CONTROL OF BREATHING DURING SLEEP

Control of breathing in non-rapid-eye-movement (NREM) sleep is believed to be driven by chemoreflexes underlying a "metabolic control system," whereas during rapid-eye-movement (REM) sleep a "behavioral system," unresponsive to chemical stimuli, is thought to predominate. Meza et al. (p. 3) utilized proportional-assist ventilation to test this hypothesis in normal subjects. The authors reasoned that in NREM sleep ventilatory assist should decrease arterial CO₂ slightly and, thereby, decrease the respiratory motor output and that this should not occur during REM sleep. However, respiratory muscle output was downgraded to a comparable extent in both REM and NREM sleep when proportional-assist ventilation was supplied. The authors interpret these results as indicating that respiratory drive during sleep is dominated by chemical control and that REM and NREM sleep are similar in this regard.

	STOP-FLOW STUDIES OF PULMONARY FILTRATION

The site of filtration of various large molecules through the pulmonary vasculature during high left atrial pressure or aspiration of HCl is uncertain. Lin et al. (p. 47) used a stop-flow approach in perfused rat lungs to determine the site of filtration of fluorescein isothiocyanate-dextran and Evans blue-labeled albumin. Comparison of the movement of tritiated water to fluorescein isothiocyanate-dextran revealed that filtration occurred through vessels that were relatively venous, compared with those through which tritiated water exchange had occurred. Instillation of 0.1 N HCl greatly increased filtration, also at more venous sites.

	DOES THE PH OF MUSCLE EXTRACELLULAR FLUID STIMULATE BREATHING DURING EXERCISE?

Evans et al. (p. 90) measured changes in skeletal muscle extracellular fluid pH (pH_e) to determine wheather a decrease in this variable could provide an error signal for ventilatory control during exercise. Using anesthetized rats, the gastrocnemius muscles of which were contracted at 5 Hz by sciatic nerve stimulation, the investigators found that pH_e, measured by magnetic resonance spectroscopy, decreased from a resting level of 7.40 ± 0.01 to 7.16 ± 0.04. pH_e remained acidic throughout the stimulation protocol, even though arterial pH was unchanged. The authors concluded that extracellular fluid pH of contracting skeletal muscle meets the temporal and qualitative criteria necessary for evoking a ventilatory metaboreflex.

	RECENT CONTRACTILE HISTORY INFLUENCES MUSCLE PERFORMANCE

A conditioning stretch of the muscle-tendon complex has been shown to facilitate subsequent concentric muscle contractile performance. The candidate mechanisms underlying this potentiating effect include restitution of elastic strain energy, myoelectric potentiation, and chemomechanical potentiation. However, there has been some controversy as to whether those potentiating mechanisms are of any functional benefit during dynamic multijoint movements. Walshe et al. (p. 97) demonstrated in human subjects that early (first 300 ms) work output produced during isokinetic squats was significantly augmented by prior isometric loading or eccentric muscle stretching. An analysis of work output and concomitant integrated muscle electromyographic activity led the authors to conclude that the early facilitation of work output was largely due to the existence of a higher muscle active state before the start of the concentric movement and that contractile element potentiation may have been a contributing factor.

	PROLONGED MEDULLARY DYSFUNCTION AND BREATHING IN AWAKE GOATS

Whereas brain stem structures and mechanisms underlying breathing have been explored mostly in anesthetized cats and rats, the relevance of the resulting information to intact undrugged mammals, including humans, is infrequently explored. Forster and colleagues (p. 129) studied the obligatory role of the caudal ventrolateral medulla in breathing in awake goats. Distrubances in this region, particularly in the retrotrapezoid nucleus, cause profound depression of breathing in anesthetized mammals. In contrast, although injections of drugs affecting glutamate-mediated neurotransmission into this region of awake goats could produce noticeable transient responses, long-lasting effects on ventilation, even after neurotoxins, were modest, consisting chiefly of long-lasting decreases in CO₂ sensitivity.

	SURFACTANT FUNCTION IN TORPID MARSUPIALS

Torpor is an energy-conserving mechanism employed by some species of small mammals, in which body temperature and metabolic rate are greatly reduced for periods of several hours. The low temperatures associated with torpor pose a theoretical problem for the physical state of lipids, including pulmonary surfactant. Lopatko et al. (p. 146) examined the surface activity of lung lavage fluid from the dunnart, a small Australian marsupial. The fluid was collected from warm-active animals and from those that had been in torpor for 4 and 8 h. The changes in surface activity of surfactant collected during torpor correlated with changes in lipid composition measured in previous studies, in which static lung compliance did not change with torpor. The changes appear to constitute an adaptation to the low body temperatures that occur with torpor.

	WHY DOES MUSCLE STRENGTH DECLINE WITH AGE?

Aging is associated with a decline in maximum voluntary contraction (MVC) force that exceeds the loss of muscle mass. One possible explanation is that older subjects are unable to maximally activate the available muscle mass by voluntary command. De Serres and Enoka (p. 284) compared the ability of young and elderly subjects to maximally activate the biceps brachii muscle. Voluntary activation was incomplete in both groups, with elderly subjects exhibiting greater deficit. However, in both groups, there was no difference between the measured and expected MVC forces based on extrapolation of submaximal forces. Because of the lower signal-to-noise ratio associated with the extrapolation method, the authors conclude that older subjects are able to achieve complete voluntary activation of the biceps brachii during an MVC maneuver. Therefore, the decline in muscle strength with age does not appear to be related to an impairment of neural drive to the muscle.

	A NEW LOOK AT PULMONARY VASCULAR MECHANICS

The longitudinal distribution of vascular resistance and compliance in the lung has long been of interest. Present approaches use arterial and venous occlusion to partition these mechanical properties from artery to vein. Presson et al. (p. 303) revisited this topic in the isolated dog lung by adding direct visualization of flow in subpleural pulmonary vessels following vascular occlusion. It was found that 65% of vascular compliance lay in microvessels <40 µm in diameter, that most of the arterial compliance was proximal to sites of resistance, and that most of the venous compliance lay symmetrically in vessels distal to sites of resistance. These results are of significance to those wishing to understand the pulmonary hemodynamic consequences of vasoconstriction and vascular obstruction. Whether these conclusions can be generalized in other species is also of interest.

	DETERMINANTS OF DECOMPRESSION SICKNESS

When a diver surfaces from a saturation dive, the risk of decompression sickness (DCS) can be reduced either by slowing the rate of ascent or by increasing inspired PO₂, which speeds inert-gas elimination. Previous work indicated that decompression could be carried out safely at a rate of 10 feet of water per hour per atmosphere of inspired O₂. Reinertsen et al. (p. 351) have refined this work by determining the influence of decompression rate and inspired PO₂ on the appearance of bubbles in the pulmonary arteries of pigs, detected by an ultrasonic probe in the esophagus. The study shows that decompression rate and inspired PO₂ can be traded off against each other to produce similar risks of DCS. This work may lead to increased choices for decompression schedules.