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Biomedical subjects

J R Sutton

Publications and source records attributed to J R Sutton.

At least 73 records · Page 4Linked to original sources
PubMed1989

Renal responses to exercise-induced lactic acidosis.

Five healthy males performed four 30-s bouts of maximal exercise, separated by 4 min of rest, on an isokinetic cycle ergometer. Arterial blood and urine samples were taken from indwelling catheters at rest, immediately postexercise, and for 90 min of recovery. Inulin was continuously infused to measure glomerular filtration rate (GFR). Arterial plasma [Na+], [K+], and [Cl-] increased (P less than 0.05) with exercise; plasma lactate concentration ([Lac-]) increased from 1.3 +/- 0.2 to 21.0 +/- 1.0 (SE) meq/l (P less than 0.05). A significant decrease in the GFR occurred after exercise and during recovery associated with reductions in renal Na+ and K+ excretion (P less than 0.05). Renal excretion of Lac- reached a maximum of 293 +/- 79.4 mu eq.kg-1.h-1 (P less than 0.05), with Cl- excretion reaching a minimum of 4.8 +/- 0.95 mu eq.kg-1.h-1 (P less than 0.05). Urine [Lac-] was 189 +/- 25.6 meq/l, and urine [Cl-] was 6 +/- 1.7 meq/l at 30 min of recovery. There was a curvilinear relationship between urine [Cl-] and [Lac-] (r = -0.86; P less than 0.0001). Net Lac- production was estimated from arterial [Lac-] and after assuming a distribution volume. Less than 2% (13.1 meq) of the total estimated Lac- produced (678 meq) was excreted in the urine. Decreases in urine [Cl-] act to limit the fall in urine pH that accompanies increases in urine [Lac-].

Acidosis, Lactic↗
PubMed1989

Operation Everest II: plasma lipid and hormonal responses during a simulated ascent of Mt. Everest.

To examine the effect of hypobaric hypoxia on plasma lipid profiles, fasting blood samples were collected from six men (21-31 yr) at 760 Torr and periodically during a 40-day exposure to decreasing barometric pressure culminating in a final ambient pressure of 282 Torr. Preascent plasma total cholesterol concentration ([TC]) was decreased by 25% after the 40-day exposure (P less than 0.01). High-density lipoprotein concentrations ([HDL-C]) decreased 32% (P less than 0.001) with no alteration in the TC-to-HDL-C weight ratio. Plasma triglyceride concentration increased twofold during this period (P less than 0.01). There were no significant differences in fasting plasma free fatty acid concentrations or free fatty acid-to-albumin molar ratio throughout the study. Fasting plasma insulin levels were increased approximately twofold with no significant changes in glucagon concentration or the insulin-to-glucagon molar ratio. Plasma norepinephrine concentrations were increased threefold on reaching 282 Torr (P less than 0.01), with no significant changes in plasma epinephrine concentrations. Mean energy intake (kcal/day) decreased 42%, whereas mean body weights decreased by 8.9 +/- 0.8% (P less than 0.01) with exposure. Increased concentrations of insulin may lead to increased hepatic production of triglyceride-rich lipoproteins, thus eliciting metabolic changes independent of weight loss and dietary intake.

Adult↗
PubMed1989

Operation Everest II: maximal oxygen uptake at extreme altitude.

Chronic exposure to high altitude reduces maximal O2 uptake (VO2max). At extreme altitudes approaching the summit of Mt. Everest [inspiratory PO2(PIO2) = 43 Torr], mean VO2max have been determined to be 15.3 ml.kg-1.min-1 in two subjects who breathed 14% O2 at 6,300 m on Mt. Everest (West et al., J. Appl. Physiol. 54: 1188-1194, 1983). To provide a more complete description of performance near the limits of human tolerance to chronic hypoxia, we measured VO2max in volunteers in an altitude chamber before, during, and after a 40-day decompression to a barometric pressure (PB) of 240 Torr (PIO2 = 43 Torr). In five of eight subjects studied at sea level and PB of 464, 347, 289, and 240 Torr, VO2max was reduced from 4.13 to 1.17 l/min (49.1-15.3 ml.kg-1.min-1) in agreement with the prior study. Although the range decreased, the rank order among the subjects was preserved. Arterial O2 saturation at maximum effort decreased (46% by ear oximetry), but minute ventilation, respiratory frequency, and tidal volume did not. The highest minute ventilation (201 l/min BTPS) was observed at PB of 464 Torr. Arterial PCO2 in three subjects at PB of 240 Torr, at rest, and with maximum effort, averaged 10.3 and 9.6 Torr, respectively. Sustained hyperventilation was crucial to exercise performance during chronic, severe hypoxemia. VO2max was lower after altitude exposure compared with initial sea level values, indicating that exposure had not improved sea level exercise capacity.

Adult↗
PubMed1989

Operation Everest II: adaptations in human skeletal muscle.

Adaptations in skeletal muscle in response to progressive hypobaria were investigated in eight male subjects [maximal O2 uptake = 51.2 +/- 3.0 (SE) ml.kg-1.min-1] over 40 days of progressive decompression to the stimulated altitude of the summit of Mt. Everest. Samples of the vastus lateralis muscle extracted before decompression (SL-1), at 380 and 282 Torr, and on return to sea level (SL-2) indicated that maximal activities of enzymes representative of the citric acid cycle, beta-oxidation, glycogenolysis, glycolysis, glucose phosphorylation, and high-energy phosphate transfer were unchanged (P greater than 0.05) at 380 and 282 Torr over initial SL-1 values. After exposure to 282 Torr, however, representing an additional period of approximately 7 days, reductions (P less than 0.05) were noted in succinic dehydrogenase (21%), citrate synthetase (37%), and hexokinase (53%) between SL-2 and 380 Torr. No changes were found in the other enzymes. Capillarization as measured by the number of capillaries per cross-sectional area (CC/FA) was increased (P less than 0.05) in both type I (0.94 +/- 0.8 vs. 1.16 +/- 0.05) and type II (0.84 +/- 0.07 vs. 1.05 +/- 0.08) fibers between SL-1 and SL-2. This increase was mediated by a reduction in fiber area. No changes were found in fiber-type distribution (type I vs. type II). These findings do not support the hypothesis, at least in humans, that, at the level of the muscle cell, extreme hypobaric hypoxia elicits adaptations directed toward maximizing oxidative function.

Acclimatization↗
PubMed1989

Operation Everest II: comparison of four instruments for measuring blood O2 saturation.

The bias and precision of four different methods for determining O2 saturation (SO2) were evaluated during a study of hypobaric hypoxia conducted with seven male subjects exposed progressively over a 40-day period to simulated altitudes from sea level (760 Torr) to 8,840 m (240 Torr). SO2 of arterial and mixed venous blood samples were measured with the Instrumentation Laboratory 282 CO-oximeter (CO-OX), the Radiometer ABL-300 (ABL), and the Lex-O2-Con-K (LEX). Noninvasive measurements of arterial SO2 were made with a Hewlett-Packard 47201A ear oximeter (EAR-OX). The CO-OX method was used as a secondary standard for comparison with the other methods because it has been validated against the classical Van Slyke method over a wide physiological range (Maas et al., Clin. Chim. Acta 29: 303-309, 1970). The LEX results most closely approximated but consistently underestimated those of the CO-OX: LEX = 0.93 CO-OX -0.86, standard error of the estimate (SEE) = 5.17, r = 0.98, n = 670. The ABL method appeared to combine two linear trends: for SO2 greater than 75%, ABL = 0.84 CO-OX +14.4, SEE = 1.77, r = 0.97, n = 369; less than 75%, ABL = 0.98 CO-OX +5.9, SEE = 4.44, r = 0.97, n = 486. The EAR-OX results were found to approximate those of the CO-OX at SO2 values only greater than 65%: EAR-OX = 1.07 CO-OX -6.12, SEE = 7.71, r = 0.98, n = 326.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1989

Physiological responses to caffeine during endurance running in habitual caffeine users.

Several studies have found that caffeine improved endurance exercise performance, but the factors which are responsible for this are not fully understood. Possibilities include an increased free fatty acid (FFA) oxidation and a resultant sparing of muscle glycogen as well as an enhancement of neuromuscular function during exercise. In order to further examine these factors, six varsity level runners (VO2max = 63.3 ml.kg-1.min-1) were studied over 90 min of treadmill running (70% VO2max) in a thermoneutral environment in order to determine the metabolic and neuromuscular effects of caffeine (6 mg.kg-1) administered in a randomized, crossover, double-blind manner. Subjects were habitual caffeine consumers (200 mg.d-1) and were given identical diets during each 3-d testing period. Caffeine administration, 60 min prior to exercise, significantly (P less than 0.05) increased plasma FFA levels both prior to and during exercise. Caffeine administration did not alter any of the other variables examined: VO2, HR, RER, rating of perceived exertion; plasma levels of glucose, lactate, epinephrine, and norepinephrine; or neuromuscular function (maximal voluntary strength, peak twitch torque, and motor unit activation). We conclude that caffeine administration (6 mg.kg-1) in athletic, habitual caffeine consumers increased plasma FFA levels but had neither metabolic nor neuromuscular effects that would be of potential ergogenic benefit in endurance running.

Adult↗
PubMed1989

The Ontario cohort study of running-related injuries.

A cohort of 1680 runners was enrolled through two community road race events and monitored during a 12-month follow-up period for the occurrence of musculoskeletal injuries. Forty-eight percent of the runners experienced at least one injury, and 54% of these injuries were new; the remainder were recurrences of previous injuries. The risk of injury was associated with increased running mileage but was relatively unassociated with other aspects of training, such as usual pace, usual running surface, hill running, or intense training. Injury rates were equal for all age-sex groups and were independent of years of running experience. Runners injured in the previous year had approximately a 50% higher risk for a new injury during follow-up.

Adolescent↗
PubMed1988

Functional and structural adaptations in skeletal muscle of trained athletes.

Twitch contractile and ultrastructural characteristics of the human triceps surae were determined in six male strength-trained athletes, six endurance-trained athletes, six active controls, and seven sedentary controls of similar height and age. Twitch contraction time in the triceps surae complex was 20% longer in strength-trained and sedentary groups than in endurance-trained or active control groups. In the 15 subjects peak twitch torque and one-half relation time in the triceps surae were 22.6 +/- 7.9 N.m and 91.1 +/- 18.3 ms, respectively. Mean fiber area in the gastrocnemius was approximately 1.6-, 1.7-, and 2.5-fold greater in the active control, endurance-trained, and strength-trained groups, respectively, relative to the sedentary group. Despite these large differences in fiber areas, the fiber fractional volume of the sarcoplasmic reticulum-transverse tubule network averaged 3.38 +/- 0.86% and 5.50 +/- 0.94% in type I and type II fibers, respectively, in all subjects. The fractional fiber volume of cytoplasm and lipid were similar for all four groups. However, mitochondrial volume was approximately 30% lower in both fiber types of the strength-trained group relative to the other groups. This implies that with exercise-induced hypertrophy, the sarcoplasmic reticulum, cytoplasm, and lipid components increase proportionately with contractile protein, whereas the mitochondrial fraction does not. The proportion of type I fibers in the soleus, medial gastrocnemius, and lateral gastrocnemius was 75.2 +/- 8.3, 58.5 +/- 6.1, and 52.4 +/- 4.2%, respectively, and was similar in all subject groups. The results demonstrate that twitch duration is prolonged in strength-trained athletes relative to endurance athletes.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1988

Operation Everest II: oxygen transport during exercise at extreme simulated altitude.

A decrease in maximal O2 uptake has been demonstrated with increasing altitude. However, direct measurements of individual links in the O2 transport chain at extreme altitude have not been obtained previously. In this study we examined eight healthy males, aged 21-31 yr, at rest and during steady-state exercise at sea level and the following inspired O2 pressures (PIO2): 80, 63, 49, and 43 Torr, during a 40-day simulated ascent of Mt. Everest. The subjects exercised on a cycle ergometer, and heart rate was recorded by an electrocardiograph; ventilation, O2 uptake, and CO2 output were measured by open circuit. Arterial and mixed venous blood samples were collected from indwelling radial or brachial and pulmonary arterial catheters for analysis of blood gases, O2 saturation and content, and lactate. As PIO2 decreased, maximal O2 uptake decreased from 3.98 +/- 0.20 l/min at sea level to 1.17 +/- 0.08 l/min at PIO2 43 Torr. This was associated with profound hypoxemia and hypocapnia; at 60 W of exercise at PIO2 43 Torr, arterial PO2 = 28 +/- 1 Torr and PCO2 = 11 +/- 1 Torr, with a marked reduction in mixed venous PO2 [14.8 +/- 1 (SE) Torr]. Considering the major factors responsible for transfer of O2 from the atmosphere to the tissues, the most important adaptations occurred in ventilation where a fourfold increase in alveolar ventilation was observed. Diffusion from alveolus to end-capillary blood was unchanged with altitude. The mass circulatory transport of O2 to the tissue capillaries was also unaffected by altitude except at PIO2 43 Torr where cardiac output was increased for a given O2 uptake. Diffusion from the capillary to the tissue mitochondria, reflected by mixed venous PO2, was also increased with altitude. With increasing altitude, blood lactate was progressively reduced at maximal exercise, whereas at any absolute and relative submaximal work load, blood lactate was higher. These findings suggest that although glycogenolysis may be accentuated at low work loads, it may not be maximally activated at exhaustion.

2,3-Diphosphoglycerate↗
PubMed1988

Factors influencing hydrogen ion concentration in muscle after intense exercise.

To assess the importance of factors influencing the resolution of exercise-associated acidosis, measurements of acid-base variables were made in nine healthy subjects after 30 s of maximal exercise on an isokinetic cycle ergometer. Quadriceps muscle biopsies (n = 6) were taken at rest, immediately after exercise, and at 3.5 and 9.5 min of recovery; arterial and femoral venous blood were sampled (n = 3) over the same time. Intracellular and plasma inorganic strong ions were measured by neutron activation and ion-selective electrodes, respectively; lactate concentration ([La-]) was measured enzymatically, and plasma PCO2 and pH were measured by electrodes. Immediately after exercise, intracellular [La-] increased to 47 meq/l, almost fully accounting for a reduction in intracellular strong ion difference ([SID]) from 154 to 106 meq/l. At the same time, femoral venous PCO2 increased to 100 Torr and plasma [La-] to 9.7 meq/l; however, plasma [SID] did not change because of a concomitant increase in inorganic [SID] secondary to increases in [K+], [Na+], and [Ca2+]. During recovery, muscle [La-] fell to 26 meq/l by 9.5 min; [SID] remained low (101 and 114 meq/l at 3.5 and 9.5 min, respectively) due almost equally to the elevated [La-] (30 and 26 meq/l) and reductions in [K+] (from 142 meq/l at rest to 123 and 128 meq/l). Femoral venous PCO2 rose to 106 Torr at 0.5 min postexercise and fell to resting values at 9.5 min.(ABSTRACT TRUNCATED AT 250 WORDS)

Acid-Base Equilibrium↗
PubMed1988

Role of lungs and inactive muscle in acid-base control after maximal exercise.

The pulmonary responses and changes in plasma acid-base status occurring across the inactive forearm muscle were examined after 30 s of intense exercise in six male subjects exercising on an isokinetic cycle ergometer. Arterial and deep forearm venous blood were sampled at rest and during 10 min after exercise; ventilation and pulmonary gas exchange variables were measured breath by breath during exercise and recovery. Immediately after exercise, ventilation and CO2 output increased to 124 +/- 17 1/min and 3.24 +/- 0.195 l/min, respectively. The subsequent decrease in CO2 output was slower than the decrease in O2 intake (half time of 105 +/- 15 and 47 +/- 4 s, respectively); the respiratory exchange ratio was greater than 1.0 throughout the 10 min of recovery. Arterial plasma concentrations of Na+, K+, and Ca2+ increased transiently after exercise. Arterial lactate ion concentration ([La-]) increased to 14-15 meq/l within 1.5 min and remained at this level for the rest of the study. Throughout recovery there was a positive arteriovenous [La-] difference of 4-5 meq/l, associated with an increase in the arteriovenous strong ion difference ([SID]) and by a large increase in the venous Pco2 and [HCO3-]. These findings were interpreted as indicating uptake of La- by the inactive muscle, leading to a fall in the muscle [SID] and increase in plasma [SID], associated with an increase in muscle PCO2. The venoarterial CO2 content difference was 38% greater than could be accounted for by metabolism of La- alone, suggesting liberation of CO2 stored in muscle, possibly as carbamate.(ABSTRACT TRUNCATED AT 250 WORDS)

Acid-Base Equilibrium↗
PubMed1988

Operation Everest. II: Nutrition and body composition.

Progressive body weight loss occurs during high mountain expeditions, but whether it is due to hypoxia, inadequate diet, malabsorption, or the multiple stresses of the harsh environment is unknown. To determine whether hypoxia due to decompression causes weight loss, six men, provided with a palatable ad libitum diet, were studied during progressive decompression to 240 Torr over 40 days in a hypobaric chamber where hypoxia was the major environmental variable. Caloric intake decreased 43.0% from 3,136 to 1,789 kcal/day (P less than 0.001). The percent carbohydrate in the diet decreased from 62.1 to 53.2% (P less than 0.001). Over the 40 days of the study the subjects lost 7.4 +/- 2.2 (SD) kg and 1.6% (2.5 kg) of the total body weight as fat. Computerized tomographic scans indicated that most of the weight loss was derived from fat-free weight. The data indicated that prolonged exposure to the increasing hypoxia was associated with a reduction in carbohydrate preference and body weight despite access to ample varieties and quantities of food. This study suggested that hypoxia can be sufficient cause for the weight loss and decreased food consumption reported by mountain expeditions at high altitude.

Adult↗
PubMed1988

Operation Everest II: lack of an effect of extreme altitude on visual contrast sensitivity.

Contrast sensitivity thresholds were studied over 40 d during gradual ascent to a simulated terrestrial altitude of 25,000 ft in a decompression chamber. Only ambient pressure, and thus inspired oxygen pressure, was varied, thereby eliminating many of the confounding effects of cold, dehydration, malnutrition and exhaustion, inevitably encountered on very high mountains. Contrast sensitivity thresholds measured by the Ginsburg Vistech test showed no overall impairment as altitude increased. These results are different from those of other previously reported vision studies involving shorter exposures, lower altitudes, and lower test luminances. However, our results can be explained on the basis of the higher stimulus luminances used in our contrast sensitivity testing. Compared to the luminance levels involved in previously reported testing, our higher luminance stimuli would be less likely to be affected by hypoxia.

Adult↗
PubMed1987

Oxygen transport during exercise at extreme altitude: Operation Everest II.

Eight male volunteers had rest and exercise measurement to determine the mechanisms of oxygen transport during a 40-day chamber decompression simulating high-altitude exposure equivalent to the summit of Mt Everest. Five subjects completing the study decreased their maximum oxygen uptake by 72%. During maximal or near-maximal exercise, arterial PCO2 fell as low as 8 mm Hg, defending the alveolar PO2 and confirming marked hyperventilation. Alveolar-arterial diffusion did not improve and V/Q worsened. Cardiac function was unimpaired. Circulatory oxygen transport resembled that at sea level. The decrease in mixed venous PO2 was not enough to preserve fractional oxygen utilization "on the summit." The PO2 gradients from atmosphere to alveolus, alveolus to arterial blood, arterial to venous blood, and from venous (capillary) blood to mitochondria all decreased. However, hyperventilation appeared to be the primary adaptation that defended the maximum oxygen uptake.

Adult↗
PubMed1987

Voluntary strength and muscle characteristics in untrained men and women and male bodybuilders.

Eight untrained women (F), 13 untrained men (M), and 11 male bodybuilders (BB) did maximal elbow flexions on an isokinetic dynamometer at velocities of 30, 120, 180, 240, and 300 degrees/s, from which impact torque (IT), peak torque (PT), and work (W) were measured. Biceps and total flexor cross-sectional area (CSA) were measured by computerized tomographic scanning. Muscle fiber area, fiber composition, and collagen volume density were determined from single needle biopsies of biceps brachii. Biceps fiber number was estimated as the ratio of biceps CSA (corrected for connective tissue) to mean fiber area. PT and W decreased at higher velocities in M and BB but not in F; consequently, the correlation between CSA and PT and W was lower at 300 degrees/s (r = 0.58, 0.60) than 30 degrees/s (r = 0.80, 0.79). The ratio of PT to flexor CSA was similar in all groups at 30 degrees/s, whereas F had greater ratios than M and BB at the remaining velocities. F had greater W/CSA ratios than M and BB at all velocities. IT increased at higher velocities in all groups; the increase was greater in F and M than in BB. In contrast to PT and W, the correlation between IT and CSA was greater at 300 degrees/s (r = 0.67) than 30 degrees/s (r = 0.58), and there were no differences among groups in the IT/CSA ratios. Flexor CSA correlated negatively with the ratio of IT, PT, and W to CSA. Muscle fiber composition failed to correlate with any measure of strength. M and BB had greater biceps area, fiber number, and fiber area than F.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1987

Operation Everest II: elevated high-altitude pulmonary resistance unresponsive to oxygen.

High altitude increases pulmonary arterial pressure (PAP), but no measurements have been made in humans above 4,500 m. Eight male athletic volunteers were decompressed in a hypobaric chamber for 40 days to a barometric pressure (PB) of 240 Torr, equivalent to the summit of Mt. Everest. Serial hemodynamic measurements were made at PB 760 (sea level), 347 (6,100 m), and 282/240 Torr (7,620/8,840 m). Resting PAP and pulmonary vascular resistance (PVR) increased from sea level to maximal values at PB 282 Torr from 15 +/- 0.9 to 34 +/- 3.0 mmHg and from 1.2 +/- 0.1 to 4.3 +/- 0.3 mmHg.l-1 X min, respectively. During near maximal exercise PAP increased from 33 +/- 1 mmHg at sea level to 54 +/- 2 mmHg at PB 282 Torr. Right atrial and wedge pressures were not increased with altitude. Acute 100% O2 breathing lowered cardiac output and PAP but not PVR. Systemic arterial pressure and resistance did not rise with altitude but did increase with O2 breathing, indicating systemic control differed from the lung circulation. We concluded that severe chronic hypoxia caused elevated pulmonary resistance not accompanied by right heart failure nor immediately reversed by O2 breathing.

Adult↗
PubMed1987

Operation Everest II: preservation of cardiac function at extreme altitude.

Hypoxia at high altitude could depress cardiac function and decrease exercise capacity. If so, impaired cardiac function should occur with the extreme, chronic hypoxemia of the 40-day simulated climb of Mt. Everest (8,840 m, barometric pressure of 240 Torr, inspiratory O2 pressure of 43 Torr). In the five of eight subjects having resting and exercise measurements at the barometric pressures of 760 Torr (sea level), 347 Torr (6,100 m), 282 Torr (7,620 m), and 240 Torr, heart rate for a given O2 uptake was higher with more severe hypoxia. Slight (6 beats/min) slowing of the heart rate occurred only during exercise at the lowest barometric pressure when arterial blood O2 saturations were less than 50%. O2 breathing reversed hypoxemia but never increased heart rate, suggesting that hypoxic depression of rate, if present, was slight. For a given O2 uptake, cardiac output was maintained. The decrease in stroke volume appeared to reflect decreased ventricular filling (i.e., decreased right atrial and wedge pressures). O2 breathing did not increase stroke volume for a given filling pressure. We concluded that extreme, chronic hypoxemia caused little or no impairment of cardiac rate and pump functions.

Adult↗