The purpose of the study was to evaluate the recuperative efficacy of pre-exercise napping on physical capacity after military sustained operations (SUSOPS) with partial sleep deprivation. Before and after a 2-day SUSOPS, 61 cadets completed a battery of questionnaires, and performed a 2-min lunges trial and a 3,000-m running time-trial. After the completion of SUSOPS, subjects were randomized to either a control [without pre-exercise nap (CON); n = 32] or a nap [with a 30-min pre-exercise nap (NAP); n = 29] group. SUSOPS enhanced perceived sleepiness and degraded mood in both groups. Following SUSOPS, the repetitions of lunges, in the CON group, were reduced by similar to 2.3%, albeit the difference was not statistically significant (p = 0.62). In the NAP group, however, the repetitions of lunges were increased by similar to 7.1% (p = 0.01). SUSOPS impaired the 3,000-m running performance in the CON group (similar to 2.3%; p = 0.02), but not in the NAP group (0.3%; p = 0.71). Present results indicate, therefore, that a relatively brief pre-exercise nap may mitigate physical performance impairments ensued by short-term SUSOPS.

Background: Echocardiography is usually performed with the subject/patient lying in the left lateral position (LLP), because the acoustic window is better in this than in the supine position (SP). The aim was to investigate cardiac responses to rotational changes of position in the transversal plane, from SP to LLP while horizontal, and from leaning on the back (HUT-LB) to leaning on the left side (HUT-LL) while tilted 60° head-up from the horizontal. Methods: Healthy men (n = 12) underwent 10-min HUT provocations. Cardiac variables were measured using two-dimensional echocardiography, Doppler, tissue Doppler imaging and arterial pressures using a volume-clamp method. Results: In horizontal posture, cardiac volumes were smaller in SP than in LLP: end-diastolic volume (EDV) by 14%, end-systolic volume (ESV) by 13%, stroke volume (SV) by 14%, and cardiac output (CO) by 16% (P<0·03). In addition, the mitral annular plane systolic excursion (MAPSE) was 11% smaller (P = 0·001) and the left ventricle isovolumic relaxation time (IVRT) 27% longer in SP than in LLP. The ejection fraction, heart rate, arterial pressure and pulmonary ventilation were similar in SP and LLP. During HUT, EDV, SV, CO and MAPSE were smaller, and IVRT was longer, in HUT-LB than in HUT-LL, by −19%, −20%, −17%, −18% and +35%, respectively (P<0·04). Conclusions: Cardiac performance is enhanced in LLP versus SP and in HUT-LL versus HUT-LB, which can be attributed to improved venous return, conceivably, wholly or in part, due to increased hydrostatic pressure gradients between the caval veins and the heart in the LLP and HUT-LL positions.

The study examined the effects of short-term field-based military training with partial sleep deprivation on whole-body endurance performance in well-trained individuals. Before and after a 2-day sustained operations (SUSOPS), 14 cadets performed a 15-min constant-load cycling at 65% of peak power output (PPO; CLT65), followed by an exhaustive constant-load trial at 85% of PPO (CLT85). Physiological [oxygen uptake (O-2), heart rate (HR), mean arterial pressure (MAP), cardiac output (CO), and regional oxygenation (TOI) in the frontal cerebral cortex and vastus lateralis muscle] and psychological [effort perception (RPE), affective valence (FS), and perceived activation (FAS)] variables were monitored during exercise. SUSOPS reduced time to exhaustion in CLT85 by 29.1% (p = 0.01). During the CLT65 trial, SUSOPS potentiated the exercise-induced elevations in O-2 and HR (p < 0.05), and blunted MAP (p = 0.001). CO did not differ between trials. Yet, towards the end of both CLT85 trials, CO tended to decline (p 0.08); a response that occurred at an earlier stage in the SUSOPS trial. During CLT65, SUSOPS altered neither cerebral nor muscle TOI. The SUSOPS CLT85 trial, however, was terminated at similar leg-muscle deoxygenation (p > 0.05) and lower prefrontal cortex deoxygenation (p < 0.01). SUSOPS increased RPE at submaximal intensities (p = 0.05), and suppressed FAS and FS throughout (p < 0.01). The present findings indicate, therefore, that a brief period of military sustained operations with partial sleep deprivation augment cardiorespiratory and psychological strain, limiting high-intensity endurance capacity.

Skeletal muscle oxidative function was evaluated in 11 healthy males (mean +/- SD age 27 +/- 5years) prior to (baseline data collection, BDC) and following a 21day horizontal bed rest (BR), carried out in normoxia (P-IO2=133 mmHg; N-BR) and hypoxia (P-IO2=90 mmHg; H-BR). H-BR was aimed at simulating reduced gravity habitats. The effects of a 21day hypoxic ambulatory confinement (P-IO2=90 mmHg; H-AMB) were also assessed. Pulmonary O-2 uptake (<(V) over dot>O-2), vastus lateralis fractional O-2 extraction (changes in deoxygenated haemoglobin+myoglobin concentration, Delta[deoxy(Hb+Mb)]; near-infrared spectroscopy) and femoral artery blood flow (ultrasound Doppler) were evaluated during incremental one-leg knee-extension exercise (reduced constraints to cardiovascular O-2 delivery) carried out to voluntary exhaustion in a normoxic environment. Mitochondrial respiration was evaluated ex vivo by high-resolution respirometry in permeabilized vastus lateralis fibres. <(V) over dot>(O2peak) decreased (P<0.05) after N-BR (0.98 +/- 0.13 L min(-1)) and H-BR (0.96 +/- 0.17 L min(-1)) vs. BDC (1.05 +/- 0.14 L min(-1)). In the presence of a decreased (by similar to 6-8%) thigh muscle volume, <(V) over dot>(O2peak) normalized per unit of muscle mass was not affected by both interventions. Delta[deoxy(Hb+Mb)](peak) decreased (P<0.05) after N-BR (65 +/- 13% of limb ischaemia) and H-BR (62 +/- 12%) vs. BDC (73 +/- 13%). H-AMB did not alter <(V) over dot>(O2peak) or Delta[deoxy(Hb+Mb)](peak). An overshoot of Delta[deoxy(Hb+Mb)] was evident during the first minute of unloaded exercise after N-BR and H-BR. Arterial blood flow to the lower limb during both unloaded and peak knee extension was not affected by any intervention. Maximal ADP-stimulated mitochondrial respiration decreased (P<0.05) after all interventions vs. control. In 21day N-BR, a significant impairment of oxidative metabolism occurred downstream of cardiovascular O-2 delivery, affecting both mitochondrial respiration and presumably the intramuscular matching between O-2 supply and utilization. Superposition of H on BR did not worsen the impairment induced by BR alone.

Supra-tolerance head-to-foot directed gravitoinertial load (+Gz) typically induces a sequence of symptoms/signs, including loss of: peripheral vision-central vision-consciousness. The risk of unconsciousness is greater when anti-G-garment failure occurs after prolonged rather than brief exposures, presumably because, in the former condition, mental signs are not consistently preceded by impaired vision. The aims were to investigate if prolonged exposure to moderately elevated +Gz reduces intraocular pressure (IOP; i.e., improves provisions for retinal perfusion), or the cerebral anoxia reserve. Subjects were exposed to 4-min +Gz plateaux either at 2 and 3 G (n = 10), or at 4 and 5 G (n = 12). Measurements included eye-level mean arterial pressure (MAP), oxygenation of the cerebral frontal cortex, and at 2 and 3 G, IOP. IOP was similar at 1 (14.1 +/- 1.6 mmHg), 2 (14.0 +/- 1.6 mmHg), and 3 G (14.0 +/- 1.6 mmHg). During the G exposures, MAP exhibited an initial prompt drop followed by a partial recovery, end-exposure values being reduced by ae<currency>30 mmHg. Cerebral oxygenation showed a similar initial drop, but without recovery, and was followed by either a plateau or a further slight decrement to a minimum of about -14 mu M. Gz loading did not affect IOP. That cerebral oxygenation remained suppressed throughout these G exposures, despite a concomitant partial recovery of MAP, suggests that the increased risk of unconsciousness upon G-garment failure after prolonged +Gz exposure is due to reduced cerebral anoxia reserve.

NEW FINDINGS: What is the central question of this study? What are the distinct and interactive effects of a 10 day exposure to hypoxia and horizontal bedrest on the whole-body peak oxygen uptake and on the regional cerebral and skeletal muscle tissue oxygenation during upright cycle ergometry in male lowlanders? What is the main finding and its importance? A 10 day sustained exposure to hypoxia aggravates the bedrest-induced reduction in peak oxygen uptake during dynamic exercise engaging large muscle groups, but mitigates the skeletal muscle oxidative capacity impairment elicited by bedrest. The study examined the interactive effects of a 10 day exposure to hypoxia and bedrest on the whole-body peak oxygen uptake (V̇O2 peak ) during maximal exercise and on skeletal muscle and cerebral oxygenation during submaximal exercise. Nine males underwent three 10 day confinements, in a Latin-square order, as follows: (i) a normoxic bedrest [NBR; partial pressure of inspired O2 (PI,O2) = 134.2 ± 0.7 mmHg]; (ii) a hypoxic bedrest (HBR; PI,O2 = 102.9 ± 0.1 mmHg at day 1, 91.5 ± 1.2 mmHg at days 3-10); and (iii) a hypoxic ambulation (HAMB; PI,O2 as in HBR). Before, 1 (R+1) and 3 days (R+3) after each confinement, subjects performed exhaustive, incremental-load and moderate-intensity constant-load (CLTs) cycle-ergometry trials, while breathing either room air or a hypoxic gas mixture. During the CLTs, changes in the regional oxygenation of the cerebral frontal cortex and the vastus lateralis and intercostal muscles were monitored with near-infrared spectroscopy. At R+1, the confinement-related impairment in V̇O2 peak was greater after HBR than after NBR or HAMB, regardless of whether the trial was performed in room air or hypoxia (HBR, -16.2%; NBR, -8.3%; HAMB, -4.1%; P = 0.001). During the CLTs, bedrest aggravated the exercise-induced reduction in locomotor and respiratory muscle oxygenation (P ≤ 0.05); an effect that was less after HBR than after NBR (P ≤ 0.05). The hypoxic exercise-induced cerebral vasodilatory response was blunted by HBR, probably because of the marked hyperventilation-dependent hypocapnia, attendant to the sustained hypoxic stimulus. Hence, short-term exposure to hypoxia potentiates the reduction in V̇O2 peak , but it mitigates the impairment in skeletal muscle oxidative capacity induced by bedrest.

PURPOSE: The purpose was to examine whether associations exist between temperature responses in the fingers vs. toes and hand vs. foot during local cold-water immersion and rewarming phases.

METHODS: Seventy healthy subjects (58 males, 12 females) immersed their right hand or right foot, respectively, in 8 °C water for 30 min (CWI phase), followed by a 15-min spontaneous rewarming (RW) in 25 °C air temperature.

RESULTS: Temperature was lower in the toes than the fingers during the baseline phase (27.8 ± 3.0 vs. 33.9 ± 2.5 °C, p < 0.001), parts of the CWI phase (min 20-30: 8.8 ± 0.7 vs. 9.7 ± 1.4 °C, p < 0.001), and during the RW phase (peak temperature: 22.5 ± 5.1 vs. 32.7 ± 3.6 °C, p < 0.001). Cold-induced vasodilatation (CIVD) was more common in the fingers than in the toes (p < 0.001). Within the first 10 min of CWI, 61% of the subjects exhibited a CIVD response in the fingers, while only 6% of the subjects had a CIVD response in the toes. There was a large variability of temperature responses both within and between extremities, and there was a weak correlation between finger- and toe temperature both during the CWI (r = 0.21, p = 0.08) and the RW phases (r = 0.26, p = 0.03).

CONCLUSIONS: Results suggest that there is generally a lower temperature in the toes than the fingers after a short time of local cold exposure and that the thermal responses of the fingers/hands are not readily transferable to the toes/foot.

Exposure to high altitude is commonly considered a predisposing factor for local cold injury. A number of field studies have indeed confirmed that local cold tolerance is impaired in low-oxygen environments, presumably due to hypoxia-induced cutaneous vasoconstriction. However, during acute and long-term high-altitude exposure, the hypoxic stressor typically co-exists with other environmental and behavioral components, viz. hypothermia, malnutrition and physical fatigue, which independently or interactively may affect peripheral blood-flow responses. Laboratory-based, control studies have demonstrated that acute exposure to hypoxia, isolated from other confounding factors, does not potentiate vasoconstriction during local cold stress, but delays spontaneous rewarming following such cold stress. Conversely, it appears that long-term exposure to hypoxia elicits adaptive processes, in particular when the high-altitude acclimatization regimen is combined with physical exercise, that reverse the hypoxia-induced vasoconstriction after local limb cooling. Such adaptive responses do, however, not seem to be transferable to sea-level conditions, i.e. they do not reduce vasoconstriction during normoxic conditions, nor to be homogeneous across the limbs.