Journal of Applied Physiology
Vol. 83, No. 1, pp. 1-2, July 1997

This Month in the Journal

EXERCISE AND LEPTIN

AGE, EXERCISE TRAINING, AND NEUROMUSCULAR JUNCTIONS

HE-O₂ BREATHING DURING EXERCISE

LIVING HIGH AND TRAINING LOW

SKELETAL MUSCLE CHANGES IN RATS WITH CHRONIC HEART FAILURE

POSTURE, BODY HEAT EXCHANGE, AND SLEEPINESS

MIDBRAIN NEURONS AND RESPIRATORY SENSATION

AROUSAL BEHAVIORS IN SLEEPING INFANTS

CO₂ TRANSPORT IN ANEMIA

EXERCISE AND LEPTIN

Leptin, a 146-amino acid protein released into plasma by adipocytes, appears to act as a hormone to regulate body weight and composition. Obese (ob/ob) mice, which lack leptin, decrease food intake and become less obese when leptin is administered to them. In human subjects, plasma leptin is decreased by fasting and increased by overfeeding. Perusse et al. (p. 5) measured plasma leptin in sedentary subjects before and after an acute bout of exercise and over the course of 20 wk of exercise training. Leptin levels correlated with body fat but did not appear to be independently influenced by acute or chronic exercise. The report is discussed in an Invited Editorial by Considine (p. 3).

AGE, EXERCISE TRAINING, AND NEUROMUSCULAR JUNCTIONS

With age, there are well-documented changes in the morphology and physiology of the neuromuscular junction (NMJ), but whether these changes are primary or secondary to reduced activity with age is not known. Fahim (p. 59) examined the effects of exercise training on NMJs in young compared with aging mice. In young mice, NMJs hypertrophied in response to training. By contrast, in older mice, training reduced the size and capacity of NMJs. This age-related difference in the response to training is of interest as more elderly people engage in endurance exercise.

HE-O₂ BREATHING DURING EXERCISE

The substitution of a normoxic He-O₂ mixture for air during heavy exercise causes an increase in ventilation. To explore the responsible mechanism, Krishnan et al. (p. 82) examined the response to an He-O₂ mixture in normal exercising subjects, with and without topical anesthesia of the airways. Airway anesthesia had no influence on the steady-state hyperventilatory response to He-O₂ breathing but blunted the transient response during the first few breaths of He-O₂ mixture. These results suggest that airway afferents play an important role in the transient ventilatory response to He-O₂ breathing but do not account for the sustained increase in ventilation.

LIVING HIGH AND TRAINING LOW

Despite popular opinion, living and training at high altitude have not been shown to confer an advantage on maximal O₂ consumption (O_{2 max}) or endurance exercise performance, possibly because of the detraining effects on skeletal muscle associated with reduced exercise capacity in hypoxia. Levine and Stray-Gundersen (p. 102) reasoned that athletes could acquire the advantage of training at high altitude without these deleterious effects by "living high" and training daily at low altitudes. In a carefully controlled study in a large group of highly trained athletes, O_{2 max}, endurance performance, and velocity of running at maximal exercise all increased significantly as a result of daily training in normoxia superimposed on chronic hypoxic exposure. These improvements coincided with an increased red cell mass.

SKELETAL MUSCLE CHANGES IN RATS WITH CHRONIC HEART FAILURE

Decreased work capacity is a hallmark of chronic heart failure. The reduced ability to perform physical work is not simply attributable to diminished cardiac output. In rats with chronic heart failure due to induced myocardial infarctions, Pickar et al. (p. 113) studied the number and affinity of [³H]ouabain-binding sites as an assay for Na⁺-K⁺-adenosinetriphosphatase activity in muscle homogenates. The number of binding sites was reduced in the animals with heart failure, but the sites' affinity for [³H]ouabain was not altered. The relationship between these findings and the reduced exercise capacity in individuals with heart failure remains to be determined.

POSTURE, BODY HEAT EXCHANGE, AND SLEEPINESS

In humans, circadian rhythms affect numerous variables, including heart rate, core body temperature (CBT), and secretion of the pineal hormone melatonin. Additionally, for behavioral reasons, body position changes as individuals go to sleep. To better distinguish among the effects of melatonin and other factors related to sleepiness, Krauchi et al. (p. 134) utilized two experimental maneuvers. They asked subjects to change from upright to supine position during daylight hours. Associated with the change in body posture, cutaneous vasodilatation caused skin temperature to rise, which increased cutaneous heat loss and reduced CBT. Sleepiness in subjects increased. Also in daylight, subjects were given exogenous melatonin or placebo. Melatonin was associated with a rise in peripheral skin temperature, decrease in CBT, and increased sleepiness. From these observations, the authors conclude that under comfortable ambient conditions core cooling from distal heat loss is a key mechanism for induction of sleepiness.

MIDBRAIN NEURONS AND RESPIRATORY SENSATION

As the drive to breathe increases in response to exercise or other stimuli, respiratory sensations increase in intensity and eventually lead to dyspnea, especially in the presence of respiratory disease. Chen and Eldridge (p. 196) postulate that mesencephalic neurons that exhibit respiratory rythm when drive is high are a key link between respiratory afferents and brain stem and cortical circuits that mediate sensation. They demonstrate in decerebrate cats that the excitability of these neurons is modulated by upper airway and nasal afferents, suggesting a pathway whereby these afferents could influence the sensation of dyspnea.

AROUSAL BEHAVIORS IN SLEEPING INFANTS

Because failure of normal arousal mechanisms in sleep is suspected to be a cause of the sudden infant death syndrome, Lijowska et al. (p. 219) made detailed observations of normal sleeping infants made hypercapnic by rebreathing with the face covered with bedding or by increasing the inspired CO₂ concentration. A stereotypical sequence of behavior was observed, often in clusters. The sequence consisted of a sigh coupled with a startle, then thrashing limb movements, and, finally, full arousal. As CO₂ increased, incomplete sequences recurred with increasing frequency until the airway was clear or full arousal was achieved. Similar sequences occurred spontaneously in sleeping infants. The authors suggest that this complex behavioral sequence leading to arousal may be endogenously regulated and may be inadequate in susceptible infants.

CO₂ TRANSPORT IN ANEMIA

Oxygen transport depends critically on the hemoglobin concentration of blood, and tissue hypoxia is the primary respiratory consequence of anemia. CO₂ transport is also predictably altered in anemia because of impairment of hemoglobin's roles in binding CO₂ as carbamate and in buffering protons produced by dissociation of carbonic acid. Deem et al. (p. 240) studied CO₂ transport in anesthetized rabbits over the course of progressive isovolemic anemia induced by exchange transfusion. The results show full compensation of CO₂ elimination, chiefly owing to increases in cardiac output and an augmented Haldane effect due to increased O₂ extraction.