Biomedical subjects

J R Sutton

Publications and source records attributed to J R Sutton.

At least 55 records · Page 3Linked to original sources

PubMed1992

Limitations to maximal oxygen uptake.

An increase in exercise capacity depends on the magnitude of increase in maximum aerobic capacity. Central and peripheral factors may limit oxygen uptake. Central oxygen delivery depends on cardiac output and maximal arterial oxygen content. Peripheral extraction of the delivered oxygen is expressed as a-v O2. With increasing intensities of exercise, the respiratory system may become limiting in some trained individuals. Most studies have shown a higher stroke volume in maximal as well as submaximal exercise in the trained vs untrained individuals. A variety of peripheral factors determine vascular tone. Maximal oxygen uptake depends on all components of the oxygen transporting system, but stroke volume appears to be the prime determinant in the trained subject. At maximum exercise the capacity of the muscle capillary network is never reached.

Cardiovascular Physiological Phenomena↗

PubMed1992

Mountain sickness.

This article outlines the fundamental physiology and pathology of high altitude. It covers the latest findings from the unique experiment Operation Everest II in which eight persons were gradually decompressed to the "summit" of Mt. Everest and extensive physiologic studies done. The article contains an examination of the various high altitude pathologies, including acute mountain sickness, high altitude pulmonary edema, high altitude cerebral edema, and high altitude retinal hemorrhage. Information on prevention and current approaches to treatment conclude the article.

Acclimatization↗

PubMed1992

VO2max--new concepts on an old theme.

This symposium "VO2max--new concepts on an old theme" is dedicated to the memory of Hermann Rahn, whose inspiration has led many young investigators to explore new horizons. In the debate on factors limiting VO2max at altitude Hermann Rahn stimulated further discussion between those camps supporting the central circulation as limiting VO2max and those proposing a peripheral diffusion limitation.

Altitude↗

PubMed1992

Oxygen transport during exercise at altitude and the lactate paradox: lessons from Operation Everest II and Pikes Peak.

It seems unlikely that oxygen-limited metabolism explains the increased lactate concentrations in blood or muscle during exercise at high altitude compared with sea level values because: 1. Even marked hypoxia equivalent to that at the summit of Mt. Everest may not be sufficiently severe to impair function or to impair muscle oxidative metabolism markedly during exercise; 2. At this very high altitude, muscle hypoxemia is probably not the limiting factor for exercise performance; other systems, i.e., the cerebral cortex [24, 33], probably fail before hypoxemia impairs muscle metabolism; 3. The traditional view of oxygen-limited aerobic metabolism during exercise at high altitude does not explain a long-standing dilemma in altitude physiology, the lactate paradox (in which blood lactate accumulation during exercise is increased on arrival at high altitude but falls with acclimatization), because the lactate fall is independent of muscle oxygenation; 4. Net lactate release by the leg during exercise is independent of oxygenation; 5. Kinetic studies show that lactate appearance and disappearance are closely linked and both increase with acute altitude exposure and decrease with acclimatization; 6. Lactate appearance rate is strongly correlated with, and may be influenced by, the extent of beta-adrenergic stimulation; 7. The beta-adrenergic stimulation may be, in part, determined by the degree of arterial oxygenation.

Acclimatization↗

PubMed1991

Heat stroke following Rugby League football.

OBJECTIVE: To present a case of severe heat stroke after Rugby League football. CLINICAL FEATURES: A 29-year-old Rugby League forward with a mild infection of the upper respiratory tract collapsed while playing football in late March, when the ambient temperature was 24.1 degrees C and the relative humidity up to 73%. He was initially thought to have sustained a head injury and was markedly dehydrated. He suffered severe disseminated intravascular coagulation and gross neurological, renal and hepatic disturbances. INTERVENTION AND OUTCOME: He required repeated haemodialysis, assisted ventilation and supportive therapy and remained unconscious for 10 days. He then recovered fully. CONCLUSION: Heat stroke is potentially fatal and can be easily mistaken for head injury in contact sports. When players are dehydrated, have febrile illness and play in warm conditions, they may succumb to heat stroke.

Adult↗

PubMed1991

Increased vital and total lung capacities in Tibetan compared to Han residents of Lhasa (3,658 m).

Larger chest dimensions and lung volumes have been reported for Andean high-altitude natives compared with sea-level residents and implicated in raising lung diffusing capacity. Studies conducted in Nepal suggested that lifelong Himalayan residents did not have enlarged chest dimensions. To determine if high-altitude Himalayans (Tibetans) had larger lung volumes than acclimatized newcomers (Han "Chinese"), we studied 38 Tibetan and 43 Han residents of Lhasa, Tibet Autonomous Region, China (elevation 3,658 m) matched for age, height, weight, and smoking history. The Tibetan compared with the Han subjects had a larger total lung capacity [6.80 +/- 0.19 (mean +/- SEM) vs 6.24 +/- 0.18 l BTPS, P less than 0.05], vital capacity (5.00 +/- 0.08 vs 4.51 +/- 0.10 1 BTPS, P less than 0.05), and tended to have a greater residual volume (1.86 +/- 0.12 vs 1.56 +/- 0.09 1 BTPS, P less than 0.06). Chest circumference was greater in the Tibetan than the Han subjects (85 +/- 1 vs 82 +/- 1 cm, P less than 0.05) and correlated with vital capacity in each group as well as in the two groups combined (r = 0.69, P less than 0.05). Han who had migrated to high altitude as children (less than or equal to 5 years old, n = 6) compared to Han adult migrants (greater than or equal to 18 years old, n = 26) were shorter but had similar lung volumes and capacities when normalized for body size. The Tibetans' vital capacity and total lung capacity in relation to body size were similar to values reported previously for lifelong residents of high altitude in South and North America. Thus, Tibetans, like North and South American high-altitude residents, have larger lung volumes. This may be important for raising lung diffusing capacity and preserving arterial oxygen saturation during exercise.

Adult↗

PubMed1991

Early adaptations in gas exchange, cardiac function and haematology to prolonged exercise training in man.

In order to determine the effect of short-term training on central adaptations, gas exchange and cardiac function were measured during a prolonged submaximal exercise challenge prior to and following 10-12 consecutive days of exercise. In addition, vascular volumes and selected haematological properties were also examined. The subjects, healthy males between the ages of 19 and 30 years of age, cycled for 2 h per day at approximately 59% of pre-training peak oxygen consumption (VO2) i.e., maximal oxygen consumption (VO2max). Following the training, VO2max (l.min-1) increased (P less than 0.05) by 4.3% (3.94, 0.11 vs 4.11, 0.11; mean, SE) whereas maximal exercise ventilation (VE,max) and maximal heart rate (fc,max) were unchanged. During submaximal exercise, VO2 was unaltered by the training whereas carbon dioxide production (VE) and respiratory exchange ratio were all reduced (P less than 0.05). The altered activity pattern failed to elicit adaptations in either submaximal exercise cardiac output or arteriovenous O2 difference. fc was reduced (P less than 0.05). Plasma volume (PV) as measured by 125I human serum albumin increased by 365 ml or 11.8%, while red cell volume (RCV) as measured by 51chromium-labelled red blood cells (RBC) was unaltered. The increase in PV was accompanied by reductions (P less than 0.05) in haematocrit, haemoglobin concentration (g.100 ml-1), and RBCs (10(6) mm-3). Collectively these changes suggest only minimal adaptations in maximal oxygen transport during the early period of prolonged exercise training. However, as evidenced by the changes during submaximal exercise, both the ventilatory and the cardiodynamic response were altered.(ABSTRACT TRUNCATED AT 250 WORDS)

Adaptation, Physiological↗

PubMed1991

The effect of amenorrhea on calcaneal bone density and total bone turnover in runners.

To examine in athletes the effect of long-term amenorrhea on the skeleton, measurements of calcaneal density and whole body retention of 99mTc-imidodiphosphate were made in 42 women who could be allocated to one of 3 groups defined by their level of physical activity and by menstrual status. There was no difference in bone density between eumenorrheic normoactive females and either eumenorrheic or amenorrheic athletes. However, calcaneal density was significantly greater for each group than for previously measured sedentary controls. Total body bone turnover was greater in both eumenorrheic and amenorrheic athletes than in eumenorrheic normoactive women. Sustained, intense physical activity does not significantly increase calcaneal bone density over and above the increase associated with normal levels of activity. This is despite a significant increase in the rate of total body bone mineral turnover.

Adult↗

PubMed1991

Operation Everest II: structural adaptations in skeletal muscle in response to extreme simulated altitude.

Alterations in skeletal muscle structure were investigated in 6 male subjects who underwent 40 days of progressive decompression in a hypobaric chamber simulating an ascent to the summit of Mount Everest. Needle biopsies were obtained from vastus lateralis of 5 subjects before and immediately after confinement in the chamber, and were examined for various structural and ultrastructural parameters. In addition, total muscle area was calculated in 6 subjects from CT scans of the thighs and upper arms. Muscle area at these sites was found to decrease significantly (by 13 and 15%) as a result of the hypobaric confinement. This was substantiated by significant (25%) decreases in cross sectional fibre areas of the Type I fibres and 26% decreases (non significant) in Type II fibre area. Capillary to fibre ratios remained unchanged following hypoxia as did capillary density although there was a trend (non significant) towards an increase in capillary density. There were no significant increases in mitochondrial volume density or other morphometric parameters. These data indicate that chronic, severe hypoxia on its own does not result in an increase in absolute muscle capillary number or a de novo synthesis of mitochondria. The trends toward an increase in capillary density and mitochondrial volume density were interpreted as being secondary occurrences in response to the pronounced muscle atrophy which occurred.

Acclimatization↗

PubMed1991

Arterial catecholamine responses during exercise with acute and chronic high-altitude exposure.

Exercise at high altitude is a stress that activates the sympathoadrenal systems, which could affect responses to acute altitude exposure and promote adaptations during chronic altitude exposure. However, catecholamine levels are not clearly described over time at high altitude. In seven male volunteers (23 yr, 72 kg), resting arterial norepinephrine concentrations (ng/ml) on arrival at Pikes Peak (0.338 +/- 0.041) decreased compared with sea-level values (0.525 +/- 0.034) but increased to above sea-level values after 21 days at 4,300 m (0.798 +/- 0.052). Furthermore, during 45 min of constant submaximal exercise, values were similar at sea level (1.670 +/- 0.221) and on acute exposure to 4,300 m (2.123 +/- 0.086) but increased after 21 days of chronic exposure (2.693 +/- 0.216). By contrast, resting arterial epinephrine values (ng/ml) during acute and chronic exposure (0.708 +/- 0.033 vs. 0.448 +/- 0.026) both exceeded those of sea level (0.356 +/- 0.020). During exercise values on arrival were greater than at sea level (0.921 +/- 0.024 vs. 0.397 +/- 0.035) but fell to 0.612 +/- 0.025 ng/ml after 21 days. Exercise norepinephrine levels were related to systemic vascular resistance measurements (r = 0.93), whereas epinephrine levels were related to circulating lactate (r = 0.95). We conclude that during exercise at altitude there is a dissociation between norepinephrine, an indicator of sympathetic neural activity, and epinephrine, an indicator of adrenal medullary response. These actions may account for different metabolic and physiological responses to acute vs. chronic altitude exposure.

Adult↗

PubMed1991

Increased dependence on blood glucose after acclimatization to 4,300 m.

To evaluate the hypothesis that altitude exposure and acclimatization result in increased dependency on blood glucose as a fuel, seven healthy males (23 +/- 2 yr, 72.2 +/- 1.6 kg, mean +/- SE) on a controlled diet were studied in the postabsorptive condition at sea level (SL), on acute altitude exposure to 4,300 m (AA), and after 3 wk of chronic altitude exposure to 4,300 m (CA). Subjects received a primed continuous infusion of [6,6-2D]glucose and rested for a minimum of 90 min, followed immediately by 45 min of exercise at 101 +/- 3 W, which elicited 51.1 +/- 1% of the SL maximal O2 consumption (VO2 max; 65 +/- 2% of altitude VO2 max). At SL, resting arterial glucose concentration was 82.4 +/- 3.2 mg/dl and rose significantly to 91.2 +/- 3.2 mg/dl during exercise. Resting glucose appearance rate (Ra) was 1.79 +/- 0.02 mg.kg-1.min-1; this increased significantly during exercise at SL to 3.71 +/- 0.08 mg.kg-1.min-1. On AA, resting arterial glucose concentration (85.8 +/- 4.1 mg/dl) was not different from sea level, but Ra (2.11 +/- 0.14 mg.kg-1.min-1) rose significantly. During exercise on AA, glucose concentration rose to levels seen at SL (91.4 +/- 3.0 mg/dl), but Ra increased more than at SL (to 4.85 +/- 0.15 mg.kg-1.min-1; P less than 0.05). Resting arterial glucose was significantly depressed with CA (70.8 +/- 3.8 mg/dl), but resting Ra increased to 3.59 +/- 0.08 mg.kg-1.min-1, significantly exceeding SL and AA values.(ABSTRACT TRUNCATED AT 250 WORDS)

Acclimatization↗

PubMed1991

Oxygen transport during steady-state submaximal exercise in chronic hypoxia.

Arterial O2 delivery during short-term submaximal exercise falls on arrival at high altitude but thereafter remains constant. As arterial O2 content increases with acclimatization, blood flow falls. We evaluated several factors that could influence O2 delivery during more prolonged submaximal exercise after acclimatization at 4,300 m. Seven men (23 +/- 2 yr) performed 45 min of steady-state submaximal exercise at sea level (barometric pressure 751 Torr), on acute ascent to 4,300 m (barometric pressure 463 Torr), and after 21 days of residence at altitude. The O2 uptake (VO2) was constant during exercise, 51 +/- 1% of maximal VO2 at sea level, and 65 +/- 2% VO2 at 4,300 m. After acclimatization, exercise cardiac output decreased 25 +/- 3% compared with arrival and leg blood flow decreased 18 +/- 3% (P less than 0.05), with no change in the percentage of cardiac output to the leg. Hemoglobin concentration and arterial O2 saturation increased, but total body and leg O2 delivery remained unchanged. After acclimatization, a reduction in plasma volume was offset by an increase in erythrocyte volume, and total blood volume did not change. Mean systemic arterial pressure, systemic vascular resistance, and leg vascular resistance were all greater after acclimatization (P less than 0.05). Mean plasma norepinephrine levels also increased during exercise in a parallel fashion with increased vascular resistance. Thus we conclude that both total body and leg O2 delivery decrease after arrival at 4,300 m and remain unchanged with acclimatization as a result of a parallel fall in both cardiac output and leg blood flow and an increase in arterial O2 content.(ABSTRACT TRUNCATED AT 250 WORDS)

Acclimatization↗

PubMed1991

Response of red cell and plasma volume to prolonged training in humans.

To clarify the role of progressive heavy training on vascular volumes and hematologic status, seven untrained males [maximal O2 uptake (VO2max) = 45.1 +/- 1.1 (SE) ml.kg-1.min-1] cycled 2 h/day at an estimated 62% of VO2max. Training was conducted five to six times per week for approximately 8 wk. During this time, VO2max increased (P less than 0.05) by 17.2%. Plasma volume (PV) measured by 125I increased (P less than 0.05) from 3,068 +/- 104 ml at 0 wk to 3,490 +/- 126 ml at 4 wk and then plateaued during the remaining four wk (3,362 +/- 113 ml). Red cell (RBC) mass (RCM) measured by 51Cr-labeled RBC did not change during the initial 4 wk of training (2,247 +/- 66 vs. 2,309 +/- 128 ml). As well, no apparent change occurred in RCM during the final 4 wk of training when RCM was estimated using PV and hematocrit (Hct). Collectively, PV plus RCM, expressed as total blood volume (TBV), increased (P less than 0.05) by 10% at 4 wk and then stabilized for the final 4 wk. During the initial phase of training, reductions (P less than 0.05) were also noted in Hct (4.6%), hemoglobin (Hb, 4.0%), and RBC count (6.3%). In contrast, an increase in mean cell volume (MCV, 1.7%) and mean cell Hb (2.3%) was observed (P less than 0.05). From 4 to 8 wk, no further changes (P greater than 0.05) in Hb, RBC, and MCV were found, whereas both mean cell Hb and Hct returned to pretraining levels.(ABSTRACT TRUNCATED AT 250 WORDS)

Adaptation, Physiological↗

PubMed1991

Decreased reliance on lactate during exercise after acclimatization to 4,300 m.

We hypothesized that the increased exercise arterial lactate concentration on arrival at high altitude and the subsequent decrease with acclimatization were caused by changes in blood lactate flux. Seven healthy men [age 23 +/- 2 (SE) yr, wt 72.2 +/- 1.6 kg] on a controlled diet were studied in the postabsorptive condition at sea level, on acute exposure to 4,300 m, and after 3 wk of acclimatization to 4,300 m. Subjects received a primed-continuous infusion of [6,6-2D]glucose (Brooks et al. J. Appl. Physiol. 70:919-927, 1991) and [3-13C]lactate and rested for a minimum of 90 min followed immediately by 45 min of exercise at 101 +/- 3 W, which elicited 51.1 +/- 1% of the sea level peak O2 consumption (VO2peak; 65 +/- 2% of both acute altitude and acclimatization). During rest at sea level, lactate appearance rate (Ra) was 0.52 +/- 0.03 mg.kg-1.min-1; this increased sixfold during exercise to 3.24 +/- 0.19 mg.kg-1.min-1. On acute exposure, resting lactate Ra rose from sea level values to 2.2 +/- 0.2 mg.kg-1.min-1. During exercise on acute exposure, lactate Ra rose to 18.6 +/- 2.9 mg.kg-1.min-1. Resting lactate Ra after acclimatization (1.77 +/- 0.25 mg.kg-1.min-1) was intermediate between sea level and acute exposure values. During exercise after acclimatization, lactate Ra (9.2 +/- 0.7 mg.kg-1.min-1) rose from resting values but was intermediate between sea level and acute exposure values. The increased exercise arterial lactate concentration response on arrival at high altitude and subsequent decrease with acclimatization are due to changes in blood lactate appearance.(ABSTRACT TRUNCATED AT 250 WORDS)

Adaptation, Physiological↗

PubMed1990

Gender differences in substrate for endurance exercise.

The effects of gender on substrate utilization during prolonged submaximal exercise were studied in six males and six equally trained females. After 3 days on a controlled diet (so that the proportions of carbohydrate, protein, and fat were identical), subjects ran on a treadmill at a velocity requiring an O2 consumption of approximately 65% of maximal. They ran a total "distance" of 15.5 km with a range in performance time of 90-101 min. Plasma glycerol, glucose, free fatty acids, and selected hormones (catecholamines, growth hormone, insulin, and glucagon) were measured throughout and after the run by sampling from an indwelling venous catheter, and glycogen utilization was calculated from pre- and postexercise needle biopsies of vastus lateralis. Exercise protein catabolism was estimated from 24-h urinary urea nitrogen excretion over the test day and a nonexercise day. The males were found to have significantly higher respiratory exchange ratios (mean 0.94 vs. 0.87), greater muscle glycogen utilization (by 25%), and greater urea nitrogen excretion (by 30%) than the females. No gender differences were evident in the hormonal response to the exercise with the exception of a lower insulin concentration and a higher epinephrine concentration in the males. We conclude that, during moderate-intensity long-duration exercise, females demonstrate greater lipid utilization and less carbohydrate and protein metabolism than equally trained and nourished males.

Adult↗

PubMed1990

Operation Everest II: neuromuscular performance under conditions of extreme simulated altitude.

The force output of the ankle dorsiflexors was studied during a 40-day simulated ascent of Mt. Everest in a hypobaric chamber; both electrically activated and maximal voluntary contractions (MVCs) were employed. The purpose of this study was to establish whether, under conditions of progressive chronic hypoxia, there was a decrease in muscle force output and/or increased fatigability. We also attempted to identify the main site of any failure, i.e., central nervous system, neuromuscular junction, or muscle fiber. Muscle twitch torque (Pt), tetanic torque (Po), MVC torque, and evoked muscle compound action potential (M wave) were monitored during 205-s exercise periods in five subjects at three simulated altitudes (760, 335, and 282 Torr). All three types of torque measurement were well preserved at the three altitudes. In some subjects, the responses to stimuli interpolated during repeated MVCs provided evidence of "central" fatigue at altitude. In addition, the rate of fatigue during 20-Hz electrical stimulation was greater (P less than 0.01) at altitude and there was increased fatigability of the twitch (P less than 0.025); however, the M wave amplitude was maintained. We conclude that central motor drive becomes more precarious at altitude and is associated with increased muscle fatigue at low excitation frequencies; the latter is the result, in part, of chronic hypoxia and occurs in the muscle fiber interior because no impairment in neuromuscular transmission could be demonstrated.

Adult↗

PubMed1990

Operation Everest II: ventilatory adaptation during gradual decompression to extreme altitude.

To assess the ventilatory adaptation during gradual ascent to extreme altitude, we studied seven healthy males as part of the 40 d simulated ascent of Mt. Everest in a hypobaric chamber. We measured resting ventilation (VE, l.min-1), arterial oxygen saturation (SaO2%), the ventilatory response to oxygen breathing, isocapnic hypoxic ventilatory response (HVR), and hypercapnic ventilatory response (HCVR) at sea level prior to the ascent (760 torr), 14,000 feet (428 torr), 24,000 feet (305 torr), and within 24 h of descent (765 torr). VE increased from 9.3 +/- 1.1 l.min-1 at 760 torr to 23.4 +/- 1.3 l.min-1 at 305 torr and remained elevated at 14.7 +/- 0.7 l.min-1 after descent. Oxygen breathing decreased VE by 9.6 +/- 1.3 l.min-1 at 305 torr. Isocapnic HVR (expressed as a positive slope of VE/SaO2, l.min-1.%SaO2(-1) increased from 0.18 +/- 0.07 at 760 torr to 0.34 +/- 0.11 and 0.38 +/- 0.5 at 428 torr and 305 torr (P less than 0.05) respectively. HVR was elevated further upon return to sea level (0.8 +/- 0.09, P less than 0.05). HCVR (S = VE/PETCO2, l.min-1.torr-1) increased from sea level (S = 4.4 +/- 0.09) to 305 torr (S = 18.7 +/- 3.5, P less than 0.01) and remained elevated upon return to sea level (S = 10.7 +/- 4.6, P less than 0.001). This study is the first to investigate the ventilatory response to such extreme altitude and so soon after descent and shows that hypoxic and hypercapnic responses increase during prolonged progressive hypoxic exposure and remain significantly elevated from pre-ascent levels immediately upon descent.

Acclimatization↗

PubMed1989

The cost to the central nervous system of climbing to extremely high altitude.

To assess the possibility that climbing to extremely high altitude may result in hypoxic injury to the brain, we performed neuropsychological and physiologic testing on 35 mountaineers before and 1 to 30 days after ascent to altitudes between 5488 and 8848 m, and on 6 subjects before and after simulation in an altitude chamber of a 40-day ascent to 8848 m. Neuropsychological testing revealed a decline in visual long-term memory after ascent as compared with before; of 14 visual items of information on the Wechsler Memory Scale, fewer were recalled after ascent by both the simulated-ascent group (a mean [+/- SD] of 10.14 +/- 1.68 items before, as compared with 7.00 +/- 3.35 items after; P less than 0.05) and the mountaineers (12.33 +/- 1.96 as compared with 11.36 +/- 1.88; P less than 0.05). Verbal long-term memory was also affected, but only in the simulated-ascent group; of a total of 10 words, an average of 8.14 +/- 1.86 were recalled before simulated ascent, but only 6.83 +/- 1.47 afterward (P less than 0.05). On the aphasia screening test, on which normal persons make an average of less than one error in verbal expression, the mountaineers made twice as many aphasic errors after ascent (1.03 +/- 1.10) as before (0.52 +/- 0.80; P less than 0.05). A higher ventilatory response to hypoxia correlated with a reduction in verbal learning (r = -0.88, P less than 0.05) and with poor long-term verbal memory (r = -0.99, P less than 0.01) after ascent. An increase in the number of aphasic errors on the aphasia screening test also correlated with a higher ventilatory response to hypoxia in both the simulated-ascent group (r = 0.94, P less than 0.01) and a subgroup of 11 mountaineers (r = 0.59, P less than 0.05). We conclude that persons with a more vigorous ventilatory response to hypoxia have more residual neurobehavioral impairment after returning to lower elevations. This finding may be explained by poorer oxygenation of the brain despite greater ventilation, perhaps because of a decrease in cerebral blood flow caused by hypocapnia that more than offsets the increase in arterial oxygen saturation.

Adult↗