Significant changes in VLDL-Triacylglycerol and glucose tolerance in obese subjects following ten days of training

We characterized the effect of ten days of training on lipid metabolism in 6 [age 37.2 (2.3) years] sedentary, obese [BMI 34.4?(3.0)?kg?·?m^?2] males with normal glucose tolerance. An oral glucose tolerance test was performed prior to and at the end of the 10?d of training period. The duration of each daily exercise session was 40?min at an intensity equivalent to ?75% of the age predicted maximum heart rate. Blood measurements were performed after an overnight fast, before and at the end of the 10?d period. Plasma triacylglycerol was significantly (p??1). Very low density lipoprotein-triacylglycerol was also significantly?(p??1). No significant changes in high density lipoprotein-cholesterol were observed as a result of training. Following training fasting plasma glucose and fasting plasma insulin were significantly reduced [Glucose: 5.9 (0.2)?mmol?·?l^?1 vs.?5.3 (0.22)?mmol?·?l^?1 (p??1 vs. 200.9 (30.1) ρ?·?mol?·?l^?1, p?=?0.05]. The total area under the glucose curve during the OGTT decreased significantly (p?相似文献   

Effects of 3 days of carbohydrate supplementation on muscle glycogen content and utilisation during a 1-h cycling performance

This study compared the effects of supplementing the normal diets of six trained cyclists [maximal oxygen uptake $(\dot {V}$ O_2max) 4.5 (0.36)l · min^?1; values are mean (SD)] with additional carbohydrate (CHO) on muscle glycogen utilisation during a 1-h cycle time-trial (TT). Using a randomised crossover design, subjects consumed either their normal diet (NORM) for 3 days, which consisted of 426 (137) g · day^?1 CHO [5.9 (1.4) g · kg^?1 body mass (BM)], or additional CHO (SUPP) to increase their intake to 661 (76) g · day^?1 [9.3 (0.7) g · kg^?1 BM]. The SUPP diet elevated muscle glycogen content from 459?(83) to 565?(62) mmol?·?kg^?1 dry weight (d.w.) (P < 0.05). However, despite the increased pre-exercise muscle glycogen stores, there was no difference in the distance cycled during the TT [40.41 (1.44) vs 40.18 (1.76)?km for NORM and SUPP, respectively]. With NORM, muscle glycogen declined from 459 (83) to 175?(64) mmol?·?kg^?1 d.w., whereas with SUPP the corresponding values were 565?(62) and 292?(113) mmol?·?kg^?1 d.w. Accordingly, both muscle glycogen utilisation [277?(64) vs 273?(114) mmol?·?kg^?1 d.w.] and total CHO oxidation [169 (20) vs 165?(30)?g?·?h^?1 for NORM and SUPP, respectively] were similar. Neither were there any differences in plasma glucose or lactate concentrations during the two experimental trials. Plasma glucose concentration averaged 5.5 (0.5) and 5.6 (0.6) mmol?·?l^?1, while plasma lactate concentration averaged 4.4 (1.9) and 4.4 (2.3) mmol?·?l^?1 for NORM and SUPP, respectively. The results of this study show that when well-trained subjects increase the CHO content of their diet for 3 days from 6 to 9 g?·?kg^?1 BM there is only a modest increase in muscle glycogen content. Since supplementary CHO did not improve TT performance, we conclude that additional CHO provides no benefit to performance for athletes who compete in intense, continuous events lasting 1?h. Furthermore, the substantial muscle CHO reserves observed at the termination of exercise indicate that whole-muscle glycogen depletion does not determine fatigue at this exercise intensity and duration.     

Stroke volume response to cycle ergometry in trained and untrained older men

The aims of this study were threefold: (1) to investigate the stroke volume (SV) response of trained older male cyclists [Cyclists: 65 (2.1) years; n?=?10] during incremental cycle ergometry (20 W?·?min^?1); (2) to determine the SV dynamics and total peripheral resistance response of untrained, but healthy and active older male controls [Controls: 66 (1.1) years; n?=?10]; (3) to compare the maximum oxygen consumption (˙VO_2max) and SV response of trained older male runners [Runners: 65 (3.4) years; n?=?11] with that of age-matched Cyclists. Impedance cardiography was used to assess the response of cardiac output (CO), SV and total peripheral resistance to exercise involving cycle ergometry. The mean ˙VO_2max of the trained Cyclists [54 (1.6) ml?·?kg^?1?·?min^?1] was significantly higher (P??1?·?min^?1], whereas both groups possessed a significantly higher ˙VO_2max than the Controls [28 (1.3) ml?·?kg^?1?·?min^?1]. During exercise, at a heart rate of 90 beats?·?min^?1, the SV of the Cyclists increased by 41%, that of the Runners increased by 47%, and that of the Controls increased by 31%. However, the Cyclists' and Runners' SV response was significantly greater than that of the Controls. The SV for cyclists and controls peaked at 30% of ˙VO_2max. This early increase in SV was a major factor underlying the increase in CO during exercise in both the trained and the untrained subjects. In addition, all three groups showed a significant decrease in total peripheral resistance throughout exercise. The finding that older male runners possessed a large exercise SV and high ˙VO_2max suggests that run training results in enhanced cardiovascular performance during cycle ergometry.     

Effect of work and recovery duration on skeletal muscle oxygenation and fuel use during sustained intermittent exercise

The purpose of this study was to compare rates of substrate oxidation in two protocols of intermittent exercise, with identical treadmill speed and total work duration, to reduce the effect of differences in factors such as muscle fibre type activation, hormonal responses, muscle glucose uptake and non-esterified fatty acid (NEFA) availability on the comparison of substrate utilisation. Subjects (n?=?7) completed 40?min of intermittent intense running requiring a work:recovery ratio of either 6?s:9?s (short-interval exercise, SE) or 24?s:36?s (long-interval exercise, LE), on separate days. Another experiment compared O₂ availability in the vastus lateralis muscle across SE (10?min) and LE (10?min) exercise using near-infrared spectroscopy (RunMan, NIM. Philadelphia, USA). Overall (i.e. work and recovery) O₂ consumption (V˙O₂) and energy expenditure were lower during LE (P?P?V˙O_2peak), was [mean (SEM)] 64.9?(2.7)% V˙O_2peak (LE) and 71.4?(2.4)% V˙O_2peak (SE). Fat oxidation was three times lower (P?P?P?P?P?n?=?4) or plasma noradrenaline and adrenaline. Muscle oxygenation declined in both protocols (P?P?r?=?0.68; P?n?=?12). Lower levels of fat oxidation occurred concurrent with accelerated carbohydrate metabolism, increases in lactate and pyruvate and reduced muscle O₂ availability. These changes were associated with proportionately longer work and recovery periods, despite identical treadmill speed and total work duration. The proposal that a metabolic regulatory factor within the muscle fibre retards fat oxidation under these conditions is supported by the current findings.     

The effect of a thiamin derivative on exercise performance

The purpose of this study was to investigate the effect of a thiamin derivative, thiamin tetrahydrofurfuryl disulfide (TTFD), on oxygen uptake (˙VO₂), lactate accumulation and cycling performance during exercise to exhaustion. Using a randomized, double-blind, cross-over design with a 10-day washout between trials, 14 subjects ingested either 1 g?·?day^?1 of TTFD or a placebo (PL) for 4 days. On day 3, subjects performed a progressive exercise test to exhaustion on a cycle ergometer for the determination of ˙VO_2submax, ˙VO_2peak, lactate concentration ([La^??]), lactate threshold (Th_La) and heart rate (?f _c). On day 4, subjects performed a maximal 2000-m time trial on a cycle ergometer. A one-way analysis of variance (ANOVA) with repeated measures was used to determine significant differences between trials. There were no significant differences detected between trials for serial measures of ˙VO_2submax, [La^?] or f _c. Likewise, ˙VO_2peak [PL 4.06 (0.19) TTFD 4.12 (0.19) l?·?min^?1, P?=?0.83], Th_La [PL 2.47 (0.17), TTFD 2.43 (0.16) l?·?min^?1, P?=?0.86] and 2000-m performance time [PL 204.5 (5.5), TTFD 200.9 (4.3)?s, P?=?0.61] were not significantly different between trials. The results of this study suggest that thiamin derivative supplementation does not influence high-intensity exercise performance.     

The effect of a low-carbohydrate diet on performance, hormonal and metabolic responses to a 30-s bout of supramaximal exercise

The aim of this study was to find out whether a low-carbohydrate diet (L-CHO) affects: (1) the capacity for all-out anaerobic exercise, and (2) hormonal and metabolic responses to this type of exercise. To this purpose, eight healthy subjects underwent a 30-s bicycle Wingate test preceded by either 3 days of a controlled mixed diet (130?kJ/kg of body mass daily, 50% carbohydrate, 30% fat, 20% protein) or 3 days of an isoenergetic L-CHO diet (up to 5% carbohydrate, 50% fat, 45% protein) in a randomized order. Before and during 1?h after the exercise venous blood samples were taken for measurement of blood lactate (LA), β-hydroxybutyrate (β-HB), glucose, adrenaline (A), noradrenaline (NA) and insulin levels. Oxygen consumption (V˙O₂) was also determined. It was found that the L-CHO diet diminished the mean power output during the 30-s exercise bout [533 (7)?W vs 581 (7)?W, P??1, P??1, P??1, P??1] were lower. The 1-h post-exercise excess of V˙O₂ [9.1 (0.25)?vs 10.6 (0.25)?l, P??1, P??1 and 14.30 (1.41)?vs 8.20 (1.31)?nmol?·?l^?1, P?相似文献   

Substrate use during and following moderate- and low-intensity exercise: Implications for weight control

Substrate utilization during and after low- and moderate-intensity exercise of similar caloric expenditure was compared. Ten active males [age: 26.9?(4.8) years; height: 181.1?(4.8)?cm; Mass: 75.7?(8.8)?kg; maximum O₂ consumption (V˙O_{2 max} ): 51.2?(4.8)?ml?·?kg^?1?· min^?1] cycled at 33% and 66% V˙O_{2 max} on separate days for 90 and 45 min, respectively. After exercise, subjects rested in a recumbent position for 6?h. Two?h post-exercise, subjects ate a standard meal of 66% carbohydrate (CHO), 11% protein, and 23% fat. Near-continuous indirect calorimetry and measurement of urinary nitrogen excretion were used to determine substrate utilization. Total caloric expenditure was similar for the two trials; however, significantly (P<0.05) more fat [42.4?(3.6)?g versus 24.0?(12.2)?g] and less CHO [142.5?(28.5)?g versus 188.8?(45.2)?g] was utilized as a substrate during the low-intensity compared to the moderate-intensity trial. Protein utilization was similar for the two trials. The difference in substrate use can be attributed to the exercise period because over twice as much fat was utilized during low-intensity [30.0?(11.0)?g] compared to moderate-intensity exercise [13.6?(6.6)?g]. Significantly more (P<0.05) CHO was utilized during the moderate-intensity [106.0?(27.8)?g] compared to the low-intensity exercise [68.7?(20.0)?g]. Substrate use during the recovery period was not significantly different. We conclude that low-intensity, long-duration exercise results in a greater total fat oxidation than does moderate intensity exercise of similar caloric expenditure. Dietary-induced thermogenesis was not different for the two trials.     

Plasma hypoxanthine and ammonia in humans during prolonged exercise

In this study we examined the time course of changes in the plasma concentration of oxypurines [hypoxanthine (Hx), xanthine and urate] during prolonged cycling to fatigue. Ten subjects with an estimated maximum oxygen uptake (V˙O_2max) of 54 (range 47–67) ml?·?kg^?1?·?min^?1 cycled at [mean?(SEM)] 74?(2)% of V˙O_2max until fatigue [79?(8) min]. Plasma levels of oxypurines increased during exercise, but the magnitude and the time course varied considerably between subjects. The plasma concentration of Hx ([Hx]) was 1.3?(0.3)?μmol/l at rest and increased eight fold at fatigue. After 60?min of exercise plasma [Hx] was >10?μmol/l in four subjects, whereas in the remaining five subjects it was <5?μmol/l. The muscle contents of total adenine nucleotides (TAN?=?ATP+ADP+AMP) and inosine monophosphate (IMP) were measured before and after exercise in five subjects. Subjects with a high plasma [Hx] at fatigue also demonstrated a pronounced decrease in muscle TAN and increase in IMP. Plasma [Hx] after 60?min of exercise correlated significantly with plasma concentration of ammonia ([NH₃], r?=?0.90) and blood lactate (r?=?0.66). Endurance, measured as time to fatigue, was inversely correlated to plasma [Hx] at 60?min (r?=??0.68, P?3] or blood lactate. It is concluded that during moderate-intensity exercise, plasma [Hx] increases, but to a variable extent between subjects. The present data suggest that plasma [Hx] is a marker of adenine nucleotide degradation and energetic stress during exercise. The potential use of plasma [Hx] to assess training status and to identify overtraining deserves further attention.     

Decreased exercise blood lactate concentrations after respiratory endurance training in humans

For many years, it was believed that ventilation does not limit performance in healthy humans. Recently, however, it has been shown that inspiratory muscles can become fatigued during intense endurance exercise and decrease their exercise performance. Therefore, it is not surprising that respiratory endurance training can prolong intense constant-intensity cycling exercise. To investigate the effects of respiratory endurance training on blood lactate concentration and oxygen consumption (V˙O₂) during exercise and their relationship to performance, 20?healthy, active subjects underwent 30?min of voluntary, isocapnic hyperpnoea 5 days a week, for 4 weeks. Respiratory endurance tests, as well as incremental and constant-intensity exercise tests on a cycle ergometer, were performed before and after the 4-week period. Respiratory endurance increased from 4.6 (SD 2.5) to 29.1?(SD 4.0)?min (P?P?V˙O₂ did not change at any exercise intensity whereas blood lactate concentration was lower at the end of the incremental [10.4 (SD 2.1) vs 8.8?(SD 1.9)?mmol?·?l^?1, P??1, P?相似文献   

Competitive sustained exercise in humans, lymphokine activated killer cell activity, and glutamine – an intervention study

This study examined whether oral glutamine supplementation abolishes some of the exercise-induced changes in lymphocyte functions following long-term intense exercise. A group of 16 marathon runners participating in The Copenhagen Marathon 1996 were placed randomly in either a placebo (n?=?7) or a glutamine receiving group (n?=?9). Each subject received four doses of either placebo or glutamine (100?mg?·?kg^?1) administered at 0, 30, 60, and 90-min post-race. In the placebo group the plasma glutamine concentrations were lower than pre-race values during the post-exercise period [mean 647 (SEM 32) compared to 470 (SEM 22)?μmol?·?l^?1 90-min post-race, P??1). Glutamine supplementation in vivo had no effect on the lymphokine activated killer (LAK) cell activity, the proliferative responses or the exercise-induced changes in concentrations or percentages of any of the leucocyte subpopulations examined. Glutamine addition in in vitro studies enhanced the proliferative response in both groups. These data would suggest that decreased plasma glutamine concentrations post-exercise are not responsible for exercise-induced decrease in LAK activity and that the influence of glutamine in vitro is not dependent on the plasma glutamine concentration at the time of sampling.     

Dehydration in soldiers during walking/running exercise in the heat and the effects of fluid ingestion during and after exercise

The aim of this study was to examine whether ingesting water alone, or dextrose (7.5?g?·?100?ml^?1) with electrolytes, or fructose/corn solids (7.5?g?·?100?ml^?1) (400?ml every 20?min) would reduce the perceived exertion associated with 16?km (3?h) walking/running in the heat compared with that perceived during exercise with no fluid intake. Perceived exertion was assessed at 1-h intervals during exercise. Blood samples, required for analysis of blood glucose, plasma sodium, plasma osmolality and plasma volume, were obtained prior to exercise and at 1-h intervals during the exercise; further samples were obtained 1-h intervals for 3?h following the exercise. Drinking fluids at regular intervals reduced the level of perceived exertion. In the test during which no fluid was ingested, body mass decreased by 4.9 (0.4)?kg [mean (SEM)], but decreased less with ingestion of either the dextrose/electrolytes or fructose/corn solids solutions, or water alone [1.3 (0.2)?kg, 1.6 (0.3)?kg and 2.0 (0.1)?kg, respectively]. Plasma volume fell by 17% when taking no fluid, but fell less when ingesting fluids. Blood glucose fell significantly (P<0.01) when taking no fluid and rose to 8.4 (1.3)?mmol?·?l^?1 (P<0.001) and 6.8 (1.1) mmol?·?l^?1 (P<0.01) with ingestion of the dextrose/electrolytes or fructose/corn solids solutions, respectively. Urine output was greater with ingestion of water than with any of the other drinks. Six subjects experienced fatigue during exercise with no fluid and failed to complete the exercise. These results suggest that fatigue was caused by several interacting factors: a fall in blood glucose and plasma volume, dehydration, and neuroglycopenia. Taking fluids during exercise reduced the strain and the rating of perceived exertion; this was better achieved by ingesting a dextrose/electrolytes solution.     

Carbon dioxide storage and nonbicarbonate buffering in the human body before and after an Himalayan expedition

Before and 7–12 days after an Himalayan expedition CO₂ equilibration curves were determined in the blood plasma of 12 mountaineers by in vitro and in vivo CO₂ titration; in vivo osmolality changes (ΔOsm?·?ΔPCO₂ ^?1, ΔOsm?·?ΔpH^?1, where PCO₂ is the partial pressure of CO₂) during the latter experiments yielded estimates of whole body CO₂ storage. In vitro ?Δ[HCO₃ ^?]?·?ΔpH^?1 [nonbicarbonate buffer capacity (β) of blood] was increased 7 days after descent [before 31.3 (SEM 0.4) mmol?·?kgH₂O^?1, after?38.3?(SEM 3.9)?mmol?·?kgH₂O^?1; P<0.05] resulting from an increased proportion of young erythrocytes; in additional experiments an augmented β was found in young (low density cells) compared to old cells [<1.097 g?·?ml^?1: 0.216 (SEM 0.028) mmol?·?gHb^?1, >1.100?g?·?ml^?1: 0.145?(SEM 0.013)?mmol?·?gHb^?1, where Hb is haemoglobin; P<0.02]. In spite of increased Hb mass in vivo Δ[CO_2total]?·?ΔPCO₂ ^?1 [0.192?(SEM 0.010)?mmol?·?kgH₂O^?1?·?mmHg^?1] and ?Δ[HCO₃ ^?]?·?ΔpH^?1 [17.9?(SEM 1.0)?mmol?·?kgH₂O^?1] as indicators of extracellular β rose only slightly after altitude (7 days +16%, P<0.02; +7%, NS) because of haemodilution. The ΔOsm?·?ΔPCO₂ ^?1 [0.230?(SEM 0.015) mosmol?·?kgH₂O^?1?·?mmHg^?1] remained unchanged. Prealtitude differences in ΔOsm?·?ΔpH^?1 between hypercapnia [?41?(SEM 5)?mosmol?·?kgH₂O^?1] and hypo-capnia [?20?(SEM 3)?mosmol?·?kgH₂O^?1; P<0.01] disappeared temporarily after return since the former slope was reduced. The high value during hypercapnia before ascent probably resulted from mechanisms stabilizing intracellular pH during moderate hypercapnia which were attenuated after descent.     

Body fluid homeostasis and cardiovascular adjustments during submaximal exercise: influence of chewing coca leaves

The present study was undertaken to determine the haematological and cardiovascular status, at rest and during prolonged (1?h) submaximal exercise (approximately 70% of peak oxygen uptake) in a group (n?=?12) of chronic coca users after chewing approximately 50?g of coca leaves. The results were compared to those obtained in a group (n?=?12) of nonchewers. At rest, coca chewing was accompanied by a significant increase in heart rate [from 60 (SEM?4) TO 76?(SEM?3) beats?·?min^?1], in haematocrit [from 53.2 (SEM 1.2) to 55.6 (SEM 1.1)%] in haemoglobin concentration, and plasma noradrenaline concentration [from 2.8 (SEM?0.4) to 5.0?(SEM?0.5)?μmol?·?l^?1]. It was calculated that coca chewing for 1?h resulted in a significant decrease in blood [?4.3?(SEM?2.2)%] and plasma [?8.7?(SEM?1.2)%] volume. During submaximal exercise, coca chewers displayed a significantly higher heart rate and mean arterial blood pressure. The exercise-induced haemoconcentration was blunted in coca chewers compared to nonchewers. It was concluded that the coca-induced fluid shift observed at rest in these coca chewers was not cumulative with that of exercise, and that the hypovolaemia induced by coca chewing at rest compromised circulatory adjustments during exercise.     

Sex-related differences in thermoregulatory responses while wearing protective clothing

This study examined the thermoregulatory responses of men (group M) and women (group F) to uncompensable heat stress. In total, 13?M [mean (SD) age 31.8 (4.7) years, mass 82.7 (12.5)?kg, height?1.79?(0.06)?m, surface area to mass ratio 2.46?(0.18)?m²?·?kg^?1?·?10^?2, Dubois surface area 2.01 (0.16)?m², %body fatness 14.6 (3.9)%, V˙O_2peak 49.0?(4.8)?ml?·?kg^?1?·?min^?1] and 17 F [23.2 (4.2) years, 62.4 (7.7)?kg, 1.65 (0.07)?m, 2.71 (0.14)?m²?·?kg^?1?·?10^?2, 1.68 (0.13)?m², 20.2 (4.8)%, 43.2 (6.6)?ml?·?kg^?1?·?min^?1, respectively] performed light intermittent exercise (repeated intervals of 15?min of walking at 4.0?km?·?h^?1 followed by 15?min of seated rest) in the heat (40°C, 30% relative humidity) while wearing nuclear, biological, and chemical protective clothing (0.29?m²?·°C · W^?1 or 1.88 clo, Woodcock vapour permeability coefficient 0.33?i _m). Group F consisted of eight non-users and nine users of oral contraceptives tested during the early follicular phase of their menstrual cycle. Heart rates were higher for F throughout the session reaching 166.7 (15.9) beats?·?min^?1 at 105?min (n?=?13) compared with 145.1 (14.4)?beats?·?min^?1 for M. Sweat rates and evaporation rates from the clothing were lower and average skin temperature ( ) was higher for F. The increase in rectal temperature (T _re) was significantly faster for the F, increasing 1.52 (0.29)°C after 105?min compared with an increase of 1.37?(0.29)°C for M. Tolerance times were significantly longer for M [142.9?(24.5)?min] than for F [119.3?(17.3)?min]. Partitional calorimetric estimates of heat storage (S) revealed that although the rate of S was similar between genders [42.1?(6.6) and 46.1?(9.7) W?·?m^?2 for F and M, respectively], S expressed per unit of total mass was significantly lower for F [7.76?(1.44)?kJ?·?kg^?1] compared with M [9.45?(1.26) kJ?·?kg^?1]. When subjects were matched for body fatness (n?=?8?F and 8?M), tolerance times [124.5?(14.7) and 140.3?(27.4)?min for F and M, respectively] and S [8.67?(1.44) and 9.39?(1.05)?kJ?·?kg^?1 for F and M, respectively] were not different between the genders. It was concluded that females are at a thermoregulatory disadvantage compared with males when wearing protective clothing and exercising in a hot environment. This disadvantage can be attributed to the lower specific heat of adipose versus non-adipose tissue and a higher percentage body fatness.     

Detection of the change point in oxygen uptake during an incremental exercise test using recursive residuals: relationship to the plasma lactate accumulation and blood acid base balance

The purpose of this study was to develop a method to determine the power output at which oxygen uptake (V˙O₂) during an incremental exercise test begins to rise non-linearly. A group of 26 healthy non-smoking men [mean age 22.1?(SD 1.4)?years, body mass 73.6?(SD 7.4)?kg, height 179.4?(SD 7.5)?cm, maximal oxygen uptake (V˙O_2max) 3.726?(SD 0.363)?l?·?min^?1], experienced in laboratory tests, were the subjects in this study. They performed an incremental exercise test on a cycle ergometer at a pedalling rate of 70?rev?·?min^?1. The test started at a power output of 30?W, followed by increases amounting to 30?W every 3?min. At 5?min prior to the first exercise intensity, at the end of each stage of exercise protocol, blood samples (1?ml each) were taken from an antecubital vein. The samples were analysed for plasma lactate concentration [La]_pl, partial pressure of O₂ and CO₂ and hydrogen ion concentration [H⁺]_b. The lactate threshold (LT) in this study was defined as the highest power output above which [La^?]_pl showed a sustained increase of more than 0.5?mmol?·?l^?1?·?step^?1. The V˙O₂ was measured breath-by-breath. In the analysis of the change point (CP) of V˙O₂ during the incremental exercise test, a two-phase model was assumed for the 3rd-min-data of each step of the test: X _i =at _i +b+? _i for i=1,2,…,T, and E(X _i )>at _i +b for i =T+1,…,n, where X ₁, … , X _n are independent and ? _i ～N(0,σ²). In the first phase, a linear relationship between V˙O₂ and power output was assumed, whereas in the second phase an additional increase in V˙O₂ above the values expected from the linear model was allowed. The power output at which the first phase ended was called the change point in oxygen uptake (CP-V˙O₂). The identification of the model consisted of two steps: testing for the existence of CP and estimating its location. Both procedures were based on suitably normalised recursive residuals. We showed that in 25 out of 26 subjects it was possible to determine the CP- O₂ as described in our model. The power output at CP-V˙O₂ amounted to 136.8?(SD 31.3)?W. It was only 11?W – non significantly – higher than the power output corresponding to LT. The V˙O₂ at CP-V˙O₂ amounted to 1.828?(SD 0.356)?l?·?min^?1 was [48.9?(SD 7.9)% V˙O_{2 max} ]. The [La^?]_pl at CP-V˙O₂, amounting to 2.57?(SD 0.69)?mmol?·?l^?1 was significantly elevated (P<0.01) above the resting level [1.85?(SD 0.46)?mmol?·?l^?1], however the [H⁺]_b at CP-V˙O₂ amounting to 45.1 (SD 3.0)?nmol?·?l^?1, was not significantly different from the values at rest which amounted to 44.14?(SD 2.79)?nmol?·?l^?1. An increase of power output of 30?W above CP-V˙O₂ was accompanied by a significant increase in [H⁺]_b above the resting level (P=0.03).     

Effects of decreased plasma glutamine concentrations on peripheral lymphocyte proliferation in rats

The relationship between exercise-induced lowering of plasma glutamine concentrations and proliferation of peripheral lymphocytes was investigated in male Wistar rats. The T-lymphocyte proliferative responses to the mitogen, concanavalin A, were determined by incorporation of radiolabelled thymidine into the DNA in vitro. The rats ran 2 h?·?day^?1, 6 days?· week^?1 for 4 weeks. Analysis immediately after the final period of exercise showed T-lymphocyte proliferation to be significantly depressed, together with a marked decrease in plasma glutamine concentrations. There were also significant increases in serum corticosterone concentrations immediately after exercise. However, following 24-h recovery, this exercise-induced immunosuppression was not statistically significant when compared with the age-matched control group. In the second experiment, in order to clarify the importance of glutamine for immunological function in vivo, methionine sulfoximine, an effective inhibitor of glutamine synthetase was injected intraperitoneally (12.5 mg?·?kg body mass^?1). Plasma glutamine concentrations were decreased 4 h after the injection, compared with the placebo control group, and this resulted in a significant decrease in the rate of T-lymphocyte proliferation. This treatment had no effects on serum corticosterone concentrations. These results would suggest that the chronic exercise-induced reduction in proliferation of peripheral T-lymphocytes is a transient reversible phenomenon, which returns to normal levels within 24 h of the final training period. It is also conceivable that this exercise-induced immunosuppression is associated with a decrease in circulating glutamine concentrations.     

A comparison of skeletal muscle oxygenation and fuel use in sustained continuous and intermittent exercise

In this study we compared substrate oxidation and muscle oxygen availability during sustained intermittent intense and continuous submaximal exercise with similar overall (i.e. work and recovery) oxygen consumption (V˙O₂). Physically active subjects (n?=?7) completed 90?min of an intermittent intense (12?s work:18?s recovery) and a continuous submaximal treadmill running protocol on separate days. In another experiment (n?=?5) we compared oxygen availability in the vastus lateralis muscle between these two exercise protocols using near-infrared spectroscopy. Initially, overall V˙O₂ (i.e. work and recovery) was matched, and from 37.5?min to 67.5?min of exercise was similar, although slightly higher during continuous exercise (8%; P??1?·?kg^?1] and continuous submaximal [0.85 (0.01)?kJ?·?min^?1?·?kg^?1] exercise. Overall exercise intensity, represented as a proportion of peak aerobic power (V˙O_2peak), was 68.1 (2.5)% V˙O_2peak and 71.8 (1.8)% V˙O_2peak for intermittent and continuous exercise protocols, respectively. Fat oxidation was almost 3 times lower (P?P?P?P?P?r?=?0.72; P?V˙O₂ and identical energy expenditure.     

The Impact of heat exposure and repeated exercise on circulating stress hormones

To determine if heat exposure alters the hormonal responses to moderate, repeated exercise, 11 healthy male subjects [age?=?27.1 (3.0) years; maximal oxygen consumption, V˙O_2max?=?47.6 (6.2) ml?·?kg?· min^?1; mean (SD)] were assigned to four different experimental conditions according to a randomized-block design. While in a thermoneutral (23°C) or heated (40°C, 30% relative humidity) climatic chamber, subjects performed either cycle ergometer exercise (two 30-min bouts at ≈50% V˙O_2max, separated by a 45-min recovery interval, CEx and HEx conditions), or remained seated for 3?h (CS and HS conditions). Blood samples were analyzed for various exercise stress hormones [epinephrine (E), norepinephrine (NE), dopamine, cortisol and human growth hormone (hGH)]. Passive heating did not alter the concentrations of any of these hormones significantly. During both environmental conditions, exercise induced significant (P < 0.001) elevations in plasma E, NE and hGH levels. At 23°C during bout 1: E?=?393 (199) pmol?·?l^?1 (CEx) vs 174 (85) pmol?·?l^?1 (CS), NE?=?4593 (2640) pmol?·?l^?1 (CEx) vs 1548 (505) pmol?·?l^?1 (CS), and hGH?=?274 (340) pmol?·?l^?1 (CEx)vs 64 (112) pmol?·?l^?1 (CS). At 40°C, bout 1: E?=?596 (346) pmol?·?l^?1 (HEx) vs 323 (181) pmol?·?l^?1 (HS), NE?=?7789 (5129) pmol?·?l^?1 (HEx) vs 1527 (605) pmol?·?l^?1 (HS), and hGH?=?453 (494) pmol?·?l^?1 (HEx) vs 172 (355) pmol?·?l^?1 (HS). However, concentrations of plasma cortisol were increased only in response to exercise in the heat [HEx?=?364 (168) nmol?·?l^?1 vs HS?=?295 (114) nmol?·?l^?1). Compared to exercise at room temperature, plasma levels of E, NE and cortisol were all higher during exercise in the heat (P < 0.001 in all cases). The repetition of exercise did not significantly alter the pattern of change in cortisol or hGH levels in either environmental condition. However, repetition of exercise in the heat increased circulatory and psychological stress, with significantly (P < 0.001) higher plasma concentrations of E and NE. These results indicate a differential response of the various stress hormones to heat exposure and repeated moderate exercise.     

Effect of repeated bouts of short-term exercise on plasma free and sulphoconjugated catecholamines in humans

We tested the hypothesis that measurement of plasma catecholamine sulphate concentration after exercise reflects the overall activation of the sympathoadrenergic system during the whole period of repeated bouts of short-term exercise. A group of 11 male athletes performed two exercise tests at similar average power outputs consisting of three sets each. The tests either started with one set of three very intense sprints (95% of maximal running speed) followed by two sets of three less intense sprints (85% of maximal running speed; HLX) or vice versa (LHX). Similar mean areas under the curve of free noradrenaline (NA) during HLX and LHX [622 (SEM 13) vs 611 (SEM 14) nmol?·?l^?1?·?min) as well as similar mean heart rates [143 (SEM 9) vs 143 (SEM 8) beats?·?min^?1] indicated comparable sympathetic activation during both exercise tests. Even so, plasma concentration of free NA was still significantly higher at the end of LHX than of HLX [35.7 (SEM 3.5) vs 22.5 (SEM 2.1) nmol?·?l^?1, respectively], i.e. when exercise ended with the more intense set of sprints. Plasma noradrenaline sulphate (NA-S) increased with exercise intensity showing higher mean increments after the first set of HLX compared to LHX [1.83 (SEM 0.42) vs 1.18 (SEM 0.29) nmol?·?l^?1; P?0.05]. However, after the end of HLX and LHX, increments in plasma NA-S were similar [4.52 (SEM 0.76) vs 4.06 (SEM 0.79) nmol?·?l^?1], suggesting that NA-S response changed in parallel with the overall activation of the sympathetic nervous system during repeated bouts of short-term exercise. The results supported the hypothesis that measurement of plasma NA-S immediately after repeated bouts of short-term exercise reflects overall activation of the sympathetic nervous system during prolonged periods of this type of exercise.