous epithelium cycle on day 7 and 14 post exposure to heat stress with involvement of all stages of seminiferous epithelium 16h following heat stress. Reduction in germ cell apoptosis was evident 21 days post exposure. To determine the mechanism of germ cell apoptosis, caspase-3 proteins were detected in apoptotic germ cells following heat stress which showed strong positivity. Hence, we concluded that whole body heat stress results in caspase-3 mediated germ cell apoptosis. Furthermore, changes in cauda epididymal spermatozoa were investigated to determine sperm apoptosis following heat stress. Sperm apoptosis was detected by the exteriorization of phosphotidylserine (PS) on the outer layer of the plasma membrane. The results showed an early and late apoptosis in caudal epididymal spermatozoa 16hr following heat treatment. A second experiment was conducted to determine the time of appearance of changes in spermatozoa following whole body heat stress for which the duration of exposure to heat of 37-38°C was reduced to one-day period. This showed more spermatozoa in the early phase of apoptosis with fewer dead spermatozoa, which is suggestive of a time and temperature dependant pattern of sperm apoptosis. Arid-adapted Notomys alexis (hopping mice) were also investigated to determine whether differences in response to whole body heat have evolved in extreme climate conditions. Therefore hopping mice were exposed to similar temperatures as laboratory mice to investigate heat influences on germ cells and spermatozoa. Like the laboratory mice, germ cells and spermatozoa of hopping mice also showed apoptosis. However, unlike in laboratory mice, stage specificity in apoptosis could not be determined in hopping mice because of the presence of more than one cell association within the cross sections of the seminiferous tubules. Similar to laboratory mice, germ cell apoptosis in hopping mice was caspase-3 mediated. The vasculature of hopping mice was also determined to look for any variations in the cooling mechanisms, which could have resulted in germ cell apoptosis. We found the absence of a coiled testicular artery suggestive of a lack of such a cooling mechanism in hopping mice that could have resulted in germ cell and sperm apoptosis. We also investigated changes in germ cells following experimental cryptorchidism, which showed tubular degeneration with low numbers of germ cells lining the seminiferous epithelium. Thus the findings indicated that whole body heat had a detrimental effect on developing germ cells and spermatozoa. It is also known that heat stress changes other bodily functions to maintain body homeostasis. Heat stress is associated with an activation of the hypothalamic-pituitary axis, which is followed by an increase in blood cortisol levels in the circulation as a result of increased synthesis of corticosteroids from the adrenocortical cells. Hence the current study also determined changes, if any, in the adrenal glands, especially the adrenocortical cells of laboratory and hopping mice following whole body heat exposure. Heat stress resulted in the formation of vacuoles, dilated capillaries and interstitial fibrosis in cortical areas of the adrenal glands in both the species. In addition, large syncytial bodies were evident in hopping mice adrenal cortical cells. Thus it is evident from the study that germ cell and sperm apoptosis are a result of either a direct effect of heat on germ cells and/ or due to changes in the body hormonal milieu following whole body heat stress. Thus this study showed an activation of caspases in producing germ cell apoptosis and externalization of PS in inducing sperm apoptosis following whole body heat stress with changes in the adrenocortical cells following heat stress. This study demonstrated that an aridadapted species Notomys alexis, although evolved in extreme environmental conditions, also is affected by high temperatures. Hence, this study gives some insight in the reasons for reduced fertility following whole body heat stress.
Thesis (Ph.D.) (Research by Publication) -- University of Adelaide, School of Medicine, 2015.

Thesis (M.S.)--University of Wisconsin--Madison, 1985.
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Tese de Doutoramento em Engenharia Industrial e de Sistemas (PDEIS)
Atualmente, é possível definir a saúde como o bem-estar físico, mental e social, em que o ser humano goza o grau máximo de saúde em determinado tempo e lugar. No entanto, para o ambiente de trabalho ser considerado salubre ele deve respeitar os limites de tolerância previstos pelas legislações e diretivas internacionais. No geral, a literatura evidencia que dois riscos ocupacionais combinados, podem produzir respostas orgânicas diferentes de quando considerados de forma isolada. À princípio, os mesmos teriam o potencial de ser mais nocivos à saúde do trabalhador, mesmo em baixos níveis. Tal fato possibilita a discussão sobre os métodos tradicionais de avaliação ocupacional, cujas metodologias consideram os fatores de riscos de forma isolada. Com isso, o objetivo do trabalho foi identificar os efeitos resultantes da exposição simultânea a fatores de risco físico sobre a saúde de operadores de equipamentos na indústria da construção civil, relativos aos aspectos fisiológicos e cognitivos, a fim de desenvolver uma metodologia para análise combinada dos fatores de risco físico. Para isto foram realizadas 50 medições ocupacionais de ruído, estresse térmico e vibrações de corpo inteiro em operadores de equipamentos da construção civil (ECC) durante a toda a jornada de trabalho. Também foram coletados dados de frequência cardíaca (FC) e desempenho em teste de atenção (TMR) durante a jornada de trabalho. Os dados foram tratados estatisticamente, cujos resultados mostram que o ruído possui o Lavg médio de 77,7 dB(A), enquanto o índice WBGT é de 26,0°C e a vibração de corpo inteiro possui AREN de 0,570 m/s2. Esses valores indicam que as operações com ECC ocorrem com os fatores de risco abaixo dos limites de tolerância. Tendo em vista que para o ruído o limite é de 85,0 dB(A). Enquanto o para o estresse térmico é de 30,5°C e para as vibrações de corpo inteiro é de 1,15m/s2. Os fatores de risco físico quando analisados em separado possuem fraca correlação estatística com as respostas orgânicas (FC e TMR). Contudo, quando analisados em simultâneo por meio de modelos de regressão linear múltipla (RLM) as respostas orgânicas podem ser explicadas pela combinação do ruído, das vibrações de corpo inteiro e do calor. Não foi possível perceber se os fatores de risco físico quando combinados tornavam-se mais agressivos do que quando avaliados em separado. O que foi possível constatar é que durante a jornada, a FC e o TMR variam em torno de valores médios. A sinergia entre os fatores de risco observados, não pôde ser relacionada a capacidade de ser mais agressivo ao ser humano durante a exposição, mas sim ao fato dos dados das respostas orgânicas obtidos só puderem ser explicados pela combinação dos mesmos. Ao ponto de quando o dado de um dos fatores ser retirado da análise, o modelo perder totalmente sua precisão e capacidade de explicação numérica das respostas orgânicas.
Currently, it is possible to define health as physical, mental and social well-being, in which the human being enjoys the maximum degree of health at a given time and place. However, for the working environment to be considered salubrious it must respect the limits of tolerance provided by international laws and directives. Overall, the literature shows that two combined occupational hazards may produce different organic responses than when considered in isolation. At first, they would have the potential to be more harmful to worker health, even at low levels. This fact makes possible the discussion about the traditional methods of occupational evaluation, whose methodologies consider the risk factors in isolation. The objective of this study was to identify the effects of simultaneous exposure to physical risk factors on the health of equipment operators in the construction industry, related to physiological and cognitive aspects, to develop a methodology for the combined analysis of physical risk factors. For this, 50 occupational measurements of noise, heat and full body vibrations were performed on construction equipment operators (CEO) during the working day. Also collected heart rate (HR) data and performance in attention test (MRT) during the work day. The data were analyzed statistically, whose results show that the noise has the Lavg of 77.7 dB (A), while the index WBGT is 26.0°C and whole body vibration has AREN of 0.570 m/s2. These values indicate that CEO operations occur with risk factors below the tolerance limits. Considering that the noise limit is 85.0 dB (A). While the for the heat stress is 30.5 ° C and for the whole-body vibrations is 1.15m/s2. Physical risk factors when analyzed separately have a low statistical correlation with the physiological responses (HR and MRT). However, when analyzed simultaneously by multiple linear regression (MLR) models the physiological responses can be explained by the combination of noise, whole-body vibrations and heat. It was not possible to see if the physical risk factors when combined became more aggressive than when assessed separately. What was possible to verify is that during the day, the HR and TMR vary around average values. The synergy between the observed risk factors could not be related to the capacity to be more aggressive to humans during the exposure, but to the fact that the data of the physiological responses obtained can only be explained by the combination of the same. To the extent that when the data of one of the factors is removed from the analysis the model totally loses its accuracy and numerical explanation capacity of the physiological responses.