Sleep deprivation and cardiorespiratory function

The effects of 64 h of sleep deprivation upon cardiorespiratory function was studied in 11 young men ( \(\dot V_{{\text{O}}_{{\text{ 2 max}}} } = 55.5{\text{ ml kg}}^{ - 1} {\text{ min}}^{ - 1} ,{\text{ STPD}}\) ). Six subjects engaged in normal sedentary activities, while the others walked on a treadmill at 28% \(\dot V_{{\text{O}}_{{\text{ 2 max}}} } \) for one hour in every three; eight weeks later, sleep deprivation was repeated with a crossover of subjects. Immediate post-deprivation measurement of \(\dot V_{{\text{O}}_{{\text{ 2 max}}} } \) showed a small but statistically significant decrease (−3.8 ml min⁻¹ kg⁻¹, STPD), with no difference between exercise and control trials. The final decrement in aerobic power was not due to a loss of motivation, as 88% (21 of 24) of post-deprivation tests still showed a plateau of \(\dot V_{{\text{O}}_{{\text{ 2 max}}} } \) ; in addition, terminal heart rates (198 vs 195 beats min⁻¹), respiratory exchange ratios (1.14 vs 1.15) and blood lactate levels (12.1 vs 11.8 mmol l⁻¹) were not significantly different after sleep deprivation. The decrease in \(\dot V_{{\text{O}}_{{\text{ 2 max}}} } \) was associated with a lower \(\dot V_{{\text{E}}_{{\text{ 2 max}}} } \) (127 vs 142 l min⁻¹, BTPS) and a substantial haemodilution (13%). Physiological responses to sub-maximal exercise showed persistence of the normal diurnal rhythm in heart rate and oxygen consumption, with no added effects due to sleep deprivation. However, ratings of perceived exertion (Borg scale) increased significantly throughout sleep deprivation. The findings are consistent with a mild respiratory acidosis, secondary to reduced cortical arousal and/or a progressive depletion of tissue glycogen stores which are not altered appreciably by moderate physical activity.