Summary
Background
Chronic sleep debt is becoming increasingly common and affects millions of people in more-developed countries. Sleep debt is currently believed to have no adverse effect on health. We investigated the effect of sleep debt on metabolic and endocrine functions.
Methods
We assessed carbohydrate metabolism, thyrotropic function, activity of the hypothalamo-pituitary-adrenal axis, and sympathovagal balance in 11 young men after time in bed had been restricted to 4 h per night for 6 nights. We compared the sleep-debt condition with measurements taken at the end of a sleep-recovery period when participants were allowed 12 h in bed per night for 6 nights.
Findings
Glucose tolerance was lower in the sleep-debt condition than in the fully rested condition (p<0·02), as were thyrotropin concentrations (p<0·01). Evening cortisol concentrations were raised (p=0·0001) and activity of the sympathetic nervous system was increased in the sleep-debt condition (p<0·02).
Interpretation
Sleep debt has a harmful impact on carbohydrate metabolism and endocrine function. The effects are similar to those seen in normal ageing and, therefore, sleep debt may increase the severity of age-related chronic disorders.
Introduction
Voluntary sleep curtailment has become common. “Normal” average sleep duration has decreased from about 9 h per night in 1910 to about 7·5 h currently1 to create maximum time for work and leisure activities· Additionally, to meet the demands of around-the-clock production, many shift workers sleep, on average, less than 5 h per work day. Sleep curtailment is purported to be harmless and efficient. It has been suggested that a “normal” night’s sleep of about 8 h is composed of a 4–5 h period of core sleep, including most of deep non-rapid-eye-movement (non-REM) sleep, and optional sleep. It has been proposed that optional sleep could be progressively removed without inducement of increased daytime sleepiness, mood changes, or detectable decline in cognitive function. Some studies have shown that participants could adapt to a progressive curtailment of their usual sleep period by 2–3 h per night with no substantial alterations in mood and vigilance, but other studies have provided strong evidence to the contrary. Experimental extension of the time spent in bed to 14 h per day over 1 month showed that a normal 8 h night does not meet the sleep needs of healthy young adults, who may carry a substantial sleep debt even in the absence of obvious efforts to curtail sleep. No study has assessed the potential health impact of
chronic sleep debt. Despite well documented modulation by sleep of metabolic and endocrine regulation, immune function, and cardiovascular variables, the consensus is
that sleep is for the brain, not for the rest of the body, and that sleep debt has little or no effect on peripheral function. We investigated metabolic and hormonal variables in people in whom sleep had been restricted and extended.
Discussion
Less than 1 week of sleep curtailment in healthy young people is associated with striking alterations in metabolic and endocrine function. Therefore, although the primary
function of sleep may be cerebral restoration, sleep debt also has consequences for peripheral function that, if maintained chronically, could have long-term adverse effects on health. Decreased carbohydrate tolerance and increased sympathetic tone are well-recognised risk factors for the development of insulin resistance, obesity, and hypertension. Raised cortisol concentrations in the evening are thought to reflect an impairment of the negative-feedback control of the hypothalamo-pituitary-adrenal axis and to be involved in age-related insulin resistance and memory impairments. The metabolic and endocrine alterations seen during the sleep-debt condition therefore mimic some of the hallmarks of ageing, which suggests that chronic sleep loss could increase the severity of age-related pathologies, such as diabetes and hypertension.
For metabolic and endocrine variables derived from measurements in blood, sleep debt could be compared only with the sleep-recovery condition and not with the baseline condition because of limitations on blood withdrawal. For non-invasive measures such as subjective sleepiness, sympathovagal balance, and concentrations for free cortisol in the saliva, however, baseline values were intermediate between the sleep-debt and the sleep recovery conditions, which suggests that the fully rested state may represent a better functional condition than that achieved by the “normal” 8 h bedtime. Previous studies have shown that 8 h in bed may not be sufficient to satisfy the sleep needs of normal young adults. Our data further identify putative pathways by which the impact of sleep debt on the central nervous system could be translated to the periphery. Increases in sympathetic compared with parasympathetic tone, which we interpret as the most probable cause of decreased β-cell responsiveness in the sleep-debt condition, may negatively affect cardiac function, regulation of blood pressure, and kidney function. A decrease in non-insulin dependent glucose uptake is likely to reflect decreased cerebral use of glucose, which suggests another pathway linking central and peripheral manifestations of sleep debt. Diminished brain glucose uptake results in increased exposure of peripheral tissues to higher glucose concentrations, which, under chronic conditions, will probably facilitate the development of insulin resistance in predisposed individuals. The slower decrease of cortisol concentrations in the afternoon was consistent with altered hippocampal mechanisms that control negative feedback regulation of the hypothalamo-pituitary-adrenal axis. Metabolic and cognitive function could therefore be adversely affected under chronic conditions.
Irrespective of the underlying mechanisms, when compared with the sleep-recovery condition, sleep debt, which is experienced by a substantial proportion of people in more-developed countries, is clearly associated with metabolic and endocrine alterations that may have physiopathological consequences in the long term.