Effects of menthol application on the skin during prolonged immersion in cool and cold water.

The aim of the study was to compare the effect of skin surface menthol application on rectal temperature (Tre) during prolonged immersion in cool and cold water. We hypothesized that menthol application would lead to a slower Tre decline due to the reduced heat loss as a consequence of the menthol-induced vasoconstriction and that this effect would be attenuated during cold-water immersion. Six male subjects were immersed for 55 minutes in stirred cool (24°C) or cold (14°C) water immediately after attaining a Tre of 38°C by cycling at 60% of maximum heart rate on two occasions: without (ΝM) and with (M) whole-body skin application of menthol cream. Tre, the proximal-distal skin temperature gradient, and oxygen uptake were continuously measured. ANOVA with repeated measures was employed to detect differences among variables. Significance level was set at 0.05. The area under the curve for Tre was calculated and was greater in 24°C M (-1.81 ± 8.22 a.u) compared to 24°C NM (-27.09 ± 19.09 a.u., P = .03, r = .90), 14°C NM (-18.08 ± 10.85 a.u., P = .03, r = .90), and 14°C M (-11.71 ± 12.58 a.u, P = .05, r = .81). In cool water, oxygen uptake and local vasoconstriction were increased (P ≤ .05) by 39 ± 25% and 56 ± 37%, respectively, with menthol compared to ΝM, while no differences were observed in cold water. Menthol application on the skin before prolonged immersion reduces heat loss resulting in a blunted Tre decline. However, such a response is less obvious at 14°C water immersion, possibly because high-threshold cold-sensitive fibers are already maximally recruited and the majority of cold receptors saturated.

Effects of menthol application on the skin during prolonged immersion in swimmers and controls.

We hypothesized that menthol application on the skin would enhance vasoconstriction of subjects immersed in cool water, which would reduce heat loss and rectal temperature (Tre) cooling rate. Furthermore, it was hypothesized that this effect would be greater in individuals acclimatized to immersion in 24 °C water, such as swimmers. Seven swimmers (SW) and seven physical education students (CON) cycled at 60% VO2 max until Tre attained 38 °C, and were then immediately immersed in stirred water maintained at 24 °C on two occasions: without (NM) and with (M; 4.6 g per 100 mL of water) whole-body skin application of menthol cream. Heart rate, Tre, proximal-distal skin temperature gradient, oxygen uptake (VO2 ), electromyographic activity (EMG), and thermal sensation were measured. Tre reduction was similar among SW and CON in NM and CON in M (-0.71±0.31 °C in average), while it was smaller for SW in M (-0.37±0.18 °C, P < 0.01). VO2 and heart rate were greater in M compared with NM condition (P = 0.01). SW in M exhibited a shift of the threshold for shivering, as reflected in increased VO2 and EMG activity, toward a higher Tre compared with the other trials. Menthol application on the skin before immersion reduces heat loss, but defends Tre decline more effectively in swimmers than in non-swimmers.

A new equation to estimate temperature-corrected PaCO2 from PET CO2 during exercise in normoxia and hypoxia.

End-tidal PCO2 (PET CO2 ) has been used to estimate arterial pressure CO2 (Pa CO2 ). However, the influence of blood temperature on the Pa CO2 has not been taken into account. Moreover, there is no equation validated to predict Pa CO2 during exercise in severe acute hypoxia. To develop a new equation to predict temperature-corrected Pa CO2 values during exercise in normoxia and severe acute hypoxia, 11 volunteers (21.2 ± 2.1 years) performed incremental exercise to exhaustion in normoxia (Nox, PI O2 : 143 mmHg) and hypoxia (Hyp, PI O2 : 73 mmHg), while arterial blood gases and temperature (ABT) were simultaneously measured together with end-tidal PCO2 (PET CO2 ). The Jones et al. equation tended to underestimate the temperature corrected (tc) Pa CO2 during exercise in hypoxia, with greater deviation the lower the Pa CO2 tc (r = 0.39, P < 0.05). The new equation has been developed using a random-effects regression analysis model, which allows predicting Pa CO2 tc both in normoxia and hypoxia: Pa CO2 tc = 8.607 + 0.716 × PET CO2 [R(2) = 0.91; intercept SE = 1.022 (P < 0.001) and slope SE = 0.027 (P < 0.001)]. This equation may prove useful in noninvasive studies of brain hemodynamics, where an accurate estimation of Pa CO2 is needed to calculate the end-tidal-to-arterial PCO2 difference, which can be used as an index of pulmonary gas exchange efficiency.

Reduced metaboreflex control of blood pressure during exercise in individuals with intellectual disability: a possible contributor to exercise intolerance.

The aim was to investigate the hemodynamic responses to isometric handgrip exercise (HG) and examine the role of the muscle metaboreflex in the exercise pressor response in individuals with intellectual disability (IID) and non-disabled control subjects. Eleven males with mild-moderate intellectual disabilities and eleven non-disabled males performed a testing protocol involving 3-min periods of baseline, HG exercise (at 30% MVC), circulatory occlusion, and recovery. The same protocol was repeated without occlusion. At baseline, no differences were detected between groups in beat-to-beat mean arterial pressure (MAP), heart rate (HR), stroke volume, and peripheral resistance. IID were able to sustain an exercise MAP response at comparable levels to the control group exerting similar peripheral resistance; however, IID exhibited a blunted chronotropic response to HG and a diminished exercise vagal withdrawal compared to controls. During occlusion, IID exhibited a lower pressor response than their control peers, associated with a lower increase in peripheral resistance during this task. In conclusion, although intellectual disabilities can be the consequence of many different genes, IID share common deficits in the chronotropic response to exercise and a blunted metaboreflex-induced pressor response.

On- and off-exercise kinetics of cardiac output in response to cycling and walking in COPD patients with GOLD Stages I-IV.

Exercise-induced dynamic hyperinflation and large intrathoracic pressure swings may compromise the normal increase in cardiac output (Q) in Chronic Obstructive Pulmonary Disease (COPD). Therefore, it is anticipated that the greater the disease severity, the greater would be the impairment in cardiac output during exercise. Eighty COPD patients (20 at each GOLD Stage) and 10 healthy age-matched individuals undertook a constant-load test on a cycle-ergometer (75% WR(peak)) and a 6min walking test (6MWT). Cardiac output was measured by bioimpedance (PhysioFlow, Enduro) to determine the mean response time at the onset of exercise (MRTon) and during recovery (MRToff). Whilst cardiac output mean response time was not different between the two exercise protocols, MRT responses during cycling were slower in GOLD Stages III and IV compared to Stages I and II (MRTon: Stage I: 45±2, Stage II: 65±3, Stage III: 90±3, Stage IV: 106±3s; MRToff: Stage I: 42±2, Stage II: 68±3, Stage III: 87±3, Stage IV: 104±3s, respectively). In conclusion, the more advanced the disease severity the more impaired is the hemodynamic response to constant-load exercise and the 6MWT, possibly reflecting greater cardiovascular impairment and/or greater physical deconditioning.

Does recombinant human Epo increase exercise capacity by means other than augmenting oxygen transport?

This study was performed to test the hypothesis that administration of recombinant human erythropoietin (rHuEpo) in humans increases maximal oxygen consumption by augmenting the maximal oxygen carrying capacity of blood. Systemic and leg oxygen delivery and oxygen uptake were studied during exercise in eight subjects before and after 13 wk of rHuEpo treatment and after isovolemic hemodilution to the same hemoglobin concentration observed before the start of rHuEpo administration. At peak exercise, leg oxygen delivery was increased from 1,777.0+/-102.0 ml/min before rHuEpo treatment to 2,079.8+/-120.7 ml/min after treatment. After hemodilution, oxygen delivery was decreased to the pretreatment value (1,710.3+/-138.1 ml/min). Fractional leg arterial oxygen extraction was unaffected at maximal exercise; hence, maximal leg oxygen uptake increased from 1,511.0+/-130.1 ml/min before treatment to 1,793.0+/-148.7 ml/min with rHuEpo and decreased after hemodilution to 1,428.0+/-111.6 ml/min. Pulmonary oxygen uptake at peak exercise increased from 3,950.0+/-160.7 before administration to 4,254.5+/-178.4 ml/min with rHuEpo and decreased to 4,059.0+/-161.1 ml/min with hemodilution (P=0.22, compared with values before rHuEpo treatment). Blood buffer capacity remained unaffected by rHuEpo treatment and hemodilution. The augmented hematocrit did not compromise peak cardiac output. In summary, in healthy humans, rHuEpo increases maximal oxygen consumption due to augmented systemic and muscular peak oxygen delivery.

Anthropometric, body composition and somatotype differences of Greek elite female basketball, volleyball and handball players.

AIM: The aims of the present study were: a) to determine the anthropometric profile, body composition and somatotype of elite Greek female basketball (B), volleyball (V) and handball (H) players, b) to compare the mean scores among sports and c) to detect possible differences in relation to competition level. METHODS: A total of 518 female athletes, all members of the Greek first National League (A1 and A2 division) in B, V and H sport teams participated in the present study. Twelve anthropometric measures required for the calculation of body composition indexes and somatotype components were obtained according to the established literature. RESULTS: V athletes were the tallest (P<0.001) among the three groups of athletes, had the lowest values of body fat (P<0.001) and their somatotype was characterized as balanced endomorph (3.4-2.7-2.9). B athletes were taller (P<0.01) and leaner (P<0.001) than H players, with a somatotype characterized as mesomorph-endomorph (3.7-3.2-2.4). H athletes were the shortest of all (P<0.01), had the highest percentage of body fat (P<0.001) and their somatotype was mesomorph-endomorph (4.2-4.7-1.8). In comparison with their A2 counterparts the A1 division players were taller (P<0.001) and heavier (P<0.01), but at the same time leaner (P<0.001), and exhibited higher homogeneity in somatotype characteristics (P<0.05). CONCLUSIONS: Anthropometric, body composition and somatotype variables of Greek female elite teamball players varied among sports; selection criteria, hours of training and sport-specific physiological demands during the game could explain the observed differences. More data are certainly needed to define the anthropometric profile of B, V and H female athletes internationally.

Arterial O2 content and tension in regulation of cardiac output and leg blood flow during exercise in humans.

A universal O2 sensor presumes that compensation for impaired O2 delivery is triggered by low O2 tension, but in humans, comparisons of compensatory responses to altered arterial O2 content (CaO2) or tension (PaO2) have not been reported. To directly compare cardiac output (QTOT) and leg blood flow (LBF) responses to a range of CaO2 and PaO2, seven healthy young men were studied during two-legged knee extension exercise with control hemoglobin concentration ([Hb] = 144.4 +/- 4 g/l) and at least 1 wk later after isovolemic hemodilution ([Hb] = 115 +/- 2 g/l). On each study day, subjects exercised twice at 30 W and on to voluntary exhaustion with an FIO2 of 0.21 or 0.11. The interventions resulted in two conditions with matched CaO2 but markedly different PaO2 (hypoxia and anemia) and two conditions with matched PaO2 and different CaO2 (hypoxia and anemia + hypoxia). PaO2 varied from 46 +/- 3 Torr in hypoxia to 95 +/- 3 Torr (range 37 to >100) in anemia (P < 0.001), yet LBF at exercise was nearly identical. However, as CaO2 dropped from 190 +/- 5 ml/l in control to 132 +/- 2 ml/l in anemia + hypoxia (P < 0.001), QTOT and LBF at 30 W rose to 12.8 +/- 0.8 and 7.2 +/- 0.3 l/min, respectively, values 23 and 47% above control (P < 0.01). Thus regulation of QTOT, LBF, and arterial O2 delivery to contracting intact human skeletal muscle is dependent for signaling primarily on CaO2, not PaO2. This finding suggests that factors related to CaO2 or [Hb] may play an important role in the regulation of blood flow during exercise in humans.

Skeletal muscle blood flow in humans and its regulation during exercise.

Regional limb blood flow has been measured with dilution techniques (cardio-green or thermodilution) and ultrasound Doppler. When applied to the femoral artery and vein at rest and during dynamical exercise these methods give similar reproducible results. The blood flow in the femoral artery is approximately 0.3 L min(-1) at rest and increases linearly with dynamical knee-extensor exercise as a function of the power output to 6-10 L min[-1] (Q= 1.94 + 0.07 load). Considering the size of the knee-extensor muscles, perfusion during peak effort may amount to 2-3 L kg(-1) min(-1), i.e. approximately 100-fold elevation from rest. The onset of hyperaemia is very fast at the start of exercise with T 1/2 of 2-10 s related to the power output with the muscle pump bringing about the very first increase in blood flow. A steady level is reached within approximately 10-150 s of exercise. At all exercise intensities the blood flow fluctuates primarily due to the variation in intramuscular pressure, resulting in a phase shift with the pulse pressure as a superimposed minor influence. Among the many vasoactive compounds likely to contribute to the vasodilation after the first contraction adenosine is a primary candidate as it can be demonstrated to (1) cause a change in limb blood flow when infused i.a., that is similar in time and magnitude as observed in exercise, and (2) become elevated in the interstitial space (microdialysis technique) during exercise to levels inducing vasodilation. NO appears less likely since NOS blockade with L-NMMA causing a reduced blood flow at rest and during recovery, it has no effect during exercise. Muscle contraction causes with some delay (60 s) an elevation in muscle sympathetic nerve activity (MSNA), related to the exercise intensity. The compounds produced in the contracting muscle activating the group IIl-IV sensory nerves (the muscle reflex) are unknown. In small muscle group exercise an elevation in MSNA may not cause vasoconstriction (functional sympatholysis). The mechanism for functional sympatholysis is still unknown. However, when engaging a large fraction of the muscle mass more intensely during exercise, the MSNA has an important functional role in maintaining blood pressure by limiting blood flow also to exercising muscles.

Cardiovascular responses to dynamic exercise with acute anemia in humans.

We hypothesized that reducing arterial O2 content (CaO2) by lowering the hemoglobin concentration ([Hb]) would result in a higher blood flow, as observed with a low PO2, and maintenance of O2 delivery. Seven young healthy men were studied twice, at rest and during two-legged submaximal and peak dynamic knee extensor exercise in a control condition (mean control [Hb] 144 g/l) and after 1-1.5 liters of whole blood had been withdrawn and replaced with albumin [mean drop in [Hb] 29 g/l (range 19-38 g/l); low [Hb]]. Limb blood flow (LBF) was higher (P < 0.01) with low [Hb] during submaximal exercise (i.e., at 30 W, LBF was 2.5 +/- 0.1 and 3.0 +/- 0.1 l/min for control [Hb] and low [Hb], respectively; P < 0.01), resulting in a maintained O2 delivery and O2 uptake for a given workload. However, at peak exercise, LBF was unaltered (6.5 +/- 0.4 and 6.6 +/- 0.6 l/min for control [Hb] and low [Hb], respectively), which resulted in an 18% reduction in O2 delivery (P < 0.01). This occurred despite peak cardiac output in neither condition reaching >75% of maximal cardiac output (approximately 26 l/min). It is concluded that a low CaO2 induces an elevation in submaximal muscle blood flow and that O2 delivery to contracting muscles is tightly regulated.

Hypoxia and the cardiovascular response to dynamic knee-extensor exercise.

Hypoxia affects O2 transport and aerobic exercise capacity. In two previous studies, conflicting results have been reported regarding whether O2 delivery to the muscle is increased with hypoxia or whether there is a more efficient O2 extraction to allow for compensation of the decreased O2 availability at submaximal and maximal exercise. To reconcile this discrepancy, we measured limb blood flow (LBF), cardiac output, and O2 uptake during two-legged knee-extensor exercise in eight healthy young men. They completed studies at rest, at two submaximal workloads, and at peak effort under normoxia (inspired O2 fraction 0.21) and two levels of hypoxia (inspired O2 fractions 0.16 and 0.11). During submaximal exercise, LBF increased in hypoxia and compensated for the decrement in arterial O2 content. At peak effort, however, our subjects did not achieve a higher cardiac output or LBF. Thus O2 delivery was not maintained and peak power output and leg O2 uptake were reduced proportionately. These data are consistent then with the findings of an increased LBF to compensate for hypoxemia at submaximal exercise, but no such increase occurs at peak effort despite substantial cardiac capacity for an elevation in LBF.

Arterial hypoxemia and performance during intense exercise.

In order to determine the level of hypoxemia which is sufficient to impair maximal performance, seven well-trained male cyclists [maximum oxygen consumption (VO2max) > or = 5 l.min-1 or 60 ml.kg-1.min-1] performed a 5-min performance cycle test to exhaustion at maximal intensity as controlled by the subject, under three experimental conditions: normoxemia [percentage of arterial oxyhemoglobin saturation (%SaO2) > 94%], and artificially induced mild (%SaO2 = 90 +/- 1%) and moderate (% SaO2 = 87 +/- 1%) hypoxemia. Performance, evaluated as the total work output (Worktot) performed in the 5-min cycle test, progressively decreased with decreasing % SaO2 [mean (SE) Worktot = 107.40 (4.5) kJ, 104.07 (5.6) kJ, and 102.52 (4.7) kJ, under normoxemia, mild, and moderate hypoxemia, respectively]. However, only performance in the moderate hypoxemia condition was significantly different than in normoxemia (P = 0.02). Mean oxygen consumption and heart rate were similar in the three conditions (P = 0.18 and P = 0.95, respectively). End-tidal partial pressure of CO2 was significantly lower (P = 0.005) during moderate hypoxemia compared with normoxemia, and ventilatory equivalent of CO2 was significantly higher (P = 0.005) in both hypoxemic conditions when compared with normoxemia. It is concluded that maximal performance capacity is significantly impaired in highly trained cyclists working under an % SaO2 level of 87% but not under a milder desaturation level of 90%.