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PubMed1997

Skeletal muscle resting metabolism in cold-acclimated rats: effect of age, noradrenaline and hyperosmolarity.

1. A myothermic technique has been used to measure the resting metabolism of small bundles of a fast twitch muscle, extensor digitorum longus (EDL), and a slow twitch muscle, soleus (SOL), in 7-week-old rats. At 27 degrees C, mean (+/-SEM) resting heat rates were 2.33 +/- 0.41 and 2.09 +/- 0.37 mW/g in EDL and SOL, respectively (n = 16). 2. Seven-week-old rats were cold acclimatized at 4 degrees C for 1-4 weeks and the metabolic rates of the fast and slow twitch muscles were monitored and compared with 7- and 11-week-old controls. There was a 160% increase in metabolic rate from week 7 to week 11, but the increase also occurred in the control group. 3. In accordance with several literature reports, noradrenaline at concentrations of 10(-7) and 10(-6) mol/L had no effect on either the control or cold-acclimatized resting heat rate. 4. The osmolarity of the physiological solution bathing the muscle bundles was increased by 100 mosmol using sodium sulphate. Basal metabolism increased by similar amounts (approximately 250%) in both the fast and slow muscle bundles. Periods of cold exposure had no significant effect on the magnitude of the increment. 5. Bumetanide, a potent inhibitor of Na(+)-Cl- co-transport, produced only a slight reduction in the heat increments caused by hyperosmolar challenge.

Acclimatization↗
PubMed2004

Central and obstructive sleep apnoea during ascent to high altitude.

OBJECTIVE: The aim of the study was to investigate the relationship between central sleep apnoea (CSA) at high altitude and arterial blood gas tensions, and by inference, ventilatory responsiveness. METHODOLOGY: Fourteen normal adult volunteers were studied by polysomnography during sleep, and analysis of awake blood gases during ascent over 12 days from sealevel to 5050 m in the Nepal Himalayas. RESULTS: Thirteen subjects developed CSA. Linear regression analysis showed tight negative correlations between mean CSA index and mean values for sleep SaO2, PaCO2 and PaO2 over the six altitudes (r2 > or = 0.74 for all, P < 0.03). Paradoxically there was poor correlation between the individual data for CSA index and those parameters at the highest altitude (5050-m) where CSA was worst (r2 < 0.12 for all, NS), possibly due to variation in degree of acclimatization between subjects. In addition, CSA replaced mild obstructive sleep apnoea during ascent. Obstructive sleep apnoea index fell from 5.5 +/- 6.9/h in rapid eye movement sleep at sealevel to 0.1 +/- 0.3/h at 5050 m (P < 0.001, analysis of variance), while CSA index rose from 0.1 +/- 0.3/h to 55.7 +/- 54.4/h (P < 0.001). CONCLUSION: There was a general relationship between decreasing PaCO2 and CSA, but there were significant effects from variations in acclimatization that would make hypoxic ventilatory response an unreliable predictor of CSA in individuals.

Acclimatization↗
PubMed1999

Ventilatory responses to hypercapnia and hypoxia after 6 h passive hyperventilation in humans.

1. Acute exposure to hypoxia stimulates ventilation and induces hypocapnia. Long-term exposure to hypoxia generates changes in respiratory control known as ventilatory acclimatization to hypoxia. The object of this study was to investigate the degree to which the hyperventilation and hypocapnia can induce the changes known as ventilatory acclimatization to hypoxia, in the absence of the primary hypoxic stimulus itself. 2. Three 6 h protocols were each performed on twelve healthy volunteers: (1) passive hypocapnic hyperventilation, with end-tidal CO2 pressure (PET,CO2) held 10 Torr below the eupnoeic value; (2) passive eucapnic hyperventilation, with PET,CO2 maintained eucapnic; (3) control. 3. Ventilatory responses to acute hypercapnia and hypoxia were assessed before and half an hour after each protocol. 4. The presence of prior hypocapnia, but not prior hyperventilation, caused a reduction in air-breathing PET,CO2 (P < 0.05, ANOVA), and a leftwards shift of the ventilatory response to hypercapnia (P < 0.05). The presence of prior hyperventilation, but not prior hypocapnia, caused an increase in the ventilatory sensitivity to CO2 (P < 0.05). No significant effects of any protocol were detected on the ventilatory sensitivity to hypoxia. 5. We conclude that following 6 h of passive hyperventilation: (i) the left shift of the VE-PET,CO2 relationship is due to alkalosis and not to hyperventilation; (ii) the increase in slope of the VE-PET,CO2 relationship is due to the hyperventilation and not the alkalosis; and (iii) ventilatory sensitivity to hypoxia is unaltered.

Acclimatization↗
PubMed1977

Work-heat tolerance of distance runners.

Physical training in a cool environment by subjects not previously trained improves their work-heat tolerance, but can not replace heat acclimatization to the standard heat stress conditions employed by a variety of investigators. This is attributed to the inability of these subjects to sustain prolonged work at high metabolic rates. Thus, they are not maintaining high core body temperatures long enough to bring about an adaptive change to heat. On the other hand, the intense and prolonged (years) training of long distance runners in a temperature environment at high metabolic rates has acclimatized them for at least 4 hours of mild work (MR 160 kcal/m2-hr) in both hot dry (50/27 C db/wb) and hot wet (36.7/33.1 C db/wb) environments, but not for work at high energy expenditures (MR 540 kcal/m2-hr) in a less severe thermal stress (35/21 C db/wb). These highly trained athletes can improve their work-heat tolerance at high metabolic rates in a warm climate by training at competitive speeds in a cool environment dressed in sweat clothing or by training at near competitive speeds in the heat. In either of these situations the athlete is cautioned to consume water at frequent intervals to offset the dehydration associated with excessive sweating under these conditions.

Acclimatization↗
PubMed1968

Finger blood flow in Antarctica.

1. Finger blood flow was estimated, by strain-gauge plethysmography, before and during a 1 hr immersion in ice water, on twenty-five men throughout a year at Wilkes, Antarctica. A total of 121 satisfactory immersions were made.2. Blood flow before and during immersion decreased significantly in the colder months of the year, and the increase caused by cold-induced vasodilatation (CIVD) became less as the year progressed. The time of onset, blood flow at onset, and frequency of the cycles of CIVD showed no significant relation to the coldness of the weather (as measured by mean monthly wind chill) or the time in months. Comparisons of blood flow before and after five field trips (average duration 42 days), on which cold exposure was more severe than at Wilkes station, gave similar results.3. The results suggest that vasoconstrictor tone increased. This interpretation agrees with previous work on general acclimatization in Antarctica, but contrasts with work elsewhere on local acclimatization of the hands.

Acclimatization↗
PubMed1987

The origin of proteinuria at high altitude.

Urinary protein excretion was measured before and after the intravenous infusion of lysine in 14 normal subjects after 4-6 days' acclimatization at 4846 m. Urinary albumin excretion before lysine was elevated in 11 subjects but alpha 1-microglobulin was detected in only four. After lysine a large increase in albumin excretion occurred in all subjects. Together with the absence of alpha 1-microglobulin before lysine this implies that increased glomerular capillary permeability is the major cause of proteinuria after acclimatization to high altitude. The estimated minimum glomerular fluid albumin concentration was increased two to three fold above the published values in normal controls.

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PubMed1980

Persistence of impaired heat tolerance from artificially induced miliaria rubra.

Ten volunteers were heat acclimatized to 48.9 degrees C (Ta), 20% rh for 7 days to complete a 100-min walk on a level treadmill (1.56 m x s-1). Subjects were then divided into experimental (n = 6) and control (n = 4) groups. Miliaria rubra (heat rash) was then induced on the experimental subjects by wrapping them for 3 days in polyethylene plastic. All six developed marked miliaria with involvement of 40-70% of the total body surface area. All subjects were reexposed to walking in the heat on the 7th day after unwrapping, by which time rash was clinically indetectable, and again 14 days after unwrapping. On the first test (day 7) only one of the rashed group, and on the second test (day 14) only two could complete the 100-min walk; the control group finished without difficulty on both days. Body heat storage for the rash group was 2.5 times that of the control group on day 7 and 1.5 as great on day 14; measurements of mean body temperature (Tb) on the rash group indicated a much greater heat stress when compared to their own prerash-acclimatized values or those of the control group. These data demonstrate the potential of "healed" miliaria in the etiology of clinical heat illness.

Acclimatization↗
PubMed1980

Heat intolerance as a function of percent of body surface involved with miliaria rubra.

Twenty-four heat-acclimatized male volunteers were wrapped as previously described (Am. J. Physiol. 239 (Regulatory Integrative Comp. Physiol. 8): R226-R232, 1980) but to produce miliaria rubra (heat rash) in specific regions of the body. Three experimental rash groups were involved: 1) the torso (17% total skin surface rashed, n = 6), 2) torso and arms (38%, n = 8), or 3) legs (41%, n = 6), while four subjects served as controls. All subjects were reexposed to walking in the heat on the 7th day after unwrapping, and again 14, 21, and 28 days after unwrapping. When compared to responses for the last heat acclimatization day, tolerance time and sweat rate were lower and mean body temperature and delta heat storage significantly higher for experimental rash subjects contrasted to the controls for up to 21 days; however, no significant differences between the three rashed groups were found. The critical amount of surface area for heat intolerance from heat rash appears to be related to the specific region of the body and associated sweating responses; smaller rashed areas of the trunk, because they have greater potential for abundant sweating, may produce similar responses to heat stress as larger rashed areas of the limbs. Heat intolerance due to rash was not resolved until after 21 days.

Acclimatization↗
PubMed1991

Nonshivering thermogenesis in king penguin chicks. II. Effect of fasting.

The effect of fasting on the energy metabolism of skeletal muscle and liver was investigated in cold-acclimatized short-term fasting (STF) (3 wk) and naturally long-term fasting (LTF) (4-5 mo) king penguin chicks, both groups exhibiting nonshivering thermogenesis (NST). A comparison was made with nourished cold-acclimatized controls. In these chicks, no brown adipose tissue deposits could be found on electron-microscopic observations of fat deposits. Protein content and cytochrome oxidase (CO) activity of tissue homogenates were measured in liver and pectoralis and gastrocnemius muscles, as were protein content, CO activity, and respiration rates of mitochondria isolated from these organs. Fasting-induced protein loss affected the pectoralis more than the gastrocnemius muscle, thus preserving locomotor function. In STF chicks, specific mitochondrial protein content and specific tissue CO activity were preserved but total organ CO capacity was reduced by half in pectoralis and liver following the fall in organ mass. In LTF chicks, both specific and total CO activity were drastically reduced in muscles, whereas specific CO activity was preserved in liver. In these LTF chicks, muscle mitochondria showed an energized configuration associated with an increased area of inner membrane in gastrocnemius. A reduction of respiratory control ratio (RCR) was observed in subsarcolemmal muscle mitochondria of STF chicks, whereas intermyofibrillar and liver mitochondria kept high RCR values.(ABSTRACT TRUNCATED AT 250 WORDS)

Acclimatization↗
PubMed1998

Poor relationship between arterial [lactate] and leg net release during exercise at 4,300 m altitude.

We evaluated the hypotheses that on acute exposure to hypobaric hypoxia, sympathetic stimulation leads to augmented muscle lactate production and circulating [lactate] through a beta-adrenergic mechanism and that beta-adrenergic adaptation to chronic hypoxia is responsible for the blunted exercise lactate response after acclimatization to altitude. Five control and 6 beta-blocked men were studied during rest and exercise at sea level (SL), on acute exposure to 4,300 m (A1), and after a 3-wk sojourn at altitude (A2). Exercise was by leg cycling at 49% of SL peak O2 consumption (VO2 peak) (65% of altitude VO2 peak or 87 +/- 2.6 W); beta-blockade was by propranolol (80 mg 3x daily), femoral arterial and venous blood was sampled; leg blood flow (Q) was measured by thermodilution, leg lactate net release [ = (2) (1-leg Q) venous-arterial concentrationL] was calculated, and vastus lateralis needle biopsies were obtained. Muscle [lactate] increased with exercise and acute altitude exposure but regressed to SL values with acclimatization; beta-blockade had no effect on muscle [lactate]. Arterial [lactate] rose during exercise at SL (0.9 +/- 0.1 to 1.5 +/- 0.3 mM); exercise at A1 produced the greatest arterial [lactate] (4.4 +/- 0.8 mM), and exercise at A2 an intermediate response (2.1 +/- 0.6 mM). beta-Blockade reduced circulating [lactate] approximately 45% during exercise under all altitude conditions. increased transiently at exercise onset but then declined over time under all conditions. Blood and muscle "lactate paradoxes" occurred independent of beta-adrenergic influences, and the hypotheses relating the blood lactate response at altitude to beta-adrenergic mechanisms are rejected. During exercise at altitude, arterial [lactate] is determined by factors in addition to hypoxemia, circulating epinephrine, and net lactate release from active muscle beds.

Acclimatization↗
PubMed1975

Changes of thermal balance induced by passive heating in resting man.

Heat acclimatization has been induced in 12 resting healthy men by 90-min exposure to 45C dry bulb and 24% relative humidity for 9 successive days. The most significant results ovserved were 1) increased sensitivity of sweating with marked quickening of sweat measured, 2) decreased rate of body heat storage associated with a lower rectal temperature at end of exposure, as follows: 14.07 plus or minus 1.58 Wtimeshtimeskg-1 before and 9.39 plus or minus 1.69 afterward for body heat storage; 37.55 plus or minus 0.15C before and 36.99 plus or minus 0.24C afterward for rectal temperature. In contrast, no significant changes were observed in the final sweat rates, mean skin temperatures, or the heat conductance between the body interior and skin surface. The quickness of the heat dissipation process caused by both increased sensitivity of sweating and lower internal body temperature is the major factor in achieving a thermal balance and a decreased body heat content after acclimatization.

Acclimatization↗
PubMed1975

Thermoregulation during marathon running in cool, moderate, and hot environments.

A well-trained subject, age 38, ran continously for periods ranging from 60 to 165 min on a motor-driven treadmill at 255.7 m/min while confronted with an airflow equivalent to running speed in cool, moderate, and hot environments. After a period of intensive heat acclimatization, treadmill runs were repeated in the moderate and hot conditions. Measurements were also obtained outdoors in a competitive marathon race. Sweat rate (SR) and mean skin temperature (Ts) were linearly related to Tdb. Acclimatization did not alter VO2max or metabolic rate during the treadmill runs, but heart rat (HR),rectal temperature (Tre), and Ts were lower, SR was higher, and maximal run duration longer in the hot environment, postacclimatization. Maximum runs in the hot environment were terminated by a spiralling increase in Tre to hyperthermic levels, due largely to a marked reduction in cutaneous blood flow, probably reflecting cardiovascular overload from the combined muscular and thermoregulatory blood flow demands, coupled with the effects of progressive dehydration. Utilizing partitional calorimetry and the subject's metabolic heat production, two examples of limiting environmental conditions for his marathon running speed were given.

Acclimatization↗
PubMed1976

Body fluid responses of heat-tolerant and intolerant men to work in a hot wet environment.

Acclimatization to heat before proceeding underground is a requirement for each South African mine laborer. Certain individuals among this large population cannot be acclimatized to heat (33.3 degrees C db, 31.7 degrees C wb) and are classified as heat intolerant. In this study certain body fluid responses to heat and work were compared between a group of 19 heat-tolerant (HT) and of 15 heat-intolerant (HI) subjects. To the factors known to affect heat tolerance such as age, weight, and oxygen consumption must now be added differences in body fluid responses. The HI group of subjects failed to hemodilute to the same degree as the HT group though working at the same relative work loads (30% and 50% VO2 max). As the 4-h work period (33.3 degrees C db, 31.7 degrees C wb) continued, the HI group did not maintain hemodilution in spite of the lower absolute work loads, sweat rates, and water deficits suffered by this group. From analysis of blood constituent changes it was suggested that the reason for the differences noted in body fluid dynamics concerned plasma protein equilibrium across capillary walls as well as the protein population of interstitial spaces.

Acclimatization↗
PubMed1977

Increase in sweating sensitivity by endurance conditioning in man.

Sweating sensitivity has been evaluated at rest in 10 competitive athletes (cross-country skiers and swimmers). Three sedentary men underwent a 3-mo period of endurance training in a temperate climate, (dry bulb temperature (Tdb): 18 degrees C) and had their sweating sensitivity measured before and after the training period. Mean maximum oxygen uptake (Vo2max, ml.min(-1).kg(-1)) was: skiers: 66.5; swimmers 65.8; sedentary men, pretraining 40.9; posttraining: 48.3 (+18%). Sweat output of athletes under a given stress (passive heating) was markedly higher than that of sedentary men. Skiers exhibited a high level of heat tolerance and were better acclimatized than swimmers, although they had never experienced exposure to heat. The increase in Vo2max of sedentary men was accompanied by 1) an increase in sweating sensitivity with a decrease of body heat storage at steady state (pretraining: 5.4 kJ.kg(-1); posttraining: 3.5 kJ.kg(-1); P less than 0.05); 2) significant shift down the temperature scale with reduced rectal temperature (Tre) for sweat onset; 3) an increase of gain constants of sweating (W.m-2 degrees C(-1) (pretraining: 168; posttraining: 269; gain constant of swimmers: 222). It was suggested that endurance training in cold or temperate conditions with significant increase of Vo2max could act on the thermoregulatory function in a way similar to body heating procedures, such as work in heat, and could contribute to heat acclimatization.

Acclimatization↗
PubMed1986

Reduced hyperpnea-induced bronchospasm following repeated cold air challenge.

This study assessed reduction in expiratory function in 12 asthmatic subjects both after 5 min of cold air provocation (CAP) with dry air conditioned to approximately 0 degrees C and after exercise (to 85% of predicted maximum heart rate) while breathing ambient room air (approximately 21 degrees C and 40% relative humidity). These assessments were done both before and after the following training protocol. Three 5-min periods of isocapnic cold air hyperpnea separated by 5-min rest periods were performed breathing 0 degrees to -10 degrees C air, for 36 sessions over 12 wk. As expected, pretraining expiratory function was significantly reduced (P less than 0.001) after both CAP and exercise. The posttraining reduction in expiratory function after CAP and exercise, however, was significantly less pronounced (largest P less than 0.05). These data support our hypothesis that repeated bouts of cold air challenge result in airway acclimatization to cold air and consequent decrease in exercise-induced bronchospasm. Acclimatization may result directly either by habituation of the airways or by vasodilation leading to increased bronchial blood flow and consequent reduced airway cooling. An unanticipated finding, though, is that repeated cold air challenge may also cause long-term inflammatory changes in the airways. A significant percentage of subjects experienced reduced base-line pulmonary function and overall exacerbation of asthma symptoms during the training period.

Acclimatization↗
PubMed1993

Effect of chronic hypoxia on hypoxic ventilatory response in awake rats.

We compared the hypoxic ventilatory response (HVR) of two groups of unrestrained awake male rats (300-550 g): those acclimatized to hypoxia > 7 wk at simulated altitude (380 Torr, n = 12) and sea level controls (n = 8). Chronic catheters were placed in the iliac artery and vein 3-7 days before study. An "on-line" system was used to measure arterial PO2 and PCO2. Arterial blood was drawn via a roller pump past O2 and CO2 electrodes and returned to the vein. Batch samples were taken before and after HVR measurements for calibrating and determining arterial pH and hematocrit. Inspired ventilation, tidal volume, and respiratory frequency were measured with barometric pressure plethysmography at several levels of inspired O2 fraction (0.08-0.30) maintained for 15 min. For isocapnic HVR, inspired CO2 fraction was increased as necessary to maintain arterial PCO2 at the hyperoxic level. In both groups, poikilocapnic HVRs (inspired CO2 fraction = 0) were significantly less than isocapnic HVRs. Isocapnic HVRs were significantly greater in hypoxia-acclimatized (2,783 +/- 233 ml.min-1.kg-1) than in sea level control rats (1,826 +/- 106 ml.min-1.kg-1), mainly due to a significant increase in tidal volume (P < 0.05). In conclusion, relieving hypocapnia in hypoxia, by maintaining isocapnia, reveals a significant increase in the ventilatory response to arterial PO2 in awake rats with chronic hypoxia.

Acclimatization↗
PubMed1994

Higher exercise performance and lower VO2max in Tibetan than Han residents at 4,700 m altitude.

To examine the hypothesis that the pathway of adaptation to high altitude in natives differs considerably from that in newcomers, we measured maximal O2 uptake (VO2max), minute ventilation, anaerobic threshold (AT), blood lactate, and blood gases during maximal exercise in 17 lifelong Tibetan residents and 14 acclimatized Han Chinese newcomers living at the altitude of 4,700 m. The two groups were similar in age, height, and weight, and the subjects were nonathletes. Although VO2max was significantly lower in the Tibetans than in the Hans (30.4 +/- 1.5 vs. 36.0 +/- 1.9 ml.min-1.kg-1 STPD; P < 0.05), at maximal exercise effort the exercise workload was greater (167.7 +/- 4.2 vs. 150.0 +/- 5.9 W; P < 0.05). The mean AT values (in % VO2max) in the Tibetan and Han subjects were 84.1 and 61.6%, respectively (P < 0.01). Minute ventilation at maximal exercise was significantly lower in the Tibetans than in the Hans (68.4 +/- 3.4 vs. 79.7 +/- 4.1 l/min BTPS; P < 0.05), whereas heart rate at maximal effort was equivalent in the two groups. The Tibetans showed lower blood lactate value than did the Hans both before and at the end of exercise. We conclude that the Tibetan natives have higher exercise performance and AT but lower VO2max and blood lactate concentration than do acclimatized Han newcomers. These results may reflect the effects of genetic or peripheral adaptation factors in the Tibetan natives.

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PubMed1994

Sympathetic and parasympathetic indicators of heart rate control at altitude studied by spectral analysis.

The adaptive responses of the cardiovascular system to altitude appear to be dominated by increased sympathetic neural activity. We investigated the combined roles of the sympathetic and parasympathetic nervous systems (SNS and PNS, respectively) in the early (days 4-5) and subsequent (days 11-12) phases of acclimatization on Pike's Peak, CO (4,300 m), by spectral analysis of heart rate variability. Male subjects were randomly assigned to groups receiving oral propranolol (240 mg/day; n = 6) or a matched placebo (n = 3). On ascent to altitude, the high-frequency, fractal, and total spectral powers were reduced in the placebo group during days 4-5 and 11-12. At altitude during days 4-5, all three placebo group subjects increased SNS and decreased PNS activities compared with at sea level, and during days 11-12 SNS decreased and PNS increased compared with days 4-5. Relative to the placebo group, propranolol caused lengthening of the R-R interval; increases in high-frequency power, total spectral power, and the PNS indicator; and a decrease in the SNS indicator. Total spectral power tended to decrease at altitude, but there were no effects of altitude on PNS and SNS indicators in the propranolol group. The data from the placebo and propranolol groups suggest that both the PNS and SNS are involved in the elevated heart rate during the early phase of altitude acclimatization. Changes in heart rate variability during days 11-12 at altitude must be considered in light of the possible reductions in sympathetic receptor number noted in previous studies.

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