Plasma lipid and lipoprotein profile in elderly female runners.

Plasma lipid and lipoprotein profiles were compared in elderly female runners (RU: n = 15, aged 66 +/- 5 years, body fat 20 +/- 4%, training distance 35 +/- 15 km week-1, VO2max 36 +/- 4 ml kg-1 min-1, mean +/- SD) and age-matched untrained women (UT: n = 28, 66 +/- 4 years, body fat 26 +/- 6%, VO2max 26 +/- 3 ml kg-1 min-1). There were insignificant differences in total cholesterol (RU: 5.04 +/- 0.60 vs. UT: 5.48 +/- 0.85 mmol l-1), HDL-cholesterol (RU: 1.97 +/- 0.41 vs. UT: 1.91 +/- 0.36 mmol l-1) and LDL-cholesterol (RU: 2.72 +/- 0.59 vs. UT: 3.03 +/- 0.80 mmol l-1) between the two groups. Plasma triglyceride concentration of the runners was significantly lower than that of the untrained women (RU: 0.80 +/- 0.27 vs UT: 1.14 +/- 0.36 mmol l-1, P less than 0.01). No difference was observed in the LDL-cholesterol/HDL-cholesterol ratio between the two groups (RU: 1.45 +/- 0.51 vs UT: 1.64 +/- 0.53 units). These results suggest that regularly performed running of 35 km week-1 in elderly women does not further elevate their HDL-cholesterol level which is already high compared to the levels found in elderly men. However, elderly female runners appear to be protected against age-related increases in the levels of triglyceride and LDL-cholesterol.     

The effect of treadmill incline on maximal oxygen uptake,gas exchange and the metabolic response to exercise in the horse

In healthy man, conditions that change muscle O2 delivery affect the achievable maximum rate of O2 uptake as well as the metabolic (e.g. lactate threshold, LT) and gas exchange (e.g. gas exchange threshold, Tge) responses to incremental exercise. Inclined (I) compared to level (L) running increases locomotory muscle EMG at a given speed in the horse, indicative of elevated metabolic demand. To our knowledge, the effect of treadmill incline on VO2,max, LT and Tge has not been addressed in the exercising quadruped. We used blood sampling and breath-by-breath expired gas analysis to test the hypothesis that I (10% gradient) would increase VO2,max and the rate of O2 uptake (VO2) at LT and Tge in six Thoroughbred horses during incremental running to volitional fatigue. VO2,max was significantly higher for I (I, 77.8 +/- 4.1; L, 65.5 +/- 5.3 1 min(-1); P < 0.05), but peak plasma lactate concentration was not (I, 28.0 +/- 3.7; L, 25.9 +/- 3.0 mM). Arterial Pco2 increased to 62.1 +/- 3.3 and 57.9 +/- 2.7 Torr (I vs. L; P < 0.05), yet despite this relative hypoventilation, a distinct Tge was present. This Tge occurred at a significantly different absolute (I, 49.6 +/- 3.2; L, 42.4 +/- 3.21 min(-1); P < 0.05), but nearly identical relative VO2 (I, 63.6 +/- 1.2; L, 63.9 +/- 1.6% VO2max) in I and L. Similarly, LT occurred at a significantly greater absolute VO2 (I, 37.3 +/- 2.8; L, 26.9 +/- 2.1 1 min(-1)), but a relative VO2 that was not different (I, 47.9 +/- 2.1; L, 43.9 +/- 4.5% VO2,max). In addition, Tge occurred at a significantly higher (P < or = 0.05) absolute and relative VO2 than LT for both I and L tests. In conclusion, VO2,max is higher during inclined than level running and both LT and Tge in the horse occur at a similar percentage of VO2,max irrespective of the absolute level of VO2,max. In contrast to humans, LT is a poor analogue of Tge in the horse.     

The effect of pedal rate on pulmonary O2 uptake kinetics during very heavy intensity exercise in trained and untrained teenage boys

This study tested the hypothesis that the VO2 kinetic response would be slowed in untrained (UT) but not trained (T) teenage participants whilst cycling at 115 rev min(-1) compared to 50 rev min(-1). Eight UT and seven T boys completed two square-wave transitions to very heavy-intensity exercise pedalling at 50 rev min(-1) and 115 rev min(-1). In UT at the higher pedal rate, the phase II VO2 was significantly (P < 0.01) slower (50 rev min(-1): 32 ± 5 vs. 115 rev min(-1): 42 ± 11 s) and the relative VO2 slow component was significantly (P < 0.01) elevated (50 rev min(-1): 10 ± 3 vs. 115 rev min(-1): 16 ± 5%). The phase II VO2 (50 rev min(-1): 26 ± 4 vs. 115 rev min(-1): 22 ± 6s) and relative VO2 slow component (50 rev min(-1): 14 ± 5 vs. 115 rev min(-1): 17 ± 3%) were unaltered by pedal rate in T (P > 0.05). These data are consistent with the notion that VO2 kinetics are influenced by muscle fibre recruitment in youth but this effect is attenuated in endurance trained teenage boys.     

Blood glucose concentration dependent ACTH and cortisol responses to prolonged exercise

The purpose of this study is to investigate responses of serum ACTH and cortisol concentration to low intensity prolonged exercise. In experiment 1, 10 subjects fasted for 12 h and performed bicycle exercise at 49.3% VO2max (+/- 4.3%) until exhaustion or up to 3 h. During the early part of the exercise, serum ACTH and cortisol concentrations did not increase from the pre-exercise values (ACTH: 44 +/- 5 micrograms/l, cortisol: 139 +/- 52 micrograms/l). Whilst the time to serum ACTH concentration increasing varied among the subjects (60-180 min), the increases of this hormone occurred for all subjects (175 +/- 85 ng/l, P less than 0.05) when blood glucose concentration decreased to a critical level of 3.3 mmol/l. At the end of the exercise, blood glucose concentration decreased to 2.60 +/- 0.21 mmol/l, and serum ACTH and cortisol concentrations increased to 313 +/- 159 ng/l and 371 +/- 151 micrograms/l, respectively. In experiment 2, four subjects performed the same intensity exercise until exhaustion, and were then given 600 ml of 20 g glucose solution, and immediately afterwards, they were asked to repeat the same exercise. The subjects continued the exercise for between 30 to 90 min until again reaching exhaustion. During the second exercise, blood glucose concentration increased to the pre-exercise value (2.72 +/- 0.58 to 4.00 +/- 0.22 mmol/l, P less than 0.05) and simultaneously, serum ACTH concentration decreased considerably (354 +/- 22 to 119 +/- 54 ng/l, P less than 0.05). The results of the present study suggest that serum ACTH and cortisol concentration during low intensity prolonged exercise may be dependent on blood glucose concentration.     

Oxygen deficit is not affected by the rate of transition from rest to submaximal exercise

Five subjects cycled on an ergometer at power outputs corresponding to 20, 40, 60 and 80% of their maximal oxygen uptake (VO2 max). On one occasion the transition from rest to work was direct (D), while on the other occasion the power output was increased slowly (S) in a stepwise manner for 6-15 min prior to exercise at the predetermined intensity. Oxygen uptake (VO2) was measured, and O2 deficit and O2 debt were calculated. Oxygen deficit increased with the exercise intensities, the peak values being 2.1 +/- 0.2 and 1.9 +/- 0.1 litres (mean +/- SEM) at 80% of VO2 max after D and S respectively. No significant difference was observed in O2 deficit or O2 debt between D and S at any exercise intensity (P less than 0.05). The O2 debt was similar to the O2 deficit at 20, 40 and 60% of VO2 max but lower than the O2 deficit (P less than 0.05) at 80% of VO2 max. Femoral venous blood lactate remained unchanged at 20% of VO2 max but increased at the higher exercise intensities, reaching peak values of 7.6 +/- 0.6 and 7.4 +/- 1.1 mmol l-1 at 80% of VO2 max after D and S respectively. Blood lactate was not significantly different between D and S at any exercise intensity (P greater than 0.05). It is concluded that O2 deficit, O2 debt and blood lactate are not affected by the rate of transition from rest to submaximal exercise. The data contradict the hypothesis that O2 deficit is caused by an inadequate O2 transport at the onset of exercise.     

Determinants of repeated-sprint ability in females matched for single-sprint performance

This study investigated the relationship between VO2max and repeated-sprint ability (RSA), while controlling for the effects of initial sprint performance on sprint decrement. This was achieved via two methods: (1) matching females of low and moderate aerobic fitness (VO2max: 36.4 +/- 4.7 vs 49.6 +/- 5.5 ml kg(-1) min(-1) ; p < 0.05) for initial sprint performance and then comparing RSA, and (2) semi-partial correlations to adjust for the influence of initial sprint performance on RSA. Tests consisted of a RSA cycle test (5 x 6-s max sprints every 30 s) and a VO2max test. Muscle biopsies were taken before and after the RSA test. There was no significant difference between groups for work (W1, 3.44 +/- 0.57 vs 3.58 +/- 0.49 kJ; p = 0.59) or power (P1, 788.1 +/- 99.2 vs 835.2 +/- 127.2 W; p = 0.66) on the first sprint, or for total work (W(tot), 15.2 +/- 2.2 vs 16.6 +/- 2.2 kJ; p = 0.25). However, the moderate VO2max group recorded a smaller work decrement across the five sprints (W(dec), 11.1 +/- 2.5 vs 7.6 +/- 3.4%; p = 0.045). There were no significant differences between the two groups for muscle buffer capacity, muscle lactate or pH at any time point. When a semi-partial correlation was performed, to control for the contribution of W1 to W(dec), the correlation between VO2max and W(dec) increased from r = -0.41 (p > 0.05) to r = -0.50 (p < 0.05). These results indicate that VO2max does contribute to performance during repeated-sprint efforts. However, the small variance in W(dec) explained by VO2max suggests that other factors also play a role.     

The effect of sustained heavy exercise on the development of pulmonary edema in trained male cyclists

To determine whether intense, prolonged activity can induce transient pulmonary edema, eight highly trained male cyclists (mean +/- S.D.: age, 26.9 +/- 3.0 years; height, 179.9 +/- 5.7 cm; weight, 76.1 +/- 6.5 kg) performed a 45-min endurance cycle test (ECT). V(O2,max) was determined (4.84 +/- 0.4 L min(-1), 63.7 +/- 2.6 ml min(-1) g(-1)) and the intensity of exercise for the ECT was set at 10% below ventilatory threshold (approximately 76% V(O2, max) 300 +/- 25 W). Pre- and post-exercise pulmonary diffusion (DL(CO)) measurements and magnetic resonance imaging of the lung were made. DL(CO) and pulmonary capillary blood volume (VC) decreased 1h post-exercise by 12% (P = 0.004) and 21% (P = 0.017), respectively, but no significant change in membrane diffusing capacity (DM) was found. The magnetic resonance scans demonstrated a 9.4% increase (P = 0.043) in pulmonary extravascular water 90 min post-exercise. These data support the theory that high intensity, sustained exercise in well-trained athletes can result in transient pulmonary edema.     

Reproducibility of the cycling time to exhaustion at .VO2peak in highly trained cyclists.

The purpose of the present study was to examine, in highly trained cyclists, the reproducibility of cycling time to exhaustion (T(max)) at the power output equal to that attained at peak oxygen uptake (.VO2peak) during a progressive exercise test. Forty-three highly trained male cyclists (M +/- SD; age = 25 +/- 6 yrs; weight = 75 +/- 7 kg; .VO2peak = 64.8 +/- 5.2 ml.kg-1.min-1) performed two T(max) tests one week apart. While the two measures of T(max) were strongly related (r = 0.884; p < 0.001), T(max) from the second test (245 +/- 57 s) was significantly higher than that of the first (237 +/- 57 s; p = 0.047; two-tailed). Within-subject variability in the present study was calculated to be 6 +/- 6%, which was lower than that previously reported for T(max) in sub-elite runners (25%). The mean T(max) was significantly (p < 0.05) related to both the second ventilatory turnpoint (VT(2); r = 0.38) and to .VO2peak (r = 0.34). Despite a relatively low within-subject coefficient of variation, these data demonstrate that the second score in a series of two T(max) tests may be significantly greater than the first. Moreover, the present data show that T(max) in highly trained cyclists is moderately related to VT(2) and .VO2peak.     

Angiotensin II attenuates reflex decrease in heart rate and sympathetic activity in man

Circulatory variables and hormone concentrations in arterial plasma were measured in six normal subjects during angiotensin II (ANG II) step-up infusion of 0.25 and 1.00 ng kg-1 X min. During the 1.00 ng kg-1 X min infusion ANG II plasma concentrations increased from 11 +/- 2 to 48 +/- 6 pg ml-1; i.e., similar to those obtained during acute hypotensive hypovolaemia in man. Mean arterial pressure increased (P less than 0.05) from a resting value of 89 +/- 3 to 97 +/- 5 mmHg. Heart rate and catecholamine concentrations did not change. Plasma aldosterone increased (P less than 0.05) from 36 +/- 4 to 77 +/- 10 pg ml-1 during the infusion. Plasma concentrations of vasopressin, adrenalin and pancreatic polypeptide did not change during the investigation. During the 0.25 and 1.00 ng kg-1 X min infusion subcutaneous blood flow decreased (P = 0.06) to 67 +/- 20 and 66 +/- 26%, respectively, of control. It is concluded that: (1) ANG II in physiological doses in man may augment the sympathetic activity on the circulatory system since compensatory decreases in heart rate or in plasma catecholamines were not observed during the increased arterial pressure; (2) ANG II does not induce a general decrease in vagal tone as plasma pancreatic polypeptide concentrations were unchanged; (3) the obtained plasma concentrations of ANG II do not stimulate the release of vasopressin to plasma; and (4) the threshold for reducing the subcutaneous blood flow is reached within relatively small increments in plasma ANG II.     

Comparison of VO2max and disease risk factors between perimenopausal and postmenopausal women

OBJECTIVE: This study determines whether maximal oxygen consumption (VO2 max) is higher in perimenopausal women compared with similarly aged postmenopausal women and whether the lower VO2 max in postmenopausal women is associated with a higher total and visceral fat mass, less favorable lipid and glucose metabolism, and lower bone mineral density (BMD). DESIGN: Participants were 18 perimenopausal women (mean +/- SD; irregular menstrual cycle in the past 6 months) aged 49 +/- 4 years and 18 postmenopausal women (no menstrual cycle in the past year) aged 52 +/- 2 years who were matched for body mass index and race. Women were sedentary, and none were on hormone replacement therapy. Body composition (dual-energy x-ray absorptiometry and CT), VO2 max, fasting concentrations of sex steroid hormones, lipoproteins, insulin, and glucose were determined. RESULTS: VO2 max was 17% lower (22 +/- 3 v 27 +/- 7 mL.kg.min; P 相似文献   

Brain activity and fatigue during prolonged exercise in the heat

We hypothesized that fatigue due to hyperthermia during prolonged exercise in the heat is in part related to alterations in frontal cortical brain activity. The electroencephalographic activity (EEG) of the frontal cortex of the brain was measured in seven cyclists [maximal O2 uptake (VO2max) 4.8 +/- 0.1 (SE) 1 min-1] cycling at 60% VO2max in a hot (H, 42 degrees C) and a cool (C, 19 degrees C) environment. Fast Fourier transformation of the EEG was used to obtain power spectrum areas in the alpha (8-13 Hz) and beta (13-30 Hz) frequencies. The ratio alpha/beta was calculated as an index of arousal level; an elevated alpha/beta index reflects suppressed arousal. In H, subjects fatigued after 34.4 +/- 1.4 min coinciding with an oesophageal temperature (Toes) of 39.8 +/- 0.1 degrees C, an almost maximal heart rate (HR 192 +/- 3 beats.min-1), a rating of perceived exertion (RPE) of 19.0 +/- 0.8 and significantly elevated alpha/beta index (188 +/- 71% of the value after 2 min of exercise; P < 0.05). In C, subjects cycled for a similar period while Toes was below 38 degrees C, HR and RPE were low, and the alpha/beta index was not significantly elevated (59 +/- 27% of 2 min value; P = NS). Increases in the alpha/beta index were strongly correlated to increases in Toes (r2 = 0.98; P = 0.0001).     

Effect of 4 weeks of training on the limit time at VO2 max]

The purpose of this study was to examine the effect of 4 weeks training in running on the time spent at VO2max (tlim VO2max). Eight athletes carried out, before and after an aerobic training, an incremental and five exhaustive tests at 90, 95, 100, 115% vVO2max and at the critical power at VO2max (CV'; slope of the linear relation between the tlim VO2max and the distance limit at VO2max). This training did not significantly improve VO2max (p = 0.17) or tlim VO2max (p = 0.72). However, the "tlim VO2max-intensity" curve was shifted toward the right, meaning that the athlete had to run at a higher intensity after training to obtain the same tlim VO2max. Tlim VO2max at CV' before training was significantly higher than tlim VO2max at 90, 95, 100, and 115% vVO2max (p < 0.05). This training increased CV' in absolute value (13.9 +/- 1.3 vs. 14.9 +/- 1.2 km.h-1, p < 0.05; n = 6) but not in relative value (86 +/- 4 vs. 86 +/- 5% vVO2max; p = 0.9). In conclusion, in spite of the shift of the "tlim VO2max-intensity" curve, tlim VO2max was not significantly increased by this training. Furthermore, CV' allowed subjects to spend the longest time of exercise at VO2max during a continuous exercise with constant speed, but CV', expressed in % vVO2max, did not improve with this training.     

Plasma volume and electrolyte shifts with heavy exercise in sitting and supine positions.

Plasma volume (PV) and electrolyte shifts were measured before and for 60 min after a continuous peak oxygen uptake (VO2 peak) test in four men (26-45 yr) on a bicycle ergometer. Mean (+/-SE) sitting VO2peak (3.16 +/- 0.32 1/min) was the same as supine VO2peak (3.13 +/- 0.33 1/min). In recovery (R + 1.5 min), mean PV had decreased by 477 ml (-16.1%, P less than 0.05) in the sitting and by 548 ml (-17.6%, P less than 0.05) in the supine positions, whereas total osmolality increased progressively with its peak at R + 3.5 min. The percentage losses of protein, total Ca2+, and ionized Cai2+ were about half as great as the percentage loss in PV, indicating a selective retention of these constituents. Calculated osmolality (sigma Na+, K+, Cl-, Cai2+) returned to control levels within 1.5 min after sitting exercise but required about 15 min after supine exercise. These small increases in protein concentration were not likely to significantly aid restitution of plasma volume and the ions were probably in equilibrium across the capillary membrane. So a change in hydrostatic and/or systemic blood pressures most likely provided the force for restitution of plasma volume.     

Gender differences in temperature and vascular characteristics during exercise recovery.

Temperature and vascular responses during exercise recovery were examined in men and women of similar age and fitness status (VO2max: 76 +/- 5 vs 73 +/- 5 mL O2 / kg Fat Free Mass x min). Forearm blood flow (venous occlusion plethysmography; FBF), rectal (Trectal) and forearm skin (Tskin) temperatures (degree C) were measured before and every 15 min up to 105 min (t105) during recovery from a 45-min run at 75% of VO2max. Results indicate Trectal decreased to pre-exercise levels within 25 min in men but reached and remained at values lower than baseline between 60 and 105 min of recovery in women. From 90 to 105 min of recovery, Tskin was lower in women than men (t105 : 29.0 +/- 1.3 vs 30.7 +/- 1.5; p <.05). Recovery FBF (mL/100mL x min) was higher in men than women from the start (6.2 +/- 1.9 vs 4.9 +/- 1.9) to the end of recovery (t105 = 1.7 +/- 0.6 vs 2.6 +/- 1.1) (p <.05). Heat flux calculated at the forearm was higher in women and increased throughout the last hour of recovery (p <.05). Further investigations are needed to examine mechanisms underlying failure of post-exercise core and skin temperatures in women to stabilize at pre-exercise levels.     

Thyroid hormones may influence the slow component of VO(2) in professional cyclists

We analyzed the relationship between the plasma concentrations of several hormones (testosterone [T], follicle-stimulating [FSH] and luteinizing hormone [LH], cortisol [C], 3,5,3'-triiodothyronine [T(3)], thyroxine [T(4)], and thyrotrophin [TSH]) and the magnitude of the VO(2) slow component (Delta VO(2)) in a group of nine professional road cyclists (26+/-2 years). The resting levels of the aforementioned hormones were determined before the subjects performed a 20-min cycle ergometer test at approximately 80% of VO(2 max) (or approximately 400 W). Plasma concentrations of T(3) and T(4) were inversely correlated (p<0.05) with Delta VO(2) (r=-0.72 and rr=-0.66, respectively), suggesting, at least partly, and association between thyroid basal function and the VO(2) slow component of euthyroid elite endurance athletes during constant-load intense exercise.     

During hypoxic exercise some vasoconstriction is needed to match O2 delivery with O2 demand at the microcirculatory level.

To test the hypothesis that the increased sympathetic tonus elicited by chronic hypoxia is needed to match O(2) delivery with O(2) demand at the microvascular level eight male subjects were investigated at 4559 m altitude during maximal exercise with and without infusion of ATP (80 mug (kg body mass)(-1) min(-1)) into the right femoral artery. Compared to sea level peak leg vascular conductance was reduced by 39% at altitude. However, the infusion of ATP at altitude did not alter femoral vein blood flow (7.6 +/- 1.0 versus 7.9 +/- 1.0 l min(-1)) and femoral arterial oxygen delivery (1.2 +/- 0.2 versus 1.3 +/- 0.2 l min(-1); control and ATP, respectively). Despite the fact that with ATP mean arterial blood pressure decreased (106.9 +/- 14.2 versus 83.3 +/- 16.0 mmHg, P < 0.05), peak cardiac output remained unchanged. Arterial oxygen extraction fraction was reduced from 85.9 +/- 5.3 to 72.0 +/- 10.2% (P < 0.05), and the corresponding venous O(2) content was increased from 25.5 +/- 10.0 to 46.3 +/- 18.5 ml l(-1) (control and ATP, respectively, P < 0.05). With ATP, leg arterial-venous O(2) difference was decreased (P < 0.05) from 139.3 +/- 9.0 to 116.9 +/- 8.4(-1) and leg .VO(2max) was 20% lower compared to the control trial (1.1 +/- 0.2 versus 0.9 +/- 0.1 l min(-1)) (P = 0.069). In summary, at altitude, some degree of vasoconstriction is needed to match O(2) delivery with O(2) demand. Peak cardiac output at altitude is not limited by excessive mean arterial pressure. Exercising leg .VO(2peak) is not limited by restricted vasodilatation in the altitude-acclimatized human.     

Effect of paddling cadence on time to exhaustion and VO2 kinetics at the intensity associated with VO2max in elite white-water kayakers.

The influence of paddling cadence on the time to exhaustion (t.lim) and VO2 kinetics at the intensity associated with VO2max (IVO2max) was examined in seven highly-trained white water kayakers. All subjects were engaged in national or international competitions. Subjects took part in three constant-load tests at IVO2max, each test performed at a different paddling cadence (50, 60 or 70 cycles min(-1). The VO2 kinetics recorded during these constant-load tests at IVO2max were fitted with a mono-exponential equation. A significant increase in t.lim (P <.05) was observed as the paddling cadence increased from 50 to 70 cycles min(-1). No effect was found either on values of VO2peak, post-exercise blood lactate concentration, or on the time at which VO2peak was attained (TAVO2peak). Our results suggest that experienced kayakers may choose a high paddling cadence during physiological assessments at IVO2max. Further experiments are needed in order to identify the physiological significance of t.lim at IVO2max.     

Enhanced heat loss responses induced by short-term endurance training in exercising women

We investigated the effects of short-term endurance training and detraining on sweating and cutaneous vasodilatation during exercise in young women, taking into account changes in maximal oxygen uptake (VO2max) and the phase of the menstrual cycle. Eleven untrained women participated in endurance training; cycle exercise at approximately 60% VO2max for 60 min day(-1), 4-5 days week(-1) (30 degrees C, 45% relative humidity) for three complete menstrual cycles. The standard exercise test consisted of exercise at 50% VO2max for 30 min (25 degrees C, 45% relative humidity), and was conducted before training (Pre), during training sessions (T1, T2 and T3) and after cessation of training (D1 and D2). Values of VO2max increased significantly from 32.7 +/- 1.2 to 37.8 +/- 1.2 ml min(-1) kg(-1) at the end of the training. Local sweat rate in the chest and thigh, but not in the back and forearm, were significantly greater during T1 and T2 only in women who started training from the midfollicular phase. Cutaneous blood flow did not change with training. The threshold oesophageal temperatures for heat loss responses were significantly decreased during T1 versus Pre (averaged values for each body site: sweating, 37.49 +/- 0.08 versus 37.22 +/- 0.12 degrees C; and cutaneous vasodilatation, 37.40 +/- 0.07 versus 37.17 +/- 0.10 degrees C) and maintained through T3; the sensitivities of heat loss responses were not altered. These changes returned to the Pre level by D1. Our data indicate that physical training improves heat loss responses by decreasing the threshold temperatures and that these effects occur within a month of training and disappear within a month after cessation of training. The degree of increase in sweating with training differs among body sites and might be affected by the phase of the menstrual cycle.     

VO2 responses to different intermittent runs at velocity associated with VO2max.

The purposes of this study were (1) to determine the time sustained above 90% of VO2max in different intermittent running sessions having the same overall time run at the velocity (vVO2max) associated with VO2max, and (2) to test whether the use of a fixed-fraction (50%) of the time to exhaustion at vVO2max (Tlim) leads to longer time spent at a high percentage of VO2max. Subjects were 8 triathletes who, after determination of their track vVO2max and Tlim, performed three intermittent running sessions alternating the velocity between 100% and 50% of vVO2max, termed 30 s-30 s, 60 s-30 s, and 1/2 Tlim, where the overall time at vVO2max was similar (= 3 x Tlim). VO2max achieved in the incremental test was 71.1 +/- 3.9 ml.min-1.kg-1 and Tlim was 236 +/- 49 s. VO2peak and peak heart rate were lower in 30 s-30 s than in the other intermittent runs. The time spent above 90% of VO2max was significantly (p < 0.001) longer either in 60 s-30 s (531 +/- 187 s) or in 1/2 Tlim-1/2 Tlim (487 +/- 176 s) than in 30 s-30 s (149 +/- 33 s). Tlim was negatively correlated with the time (in % of Tlim) spent above 90% of VO2max in 30 s-30 s (r = -0.75, p < 0.05). Tlim was also correlated with the difference of time spent over 90% of VO2max between 60 s-30 s and 30 s-30 s (r = 0.77, p < 0.05), or between 1/2 Tlim-1/2 Tlim and 30 s-30 s (r = 0.97, p < 0.001). The results confirm that vVO2max and Tlim are useful for setting interval-training sessions. However, the use of an individualized fixed-fraction of Tlim did not lead to longer time spent at a high percentage of VO2max compared to when using a fixed work-interval duration.