The Effect of Skeletal Muscle Oxygenation on Hemodynamics, Cerebral Oxygenation and Activation, and Exercise Performance during Incremental Exercise to Exhaustion in Male Cyclists.

This study aimed to elucidate whether muscle blood flow restriction during maximal exercise is associated with alterations in hemodynamics, cerebral oxygenation, cerebral activation, and deterioration of exercise performance in male participants. Thirteen healthy males, cyclists (age 33 ± 2 yrs., body mass: 78.6 ± 2.5 kg, and body mass index: 25.57 ± 0.91 kg·m-1), performed a maximal incremental exercise test on a bicycle ergometer in two experimental conditions: (a) with muscle blood flow restriction through the application of thigh cuffs inflated at 120 mmHg (with cuffs, WC) and (b) without restriction (no cuffs, NC). Exercise performance significantly deteriorated with muscle blood flow restriction, as evidenced by the reductions in V˙O2max (-17 ± 2%, p < 0.001), peak power output (-28 ± 2%, p < 0.001), and time to exhaustion (-28 ± 2%, p < 0.001). Muscle oxygenated hemoglobin (Δ[O2Hb]) during exercise declined more in the NC condition (p < 0.01); however, at exhaustion, the magnitude of muscle oxygenation and muscle deoxygenation were similar between conditions (p > 0.05). At maximal effort, lower cerebral deoxygenated hemoglobin (Δ[HHb]) and cerebral total hemoglobin (Δ[THb]) were observed in WC (p < 0.001), accompanied by a lower cardiac output, heart rate, and stroke volume vs. the NC condition (p < 0.01), whereas systolic blood pressure, rating of perceived exertion, and cerebral activation (as assessed by electroencephalography (EEG) activity) were similar (p > 0.05) between conditions at task failure, despite marked differences in exercise duration, maximal aerobic power output, and V˙O2max. In conclusion, in trained cyclists, muscle blood flow restriction during an incremental cycling exercise test significantly limited exercise performance. Exercise intolerance with muscle blood flow restriction was mainly associated with attenuated cardiac responses, despite cerebral activation reaching similar maximal levels as without muscle blood flow restriction.

The effect of muscle blood flow restriction on hemodynamics, cerebral oxygenation and activation at rest.

This study tested the hypothesis that muscle blood flow restriction reduces muscle and cerebral oxygenation at rest. In 26 healthy males, aged 33 ± 2 yrs, physiological variables were continuously recorded during a 10-min period in 2 experimental conditions: a) with muscle blood flow restriction through thigh cuffs application inflated at 120 mm Hg (With Cuffs, WC) and b) without restriction (No Cuffs, NC). Muscle and cerebral oxygenation were reduced by muscle blood flow restriction as suggested by the increase in both muscle and cerebral deoxygenated hemoglobin (Δ[HHb]; p < 0.01) and the decrease of muscle and cerebral oxygenation index (Δ[HbDiff]; p < 0.01). Hemodynamic responses were not affected by such muscle blood flow restriction, whereas baroreflex sensitivity was reduced (p = 0.009). The perception of leg discomfort was higher (p < 0.001) in the WC than in the NC condition. This study suggests that thigh cuffs application inflated at 120 mm Hg is an effective method to reduce muscle oxygenation at rest. These changes at the muscular level seem to be sensed by the central nervous system, evoking alterations in cerebral oxygenation and baroreflex sensitivity. Novelty: Thigh cuffs application inflated at 120 mm Hg effectively reduces muscle oxygenation at rest. Limiting muscle oxygenation appears to reduce cerebral oxygenation, and baroreflex sensitivity, at rest. Even in healthy subjects, limiting muscle oxygenation, at rest, affects neural integration.

The effect of menstrual cycle on maximal breath-hold time.

This study investigated the effect of menstrual cycle phase on breath-hold time (BHT). Twelve healthy females, aged 18-30 yrs, with regular menstrual cycles, without breath-hold (BH) experience, performed a BH protocol which included eight repeated maximal efforts with face immersion in cool water separated by 2-min intervals in two different phases of menstrual cycle; early follicular (EF) phase and midluteal (ML) phase. Respiratory, cardiovascular and hematological responses were studied before, during and after BH efforts. Maximal BHT was significantly higher during ML (115.59 ±â€¯13.95 s) compared to EF (106.10 ±â€¯12.42 s) phase of the menstrual cycle. Metabolic rate and build-up of CO2 were higher (p < 0.001) in EF compared to ML phase. In conclusion, the greater BHT observed at the ML phase of the menstrual cycle may be the result of elevated levels of estrogen and progesterone during midluteal phase affecting both ventilatory response and metabolic rate.

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.

No ergogenic effects of a 10-day combined heat and hypoxic acclimation on aerobic performance in normoxic thermoneutral or hot conditions.

PURPOSE: Hypoxic acclimation enhances convective oxygen delivery to the muscles. Heat acclimation-elicited thermoregulatory benefits have been suggested not to be negated by adding daily exposure to hypoxia. Whether concomitant acclimation to both heat and hypoxia offers a synergistic enhancement of aerobic performance in thermoneutral or hot conditions remains unresolved. METHODS: Eight young males ([Formula: see text]: 51.6 ± 4.6 mL min-1 kg-1) underwent a 10-day normobaric hypoxic confinement (FiO2 = 0.14) interspersed with daily 90-min normoxic controlled hyperthermia (target rectal temperature: 38.5 °C) exercise sessions. Prior to, and following the confinement, the participants conducted a 30-min steady-state exercise followed by incremental exercise to exhaustion on a cycle ergometer in thermoneutral normoxic (NOR), thermoneutral hypoxic (FiO2 = 0.14; HYP) and hot (35 °C, 50% relative humidity; HE) conditions in a randomized and counterbalanced order. The steady-state exercise was performed at 40% NOR peak power output (Wpeak) to evaluate thermoregulatory function. Blood samples were obtained from an antecubital vein before, on days 1 and 10, and the first day post-acclimation. RESULTS: [Formula: see text] and ventilatory thresholds were not modified in any environment following acclimation. Wpeak increased by 6.3 ± 3.4% in NOR and 4.0 ± 4.9% in HE, respectively. The magnitude and gain of the forehead sweating response were augmented in HE post-acclimation. EPO increased from baseline (17.8 ± 7.0 mIU mL-1) by 10.7 ± 8.8 mIU mL-1 on day 1 but returned to baseline levels by day 10 (15.7 ± 5.9 mIU mL-1). DISCUSSION: A 10-day combined heat and hypoxic acclimation conferred only minor benefits in aerobic performance and thermoregulation in thermoneutral or hot conditions. Thus, adoption of such a protocol does not seem warranted.

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.

Severe hypoxemia induced by prolonged expiration and reduced frequency breathing during submaximal swimming.

The purpose of this study was to examine the metabolic responses during submaximal swimming with self-selected normal breathing (N) and prolonged expiration along with reduced frequency breathing (RB). Ten male swimmers (age: 23.1 ± 2.2 years; VO2max: 47.3 ± 7.2 ml · kg-1 · min-1) performed 75-, 100-, 175-, 200-, 275-, 300-, 375- and 400-m trials with N and RB at intensity corresponding to 90% of the critical speed. In RB condition, all trials longer than 75 m were interspersed with 25 m of self-selected N in regular intervals. In RB, oxygen saturation during recovery was decreased compared to starting values after 75, 100, 175, 275 and 375 m (78-91%, P < 0.05), while it remained unchanged after all trials in N condition (98 ± 2%, P > 0.05). Lactate concentration was higher in RB than in N after 400 m (4.3 ± 1.5 vs. 3.3 ± 1.7 mmol · l-1, P < 0.05). During recovery after the 375-m trial, partial pressure of carbon dioxide was increased and pH was decreased in RB compared to N condition. Prolonged expiration along with RB provokes severe hypoxemia during the recovery period after swimming, which is restored with self-selected N during submaximal swimming.

Effect of gender on maximal breath-hold time.

This study examined the effect of gender on breath-hold time (BHT). Sixteen healthy subjects, eight males (M) and eight females (F), aged 18-30 years, without breath-hold (BH) experience, performed: (a) a pulmonary function test, (b) an incremental cycle ergometer test to exhaustion and (c) a BH protocol, which included eight repeated maximal efforts separated by 2-min intervals on two occasions: without (BHFOI) and with face immersion (BHFI) in cool water (14.8 ± 0.07 °C). Cardiovascular, ventilatory and hematological responses were studied before, during and after BH efforts. Maximal BHT was similar between genders (M: 103.90 ± 25.68 s; F: 104.97 ± 32.71 s, p > 0.05) and unaffected by face immersion (BHFOI: 105.13 ± 28.68 s; BHFI: 103.74 ± 31.19 s, p > 0.05). The aerobic capacity, lung volumes and hematological indexes were higher in males compared to females. BHT was predicted (r (2) = 0.98, p = 0.005) by aerobic capacity, total lung volume, hematocrit and hemoglobin concentration only in males. It was concluded that despite gender differences in physiological and anthropometrical traits, BH ability was not different between males and females, both not experienced in apneas.

The effect of exercise-induced hypoxemia on blood redox status in well-trained rowers.

Exercise-induced arterial hypoxemia (EIAH), characterized by decline in arterial oxyhemoglobin saturation (SaO(2)), is a common phenomenon in endurance athletes. Acute intensive exercise is associated with the generation of reactive species that may result in redox status disturbances and oxidation of cell macromolecules. The purpose of the present study was to investigate whether EIAH augments oxidative stress as determined in blood plasma and erythrocytes in well-trained male rowers after a 2,000-m rowing ergometer race. Initially, athletes were assigned into either the normoxemic (n = 9, SaO(2) >92%, [Formula: see text]: 62.0 ± 1.9 ml kg(-1) min(-1)) or hypoxemic (n = 12, SaO(2) <92%, [Formula: see text]: 60.5 ± 2.2 ml kg(-1 )min(-1), mean ± SEM) group, following an incremental [Formula: see text] test on a wind resistance braked rowing ergometer. On a separate day the rowers performed a 2,000-m all-out effort on the same rowing ergometer. Following an overnight fast, blood samples were drawn from an antecubital vein before and immediately after the termination of the 2,000-m all-out effort and analyzed for selective oxidative stress markers. In both the normoxemic (SaO(2): 94.1 ± 0.9%) and hypoxemic (SaO(2): 88.6 ± 2.4%) rowers similar and significant exercise increase in serum thiobarbituric acid-reactive substances, protein carbonyls, catalase and total antioxidant capacity concentration were observed post-2,000 m all-out effort. Exercise significantly increased the oxidized glutathione concentration and decreased the ratio of reduced (GSH)-to-oxidized (GSSG) glutathione in the normoxemic group only, whereas the reduced form of glutathione remained unaffected in either groups. The increased oxidation of GSH to GSSG in erythrocytes of normoxemic individuals suggest that erythrocyte redox status may be affected by the oxygen saturation degree of hemoglobin. Our findings indicate that exercise-induced hypoxemia did not further affect the increased blood oxidative damage of lipids and proteins observed after a 2,000-m rowing ergometer race in highly-trained male rowers. The present data do not support any potential link between exercise-induced hypoxemia, oxidative stress increase and exercise performance.

The effect of menthol application to the skin on sweating rate response during exercise in swimmers and controls.

We tested the hypothesis that menthol application would reduce the magnitude and initiation of sweating via excitation of cold-sensitive afferent pathways and concurrently via a cross-inhibition of heat loss pathways in acclimatized (swimmers, SW) and non acclimatized (control, CON) subjects in cool water. It was expected this effect to be exaggerated in SW subjects. Eight SW and eight CON subjects cycled at 60% of their VO(2)max, as long as to reach 38 degrees C in rectal temperature (Tre), without or with (4.6 g per 100 ml of water) all-body application of menthol sediment. Heart rate (HR), Tre, sweating rate (SwR), the proximal-distal skin temperature gradient (TSk(f-f)), and oxygen consumption (VO(2)) were measured continuously. VO(2) and HR were similar between groups and conditions. Menthol increased TSk(f-f), Tre threshold for SwR [+0.32 (0.01) degrees C] and Tre gain, while menthol reduced exercise time by 8.1 (4.1) min. SW group showed higher changes in Tre threshold for SwR [+0.50 (0.01) degrees C for SW vs. +0.13 (0.03) degrees C for CON], higher Tre gain, lower time for Tre increase and shorter exercise time [-10.7 (7) min for SW vs. -4.9 (4) min for CON] in menthol condition. Upon exercise initiation, previously applied menthol on the skin seems to induce vasoconstriction, results in a delayed sweating, which in turn affects the rectal temperature. Acclimatized subjects showed higher delay in SwR and earlier rise in Tre, which most probably is due to the inter-group differences in cold receptors activity.

Oxygen saturation in the triceps brachii muscle during an arm Wingate test: the role of training and power output.

The purpose of this study was to investigate the role of training and power output on muscle oxygen desaturation during and resaturation after an arm Wingate test (WAnT). Two groups of subjects were studied; the first group consisted of nine athletes participating in upper arm anaerobic sports and the second group of 11 university students. As a consequence, the group of athletes (HP) produced higher peak and mean power output (p < 0.01) than the group of university students (LP). Muscle oxygenation status was evaluated by using near infrared spectroscopy at the triceps brachii. The HP group exhibited 17.6 +/- 8.0% less muscle oxygen desaturation than the LP group (p < 0.05) but similar muscle total hemoglobin during exercise and faster (p < 0.05) muscle oxygen resaturation during recovery (tau = 12.4 +/- 5.2 sec in HP vs. tau = 24.2 +/- 11.0 sec in LP). These results indicate that the HP group exhibits less muscle desaturation during an arm WAnT and has a faster resaturation rate, probably attributed to differences in muscle mass, muscle fiber recruitment capability, and ATP production through anaerobic pathways.

Contribution of respiratory muscle blood flow to exercise-induced diaphragmatic fatigue in trained cyclists.

We investigated whether the greater degree of exercise-induced diaphragmatic fatigue previously reported in highly trained athletes in hypoxia (compared with normoxia) could have a contribution from limited respiratory muscle blood flow. Seven trained cyclists completed three constant load 5 min exercise tests at inspired O(2) fractions (FIO2) of 0.13, 0.21 and 1.00 in balanced order. Work rates were selected to produce the same tidal volume, breathing frequency and respiratory muscle load at each FIO2 (63 +/- 1, 78 +/- 1 and 87 +/- 1% of normoxic maximal work rate, respectively). Intercostals and quadriceps muscle blood flow (IMBF and QMBF, respectively) were measured by near-infrared spectroscopy over the left 7th intercostal space and the left vastus lateralis muscle, respectively, using indocyanine green dye. The mean pressure time product of the diaphragm and the work of breathing did not differ across the three exercise tests. After hypoxic exercise, twitch transdiaphragmatic pressure fell by 33.3 +/- 4.8%, significantly (P < 0.05) more than after both normoxic (25.6 +/- 3.5% reduction) and hyperoxic (26.6 +/- 3.3% reduction) exercise, confirming greater fatigue in hypoxia. Despite lower leg power output in hypoxia, neither cardiac output nor QMBF (27.6 +/- 1.2 l min(-1) and 100.4 +/- 8.7 ml (100 ml)(-1) min(-1), respectively) were significantly different compared with normoxia (28.4 +/- 1.9 l min(-1) and 94.4 +/- 5.2 ml (100 ml)(-1) min(-1), respectively) and hyperoxia (27.8 +/- 1.6 l min(-1) and 95.1 +/- 7.8 ml (100 ml)(-1) min(-1), respectively). Neither IMBF was different across hypoxia, normoxia and hyperoxia (53.6 +/- 8.5, 49.9 +/- 5.9 and 52.9 +/- 5.9 ml (100 ml)(-1) min(-1), respectively). We conclude that when respiratory muscle energy requirement is not different between normoxia and hypoxia, diaphragmatic fatigue is greater in hypoxia as intercostal muscle blood flow is not increased (compared with normoxia) to compensate for the reduction in PaO2, thus further compromising O(2) supply to the respiratory muscles.

Human respiratory muscle blood flow measured by near-infrared spectroscopy and indocyanine green.

Measurement of respiratory muscle blood flow (RMBF) in humans has important implications for understanding patterns of blood flow distribution during exercise in healthy individuals and those with chronic disease. Previous studies examining RMBF in humans have required invasive methods on anesthetized subjects. To assess RMBF in awake subjects, we applied an indicator-dilution method using near-infrared spectroscopy (NIRS) and the light-absorbing tracer indocyanine green dye (ICG). NIRS optodes were placed on the left seventh intercostal space at the apposition of the costal diaphragm and on an inactive control muscle (vastus lateralis). The primary respiratory muscles within view of the NIRS optodes include the internal and external intercostals. Intravenous bolus injection of ICG allowed for cardiac output (by the conventional dye-dilution method with arterial sampling), RMBF, and vastus lateralis blood flow to be quantified simultaneously. Esophageal and gastric pressures were also measured to calculate the work of breathing and transdiaphragmatic pressure. Measurements were obtained in five conscious humans during both resting breathing and three separate 5-min bouts of constant isocapnic hyperpnea at 27.1 +/- 3.2, 56.0 +/- 6.1, and 75.9 +/- 5.7% of maximum minute ventilation as determined on a previous maximal exercise test. RMBF progressively increased (9.9 +/- 0.6, 14.8 +/- 2.7, 29.9 +/- 5.8, and 50.1 +/- 12.5 ml 100 ml(-1) min(-1), respectively) with increasing levels of ventilation while blood flow to the inactive control muscle remained constant (10.4 +/- 1.4, 8.7 +/- 0.7, 12.9 +/- 1.7, and 12.2 +/- 1.8 ml 100 ml(-1) min(-1), respectively). As ventilation rose, RMBF was closely and significantly correlated with 1) cardiac output (r = 0.994, P = 0.006), 2) the work of breathing (r = 0.995, P = 0.005), and 3) transdiaphragmatic pressure (r = 0.998, P = 0.002). These data suggest that the NIRS-ICG technique provides a feasible and sensitive index of RMBF at different levels of ventilation in humans.

Anaerobic capacity of the upper arms in top-level team handball players.

PURPOSE: Handball is a sport with high anaerobic demands in lower body as has been indicated by Wingate test (WT) performed with the legs, but there are no data available concerning power production during a WT performed with the arms in handball players (HndP). Therefore, the purpose of this study was to explore the arm anaerobic profile of HndP during a WT. METHODS: Twenty-one elite HndP and 9 physical education students (CON), performed a 30-s arm WT. Power production and muscle oxygenation were recorded. RESULTS: Peak power (PP) as well as mean power (MP) was higher (P = .017 and 0.03, and ES = 1.00 and 0.86, respectively) for HndP (HndP PP: 7.6 +/- 0.8 W x kg(-1); CON PP: 6.7 +/- 1.1 W x kg(-1); HndP MP 5.3 +/- 0.6 W x kg(-1); CON MP 4.7 +/- 0.9 W x kg(-1)) with no significant difference in fatigue index between the two groups. Muscle oxygen saturation (StO2) declined approximately 30% with exercise with no differences between groups. During recovery the HndP group had higher StO2 (P = .01, ES= 3.04), total hemoglobin and oxygenated hemoglobin compared with the CON group (P < .01 ES = 3.29 and 0.99, respectively). StO2 returned to resting values in 29.5 +/- 2.3 s in HndP, whereas this variable did not recover after 2 min in CON. CONCLUSIONS: The arm anaerobic capacity of the HndP was "excellent," significantly higher than that by the control group. Moreover, HndP exhibited faster recovery of StO2 compared with the control group. The greater power output and the faster muscle reoxygenation of arms in HndP can be attributed to specific training adaptations related to high performance in handball.

The role of active muscle mass on exercise-induced cardiovascular drift.

The purpose of this study was to examine the role of active muscle mass on cardiovascular drift (CVdrift) during prolonged exercise. Twelve subjects with peak oxygen uptake (VO2peak) of 3.52 ± 0.52 L·min(-1) (mean ± SD) cycled for 55 min with 80 revolutions per minute with either two legs (2-legged) or one leg (1-legged). Oxygen uptake was at 60% of VO2peak throughout the 2-legged trial and at half of this value in 1- legged condition. Cardiac output (CO-CO2 rebreathing), heart rate (HR) and quadriceps integrated electromyographic activity (iEMG) were higher (p < 0.01) during 2-legged than 1- legged exercise. Changes in stroke volume from 20 to 50 min of exercise were greater in 2-legged than in 1-legged (∆SV: -20.8 ± 0.8 vs. -13.3 ± 1.3 ml·beat(-1), p < 0.05). Similarly, changes in heart rate (∆HR) were +18.5 ± 0.8 and +10.7 ± 1.0 beats·min(-1), in 2-legged and 1-legged, respectively (p < 0.01). Calculated blood volume changes declined significantly in 2-legged exercise (∆BV: -4.25 ± 0.43%, p < 0.05). Sympathetic activation as indicated by the ratio of low and high frequency in spectral analysis of HR (LF HF(-1) ratio) was higher in 2-legged than in 1- legged trial (p < 0.05). At the end of exercise, CO had a tendency to decrease from 20(th) min in 2-legged (changes in CO = -0.92 ± 0.3 L·min(-1), p = 0.07), whereas it was maintained in 1- legged cycling (∆CO = -0.15 ± 0.2 L·min(-1), p = 0.86). Multiple regression analysis showed that HR rise and blood volume decline were predictors of SV drop whereas heart rate increase was explained by rectal temperature and magnitude of muscle mass activation, as indicated by iEMG (p < 0.05) in 2-legged cycling. In conclusion, apart from the well-known factors of thermal status and blood volume decline, it seems that muscle mass involved plays also a role on the development of CVdrift. Key pointsThe magnitude of the participated muscle mass plays a critical role for the development of cardiovascular drift, when the oxygen consumption per leg is the same.Apart from thermal status and blood volume decline, central command plays a role on cardiovascular regulation during steady state exercise performed with large muscle mass.

Somatotype, size and body composition of competitive female volleyball players.

The aim of this study was to describe the morphological characteristics of competitive female volleyball players. For this purpose, body weight and height, breadths and girths as well as skinfold thickness at various body sites were assessed in 163 elite female volleyball players (age: 23.8+/-4.7 years, years of playing: 11.5+/-4.2, hours of training per week: 11.9+/-2.9, means+/-S.D.). Seventy-nine of these players were from the A1 division and the rest from the A2 division of the Greek National League. Two-way ANOVA was used to compare the differences in these characteristics between competition level and playing position. Body height ranged from 161cm to 194cm, and the mean value (177.1+/-6.5cm) was not inferior to that of international players of similar calibre. Adiposity of these players (sum of 5 skinfolds: 51.8+/-10.2mm, percent body fat: 23.4+/-2.8) was higher than that reported in other studies in which, however, different methodology was used. Volleyball athletes of this study were mainly balanced endomorphs (3.4-2.7-2.9). The A1 division players were taller and slightly leaner with greater fat-free mass than their A2 counterparts. Significant differences were found among athletes of different playing positions which are interpreted by their varying roles and physical demands during a volleyball game. The volleyball players who play as opposites were the only subgroup of players differing between divisions; the A2 opposites had more body fat than A1 opposites. These data could be added in the international literature related to the anthropometric characteristics of competitive female volleyball players.

Effects of hypoxia on diaphragmatic fatigue in highly trained athletes.

Previous work suggests that exercise-induced arterial hypoxaemia (EIAH), causing only moderate arterial oxygen desaturation (SaO2 : 92 +/- 1%), does not exaggerate diaphragmatic fatigue exhibited by highly trained endurance athletes. Since changes in arterial O2 tension have a significant effect on the rate of development of locomotor muscle fatigue during strenuous exercise, the present study investigated whether hypoxia superimposed on EIAH exacerbates the exercise-induced diaphragmatic fatigue in these athletes. Eight trained cyclists (VO2max : 67.0 +/- 2.6 ml kg(-1) min(-1); mean +/- S.E.M.) completed in balanced order four 5 min exercise tests leading to different levels of end-exercise SaO2 (64 +/- 2, 83 +/- 1, 91 +/- 1 and 96 +/- 1%) via variations in inspired O2 fraction (FiO2 : 0.13, 0.17, 0.21 and 0.26, respectively). Measurements were made at corresponding intensities (65 +/- 3, 80 +/- 3, 85 +/- 3 and 90 +/- 3% of normoxic maximal work rate, respectively) in order to produce the same tidal volume, breathing frequency and respiratory muscle load at each FiO2. The mean pressure time product of the diaphragm did not differ across the four exercise tests and ranged between 312 +/- 28 and 382 +/- 22 cmH2O s min(-1). Ten minutes into recovery, twitch transdiaphragmatic pressure (P(di,tw)) determined by bilateral phrenic nerve stimulation, was significantly (P = 0.0001) reduced after all tests. After both hypoxic tests (FiO2 : 0.13, 0.17) the degree of fall in P(di,tw) (by 26.9 +/- 2.7 and 27.4 +/- 2.6%, respectively) was significantly greater (P < 0.05) than after the normoxic test (by 20.1 +/- 3.4%). The greater amount of diaphragmatic fatigue in hypoxia at lower leg work rates (presumably requiring smaller leg blood flow compared with normoxia at higher leg work rates), suggests that when ventilatory muscle load is similar between normoxia and hypoxia, hypoxia exaggerates diaphragmatic fatigue in spite of potentially greater respiratory muscle blood flow availability.

Erythropoietin treatment elevates haemoglobin concentration by increasing red cell volume and depressing plasma volume.

Erythropoietin (Epo) has been suggested to affect plasma volume, and would thereby possess a mechanism apart from erythropoiesis to increase arterial oxygen content. This, and potential underlying mechanisms, were tested in eight healthy subjects receiving 5000 IU recombinant human Epo (rHuEpo) for 15 weeks at a dose frequency aimed to increase and maintain haematocrit at approximately 50%. Red blood cell volume was increased from 2933 +/- 402 ml before rHuEpo treatment to 3210 +/- 356 (P < 0.01), 3117 +/- 554 (P < 0.05), and 3172 +/- 561 ml (P < 0.01) after 5, 11 and 13 weeks, respectively. This was accompanied by a decrease in plasma volume from 3645 +/- 538 ml before rHuEpo treatment to 3267 +/- 333 (P < 0.01), 3119 +/- 499 (P < 0.05), and 3323 +/- 521 ml (P < 0.01) after 5, 11 and 13 weeks, respectively. Concomitantly, plasma renin activity and aldosterone concentration were reduced. This maintained blood volume relatively unchanged, with a slight transient decrease at week 11, such that blood volume was 6578 +/- 839 ml before rHuEpo treatment, and 6477 +/- 573 (NS), 6236 +/- 908 (P < 0.05), and 6495 +/- 935 ml (NS), after 5, 11 and 13 weeks of treatment. We conclude that Epo treatment in healthy humans induces an elevation in haemoglobin concentration by two mechanisms: (i) an increase in red cell volume; and (ii) a decrease in plasma volume, which is probably mediated by a downregulation of the rennin-angiotensin-aldosterone axis. Since the relative contribution of plasma volume changes to the increments in arterial oxygen content was between 37.9 and 53.9% during the study period, this mechanism seems as important for increasing arterial oxygen content as the well-known erythropoietic effect of Epo.

Importance of hemoglobin concentration to exercise: acute manipulations.

An acute reduction of blood hemoglobin concentration ([Hb]), even when the circulating blood volume is maintained, results in lower (.)V(O(2)(max) and endurance performance, due to the reduction of the oxygen carrying capacity of blood. Conversely, an increase of [Hb] is associated with enhanced (.)V(O(2)(max) and endurance capacity, that is also proportional to the increase in the oxygen carrying capacity of blood. The effects on endurance capacity appear more pronounced and prolonged than on (.)V(O(2)(max). During submaximal exercise, there is a tight coupling between O(2) demand and O(2) delivery, such that if [Hb] is acutely decreased muscle blood flow is increased proportionally and vice versa. During maximal exercise with either a small or a large muscle mass, neither peak cardiac output nor peak leg blood flow are affected by reduced [Hb]. An acute increase of [Hb] has no effect on maximal exercise capacity or (.)V(O(2)(max) during exercise in acute hypoxia. Likewise, reducing [Hb] in altitude-acclimatized humans to pre-acclimatization values has no effect on (.)V(O(2)(max) during exercise in hypoxia.