 |
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.