The Effect of Wet Conditions and Surface Combat Swimming on Shooting.

INTRODUCTION: Shooting ability is an important aspect of performance in some sports and is vital during a military operation. Load carriage, clothing, and equipment normally associated with fatigue and reduced field of vision or lack of stability at a specific point are important factors that affect the ability to aim when shooting. Additionally, gun support and equipment appear to differentially affect shooting ability with varying shooting positions. All of the studies examining these factors have taken place on dry land and not in water. However, up to date, no study has examined the effect of wet conditions, especially after surface combat swimming (sCS), on shooting ability in different shooting positions. The purpose of this study was to determine the effect of fatigue, produced by prolonged sCS, on a fighter's shooting ability. In addition, we investigated whether the effect of fatigue and wet conditions differed between the shooting positions. MATERIALS AND METHODS: Forty-five participants performed 10 shots in a shooting simulator while standing (ST) and 10 shots while kneeling (KN). This was performed twice and in three conditions: dry, wet, and after 1,000 m of sCS. RESULTS: Wet conditions did not significantly affect shooting abilities. Surface combat swimming negatively affected shooting ability when both ST and KN. The reduction in the center of gravity (COG) of the shots after sCS was 3.7 ± 2.5% for ST and 3.5 ± 0.8% for KN (P < .01). This was accompanied by the increase in horizontal and vertical movement of the gun after the sCS (P < .01). Kneeling was more stable, as shown by a higher percentage of COG of the shots by 3.3 ± 0.1% (P < .01) and by fewer gun movements in both axes (P < .01). CONCLUSIONS: In conclusion, combat swimming affects shooting ability, both in ST and in KN positions. The KN position provides better stability and improved shooting ability.

Effects of vision on energy expenditure and kinematics during level walking.

PURPOSE: We have previously observed substantially higher oxygen uptake in soldiers walking on terrain at night than when performing the same walk in bright daylight. The aims of the present study were to investigate the influence of vision on mechanical efficiency during slow, horizontal, constant-speed walking, and to determine whether any vision influence is modified by load carriage. METHODS: Each subject (n = 15) walked (3.3 km/h) for 10 min on a treadmill in four different conditions: (1) full vision, no carried load, (2) no vision, no carried load, (3) full vision with a 25.5-kg rucksack, (4) no vision with a 25.5-kg rucksack. RESULTS: Oxygen uptake was 0.94 ± 0.12 l/min in condition (1), 1.15 ± 0.20 l/min in (2), 1.15 ± 0.12 l/min in (3) and 1.35 ± 0.19 l/min in (4). Thus, lack of vision increased oxygen uptake by about 19%. Analyses of movement pattern, by use of optical markers attached to the limbs and torso, revealed considerably shorter step length (12 and 10%) in the no vision (2 and 4) than full vision conditions (1 and 3). No vision conditions (2 and 4) increased step width by 6 and 6%, and increased vertical foot clearance by 20 and 16% compared to full vision conditions (1 and 3). CONCLUSION: The results suggest that vision has a marked influence on mechanical efficiency even during entrained, repetitive movements performed on an obstacle-free horizontal surface under highly predictable conditions.

Exercise temperature regulation following a 35-day horizontal bedrest.

NEW FINDINGS: What is the central question of this study? Does a 35-day horizontal bedrest impair thermoeffector responses during whole-body submaximal exercise performed in temperate conditions? What is the main finding and its importance? Cardiovascular and muscular deconditioning ensuing from prolonged recumbency seems to augment, at least to a degree, exercise-induced increase in body core temperature, most likely due to an impairment in non-evaporative heat loss. The response is a function of the absolute exercise intensity imposed. ABSTRACT: We examined the effects of a 35-day horizontal bedrest on thermoregulation during whole-body exercise. Fifteen healthy men were randomly assigned to either a bedrest (BR; n = 10) or a control (CON; n = 5) group. Prior to bedrest, both groups performed 40-min constant-load upright cycling at 30% of their peak workload (Wpeak ; PRE). One and 2 days after bedrest, the BR group performed, in a randomised counterbalanced order, two 40-min trials at 30% of (i) the pre-bedrest Wpeak (i.e., at a fixed absolute intensity; POST-A) and (ii) the post-bedrest Wpeak (i.e., at a fixed relative intensity; POST-R). The CON group conducted only the POST-A trial, at the same time intervals. During the trials, rectal (Trec ) and skin ( T¯sk ) temperatures, and the forehead sweating rate (SwR) were monitored. In the CON group, no differences were observed between the trials. Bedrest potentiated moderately the Trec elevation during the latter part of POST-A (∼0.10°C; P ≤ 0.05), but not of POST-R (∼0.04°C; P = 0.11). In both post-bedrest trials, T¯sk was attenuated by ∼1.5-2.0°C throughout (P < 0.01), whereas the forehead SwR was not modulated. Trec and T¯sk were similar in POST-A and POST-R, yet the forehead SwR was more dependent on the relative workload imposed (P = 0.04). The present findings therefore suggest that the cardiovascular and muscular deconditioning ensuing from a 35-day bedrest may aggravate the exercise-induced increase in body core temperature when working at a given absolute intensity, most likely due to an impairment in non-evaporative heat loss.

The Effect of a Surface Combat Swimming Training Program on Swimming Performance.

In this study the effect of a surface combat swimming (sCS) training program on performance in freestyle swimming and sCS was examined. Forty-five officer cadets were divided into three equivalent groups: a control group (CG), a group that was trained only with a swimsuit and fins (SF), and a group that was trained with combat uniform and equipment (UE). Groups SF and UE followed a 60-min training program with sCS for 4 weeks, 4 times per week. Before and after the training program all groups performed 4×50 and 400-m freestyle swimming, 250-m sCS with a uniform and equipment, 350-m with a swimsuit and fins, and 300-m with a swimsuit. The UE group showed improved performance in 4×50-m (mean±SD 14±9 s) and in 250-m sCS (24±14 s) (p<0.01). Both the SF group and the UE group improved in 300-m sCS, in 350-m sCS and in 400-m freestyle (p<0.05). We conclude that the training adaptations seemed to be specific, not only with regard to the activity performed, but also in terms of the actual conditions of an operation, which also include equipment.

Second Ventilatory Threshold Assessed by Heart Rate Variability in a Multiple Shuttle Run Test.

Many studies have focused on heart rate variability in association with ventilatory thresholds. The purpose of the current study was to consider the ECG-derived respiration and the high frequency product of heart rate variability as applicable methods to assess the second ventilatory threshold (VT2). Fifteen healthy young soccer players participated in the study. Respiratory gases and ECGs were collected during an incremental laboratory test and in a multistage shuttle run test until exhaustion. VΤ2 was individually calculated using the deflection point of ventilatory equivalents. In addition, VT2 was assessed both by the deflection point of ECG-derived respiration and high frequency product. Results showed no statistically significant differences between VT2, and the threshold as determined with high frequency product and ECG-derived respiration (F(2,28)=0.83, p=0.45, η2=0.05). A significant intraclass correlation was observed for ECG-derived respiration (r=0.94) and high frequency product (r=0.95) with VT2. Similarly, Bland Altman analysis showed a considerable agreement between VT2 vs. ECG-derived respiration (mean difference of -0.06 km·h-1, 95% CL: ±0.40) and VT2 vs. high frequency product (mean difference of 0.02 km·h-1, 95% CL: ±0.38). This study suggests that, high frequency product and ECG-derived respiration are indeed reliable heart rate variability indices determining VT2 in a field shuttle run test.

Thermoregulatory and cardiovasculareffects of capsaicin application on human skin during dynamic exercise to temperate and warm conditions.

Thermoregulatory and cardiovascular responses during cycling in temperate and warm environments without and with application of capsaicin on the skin were investigated. We hypothesized that regardless of environmental temperature, capsaicin application would activate heat loss mechanisms attenuating exercise-induced rectal temperature (Tre) and blood pressure increase. Eight males cycled at 55% of their maximal aerobic power so long as to reach 38.2°C Tre at 20.8 ± 1.0°C and at 30.6 ± 1.1°C ambient temperatures twice: without (NCA) and with (CA) application of capsaicin patches (12 × 18 cm, 4.8 mg). Patches were applied on pectoralis major, trapezius and vastus lateralis muscles. Thermoregulatory (Tre, proximal-distal skin temperature gradient, sweating rate), cardiovascular variables and oxygen uptake were continuously recorded. In both ambient conditions, during the first 14 min of exercise, the local vasoconstrictive tone as a function of the relative change in Tre was lower in CA than NCA (p < .05, d = 0.84-1.15). Further, sweating rate was higher and occurred at a lower Tre increase in CA compared to NCA (p = .03, d = 0.6) resulting in extended time to reach 38.2°C Tre (p = .03, d = 0.9). Moreover, oxygen consumption was higher in CA than in NCA (p < .001, d = 0.8). Mean arterial pressure was lower during cycling in warm compared to temperate environment, but was unaffected by capsaicin. We conclude that activation of thermal sensors by capsaicin results in lower Tre rise during exercise, which is mediated through greater skin vasodilation along with higher rate and earlier onset of sweating. Nonetheless, capsaicin application has no extra effect on exercise cardiovascular responses.

Effects of capsaicin application on the skin during resting exposure to temperate and warm conditions.

We investigated thermoregulatory and cardiovascular responses at rest in a temperate (20°C) and in a warm (30°C) environment (40% RH) without and with the application of capsaicin on the skin. We hypothesized that regardless of environmental temperature, capsaicin application would stimulate heat loss and concomitantly deactivate heat conservation mechanisms, thus resulting in rectal temperature (Tre) and mean blood pressure decline due to excitation of heat-sensitive TRPV1. Ten male subjects were exposed, while seated, for 30 minutes to 20.8 ± 1.0°C or to 30.6 ± 1.1°C: without (NCA) and with (CA) application of capsaicin patches on the skin. Thermoregulatory (Tre, proximal-distal skin temperature gradient) and cardiovascular variables (modelflow technique) as well as oxygen uptake were continuously measured. The area under the curve for Tre decline at 20°C was smaller in CA (-2.1 ± 1.3 a.u.) than in NCA (-0.6 ± 1.1 a.u., P < 0.01, r = 0.8). Likewise, at 30°C it was smaller in CA (-2.2 ± 2.1 a.u.) compared to NCA (-0.8 ± 2.0 a.u., P = 0.02, r = 0.7). Local vasomotor tone and oxygen uptake, were significantly lower by 36.7% ± 94.2% and 12.3% ± 12.3%, respectively, with capsaicin compared to NCA (P = 0.05 and P < 0.01, respectively). Additionally, in 30°C CA mean arterial pressure was lower by 10.7% ± 5.9%, 8.9% ± 5.9%, and 10.6% ± 7.0% compared to 30°C NCA, 20°C NCA, and 20°C CA, respectively (P < 0.01, P = 0.02, and P < 0.01, respectively, d = 1.4-1.8). In conclusion, capsaicin application on the skin induced vasodilation and Tre decline. At 30°C CA, thermal responses were accompanied by arterial hypotension most likely due to the interactive effects of both stressors (warm environment and capsaicin) on cutaneous vascular regulation.

A 10-day confinement to normobaric hypoxia impairs toe, but not finger temperature response during local cold stress.

The study examined the effects of a 10-day normobaric hypoxic confinement on the finger and toe temperature responses to local cooling. Eight male lowlanders underwent a normoxic (NC) and, in a separate occasion, a normobaric hypoxic confinement (HC; FO2: 0.154; simulated altitude ~3400m). Before and after each confinement, subjects immersed for 30min their right hand and, in a different session, their right foot in 8°C water, while breathing either room air (AIR) or a hypoxic gas mixture (HYPO). Throughout the cold-water immersion tests, thermal responses were monitored with thermocouples on fingers and toes. Neither confinement influenced thermal responses in the fingers during the AIR or HYPO test. In the foot, by contrast, HC, but not NC, reduced the average toe temperature by ~1.5°C (p=0.03), both during the AIR and HYPO test. We therefore conclude that a 10-day confinement to normobaric hypoxia per se augments cold-induced vasoconstriction in the toes, but not in the fingers. The mechanism underlying this dissimilarity remains to be established.

The Effect of Normobaric Hypoxic Confinement on Metabolism, Gut Hormones, and Body Composition.

To assess the effect of normobaric hypoxia on metabolism, gut hormones, and body composition, 11 normal weight, aerobically trained (O2peak: 60.6 ± 9.5 ml·kg(-1)·min(-1)) men (73.0 ± 7.7 kg; 23.7 ± 4.0 years, BMI 22.2 ± 2.4 kg·m(-2)) were confined to a normobaric (altitude ≃ 940 m) normoxic (NORMOXIA; PIO2 ≃ 133.2 mmHg) or normobaric hypoxic (HYPOXIA; PIO was reduced from 105.6 to 97.7 mmHg over 10 days) environment for 10 days in a randomized cross-over design. The wash-out period between confinements was 3 weeks. During each 10-day period, subjects avoided strenuous physical activity and were under continuous nutritional control. Before, and at the end of each exposure, subjects completed a meal tolerance test (MTT), during which blood glucose, insulin, GLP-1, ghrelin, peptide-YY, adrenaline, noradrenaline, leptin, and gastro-intestinal blood flow and appetite sensations were measured. There was no significant change in body weight in either of the confinements (NORMOXIA: -0.7 ± 0.2 kg; HYPOXIA: -0.9 ± 0.2 kg), but a significant increase in fat mass in NORMOXIA (0.23 ± 0.45 kg), but not in HYPOXIA (0.08 ± 0.08 kg). HYPOXIA confinement increased fasting noradrenaline and decreased energy intake, the latter most likely associated with increased fasting leptin. The majority of all other measured variables/responses were similar in NORMOXIA and HYPOXIA. To conclude, normobaric hypoxic confinement without exercise training results in negative energy balance due to primarily reduced energy intake.

Pressure distension in leg vessels as influenced by prolonged bed rest and a pressure habituation regimen.

Bed rest increases pressure distension in arteries, arterioles, and veins of the leg. We hypothesized that bed-rest-induced deconditioning of leg vessels is governed by the removal of the local increments in transmural pressure induced by assuming erect posture and, therefore, can be counteracted by intermittently increasing local transmural pressure during the bed rest. Ten men underwent 5 wk of horizontal bed rest. A subatmospheric pressure (-90 mmHg) was intermittently applied to one lower leg [pressure habituation (PH) leg]. Vascular pressure distension was investigated before and after the bed rest, both in the PH and control (CN) leg by increasing local distending pressure, stepwise up to +200 mmHg. Vessel diameter and blood flow were measured in the posterior tibial artery and vessel diameter in the posterior tibial vein. In the CN leg, bed rest led to 5-fold and 2.7-fold increments (P < 0.01) in tibial artery pressure-distension and flow responses, respectively, and to a 2-fold increase in tibial vein pressure distension. In the PH leg, arterial pressure-distension and flow responses were unaffected by bed rest, whereas bed rest led to a 1.5-fold increase in venous pressure distension. It thus appears that bed-rest-induced deconditioning of leg arteries, arterioles, and veins is caused by removal of gravity-dependent local pressure loads and may be abolished or alleviated by a local pressure-habituation regimen.

Severe hypoxia during incremental exercise to exhaustion provokes negative post-exercise affects.

The post-exercise emotional response is mainly dependent on the intensity of the exercise performed; moderate exercise causes positive feelings, whereas maximal exercise may prompt negative affects. Acute hypoxia impairs peak O2 uptake (V̇O2peak), resulting in a shift to a lower absolute intensity at the point of exhaustion. Hence, the purpose of the study was to examine whether a severe hypoxic stimulus would influence the post-exercise affective state in healthy lowlanders performing an incremental exercise to exhaustion. Thirty-six male lowlanders performed, in a counter-balanced order and separated by a 48-h interval, two incremental exercise trials to exhaustion to determine their V̇O2peak, while they were breathing either room air (AIR; FiO2: 0.21), or a hypoxic gas mixture (HYPO; FiO2: 0.12). Before and immediately after each trial, subjects were requested to complete two questionnaires, based on how they felt at that particular moment: (i) the Profile of Mood States-Short Form, and (ii) the Activation Deactivation Adjective Check List. During the post-exercise phase, they also completed the Multidimensional Fatigue Inventory. V̇O2peak was significantly lower in the HYPO than the AIR trial (~15%; p<0.001). Still, after the HYPO trial, energy, calmness and motivation were markedly impaired, whereas tension, confusion, and perception of physical and general fatigue were exaggerated (p≤0.05). Accordingly, present findings suggest that an incremental exercise to exhaustion performed in severe hypoxia provokes negative post-exercise emotions, induces higher levels of perceived fatigue and decreases motivation; the affective responses coincide with the comparatively lower V̇O2peak than that achieved in normoxic conditions.

Effects of Two Short-Term, Intermittent Hypoxic Training Protocols on the Finger Temperature Response to Local Cold Stress.

The study examined the effects of two short-term, intermittent hypoxic training protocols, namely exercising in hypoxia and living in normoxia (LL-TH; n=8), and exercising in normoxia preceded by a series of brief intermittent hypoxic exposures at rest (IHE+NOR; n=8), on the finger temperature response during a sea-level local cold test. In addition, a normoxic group was assigned as a control group (NOR; n=8). All groups trained on a cycle-ergometer 1 h/day, 5 days/week for 4 weeks at 50% of peak power output. Pre, post, and 11 days after the last training session, subjects immersed their right hand for 30 min in 8°C water. In the NOR group, the average finger temperature was higher in the post (+2.1°C) and 11-day after (+2.6°C) tests than in the pre-test (p≤0.001). Conversely, the fingers were significantly colder immediately after both hypoxic protocols (LL-TH: -1.1°C, IHE+NOR: -1.8°C; p=0.01). The temperature responses returned to the pre-training level 11 days after the hypoxic interventions. Ergo, present findings suggest that short-term intermittent hypoxic training impairs sea-level local cold tolerance; yet, the hypoxic-induced adverse responses seem to be reversible within a period of 11 days.

Cadets' swimming and running performance with and without a combat uniform.

INTRODUCTION: The aim was to examine whether a combat uniform (CU) influences the cadet's exercise performance in and out of the water. METHODS: Fourteen male Army Officer cadets performed on 6 separate days: (1) a maximal 400-m freestyle swimming trial; (2) a 4 x 50-m all-out freestyle swimming trial with 10 s rest in between; (3) a 50-m swim obstacle course with a CU (CUs); (4) a 50-m swim obstacle course without a CU (NUs); (5) a 1000-m track run with a CU (CU(R)); and (6) a 1000-m track run without a CU (NUR). In each trial, performance time, oxygen uptake (Vo2), lactate concentration ([La]), and capillary oxygen saturation (SpO2) were recorded. RESULTS: The mean performance time was 44.3 +/- 3.1 s and 33.4 +/- 1.8 s in CUs and NUs trials, respectively. Peak VO2 was similar in CUs, NUs, and 400 m (CUs: 59.1 +/- 1.1 ml x kg(-1) x min(-1), NUs: 57.3 +/- 2.1 ml kg(-1) x min(-1), 400 m: 58.2 +/- 1.6 ml x kg(-1) min(-1)). [La] was higher in CUs than in NUs (CUs: 10.0 +/- 2.0 mmol x L(-1), NUs: 8.5 +/- 1.8 mmol x L(-1)), but it was lower in CUs and NUs than during the 400 m and 4 x 50 m. SpO2 was lower (approximately 4.5%) in CUs than NUs. No differences were observed between running trials. CONCLUSIONS: The results suggest that the use of CU during swimming tasks induces high demands for energy and, thus, leads to a significant impairment of the swimming performance of the cadets. However, the influence of the CU seems to be less crucial during dry land running performance.

Forearm-finger skin temperature gradient as an index of cutaneous perfusion during steady-state exercise.

The purpose of this study was to examine whether the forearm-finger skin temperature gradient (T(forearm-finger)), an index of vasomotor tone during resting conditions, can also be used during steady-state exercise. Twelve healthy men performed three cycling trials at an intensity of ~60% of their maximal oxygen uptake for 75 min separated by at least 48 h. During exercise, forearm skin blood flow (BFF ) was measured with a laser-Doppler flowmeter, and finger skin blood flow (PPG) was recorded from the left index fingertip using a pulse plethysmogram. T(forearm-finger) of the left arm was calculated from the values derived by two thermistors placed on the radial side of the forearm and on the tip of the middle finger. During exercise, PPG and BFF increased (P<0.001), and T(forearm-finger) decreased (P<0.001) from their resting values, indicating a peripheral vasodilatation. There was a significant correlation between T(forearm-finger) and both PPG (r = -0.68; P<0.001) and BFF (r = -0.50; P<0.001). It is concluded that T(forearm-finger) is a valid qualitative index of cutaneous vasomotor tone during steady-state exercise.

Cardiovascular drift in trained paraplegic and able-bodied individuals during prolonged wheelchair exercise: effect of fluid replacement.

The progressive heart rate (HR) increase and stroke volume (SV) decline during prolonged constant-load leg exercise signifies cardiovascular drift (CVdrift); fluid replacement is known to minimize this phenomenon. Like their able-bodied counterparts (AB), paraplegic athletes undergo prolonged exercise during training and competition, which could result in CVdrift. The aim of this study is to address the role of rehydration on preventing CVdrift in spinal cord injured (SCI) paraplegic athletes. Eight SCI athletes with an injury level between C7 and T6 and 9 AB subjects performed 60-min constant-load exercise on a wheelchair ergometer in a thermo-neutral environment. No fluid was taken in 1 trial, whereas 85% of sweat losses were replaced by drinking water in another trial. Cardic output (CO), SV, HR, and oral temperature (Tor) were determined during exercise. Prolonged exercise resulted in similar HR (18 beats·min(-1) for AB and 12 beats·min(-1) for SCI) and Tor (0.63 °C for AB and 0.71 °C for SCI) elevation and SV decline (-8.5 mL·beat(-1) for AB and -5.5 mL·beat(-1) for SCI), whereas CO remained unchanged. Water intake restrained the exercise-induced hyperthermia and resulted in smaller SV decline (-4.0 mL for AB and -3.0 mL for SCI, p < 0.01). In conclusion, CVdrift was similar in SCI and AB subjects during prolonged wheelchair exercise. Likewise, the beneficial effects of hydration in both groups were analogous.

Cold-induced vasodilatation response in the fingers at 4 different water temperatures.

We evaluated the cold-induced vasodilatation (CIVD) response at 4 different water temperatures. Nine healthy young male subjects immersed their right hands in 35 °C water for 5 min, and immediately thereafter for 30 min in a bath maintained at either 5, 8, 10, or 15 °C. The responses of finger skin temperatures, subjective ratings of thermal comfort and temperature sensation scores were compared between the 4 immersion trials. The number of subjects who exhibited a CIVD response was higher during immersion of the hand in 5 and 8 °C (100%) compared with 10 and 15 °C water (87.5% and 37.5%, respectively). The CIVD temperature amplitude was 4.2 ± 2.6, 3.4 ± 2.0, 2.1 ± 1.6, and 2.8 ± 2.0 °C at 5, 8, 10, and 15 °C trials, respectively; higher in 5 and 8 °C compared with 10 and 15 °C water (p = 0.003). No differences in CIVD were found between the 5 and 8 °C immersions. However, during immersion in 5 °C, subjects felt "uncomfortable" while in the other trials felt "slightly uncomfortable" (p = 0.005). The temperature sensation score was "cold" for 5 °C and "cool" for the other trials, but no statistical differences were observed. Immersion of the hand in 8 °C elicits a CIVD response of similar magnitude as immersion in 5 °C, but with less thermal discomfort.

Intermittent normobaric hypoxic exposures at rest: effects on performance in normoxia and hypoxia.

INTRODUCTION: It has been speculated that short (-1-h) exposures to intermittent normobaric hypoxia at rest can enhance subsequent exercise performance. Thus, the present study investigated the effect of daily resting intermittent hypoxic exposures (IHE) on peak aerobic capacity and performance under both normoxic and hypoxic conditions. METHODS: Eighteen subjects were equally assigned to either a control (CON) or IHE group and performed a 4-wk moderate intensity cycling exercise training (1 h x d(-1), 5 d x wk(-1)). The IHE group additionally performed IHE (60 min) prior to exercise training. IHE consisted of seven cycles alternating between breathing a hypoxic gas mixture (5 min; F1O2 = 0.12-0.09) and room air (3 min; F1O2 = 0.21). Normoxic and hypoxic peak aerobic capacity (VO2(peak)) and endurance performance were evaluated before (PRE), during (MID), upon completion (POST), and 10 d after (AFTER) the training period. RESULTS: Similar improvements were observed in normoxic VO2(peak) tests in both groups [IHE: delta(POST-PRE) = +10%; CON: delta(POST-PRE) = + 14%], with no changes in the hypoxic condition. Both groups increased performance time in the normoxic constant power test only [IHE: delta(POST-PRE) = +108%; CON: delta(POST-PRE) = +114%], whereas only the IHE group retained this improvement in the AFTER test. Higher levels of minute ventilation were noted in the IHE compared to the CON group at the POST and AFTER tests. CONCLUSION: Based on the results of this study, the IHE does not seem to be beneficial for normoxic and hypoxic performance enhancement.

Heterogeneous sensitivity of cerebral and muscle tissues to acute normobaric hyperoxia at rest.

The purpose was to investigate the effects of acute normobaric hyperoxia at rest on cerebral, respiratory and leg muscle oxygenation. Ten healthy men were studied twice in a single-blinded counterbalanced crossover study protocol. On one occasion they breathed air and on the other 100% normobaric O(2) for a 2-hour time period. Oxygenated (Δ[O(2)Hb]), deoxygenated (Δ[HHb]) and total (Δ[tHb]) hemoglobin in the cerebral frontal cortex, and in the intercostal and vastus lateralis muscles were simultaneously monitored with near-infrared spectroscopy. The hyperoxic stimulus promptly increased Δ[O(2)Hb] (~2 µM) and decreased Δ[HHb] (~3.6 µM) in the frontal cortex. These cerebral responses were directly and fully countered by resumption of normoxic air breathing. In contrast, Δ[HHb] significantly decreased due to the acute hyperoxic stimulus in both intercostal and vastus lateralis muscles. The temporal changes in muscle oxygenation were slower compared to those in the cerebral area; and they only partially recovered during the 15-min normoxic-recovery period. Acute supplementation of normobaric O(2) at rest influences cerebral, leg and respiratory muscle oxygenation of healthy individuals, but not in the same manner. Namely, the frontal cortex seems to be more sensitive to hyperoxia than are the skeletal muscle regions.

Heat production and heat loss responses to cold water immersion after 35 days horizontal bed rest.

INTRODUCTION: Bed rest is a terrestrial experimental analogue of unloading experienced during exposure to microgravity. Such unloading causes atrophy predominantly of the postural muscles, especially those of the lower limbs. METHODS: We tested the hypothesis that 35 d horizontal bed rest alters thermoregulatory responses of subjects (N = 10) immersed in 15 degrees C water, particularly the heat produced by the shivering tremor of the skeletal muscles. Before and after bed rest we measured the thickness of the gastrocnemius medialis (GM), vastus lateralis (VL), tibialis anterior (TA), and biceps brachii (BB) muscles by ultrasonography. During the immersions, we monitored rectal and skin temperatures, heat flux, heart rate, and oxygen uptake. RESULTS: After bed rest, muscle thickness decreased significantly by 12.2 +/- 8.8% and 8.0 +/- 9.1% in the GM and VL, respectively. No changes were observed in the TA and BB muscles. The 35-d bed rest caused a significant reduction in aerobic power, as reflected in maximal oxygen uptake. There were no significant differences in any of the observed thermoregulatory responses between the pre- and post-bed rest immersions. CONCLUSIONS: Cardiovascular and muscular deconditioning had no effect on the heat production and heat loss responses. Due to the significant reduction in the mass of the muscles in the lower limbs, concomitant with no change in heat production, we conclude that leg muscles do not play a significant role in shivering thermogenesis.

Cardiovascular drift and cerebral and muscle tissue oxygenation during prolonged cycling at different pedalling cadences.

We hypothesized that a faster cycling cadence could exaggerate cardiovascular drift and affect muscle and cerebral blood volume and oxygenation. Twelve healthy males (mean age, 23.4 ± 3.8 years) performed cycle ergometry for 90 min on 2 separate occasions, with pedalling frequencies of 40 and 80 r·min(-1), at individual workloads corresponding to 60% of their peak oxygen consumption. The main measured variables were heart rate, ventilation, cardiac output, electromyographic activity of the vastus lateralis, and regional muscle and cerebral blood volume and oxygenation. Cardiovascular drift developed at both cadences, but it was more pronounced at the faster than at the slower cadence, as indicated by the drop in cardiac output by 1.0 ± 0.2 L·min(-1), the decline in stroke volume by 9 ± 3 mL·beat(-1), and the increase in heart rate by 9 ± 1 beats·min(-1) at 80 r·min(-1). At the faster cadence, minute ventilation was higher by 5.0 ± 0.5 L·min(-1), and end-tidal CO(2) pressure was lower by 2.0 ± 0.1 torr. Although higher electromyographic activity in the vastus lateralis was recorded at 80 r·min(-1), muscle blood volume did not increase at this cadence, as it did at 40 r·min(-1). In addition, muscle oxygenation was no different between cadences. In contrast, cerebral regional blood volume and oxygenation at 80 r·min(-1) were not as high as at 40 r·min(-1) (p < 0.05). Faster cycling cadence exaggerates cardiovascular drift and seems to influence muscle and cerebral blood volume and cerebral oxygenation, without muscle oxygenation being radically affected.