Showing papers in "Journal of Applied Physiology in 1983"
TL;DR: It is shown that erroneous results are obtained in the presence of metabolic processes such as lipogenesis and gluconeogenesis, so that the apparently negative rates encountered in patients infused with glucose do quantitatively represent net rates of synthesis.
Abstract: This paper reviews the assumptions involved in calculating rates of carbohydrate and fat oxidation from measurements of O2 consumption, CO2 production, and urinary nitrogen excretion. It is shown t...
2,184 citations
TL;DR: For evaluating cardiopulmonary function with incremental exercise testing by either treadmill or cycle, the VO2 max was significantly higher on tests where the increment magnitude was large enough to induce test durations of 8-17 min, but the AT was independent of test duration.
Abstract: Twelve normal men performed 1-min incremental exercise tests to exhaustion in approximately 10 min on both treadmill and cycle ergometer. The maximal O2 uptake (VO2 max) and anaerobic threshold (AT) were higher (6 and 13%, respectively) on the treadmill than the cycle; the AT was reached at about 50% of VO2 max on both ergometers. Maximal CO2 output, heart rate, and O2 pulse were also slightly, but significantly higher on the treadmill. Maximal ventilation, gas exchange ratio, and ventilatory equivalents for O2 and CO2 for both forms of exercise were not significantly different. To determine the optimum exercise test for both treadmill and cycle, we exercised five of the subjects at various work rate increments on both ergometers in a randomized design. The treadmill increments were 0.8, 1.7, 2.5, and 4.2%/min at a constant speed of 3.4 mph, and 1.7 and 4.2%/min at 4.5 mph. Cycle increments were 15, 30, and 60 W/min. The VO2 max was significantly higher on tests where the increment magnitude was large enough to induce test durations of 8-17 min, but the AT was independent of test duration. Thus, for evaluating cardiopulmonary function with incremental exercise testing by either treadmill or cycle, we suggest selecting a work rate increment to bring the subject to the limit of his tolerance in about 10 min.
813 citations
TL;DR: The data generally indicated that eccentric exercise causes greater injury to the muscles, and questions remain.
Abstract: These experiments were designed to study skeletal muscle pathology resulting from eccentric-biased exercise in rats. The effects on the muscles of running on a treadmill on a 0 degrees incline (sim...
773 citations
TL;DR: The results suggest that although both groups III and IV muscle afferents contribute to the reflex cardiovascular increases evoked by static exercise, group III fibers were likely to be stimulated by the mechanical effects of muscular contraction, whereas at least some group IV fibers werelikely to be stimulating by the metabolic products of muscular contractions.
Abstract: Static contraction of the hindlimb muscles, induced by electrical stimulation of the ventral roots, reflexly increases arterial blood pressure and heart rate. Although stimulation of groups III and IV muscle afferents is believed to cause these reflex increases, the responses of these afferents to a level of static contraction that increases arterial pressure have not yet been determined. Therefore, in barbiturate-anesthetized cats, afferent impulses arising from endings in the gastrocnemius muscle were recorded from the L7 or S1 dorsal roots, while the cut peripheral end of the L7 ventral root was stimulated. In addition, the effects of capsaicin (100-200 micrograms) and bradykinin (25 micrograms) on the activity of the groups III and IV afferents stimulated by contraction were examined. Contraction of the gastrocnemius muscle to a level equal to or greater than that needed to cause a pressor response stimulated 12 of 19 (63%) group III afferents and 13 of 19 (68%) group IV afferents. However, the discharge patterns of the group III afferents stimulated by contraction were very different from those of the group IV fibers. No relationship was found between those fibers stimulated by contraction and those stimulated by chemicals. Our results suggest that although both groups III and IV muscle afferents contribute to the reflex cardiovascular increases evoked by static exercise, group III fibers were likely to be stimulated by the mechanical effects of muscular contraction, whereas at least some group IV fibers were likely to be stimulated by the metabolic products of muscular contraction.
655 citations
TL;DR: Results point toward a close relationship between variations of respiratory depth and interval and the quantity, periodicity, and timing of vagal cardiac outflow in conscious humans and suggest that, at usual breathing rates, phasic respiration-related changes ofvagal motoneuron activity began in expiration, progress slowly, and are incompletely expressed at fast breathing rates.
Abstract: Since changes of heart period follow changes of cardiac vagal efferent activity quantitatively with nearly fixed latencies, measurements of respiratory sinus arrhythmia may provide insights into human central vagal mechanisms. Accordingly, I measured intervals between heartbeats during controlled breathing (at breathing intervals of 2.5-10 s and nominal tidal volumes of 1,000 and 1,500 ml) in six healthy young men and women. As breathing interval increased, the longest heart periods became longer, the shortest heart periods became shorter, and the peak-valley P-P intervals increased asymptotically. Peak-valley P-P intervals also increased in proportion to tidal volume. However, this influence was small: a 50% increase of tidal volume increased the average peak-valley P-P interval by only about 15%. The phase angles between heart period changes and respiration varied as linear functions of breathing interval. Heart period shortening (cardioacceleration) began in inspiration at short breathing intervals and in expiration at long breathing intervals. Heart period lengthening, however, began in early expiration at all breathing intervals studied. These results point toward a close relationship between variations of respiratory depth and interval and the quantity, periodicity, and timing of vagal cardiac outflow in conscious humans. They suggest that, at usual breathing rates, phasic respiration-related changes of vagal motoneuron activity began in expiration, progress slowly, and are incompletely expressed at fast breathing rates.
613 citations
TL;DR: Fatigue was postponed by carbohydrate feeding in 7 of the 10 subjects and appeared to be mediated by prevention of hypoglycemia in only two subjects.
Abstract: This study was undertaken to determine whether carbohydrate feeding during exercise can delay the development of fatigue. Ten trained cyclists performed two bicycle ergometer exercise tests 1 wk apart. The initial work rate required 74 +/- 2% of maximum O2 consumption (VO2 max) (range 70-79% of VO2 max). The point of fatigue was defined as the time at which the exercise intensity the subjects could maintain decreased below their initial work rate by 10% of VO2 max. During one exercise test the subjects were fed a glucose polymer solution beginning 20 min after the onset of exercise; during the other they were given a placebo. Blood glucose concentration was 20-40% higher during the exercise after carbohydrate ingestion than during the exercise without carbohydrate feeding. The exercise-induced decrease in plasma insulin was prevented by carbohydrate feeding. The respiratory exchange ratio was unchanged by the glucose feeding. Fatigue was postponed by carbohydrate feeding in 7 of the 10 subjects. This effect appeared to be mediated by prevention of hypoglycemia in only two subjects. The exercise time to fatigue for the 10 subjects averaged 134 +/- 6 min (mean +/- SE) without and 157 +/- 5 min with carbohydrate feeding (P less than 0.01).
492 citations
TL;DR: The results indicated that the myoelectric signal-force relationship was primarily determined by the muscle under investigation and was generally independent of the subject group and the force rate.
Abstract: An analytic study was initiated to investigate whether the normalized surface myoelectric signal vs. normalized force relationship varies in different human muscles and whether it is dependent on training level and rate of force production. The data were obtained from experiments that involved the biceps, deltoid, and first dorsal interosseous of three pianists, four long-distance swimmers, three power lifters, and six normal subjects. The elite performers (among the world's best) were chosen because they exhibited varying degrees of fine motor control, endurance training, and power training in different muscles. Approximately 200 isometric linearly force-varying contractions peaking at 80% of the maximal voluntary contraction level were processed. The results indicated that the myoelectric signal-force relationship was primarily determined by the muscle under investigation and was generally independent of the subject group and the force rate. Whereas this relationship was quasilinear for the first dorsal interosseous, it was nonlinear for the biceps and deltoid. Several possible physiological causes of the observed behavior of the myoelectric signal-force relationship are discussed.
440 citations
TL;DR: One bout of exercise after 11 days without exercise returned insulin binding and the insulin and glucose responses to an oral 100-g glucose load almost to the initial "trained" value, which support the hypothesis that residual effects of the last bouts of exercise play an important role in this phenomenon.
Abstract: Physically trained individuals have a markedly blunted insulin response to a glucose load and yet have normal glucose tolerance. This phenomenon has generally been ascribed to long-term adaptations...
363 citations
TL;DR: It is concluded that effective ventilatory rhythmogenesis in the absence of stimuli associated with wakefulness is critically dependent on chemoreceptor stimulation secondary to PCO2-[H+].
Abstract: The effect of sleep state on ventilatory rhythmicity following graded hypocapnia was determined in two normal subjects and one patient with a chronic tracheostomy. Passive positive-pressure hyperventilation (PHV) was performed for 3 min awake and during nonrapid-eye-movement (NREM) sleep with hyperoxia [fractional inspired O2 concentration (FIO2) = 0.50], normoxia and hypoxia (FIO2 = 0.12). During wakefulness, no immediate posthyperventilation apnea was noted following abrupt cessation of PHV in 27 of 28 trials [mean hyperventilation end-tidal CO2 partial pressure (PETCO2) 29 +/- 2 Torr, range 22-35]. During spontaneous breathing in hyperoxia, PETCO2 rose from 40.4 +/- 0.7 Torr awake to 43.2 +/- 1.4 Torr during NREM sleep. PHV during NREM sleep caused apnea when PETCO2 was reduced to 3-6 Torr below NREM sleep levels and 1-2 Torr below the waking level. In hypoxia, PETCO2 increased from 37.1 +/- 0.1 awake to 39.8 +/- 0.1 Torr during NREM sleep. PHV caused apnea when PETCO2 was reduced to levels 1-2 Torr below NREM sleep levels and 1-2 Torr above awake levels. Apnea duration (5-45 s) was significantly correlated to the magnitude of hypocapnia (range 27-41 Torr). PHV caused no apnea when isocapnia was maintained via increased inspired CO2. Prolonged hypoxia caused periodic breathing, and the abrupt transition from short-term hypoxic-induced hyperventilation to acute hyperoxia caused apnea during NREM sleep when PETCO2 was lowered to or below the subject's apneic threshold as predetermined (passively) by PHV. We concluded that effective ventilatory rhythmogenesis in the absence of stimuli associated with wakefulness is critically dependent on chemoreceptor stimulation secondary to PCO2-[H+].
322 citations
TL;DR: Chez le lapin la ventilation a haute frequence ameliore les echanges gazeux pour protegent le poumon des membranes hyalines contrairement a la ventilation traditionnelle.
Abstract: Chez le lapin la ventilation a haute frequence ameliore les echanges gazeux. Les oscillations a haute frequence protegent le poumon des membranes hyalines contrairement a la ventilation traditionnelle
319 citations
TL;DR: Pulmonary effects of O3 were observed at levels much lower than that for which these effects have been previously described, and Stimulation of airway receptors is probably the mechanism responsible for the majority of observed changes.
Abstract: Because minimal data are available regarding the pulmonary effects of ozone (O3) at levels less than 0.27 ppm, six groups of healthy young males were exposed for 2.5 h to one of the following O3 concentrations: 0.0, 0.12, 0.18, 0.24, 0.30, or 0.40 ppm. Fifteen-minute periods of rest and exercise (65 l/min minute ventilation) were alternated during the first 2 h of exposure. Coughing was observed at all levels of O3 exposure. Small changes in forced-expiratory spirometric variables [forced vital capacity (FVC), forced expiratory volume in 1 s, and mean expiratory flow rate between 25 and 75% FVC] were observed at 0.12 and 0.18 ppm O3, and larger changes were found at O3 levels greater than or equal to 0.24 ppm. Changes in tidal volume and respiratory frequency during exercise, specific airway resistance, the presence of pain on deep inspiration, and shortness of breath occurred at O3 levels greater than or equal to 0.24 ppm. In conclusion, pulmonary effects of O3 were observed at levels much lower than that for which these effects have been previously described. Stimulation of airway receptors is probably the mechanism responsible for the majority of observed changes; however, the existence of a second mechanism of action is postulated.
TL;DR: It is concluded that COPD patients can increase their mean Pdi 3-fold before reaching a fatiguing pattern of breathing compared with 8-fold in normal subjects and the remaining force reserve of the diaphragm can be exhausted by even minor modifications in the breathing pattern.
Abstract: The fatigue threshold of the human diaphragm in normal subjects corresponds to a transdiaphragmatic pressure (Pdi)-inspiratory time integral (TTdi) of about 15% of Pdimax. The TTdi of resting ventilation was measured in 20 patients with chronic obstructive pulmonary disease (COPD) and ranged between 1 and 12% of Pdimax (mean 5%). TTdi was significantly related to total airway resistance (Raw) (r = 0.57; P less than 0.05). Five of these patients were asked to voluntarily modify their TI/TT (ratio of inspiratory time to total cycle duration; from 0.33 to 0.49) so as to increase their TTdi from a control value of 8% to an imposed value of 17% of Pdimax. The imposed pattern induced a progressive decline in the high-frequency (150-350 Hz)/low-frequency (20-40 Hz) power ratio (H/L) of the diaphragm electromyogram (fatigue pattern), quantitatively similar to that seen in normal subjects breathing with similar TTdi levels. The decay in H/L was followed by a progressive fall in mean Pdi meanly due to decrease in gastric pressure swings. It is concluded that 1) the force reserve of the diaphragm in COPD patients is decreased because of a decrease in Pdimax; 2) the remaining force reserve of the diaphragm can be exhausted by even minor modifications in the breathing pattern; and 3) at a TI/TT of 0.40 our COPD patients can increase their mean Pdi 3-fold before reaching a fatiguing pattern of breathing compared with 8-fold in normal subjects.
TL;DR: It is concluded that AT is not detectable using invasive methods (arterial and venous lactates); and the noninvasive gas response determination has such a large range of reviewer variability that it is unsuitable for clinical use.
Abstract: Despite the popularity of the concept of “anaerobic threshold” (AT), the noninvasive detection criteria remain subjective, and invasive validations of AT have been based on lactate data of arterial...
TL;DR: Women, with relatively higher resting ventilation, have lower responses to hypoxia and hypercapnia and male-female differences in ventilatory responses to chemical stimuli are studied.
Abstract: Previous investigation has demonstrated that progesterone, a hormone found in premenopausal women, is a ventilatory stimulant. However, fragmentary data suggest that normal women may have lower ventilatory responses to chemical stimuli than men, in whom progesterone is found at low levels. As male-female differences have not been carefully studied, we undertook a systematic comparison of resting ventilation and ventilatory responses to chemical stimuli in men and women. Resting ventilation was found to correlate closely with CO2 production in all subjects (r = 0.71, P less than 0.001), but women tended to have a greater minute ventilation per milliliter of CO2 produced (P less than 0.05) and consequently a lower CO2 partial pressure (PCO2) (men 35.1 +/- 0.5 Torr, women 33.2 +/- 0.5 Torr; P less than 0.02). Women were also found to have lower tidal volumes, even when corrected from body surface area (BSA), and greater respiratory frequency than comparable males. The hypoxic ventilatory response (HVR) quantitated by the shape parameter A was significantly greater in men [167 +/- 22 (SE)] than in women (109 +/- 13; P less than 0.05). In men this hypoxic response was found to correlate closely with O2 consumption (r = 0.75, P less than 0.001) but with no measure of size or metabolic rate in women. The hypercapnic ventilatory response, expressed as the slope of ventilation vs. PCO2, was also greater in men (2.30 +/- 0.23) than in women (1.58 +/- 0.19, P less than 0.05). Finally women tended to have higher ventilatory responses in the luteal than in the follicular menstrual phase, but this was significant only for HVR (P less than 0.05). Women, with relatively higher resting ventilation, have lower responses to hypoxia and hypercapnia.
TL;DR: It is demonstrated that in this model of acute ventricular failure, increasing intrathoracic pressure improves cardiac function and is postulate that this observed improvement is due to reduced LV wall stress in a manner analogous to that seen with arterial vasodilator therapy in congestive heart failure.
Abstract: We studied the cardiovascular effects of increasing intrathoracic pressure in an acute pentobarbital-anesthetized canine model of acute ventricular failure induced by large doses of propranolol. Left ventricular (LV) function curves were generated by volume loading from LV filling pressures of 5-20 Torr. The animals were ventilated by using intermittent positive-pressure ventilation with large tidal volumes (30 ml/kg). Chest and abdominal pneumatic binders were used to increase intrathoracic pressure. When compared with the control state, acute ventricular failure was associated with a decrease in the slope of the LV function curves (P less than 0.01). After binding the increase in intrathoracic pressure (1.1 +/- 1.6 to 12.1 +/- 2.4 Torr, P less than 0.01) was associated with an improvement in both right ventricular and LV function. Our study demonstrates that in this model of acute ventricular failure, increasing intrathoracic pressure improves cardiac function. We postulate that this observed improvement with increased intrathoracic pressure is due to reduced LV wall stress in a manner analogous to that seen with arterial vasodilator therapy in congestive heart failure.
TL;DR: It is concluded that anesthesia suppresses hypoglossal motor activities much more than those of the bulbospinal-phrenic system.
Abstract: In decerebrate, vagotomized, paralyzed, and ventilated cats, phrenic and respiratory-related hypoglossal discharges were evident at normocapnic normoxia or hyperoxia. Both increased progressively i...
TL;DR: The results underline the importance of the contractile and force generating capacity of human muscle in determining maximal power output and performance during exercise of a few seconds duration.
Abstract: In five spontaneously breathing kittens (12-13 days old), anesthetized with pentobarbital sodium, we measured the passive and active elastances and resistances of the respiratory system and the dec...
TL;DR: An integrated picture of human gas exchange at the highest point on earth is constructed for the first time due to the severe arterial hypoxemia, high pH, and extremely low PCO2 of subjects on the summit of Mt. Everest.
Abstract: Pulmonary gas exchange was studied on members of the American Medical Research Expedition to Everest at altitudes of 8,050 m (barometric pressure 284 Torr), 8,400 m (267 Torr) and 8,848 m (summit of Mt. Everest, 253 Torr). Thirty-four valid alveolar gas samples were taken using a special automatic sampler including 4 samples on the summit. Venous blood was collected from two subjects at an altitude of 8,050 m on the morning after their successful summit climb. Alveolar CO2 partial pressure (PCO2) fell approximately linearly with decreasing barometric pressure to a value of 7.5 Torr on the summit. For a respiratory exchange ratio of 0.85, this gave an alveolar O2 partial pressure (PO2) of 35 Torr. In two subjects who reached the summit, the mean base excess at 8,050 m was -7.2 meq/l, and assuming the same value on the previous day, the arterial pH on the summit was over 7.7. Arterial PO2 was calculated from changes along the pulmonary capillary to be 28 Torr. In spite of the severe arterial hypoxemia, high pH, and extremely low PCO2, subjects on the summit were able to perform simple tasks. The results allow us to construct for the first time an integrated picture of human gas exchange at the highest point on earth.
TL;DR: There is evidence that pronounced lactate accumulation occurs during supramaximal exercise of a 10-s duration, suggesting that glycolysis can occur within this time frame, in contrast to the theory that glyCOlysis does not occur until endogenous phosphagen levels reach some critically low value.
Abstract: The purpose of this study was to evaluate the extent of anaerobic glycogenolysis, as indicated by intramuscular lactate concentration, after 10 and 30 s of supramaximal exercise and to compare male and female subjects in this regard. Fifteen males and seven females performed two cycle exercise bouts against a resistance which was standardized so that one pedal revolution resulted in 4.90 J work X kg body wt-1. A muscle biopsy was obtained after 10- and 30-s exercise bouts and analyzed for lactate concentration. The lactate concentrations averaged 36 and 61 mmol X kg dry wt-1 after the 10- and 30-s exercise bouts, respectively. The male subjects had higher (P less than 0.005) lactate concentrations and generated higher (P less than 0.001) power outputs for both exercise bouts. When the mean lactate concentrations were statistically adjusted after controlling for between-group variation in power output, no difference was evident between groups for the 10- or the 30-s lactate value. The results are evidence that pronounced lactate accumulation occurs during supramaximal exercise of a 10-s duration, suggesting that glycolysis can occur within this time frame. This is in contrast to the theory that glycolysis does not occur until endogenous phosphagen levels reach some critically low value, not thought to be obtainable within the first 10 s of supramaximal exercise.
TL;DR: It was found that the VO2VAT, expressed in terms of power output (POVAT), occurred at a higher value than the POLAT (1,004 vs. 621 kg X min-1) and the elevation in muscle anaerobic glycolysis precedes both the VAT and the blood LAT in this progressive exercise test.
Abstract: The purpose of this study was to investigate the interrelationship between the ventilatory anaerobic threshold (VAT), the blood lactate anaerobic threshold (LAT), and the alteration in muscle metabolism. Ten subjects (5 men and 5 women) performed progressive exercise to exhaustion on two occasions for determination of the VAT and the LAT. For both AT criteria, the initial breakpoints (P less than 0.05) in the relationship between ventilation (VE) and O2 uptake (VO2VAT) and lactate (La) and power output (POLAT) were determined by multisegmental linear regression. During three subsequent tests the subjects performed progressive exercise to various percentages of the VO2VAT. Biopsies were obtained from the musculus vastus lateralis for determination of selected glycolytic intermediates at the cessation of exercise. It was found that the VO2VAT, expressed in terms of power output (POVAT), occurred at a higher value (P less than 0.05) than the POLAT (1,004 vs. 621 kg X min-1). Blood La values at these power outputs were 2.09 and 1.25 mM, respectively. Determination of the muscle La concentration at 79, 94, and 110% of VO2VAT indicated significant increases (P less than 0.05) from rest values of 1.59 to 4.49, 6.37, and 11.3 mmol X kg wet wt-1, respectively. It is concluded that the gas exchange AT as determined by the relationship between VE and VO2VAT and the AT as determined by blood La accumulation (LAT) are not coincidental. In addition the elevation in muscle anaerobic glycolysis precedes both the VAT and the blood LAT in this progressive exercise test.
TL;DR: The onset of the “ramp”-like increase in inspiratory activity is due to an abrupt release of inhibition and a subsequent progressively increasing synaptic excitation of inspiratory premotor neurons.
Abstract: Recent advances in several laboratories concerning the respiration-related medullary neurons, their locations, projections, interconnections, morphological and physiological properties, and pattern...
TL;DR: The cardiovascular responses to exercise are determined to a large extent by the active muscle mass and the absolute oxygen uptake, with the principal feature appearing to be the tight linkage between systemic oxygen transport and utilization.
Abstract: The roles of absolute and relative oxygen uptake (VO2 and percent of muscle group specific VO2 max) as determinants of the cardiovascular and ventilatory responses to exercise over a wide range of active muscle mass have not previously been defined. Six healthy men performed four types of dynamic exercise--one-arm curl, one-arm cranking, and one- and two-leg cycling at four different relative work loads--25, 50, 75, and 100% of VO2 max for the corresponding muscle group. VO2 during maximal one-arm curl, one-arm cranking, and one-leg cycling averaged 20, 50, and 75%, respectively, of that for maximal two-leg cycling. Cardiac output was linearly related to VO2 with a similar slope and intercept for each type of exercise. Heart rate at a given %VO2 max was higher with larger active muscle mass. In relation to %VO2 max, systemic resistance was lower and plasma catecholamine levels were higher with larger active muscle mass. The cardiovascular responses to exercise are determined to a large extent by the active muscle mass and the absolute oxygen uptake, with the principal feature appearing to be the tight linkage between systemic oxygen transport and utilization.
TL;DR: A computational model of the maximal expiratory flow-volume (MEFV) curve has been developed and will require modeling of inhomogeneous emptying in diseased lungs, perfecting noninvasive techniques of estimating pertinent airway characteristics, and improving techniques for increasing the signal-to-noise ratio in MEFV curves.
Abstract: The first major advance in understanding expiratory flow limitation of the lungs came with the description of isovolume pressure-flow curves. These curves documented the existence of a volume-dependent limit to maximal expiratory flow and led directly to the description of the maximal expiratory flow-volume (MEFV) curve. Definitive modeling of flow limitation awaited the description of a localized mechanism that dominated the flow-limiting process. The phenomenon of wave speed limitation of flow was shown to apply to the airways and provided the needed localized mechanism. Using this concept and recent data on airway mechanics and the frictional losses in the flow, a computational model of the MEFV curve has been developed. Further progress will require modeling of inhomogeneous emptying in diseased lungs, perfecting noninvasive techniques of estimating pertinent airway characteristics, and improving techniques for increasing the signal-to-noise ratio in MEFV curves.
TL;DR: The results help to explain how man can reach the highest point on earth while breathing ambient air by falling considerably at the lowest values of inspired PO2.
Abstract: Maximal exercise at extreme altitudes was studied during the course of the American Medical Research Expedition to Everest. Measurements were carried out at sea level [inspired O2 partial pressure (PO2) 147 Torr], 6,300 m during air breathing (inspired PO2 64 Torr), 6,300 m during 16% O2 breathing (inspired PO2 49 Torr), and 6,300 m during 14% O2 breathing (inspired PO2 43 Torr). The last PO2 is equivalent to that on the summit of Mt. Everest. All the 6,300 m studies were carried out in a warm well-equipped laboratory on well-acclimatized subjects. Maximal O2 uptake fell dramatically as the inspired PO2 was reduced to very low levels. However, two subjects were able to reach an O2 uptake of 1 l/min at the lowest inspired PO2. Arterial O2 saturations fell markedly and alveolar-arterial PO2 differences increased as the work rate was raised at high altitude, indicating diffusion limitation of O2 transfer. Maximal exercise ventilations exceeded 200 l/min at 6,300 m during air breathing but fell considerably at the lowest values of inspired PO2. Alveolar CO2 partial pressure was reduced to 7-8 Torr in one subject at the lowest inspired PO2, and the same value was obtained from alveolar gas samples taken by him at rest on the summit. The results help to explain how man can reach the highest point on earth while breathing ambient air.
TL;DR: The results show that some individuals with VO2max limited by impaired cardiac function can undergo adaptations to training that enable them to maintain close to a metabolic steady state during exercise that elicits VO2 max.
Abstract: Six patients with ischemic heart disease who had exercised intensely for longer than 1 yr appeared to have a disproportionately high capacity for endurance exercise relative to VO2 max. They were c...
TL;DR: It is concluded that exercise-induced increases in plasma ACTH and their correlation with circulating cortisol depend on the intensity of isotonic exercise and that plasma lactic acid may influence ACTH release during exercise.
Abstract: Adrenocorticotropic hormone (ACTH) levels were compared before and after submaximal and exhaustive isotonic exercise in six normally active college students (3 men and 3 women). Each subject participated in three experiments conducted at the same morning hour. Venous plasma was obtained before and immediately after 20-min runs at 65 and 80% of maximal O2 consumption (VO2 max) and after a run of gradually increasing work intensity which resulted in exhaustion (100% VO2 max) in 12.6 +/- 1.3 min. ACTH (mean +/- SE) was 48 +/- 15, 57 +/- 12, and 61 +/- 11 pg/ml before the 65, 80, and 100% VO2 max runs, and increased to 61 +/- 15 (NS), 128 +/- 18 (P less than 0.05), and 292 +/- 72 (P less than 0.05) pg/ml, respectively. Plasma glucose, growth hormone, cortisol, and lactic acid concentrations increased in a similar fashion. Cortisol and ACTH levels were significantly correlated at the higher levels of exertion: r = 0.18 (NS) for the 65% VO2 max run, r = 0.65 (P less than 0.05) for the 80% VO2 max run, and r = 0.64 (P less than 0.05) for the run to exhaustion. Both the change in ACTH with exercise and its postrun concentration were significantly related to the change in plasma lactic acid (r = 0.65, P less than 0.05) and the postrun plasma lactic acid (r = 0.64, P less than 0.05). We conclude that exercise-induced increases in plasma ACTH and their correlation with circulating cortisol depend on the intensity of isotonic exercise. Our observations also suggest that plasma lactic acid may influence ACTH release during exercise.
TL;DR: Rat lungs were perfused in an in vitro circuit with separate control of alveolar and pulmonary arterial O2 tension and the hypoxic pulmonary vasoconstrictor response was measured as changes of perfusion pressure to conclude that HPV is determined by PAO2 and PvO2.
Abstract: Rat lungs were perfused in an in vitro circuit with separate control of alveolar and pulmonary arterial O2 tension. With perfusion flow constant, the hypoxic pulmonary vasoconstrictor (HPV) respons...
TL;DR: The results suggest that the velocity of shortening of tonically contracted AWSM is very slow relative to the rates of cycling employed, which could account for well-known effects of volume history on airway tone.
Abstract: Strips of tonically contracted canine tracheal and bronchial airway smooth muscles (AWSM) were studied in vitro to compare dynamic muscle force during stretch-retraction cycles with static isometric muscle force at various length points within the cycling range. At any particular rate, a characteristic force-length loop was obtained by cycling over a given range of lengths. Dynamic muscle force dropped well below static isometric muscle force at lengths short of the peak length at all rates of cycling. When stretch or retraction of the muscle was stopped at any point along either path of the cycle, muscle force rose to approach the isometric force at that length. Dynamic force at the peak length of the cycle remained close to, or slightly greater than, the static isometric force. The results suggest that the velocity of shortening of tonically contracted AWSM is very slow relative to the rates of cycling employed. A slow rate of shortening of AWSM relative to the rate of change in airway caliber during breathing could account for well-known effects of volume history on airway tone.
TL;DR: The data suggested that the reduced cardiac capacity of T and HLP may also be linked to their lower maximal exercise capacity and O2 uptake, and a lack of any respiratory limit to maximal O2 delivery.
Abstract: Eight tetraplegic and 13 paraplegic subjects performed a continuous progressive loading exercise test to exhaustion on a wheelchair ergometer. Their cardiorespiratory responses at maximal O2 uptake were analyzed after initially grouping subjects according to the international system for classification of wheelchair athletes. Analysis of variance provided a basis for regrouping the subjects into tetraplegic (T), high-lesion paraplegic (HLP), and low-lesion paraplegic (LLP) groups and indicated significant differences (P less than 0.05) in maximal power output (24, 47, and 80 W) and O2 uptake (0.97, 1.62, and 2.42 l/min) for T, HLP, and LLP, respectively. T had a significantly lower maximal heart rate (110) compared with the paraplegic values (175 and 190), whereas the HLP, in contrast to the LLP, had a lower maximum ventilation (66 vs. 101 l/min) and a lower O2 pulse (9.3 vs. 12.7 ml/beat). The ventilatory equivalent for O2 was similar in all groups to values for able-bodied subjects in maximal arm crank ergometry, however, suggesting a lack of any respiratory limit to maximal O2 delivery. No differences were noted in respiratory exchange ratio or net efficiency between the groups. In addition to limitations of functional muscle mass, the data suggested that the reduced cardiac capacity of T and HLP may also be linked to their lower maximal exercise capacity and O2 uptake.
TL;DR: Experiments were conducted to test the hypothesis that injury to skeletal muscle in rats resulting from prolonged downhill running is prevented to a greater extent by prior downhill training than prior uphill training.
Abstract: Experiments were conducted to test the hypothesis that injury to skeletal muscle in rats resulting from prolonged downhill running is prevented to a greater extent by prior downhill training than by either uphill or level training. Changes in plasma creatine phosphokinase (CPK) activity and glucose-6-phosphate dehydrogenase (G-6-PDase) activity in the soleus (S), vastus intermedius (VI), and medial head of triceps brachii (TM) muscles were evaluated as markers of muscle injury 48 h after 90 min of intermittent downhill running (16 m . min -1). Prior to this acute downhill run, groups of rats were trained by either downhill (-16 degrees), level (0 degrees), or uphill (+16 degrees) running (16 m . min -1) for 30 min/day. Training duration was either 5 days or 1 day. A training effect (i.e., reduced muscle injury) was indicated if muscle G-6-PDase or plasma CPK activity in a trained group following the 90-min downhill run was not different from that of nonexercised control animals and/or if it was lower than that of nontrained runners. A significant training effect was achieved in all three muscles with 5 days of either downhill or level training, but only in S after 5 days of uphill training. Elevation of plasma CPK activity was prevented by 5 days of training on all three inclines.(ABSTRACT TRUNCATED AT 250 WORDS)