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Biomedical subjects

Igor B Mekjavic

Publications and source records attributed to Igor B Mekjavic.

14 recordsLinked to original sources

Cold-induced vasodilatation is not homogenous or generalizable across the hand and feet.

Cold-induced vasodilatation (CIVD), a paradoxical cyclical increase in finger temperature upon cold exposure, is assumed to serve against cold injury. Most existing research has focused on hand and finger responses, yet most cold injuries occur in the feet. We investigated if CIVD responses of one finger can predict the responses of other fingers, and also whether the fingers could predict CIVD responses of the feet and toes. Ten subjects immersed their left hand up to the wrist in 8 degrees C water for 30 min. They passively rewarmed for 15 min, followed by immersion of the left foot to the ankle in 8 degrees C water for 30 min. Digit temperature at the edge of the nail bed was recorded on all fingers and toes and on the hand and feet. In all subjects, toe and foot temperature gradually decreased exponentially from approximately 31 to approximately 9 degrees C. No subject exhibited CIVD in any toe or on the foot itself. Eight subjects exhibited CIVD (>1 degrees C temperature increase) in at least one digit of the hand, but no consistent pattern existed in finger response to cold. No subject had strong (>2.0 degrees C) CIVD in all fingers. Five had strong CIVD in some but not all digits, with magnitudes ranging 1.4-7.5 degrees C, while three had weak (<2 degrees C) CIVD in some but not all digits. Four exhibited asynchronous CIVD in the fingers, with cycles beginning at different times. We conclude that CIVD is highly variable across the fingers, and is not a generalizable response across digits or limbs.

Adult↗

Hip, thigh and calf muscle atrophy and bone loss after 5-week bedrest inactivity.

Unloaded inactivity induces atrophy and functional deconditioning of skeletal muscle, especially in the lower extremities. Information is scarce, however, regarding the effect of unloaded inactivity on muscle size and function about the hip. Regional bone loss has been demonstrated in hips and knees of elderly orthopaedic patients, as quantified by computerized tomography (CT). This method remains to be validated in healthy individuals rendered inactive, including real or simulated weightlessness. In this study, ten healthy males were subjected to 5 weeks of experimental bedrest and five matched individuals served as ambulatory controls. Maximum voluntary isometric hip and knee extension force were measured using the strain gauge technique. Cross-sectional area (CSA) of hip, thigh and calf muscles, and radiological density (RD) of the proximal tibial bone were measured using CT. Bedrest decreased (P < 0.05) average (SD) muscle strength by 20 (8)% in knee extension, and by 22 (12)% in hip extension. Bedrest induced atrophy (P < 0.05) of extensor muscles in the gluteal region, thigh and calf, ranging from 2 to 12%. Atrophy was more pronounced in the knee extensors [9 (4)%] and ankle plantar flexors [12 (3)%] than in the gluteal extensor muscles [2 (2)%]. Bone density of the proximal tibia decreased (P < 0.05) by 3 (2)% during bedrest. Control subjects did not show any temporal changes in muscle or bone indices (P > 0.05), when examined at similar time intervals. The present findings of a substantial loss in hip extensor strength and a smaller, yet significant atrophy of these muscles, demonstrate that hip muscle deconditioning accompanies losses in thigh and calf muscle mass after bedrest. This suggests that comprehensive quantitative studies on impaired locomotor function after inactivity should include all joints of the lower extremity. Our results also demonstrate that a decreased RD, indicating bone mineral loss, can be shown already after 5 weeks of unloaded bedrest, using a standard CT technique.

Adult↗

Motion sickness increases the risk of accidental hypothermia.

Motion sickness (MS) has been found to increase body-core cooling during immersion in 28 degrees C water, an effect ascribed to attenuation of the cold-induced peripheral vasoconstriction (Mekjavic et al. in J Physiol 535(2):619-623, 2001). The present study tested the hypothesis that a more profound cold stimulus would override the MS effect on peripheral vasoconstriction and hence on the core cooling rate. Eleven healthy subjects underwent two separate head-out immersions in 15 degrees C water. In the control trial (CN), subjects were immersed after baseline measurements. In the MS-trial, subjects were rendered motion sick prior to immersion, by using a rotating chair in combination with a regimen of standardized head movements. During immersion in the MS-trial, subjects were exposed to an optokinetic stimulus (rotating drum). At 5-min intervals subjects rated their temperature perception, thermal comfort and MS discomfort. During immersion mean skin temperature, rectal temperature, the difference in temperature between the non-immersed right forearm and 3rd finger of the right hand (DeltaTff), oxygen uptake and heart rate were recorded. In the MS-trial, rectal temperature decreased substantially faster (33%, P < 0.01). Also, the DeltaTff response, an index of peripheral vasomotor tone, as well as the oxygen uptake, indicative of the shivering response, were significantly attenuated (P < 0.01 and P < 0.001, respectively) by MS. Thus, MS may predispose individuals to hypothermia by enhancing heat loss and attenuating heat production. This might have significant implications for survival in maritime accidents.

Adult↗

Contribution of thermal and nonthermal factors to the regulation of body temperature in humans.

The set point has been used to define the regulated level of body temperature, suggesting that displacements of core temperature from the set point initiate heat production (HP) and heat loss (HL) responses. Human and animal experiments have demonstrated that the responses of sweating and shivering do not coincide at a set point but rather establish a thermoeffector threshold zone. Neurophysiological studies have demonstrated that the sensor-to-effector pathways for HP and HL overlap and, in fact, mutually inhibit each other. This reciprocal inhibition theory, presumably reflecting the manner in which thermal factors contribute to homeothermy in humans, does not incorporate the effect of nonthermal factors on temperature regulation. The present review examines the actions of these nonthermal factors within the context of neuronal models of temperature regulation, suggesting that examination of these factors may provide further insights into the nature of temperature regulation. It is concluded that, although there is no evidence to doubt the existence of the HP and HL pathways reciprocally inhibiting one another, it appears that such a mechanism is of little consequence when comparing the effects of nonthermal factors on the thermoregulatory system, since most of these factors seem to exert their influence in the region after the reciprocal cross-inhibition. At any given moment, both thermal and several nonthermal factors will be acting on the thermoregulatory system. It may, therefore, not be appropriate to dismiss the contribution of either when discussing the regulation of body temperature in humans.

Autonomic Nervous System↗

Effects of local arteriosclerosis on carotid baroreflex sensitivity and on heart rate and arterial pressure variability in humans.

The study examined whether the alterations in heart rate variability (HRV) and baroreflex sensitivity (BRS) observed in patients with coronary artery disease can also be discerned in otherwise healthy subjects with mild-to-moderate arteriosclerosis in the carotid artery bifurcation. Based on the results of carotid duplex ultrasonography, subjects were designated as either having no arteriosclerotic lesions (n = 18), unilateral (n = 19) or bilateral lesions (n = 18) in the bifurcation. Electrocardiograms were recorded and simultaneous and continuous records of arterial pressure were obtained. Resting HRV was determined by calculating the spectral power density in three frequency bands: 0-0.05 Hz [very low frequency (VLF) band], 0.05-0.15 [low frequency (LF) band] and 0.15-2 Hz (high frequency band), whereas the arterial pressure variability (APV) was determined from spectral power density of the VLF and LF bands. Carotid BRS was evaluated by measuring R-R intervals during application of pulse-synchronous graded pressures (40 to -65 mmHg) in a neck-chamber device. Analysis of variance revealed no effect of mild-to-moderate carotid arteriosclerosis on the spectral components of HRV and APV or on BRS. It thus appears that mild-to-moderate asymptomatic carotid arteriosclerosis does not affect carotid BRS, APV or HRV at rest.

Adult↗

The sweating foot: local differences in sweat secretion during exercise-induced hyperthermia.

INTRODUCTION: Little is known regarding local differences in foot sweat secretion. Since such information is important to our understanding of sweat gland control for thermoregulatory modeling and for the design of footwear we explored this topic. METHODS: Local sweat rates were investigated across core temperatures from 37-39 degrees C, achieved using endogenous (cycling) and exogenous heat (water-perfusion garment: 46 degrees C). Six healthy adults (three men, three women) performed one-legged, incremental cycling in a heated, climate-controlled chamber (36 degrees C, 60% relative humidity). Sweat rates were measured at the forehead and stationary (left) foot (capsules 3.16 cm2): three dorsal sites (base of toes, second metatarsal, and mid point), the lateral, and the central plantar surfaces. RESULTS: Terminal core temperatures ranged between 38.3-39.1 oC, with peak heart rates of 155-187 bpm. Most foot sweat rates were < 50% of that observed at the forehead: dorsal 1 (38%); dorsal 2 (54%); dorsal 3 (37%); lateral (24%); and plantar surfaces (18%). When averaged across the trial, local sweat rates were: 2.61 (forehead); 0.98 (dorsal 1); 1.39 (dorsal 2); 0.95 (dorsal 3); 0.62 (lateral); and 0.47 mg cm2 2 min-1 (plantar). CONCLUSION: Two key observations emerged. First, sweat secretion from the experimental foot averaged 30 ml x h(-1), peaking in the last 5 min at 50 ml x h(-1). Second, approximately 70% of the measured sweat flow emanated from the upper skin surfaces, with only 30% coming from the plantar surface.

Adult↗

Human temperature regulation during cycling with moderate leg ischaemia.

The effect of graded ischaemia in the legs on the regulation of body temperature during steady-state exercise was investigated in seven healthy males. It was hypothesised that graded ischaemia in the working muscles increases heat storage within the muscles, which in turn potentiates sweat secretion during exercise. Blood perfusion in the working muscles was reduced by applying a supra-atmospheric pressure (+6.6 kPa) around the legs, which reduced maximal working capacity by 29%. Each subject conducted three separate test trials comprising 30 min of steady-state cycling in a supine position. Exercise with unrestricted blood flow (Control trial) was compared to ischaemic exercise conducted at an identical relative work rate (Relative trial), as well as at an identical absolute work rate (Absolute trial); the latter corresponding to a 20% increase in relative workload. The average (SD) increases in both the rectal and oesophageal temperatures during steady-state cycling was 0.3 (0.2) degrees C and did not significantly differ between the three trials. The increase in muscle temperature was similar in the Control (2.7 (0.3) degrees C) and Absolute (2.4 (0.7) degrees C) trials, but was substantially lower (P < 0.01) in the Relative trial (1.4 (0.8) degrees C). Ischaemia potentiated (P < 0.01) sweating on the forehead in the Absolute trial (24.2 (7.3) g m(-2) min(-1)) compared to the Control trial (13.4 (6.2) g m(-2) min(-1)), concomitant with an attenuated (P < 0.05) vasodilatation in the skin during exercise. It is concluded that graded ischaemia in working muscles potentiates the exercise sweating response and attenuates vasodilatation in the skin initiated by increased core temperature, effects which may be attributed to an augmented muscle metaboreflex.

Adult↗

Human thermoregulatory function during exercise and immersion after 35 days of horizontal bed-rest and recovery.

The present study evaluated the effect of 35 days of experimental horizontal bed-rest on exercise and immersion thermoregulatory function. Fifteen healthy male volunteers were assigned to either a Control (n = 5) or Bed-rest (n = 10) group. Thermoregulatory function was evaluated during a 30-min bout of submaximal exercise on a cycle ergometer, followed immediately by a 100-min immersion in 28 degrees C water. For the Bed-rest group, exercise and immersion thermoregulatory responses observed post-bed-rest were compared with those after a 5 week supervised active recovery period. In both trials, the absolute work load during the exercise portion of the test was identical. During the exercise and immersion, we recorded skin temperature, rectal temperature, the difference in temperature between the forearm and third digit of the right hand (DeltaT(forearm-fingertip))--an index of skin blood flow, sweating rate from the forehead, oxygen uptake and heart rate at minute intervals. Subjects provided ratings of temperature perception and thermal comfort at 5-min intervals. Exercise thermoregulatory responses after bed-rest and recovery were similar. Subjective ratings of temperature perception and thermal comfort during immersion indicated that subjects perceived similar combinations of Tsk and Tre to be warmer and thermally less uncomfortable after bed-rest. The average (SD) exercise-induced increase in Tre relative to resting values was not significantly different between the Post-bed-rest (0.4 (0.2) degrees C) and Recovery (0.5 (0.2) degrees C) trials. During the post-exercise immersion, the decrease in Tre, relative to resting values, was significantly (P < 0.05) greater in the Post-bed-rest trial (0.9 (0.5) degrees C) than after recovery (0.4 (0.3) degrees C). DeltaT(forearm-fingertip) was 5.2 (0.9) degrees C and 5.8 (1.0) degrees C at the end of the post-bed-rest and recovery immersions, respectively. The gain of the shivering response (increase in VO(2) relative to the decrease in Tre; VO(2)/Tre) was 1.19 l min(-1) degrees C(-1) in the Recovery trial, and was significantly attenuated to 0.51 l min(-1) degrees C(-1) in the Post-bed-rest trial. The greater cooling rate observed in the post-bed-rest trial is attributed to the greater heat loss and reduced heat production. The former is the result of attenuated cold-induced vasoconstriction and enhanced sweating rate, and the latter a result of a lower shivering VO(2) response.

Bed Rest↗

Motion sickness decreases arterial pressure and therefore acceleration tolerance.

BACKGROUND: Motion sickness is a common aeromedical problem that may occur in pilots exposed to increased gravitoinertial load in the head-to-foot direction (+Gz). Since motion sickness may affect autonomic nervous functions including cardiovascular control, it was hypothesized that it might interfere with cardiovascular responses to high +Gz, thereby decreasing G tolerance. METHODS: G tolerance and cardiovascular responses to increased G load were studied in nine subjects in a centrifuge environment under two conditions. In the motion sickness condition, the subject was exposed to a motion sickness provocation (MSP) comprising repeated rapid changes in G load in combination with a regimen of head movements. In the control condition the subject was exposed to similar cumulative G-time stress, but without the MSP. Mean arterial pressure (MAP) was measured. An index of peripheral vascular resistance was achieved by measuring the difference in skin temperature between the forearm and fingertip (deltaT(forearm-fingertip)). RESULTS: MSP decreased gradual-onset rate G tolerance from 5.1 +/- 1.0 G (mean +/- SD) to 4.6 +/- 0.9 G. There was no change in gradual-onset rate G tolerance in the control condition. Rapid-onset rate G tolerance was lower in the motion sickness (2.9 +/- 0.5 G) than in the control (3.4 +/- 0.3 G) condition. MSP reduced MAP by 11 mmHg and deltaT(forearm-fingertip) by 4.2 +/- 4.1 degrees C. In the control condition MAP and deltaT(forearm-fingertip) were unaffected. CONCLUSIONS: Motion sickness may reduce the arterial pressure response to the extent that the capacity of an individual to withstand increased G loads in the head-to-foot direction is significantly diminished.

Acceleration↗

Effect of hypoxia on preferred hand temperature.

INTRODUCTION: Selection of preferred skin temperature is a consequence of complex central neural integration of thermoafferent information in the polysynaptic pathway for behavioral thermoregulation. The present study tested the hypothesis that hypoxia alters behavioral temperature regulation. METHODS: Eight male volunteers participated in two separate trials. In each trial they were immersed in 28 degrees C water for 90 min, and inspired either room air (air trial) or a hypoxic gas mixture (hypoxia trial; 11.5% O2/88.5% N2). Their left hand was placed in a separate bath perfused with water. At regular intervals they were instructed to adjust the temperature of the water perfusing the hand bath to a comfortable temperature, defined as the 'preferred hand temperature' (Tpref). At minute intervals, esophageal (Tes), rectal (Tre), and skin (Tsk) temperatures, along with heat flux from the skin (Q) and ventilation (VI) were recorded. The observed responses were compared with a one-way ANOVA. RESULTS: With the exception of VI, there were no significant differences in any of the recorded variables between the two conditions. During the immersion, Tes and Tre decreased by 1.0 and 0.7 degrees C, respectively, in the air trial, and by 0.8 and 0.7 degrees C, respectively, in the hypoxia trial. Concomitant with decreases in core temperature, there was a significant increase (p < 0.05) in Tpref of 2.1 degrees C in the air trial and 2.4 degrees C in the hypoxia trial. The difference in Tpref between the air and hypoxia trials was not significant. DISCUSSION: Assuming that the selection of preferred hand temperature represents a behavioral thermoregulatory response, the present results suggest that moderate normobaric hypoxia does not affect human behavioral thermoregulation.

Adult↗

Inhalation of warm and cold air does not influence brain stem or core temperature in normothermic humans.

The present study tested the hypothesis that inhalation rewarming provides a thermal increment to central neural structures adjacent to the nasopharyngeal region. Auditory-evoked brain stem responses of 14 subjects (7 men and 7 women) were monitored for 25 min while they inspired room air (24 degrees C) followed by hot air (41 degrees C) saturated with water vapor and cold dry air (-1 degrees C). The latencies of peaks I, III, and V and the interpeak latencies (IPLs) I-III, III-V, and I-V were compared among the three conditions with a repeated-measures ANOVA. Changes in IPLs are sensitive markers of changes in brain stem temperature. Tympanic temperature (T(ty)) was measured with an infrared tympanic thermometer. There were no significant differences in T(ty), peak latencies I, III, and V, and IPLs I-III, III-V, and I-V. The results indicate that inhalation of hot and cold air does not influence T(ty), nor does it influence the temperature of the brain stem. We conclude that inhalation rewarming is not capable of warming the vital central neural structures adjacent to the naropharynx.

Adult↗

Visual function after prolonged bed rest.

The present study evaluated the claim of earlier reports, that of bed rest-induced alterations in visual function. Indices of visual function were studied in 10 healthy male subjects, during 35 days of horizontal bed rest. Before and after the 35 day bed rest, both eyes of all subjects were examined for visual acuity, intraocular pressure, contrast sensitivity, stereopsis and visual field. Pre- and post-bed rest values were compared with Student's T-test. There were no significant differences in any of the measured indices of visual function.

Journal Article↗

Influence of active recovery following prolonged bed rest on static exercise pressor response.

The present study investigated the effect of active recovery, following 35 days of horizontal bed rest, on the magnitude and time course of the pressor and heart rate responses to sustained 90 minute submaximal isometric contraction of unilateral knee extensor muscles. Ten healthy male subjects were tested immediately post bed rest (Post BR) and again after 4 weeks of active recovery (Recovery). In both trials subjects sustained an absolute force equal to 30% of Post BR maximal voluntary contraction (MVC). Beat-to-beat heart rate (HR) and mean arterial blood pressure (MAP) were monitored continuously during sustained contraction using the volume-clamp technique. Despite a 24% increase in MVC, there were no significant differences in the magnitudes of HR and MAP responses between Post BR and Recovery trials, suggesting a bed rest-induced attenuation of the static exercise pressor response.

Journal Article↗

Core temperature circdian rhythm during 35 days of horizontal bed rest.

The present study evaluated whether the previously reported alterations in core temperature circadian rhythm associated with bed rest might be attributable to increased heat loss from the skin. Infra-red thermograms were obtained at weekly intervals during 5 weeks of bed rest and after 4 weeks of active recovery. Tympanic temperature (Tty) was measured at hourly intervals from 0800 to 2300 hrs on similar occasions during bed rest. There were no significant changes in mean tympanic temperature or amplitude of Tty circadian rhythm during the 5 week bed rest period. Skin temperature decreased progressively during bed rest (P<0.005), with distal regions being the most affected.

Journal Article↗