Journal of Applied Physiology AJP: Endocrinology and Metabolism
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J Appl Physiol 85: 1199-1200, 1998;
8750-7587/98 $5.00
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Vol. 85, Issue 4, 1199-1200, October 1998

This Month in the Journal

    THE NOSE AND NITROUS OXIDE

When an inert gas enters the nasal airway, it is taken up by passive solution in the capillary blood and tissues lining the airway. Kelley and DuBois (p. 1203) studied the nasal uptake of nitrous oxide, an inert gas, in human subjects who learned to isolate their nasal airways by voluntary closure of their soft palates. The results enabled the investigators to estimate the superficial capillary blood flow in the nose. Furthermore, by comparing the nitrous oxide findings with previous measurements of the nasal uptake of nitric oxide (NO), a highly reactive gas, they determined that NO uptake is 25-31 times that predicted from its solubility and the capillary blood flow. This difference is attributed to chemical reactions of NO in mucous secretions, nasal tissues, and capillary blood. The paper is discussed in an Invited Editorial by Morris (p. 1201).

    EXERCISE, INSULIN, AND GLUCOSE UPTAKE IN MUSCLE

Both muscle contraction and insulin stimulate translocation of glucose transporters (GLUT-4 isoform) to the region of the cell surface (T tubules and sarcolemma). GLUT-4 transporters are then positioned to mediate cell glucose uptake, and so exercise is said to promote the action of insulin. Using laboratory rats and a photolabeling technique applied to skeletal muscle, Hansen and associates (p. 1218) showed that a single bout of exercise increased cell surface GLUT-4 labeling and doubled glucose uptake in response to an insulin challenge 3.5 h later. Assays of insulin receptor substrate-1 tyrosine phosphorylation after exercise showed no effect of insulin. Thus, even though exercise and insulin affect GLUT-4 translocation by separate mechanisms, exercise increases insulin action by positioning transporters where they can facilitate glucose uptake.

    ACTIVITY OF EXPIRATORY NEURONS AND THE DURATION OF EXPIRATION

Models for generation of respiratory rhythm, based on neuronal recordings from anesthetized, decerebrate or in vitro preparations, are difficult to test. Using endogenous variations of the respiratory pattern in cats during sleep and wakefulness, Orem (p. 1260) examined the prediction of some models that there should be an inverse relationship between the activity of rostral medullary expiratory neurons and expiratory duration. No consistent relationship was found, so the models will have to be modified to take these findings into account.

    PLASTICITY OF THE CHEMICAL CONTROL OF BREATHING

Although the carotid body is known to play a role in normal control of breathing, the magnitude of its contribution at rest and during exercise remains uncertain. Using awake goats, Pan et al. (p. 1299) evaluated the time course of alterations in control of breathing over the first 15 days after carotid body denervation. Hypercapnic ventilatory responsesiveness was attenuated by 60% on day 4 after bilateral carotid body denervation, and arterial PCO2 during room-air breathing increased by 11 Torr. Both responsiveness and arterial PCO2 returned to normal at 15 days. The results reveal that the carotid chemoreceptor plays an important role in the ventilatory response to CO2 and that an apparent plasticity of the system provides for compensation after chronic loss of this input.

    LUNG VOLUME AND CONTRACTILE PERFORMANCE OF THE DIAPHRAGM

Polkey and colleagues (p. 1322) evaluated the effect of lung volume (from residual volume to total lung capacity) on transdiaphragmatic pressures (Pdi) elicited by bilateral anterior magnetic stimulation of the phrenic nerves in healthy human subjects. Pairs of phrenic nerve stimuli were presented, with interstimulus intervals varying from 999 to 10 ms. Changes in amplitude of the response to the second stimulus (T2 Pdi) were used to examine the dependence of Pdi on the frequency of stimulation. T2 Pdi decreased as lung volume increased, and this effect was greatest at longer interstimulus intervals, corresponding to slower stimulation frequencies. These results suggest that lung volume change has a greater effect on Pdi generated at lower frequencies of stimulation. Thus, in the human diaphragm, hyperinflation may have a disproportionately severe effect on the summation of pressure responses elicited by low stimulation frequencies.

    IMPORTANCE OF SODIUM IN REHYDRATION

Ray et al. (p. 1329) compared the effectiveness of high-sodium (chicken broth and chicken noodle soup) and low-sodium (water and a carbohydrate-electrolyte solution) beverages for initial fluid replacement in normal subjects after dehydration by 2.5% of body weight. After rehydration to replace weight loss over 2 h, plasma volume was fully restored in subjects who drank high-sodium beverages but remained below baseline in those receiving low-sodium fluids. Urine volume was greater in the low-sodium group. The results indicate that oral sodium early in rehydration increases fluid retention and improves plasma volume restoration.

    RACIAL DIFFERENCES IN REFLEX RESPONSES DURING SLEEP

Crisostomo et al. (p. 1413) examined the responses of heart rate and ventilation to phenylephrine-induced increases in blood pressure and to transient hypoxia during wakefulness and sleep in normotensive African American and Caucasian subjects. Non-rapid-eye-movement (NREM) sleep increased baroresponsiveness but did not alter the ventilatory response to hypoxia. African Americans showed a reduced baroreceptor responsiveness and an enhanced hypoxic ventilatory response in NREM, a pattern previously reported in subjects with borderline hypertension. The net effect of these responses may result in increased exposure during sleep to sympathetic vasoconstriction in susceptible subjects.

    CAFFEINE AND EXERCISE PERFORMANCE

Some athletes purposely use caffeine as a stimulant, but more often athletes are exposed incidentally to caffeine contained in coffee, tea, and other beverages. How do these athletes respond if dietary caffeine is withheld? Van Soeren and Graham (p. 1493) studied caffeine-habituated recreational athletes during leg cycling at 80-85% maximal O2 consumption. Caffeine-containing or placebo pills were given to athletes after 0, 2, or 4 days of withdrawal. Exercise endurance time as well as concentrations of blood metabolites and catecholamines were determined. Caffeine promoted exercise endurance whether subjects had withdrawn or not. Increased endurance from acute caffeine ingestion was not related to metabolite or hormone concentrations, leaving the ergogenic effect unexplained.

    ON THE OTHER HAND...

It is thought that caffeine acts to increase catecholamine levels and fat metabolism in skeletal muscle, resulting in glycogen sparing. If so, caffeine should have no impact on short-duration high-intensity exercise, in which glycogen stores are not a limiting factor. Greer and colleagues (p. 1502) evaluated the effect of caffeine ingestion on short-term high-intensity exercise (four 30-s Wingate sprints with 4 min intervening between bouts of exercise) in healthy male subjects. Caffeine ingestion had no effect on power output during the first two sprints and a negative impact on the last two bouts of intense exercise. Caffeine ingestion also had no effect on blood lactate or O2 consumption during the protocol. Despite an elevation in plasma epinepherine levels, there was no indication of an increase in anaerobic metabolism after caffeine ingestion, except for an increase in NH3 concentration. These results indicate that caffeine ingestion has no ergogenic benefit on power output during repeated bouts of short-term intense exercise.

    DISTRIBUTION OF PULMONARY PERFUSION DURING EXERCISE

Ventilation-perfusion mismatching increases during maximal exercise, especially in athletes. To explore the responsible mechanism, Hopkins et al. (p. 1523) used the multiple inert-gas infusion technique to characterize perfusion inequality over time during 1 h of moderately heavy exercise in endurance-trained athletes. The dispersion of the perfusion distribution increased with time, coinciding with a falling pulmonary arterial pressure and pulmonary vascular resistance. Among the individual subjects, nonuniformity of the perfusion distribution was tightly correlated with total lung capacity.


J APPL PHYSIOL 85(4):1199-1200
8570-7587/98 $5.00 Copyright © 1998 the American Physiological Society




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