Glycogen breakdown in different human muscle fibre types during exhaustive exercise of short duration

The rates of glycogen breakdown during exhaustive intense exercise of three different intensities were determined in type I and subgroups of type II fibres. The exercise intensity corresponded to 122 ± 2 , 150 ± 7 and 194 ± 7% of Vo_2max. Muscle biopsies were taken from both legs before and immediately after exhaustion. Muscle lactate concentration increased by 27 ± 1 , 27 ± 1 and 20 ± 2 mmolkg^-1 wet wt during the exercise at 122 , 150 and 194%Vo_2max, respectively. The rates of glycogen depletion increased in all fibre types with increasing intensity, and the decline in type I fibres was 30–35% less than in type II fibres at all intensities. No differences were observed between the glycogen depletion rates in subgroups of type II fibres (IIA, IIAB and IIB). During the exercise at 194% Vo_2max, the rates of glycogen breakdown were 0.35 ± 0.03 and 0.52 ± 0.05 mmol s^-1 kg^-1 wet wt in type I and type II fibres, respectively. For both fibre types, the rates were 32 and 69% lower during the exercise at 150 and 12296 VO_2max. These data indicate that the glycolytic capacity of type I fibres is 30–35% lower than the capacity of type II fibres, in good agreement with the differences in phosphorylase and phosphofructokinase activities (Essén et al. 1 975 , Harris et al. 1976). The data also indicate that both fibre types contribute significantly to the anaerobic energy release at powers up till almost 200%Vo_2max.     

Splanchnic and renal vasoconstrictor and metabolic responses to neuropeptide Y in resting and exercising man

The local clearance of neuropeptide Y (NPY) and whether NPY influences splanchnic and renal metabolism in man have not been investigated previously. The influence of NPY on splanchnic and renal blood flows at physiologically elevated levels has also not been investigated. The effects of a 40-min constant NPY infusion (3 pmol kg^-1 min^-1) at rest and during 130 min of exercise (50% of Vo_2max) were studied in six healthy subjects and compared with resting and exercising subjects receiving no NPY. Blood samples were drawn from arterial, hepatic and renal vein catheters for the determination of blood flows (indicators: cardiogreen and paraaminohippuric acid [PAH]), NPY, catecholamines, glucose, lactate and glycerol. NPY infusion was accompanied by: (1) significant fractional extraction of NPY-like immunoreactivity (NPY-Li) by splanchnic tissues at rest (58±5%) and during exercise (53±6%), while no arterial–venous differences could be detected across the kidney; (2) a reduction in splanchnic and renal blood flows of up to 18 and 13% respectively (P < 0.01–0.001) at rest without any additional changes during exercise; and (3) metabolic changes as reflected in: (a) a more marked fall in arterial glucose during exercise compared to the reference group (P < 0.05); (b) a 35% lower splanchnic glucose release (P < 0.01) during exercise due to diminished glycogenolysis (P < 0.01); and (c) a lower arterial lactate level (18%P < 0.05) together with unchanged splanchnic lactate uptake during exercise, suggesting reduced lactate production by extrahepatic tissues. The disappearance of plasma NPY-Li after the infusions was biphasic with two similar half-lives at rest (4 and 39 min) and during exercise (3 and 43 min).     

Effect of anaesthetizing the region of the paraventricular hypothalamic nuclei on energy metabolism during exercise in the rat

The ventromedial and posterior hypothalamic nuclei are known to influence glucoregulation during exercise. The extensive projections of the paraventricular hypothalamic nucleus (PVN) to the sympathetic nervous system suggest that the PVN also may be involved in glucoregulation during exercise. The region of the PVN was anaesthetized with bupivacaine before running (26 m min^-1) or continued rest, via previously implanted bilateral brain cannulas aimed at the dorsal aspect of the PVN. Control rats were treated identically to PVN-anaesthetized rats, but were not infused. Blood, for determination of plasma concentrations of metabolites and hormones, was drawn from a tail artery, and ³H-glucose was infused in a tail vein for glucose turnover determinations. At rest, no significant changes in plasma concentrations of metabolites or hormones were induced by anaesthesia of the region of the PVN. During exercise, glucose production and utilization and plasma concentrations of glucose, lactate, glycerol, noradrenaline, adrenaline, corticosterone, and glucagon increased (P < 0.02) and plasma insulin decreased (P < 0.02) in all rats. However, initially in exercise, adrenaline (4.3 ±0.8 vs. 7.9 ± 1.0 nmol 1^-1 in controls, P < 0.05, t= 6 min) and later corticosterone levels (1.37 ± 0.06 vs. 1.69 ± 0.10 nmol 1^-1 in controls, P < 0.05, t = 20 min) were attenuated by PVN anaesthesia. Initially during exercise, glucose utilization was higher and plasma glucose lower in PVN-anaesthetized rats compared to controls (16.6 ± 0.8 vs. 12.7 ± 0.6 μmol min^-1 100 g^-1 and 7.1 ± 0.2 vs. 8.1 ± 0.2 mmol 1^-1, respectively. P < 0.05, t= 6 min) and exercise-induced liver glycogen breakdown was only significant in the controls. In conclusion, the region of the PVN does not influence glucoregulation at rest, but affects glucoregulation during exercise, by stimulating adrenaline and corticosterone secretion during exercise.     

The effect of exercise on postprandial lipidemia in type 2 diabetic patients

To elucidate if postprandial exercise can reduce the exaggerated lipidemia seen in type 2 diabetic patients after a high-fat meal. Two mornings eight type 2 diabetic patients (males) (58 ± 1.2 years, BMI 28.0 ± 0.9 kg m⁻²) and seven non-diabetic controls ate a high-fat breakfast (680 kcal m⁻², 84% fat). On one morning, 90 min later subjects cycled 60 min at 57% . Biopsies from quadriceps muscle and abdominal subcutaneous adipose tissue were sampled after exercise or equivalent period of rest and arterialized blood for 615 min. Postprandial increases in serum total-triglyceride (TG) (incremental AUC: 1,702 ± 576 vs. 341 ± 117 mmol l⁻¹ 600 min), chylomicron-TG (incremental AUC: 1,331 ± 495 vs. 184 ± 55 mmol l⁻¹ 600 min) and VLDL-TG as well as in insulin (incremental AUC: 33,946 ± 7,414 vs. 13,670 ± 3,250 pmol l⁻¹ 600 min), C-peptide and glucose were higher in diabetic patients than in non-diabetic controls (P < 0.05). In diabetic patients these variables were reduced (P < 0.05) by exercise (total-TG incremental AUC being 1,110 ± 444, chylomicron-TG incremental AUC 1,043 ± 474 mmol l⁻¹ 600 min and insulin incremental AUC 18,668 ± 4,412 pmol l⁻¹ 600 min). Lipoprotein lipase activity in muscle (11.0 ± 2.0 vs. 24.1 ± 3.4 mU g per wet weight, P < 0.05) and post-heparin plasma at 615 min were lower in diabetic patients than in non-diabetic controls, but did not differ in adipose tissue and did not change with exercise. In diabetic patients, 210 min after exercise oxygen uptake (P < 0.05) and fat oxidation (P < 0.1) were still higher than on non-exercise days. In type 2 diabetic patients, after a high-fat meal exercise reduces the plasma concentrations of triglyceride contained in both chylomicrons and VLDL as well as insulin secretion. This suggests protection against progression of atherosclerosis and diabetes.     

Exercise and myocardial tolerance to ischaemia‐reperfusion

It is well established that both short‐term (1–5 days) and long‐term (weeks to months) high intensity exercise (i.e. 70–75%VO_2max) provides cardioprotection against ischaemia‐reperfusion injury. However, it is unclear if moderate intensity exercise will also provide cardioprotection. Aim: Therefore, these experiments compared the protective effects of moderate vs. high intensity exercise in providing defense against ischaemia‐reperfusion injury. Methods: Male Sprague–Dawley rats were randomly assigned to one of three‐experimental groups: (1) sedentary (control); (2) moderate intensity treadmill exercise (60 min day^?1 at ～55%VO_2max); or (3) high intensity treadmill exercise (60 min day^?1 at ～75%VO_2max). Hearts were exposed to 20 min of global ischaemia followed by 30 min reperfusion in an isolated working heart preparation. Results: Compared with sedentary rats, both moderate and high intensity exercised rats maintained a higher (P < 0.05) percentage of pre‐ischaemia cardiac output and cardiac work (cardiac output × systolic blood pressure) during reperfusion. No differences in the percent recovery of cardiac output and heart work existed (P > 0.05) between the two exercise groups. Conclusions: These data reveal that both moderate and high intensity exercise training provide equivalent protection against ischaemia‐reperfusion injury.     

Effect of arm-cranking on leg blood flow and noradrenaline spillover during leg exercise in man

Controversy exists whether recruitment of a large muscle mass in dynamic exercise may outstrip the pumping capacity of the heart and require neurogenic vasoconstriction in exercising muscle to prevent a fall in arterial blood pressure. To elucidate this question, seven healthy young men cycled for 70 minutes at a work load of 5540%VO_2max. At 30 to 50 minutes, arm cranking was added and total work load increased to (mean ± SE) 82 ± 4% of Vo_2max. During leg exercise, leg blood flow average 6.15 4.511 minutes^-1, mean arterial blood pressure 137 ± 4 mmHg and leg conductance 42.3 ± 2.2 ml minutes^-1 mmHg^-1. When arm cranking was added to leg cycling, leg blood flow did not change significantly, mean arterial blood pressure increased transiently to 147 ± 5 mmHg and leg vascular conductance decreased transiently to 33.5 ± 3.1 ml minutes^-1 mmHg^-1. Furthermore, arm cranking doubled leg noradrenaline spillover. When arm cranking was discontinued and leg cycling continued, leg blood flow was unchanged but mean arterial blood pressure decreased to values significantly below those measured in the first leg exercise period. Furthermore, leg vascular conductance increased transiently, and noradrenaline spillover decreased towards values measured during the first leg exercise period. It is concluded that addition of arm cranking to leg cycling increases leg noradrenaline spillover and decreases leg vascular conductance but leg blood flow remains unchanged because of a simultaneous increase in mean arterial blood pressure. The decrease in leg vascular conductance observed when arm cranking increased mean arterial blood pressure could be regarded more as a measure to prevent overperfusion than a measure to maintain arterial blood pressure.     

Fuel substrate turnover and oxidation and glycogen sparing with carbohydrate ingestion in non-carbohydrate-loaded cyclists

This study examined the effects of ingesting 500 ml/h of either a 10% carbohydrate (CHO) drink (CI) or placebo (PI) on splanchnic glucose appearance rate (endogenous + exogenous) (R _a), plasma glucose oxidation and muscle glycogen utilisation in 17, non-carbohydrate-loaded, male, endurance-trained cyclists who rode for 180 min at 70% of maximum oxygen uptake. Mean muscle glycogen content at the start of exercise was 130 ± 6 mmol/kg ww; (mean ± SEM). Total CHO oxidation was similar in CI and PI subjects and declined during the trial. R _a increased significantly during the trial (P < 0.05) in both groups. Plasma glucose oxidation also increased significantly during the trial, reaching a plateau in the PI subjects, but was significantly (P < 0.05) higher in CI than PI subjects at the end of exercise [(98 ± 14 vs. 72 ± 10 μmol/min/kg fat-free mass) (FFM) (1.34 ± 0.19 vs. 0.93 ± 0.13 g/min)]. However, mean endogenous R _a was significantly (P < 0.05) lower in the CI than PI subjects throughout exercise (35 ± 7 vs. 54 ± 6 μmol/min/kg FFM), as was the oxidation of endogenous plasma glucose, which remained almost constant in CI subjects, and reached values at the end of exercise of 42 ± 13 and 72 ± 10 μmol/min/kg FFM in the CI and PI groups respectively. Of the 150 g CHO ingested during the trial, 50% was oxidised. Muscle glycogen disappearance was identical during the first 2 h of exercise in both groups and continued at the same rate in PI subjects, however no net muscle glycogen disappearance occurred during the final hour in CI subjects. We conclude that ingestion of 500 ml/h of a 10% CHO solution during prolonged exercise in non carbohydrate loaded subjects has a marked liver glycogen-sparing effect or causes a reduction in gluconeogenesis, or both, maintains plasma glucose concentration and has a muscle glycogen-sparing effect. Received: 25 August 1995/Received after revision: 25 March 1996/Accepted: 29 April 1996     

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   

Maximal voluntary hyperpnoea increases blood lactate concentration during exercise

Ventilatory work during heavy endurance exercise has not been thought to influence systemic lactate concentration. We evaluated the effect of maximal isocapnic volitional hyperpnoea upon arterialised venous blood lactate concentration ([lac⁻]_B) during leg cycling exercise at maximum lactate steady state (MLSS). Seven healthy males performed a lactate minimum test to estimate MLSS, which was then resolved using separate 30 min constant power tests (MLSS=207±8 W, mean ± SEM). Thereafter, a 30 min control trial at MLSS was performed. In a further experimental trial, the control trial was mimicked except that from 20 to 28 min maximal isocapnic volitional hyperpnoea was superimposed on exercise. Over 20–28 min minute ventilation, oxygen uptake, and heart rate during the control and experimental trials were 87.3±2.4 and 168.3±7.0 l min⁻¹ (P<0.01), the latter being comparable to that achieved in the maximal phase of the lactate minimum test (171.9±6.8 l min⁻¹), 3.46±0.20 and 3.83 ± 0.20 l min⁻¹ (P<0.01), and 158.5±2.7 and 166.8±2.7 beats min⁻¹ (P<0.05), respectively. From 20 to 30 min of the experimental trial [lac⁻]_B increased from 3.7±0.2 to 4.7±0.3 mmol l⁻¹ (P<0.05). The partial pressure of carbon dioxide in arterialised venous blood increased approximately 3 mmHg during volitional hyperpnoea, which may have attenuated the [lac⁻]_B increase. These results show that, during heavy exercise, respiratory muscle work may affect [lac⁻]_B. We speculate that the changes observed were related to the altered lactate turnover in respiratory muscles, locomotor muscles, or both.     

The effects of 24 weeks of moderate- or high-intensity exercise on insulin resistance

This study was designed to investigate the effect of exercise intensity on insulin resistance by comparing moderate- and high-intensity interventions of equal energy cost. Maximum oxygen consumption (VO_2max), insulin, glucose and triglycerides were measured in 64 sedentary men before random allocation to a non-exercise control group, a moderate-intensity exercise group (three 400-kcal sessions per week at 60% of VO_2max) or a high-intensity exercise group (three 400-kcal sessions per week at 80% of VO_2max). An insulin sensitivity score was derived from fasting concentrations of insulin and triglycerides, and insulin resistance was assessed using the homeostasis model assessment of insulin resistance (HOMA-IR). Data were available for 36 men who finished the study. After 24 weeks, insulin concentration decreased by 2.54±4.09 and 2.37±3.35 mU l⁻¹, insulin sensitivity score increased by 0.91±1.52 and 0.79±1.37, and HOMA-IR decreased by −0.6±0.8 and −0.5±0.8 in the moderate- and high-intensity exercise groups, respectively. When data from the exercise groups were combined, one-way analysis of variance with one-tailed post hoc comparisons indicated that these changes were significantly greater than those observed in the control group (all P<0.05). Twenty-four week changes in insulin concentration, insulin sensitivity score and HOMA-IR were not significantly different between the exercise groups. These data suggest that exercise training is accompanied by a significant reduction in insulin resistance, as indicated by well-validated surrogate measures. These data also suggest that moderate-intensity exercise is as effective as high-intensity exercise when 400 kcal are expended per session.     

Effects of glucose ingestion or glucose infusion on fuel substrate kinetics during prolonged exercise

To determine if bypassing both intestinal absorption and hepatic glucose uptake by intravenous glucose infusion might increase the rate of muscle glucose oxidation above 1 g · min^–1, ten endurance-trained subjects were studied during 125 min of cycling at 70% of peak oxygen uptake (VO_{2 peak}). During exercise the subjects ingested either a 15 g · 100 ml^–1 U-¹⁴C labelled glucose solution or H₂O labelled with a U-¹⁴C glucose tracer for the determination of the rates of plasma glucose oxidation (Rox) and exogenous carbohydrate (CHO) oxidation from plasma¹⁴C glucose and¹⁴CO₂ specific activities, and respiratory gas exchange. Simultaneously, 2-³H glucose was infused at a constant rate to measure glucose turnover, while unlabelled glucose (25% dextrose) was infused into those subjects not ingesting glucose to maintain plasma glucose concentration at 5 mmol · l^–1. Despite similar plasma glucose concentrations [ingestion 5.3 (SEM 0.13) mmol · l^–1; infusion 5.0 (0.09) mmol · l^–1], compared to glucose infusion, CHO ingestion significantly increased plasma insulin concentrations [12.9 (1.0) vs 4.8 (0.5) mU · l^–1;P<0.05], raised total Rox values [9.5 (1.2) vs 6.2 (0.7) mmol · 125 min^–1 kg fat free mass^–1 (FFM);P<0.05] and rates of CHO oxidation [37.2 (2.8)vs 24.1 (3.9) mmol · 125 min^–1 kg FFM^–1;P<0.05]. An increased reliance on CHO metabolism with CHO ingestion was associated with a decrease in fat oxidation. Whereas the contribution from fat oxidation to energy production increased to 51 (10)% with glucose infusion, it only reached 18 (4)% with glucose ingestion (P<0.05). Despite these differences in plasma insulin concentration and rates of fat oxidation, the rates of glucose oxidation by muscle were similar after 125 min of exercise for both trials [ingestion 93 (8); infusion 85 (5) mol · min^–1 kg FFM^–1], suggesting that peak rates of muscle glucose oxidation were primarily dependent on blood glucose concentration which, in turn, regulated the hepatic appearance of ingested CHO.     

Reducing plasma free fatty acids by acipimox improves glucose tolerance in high‐fat fed mice

To study whether free fatty acids (FFAs) contribute to glucose intolerance in high‐fat fed mice, the derivative of nicotinic acid, acipimox, which inhibits lipolysis, was administered intraperitoneally (50 mg kg^?1) to C57BL/6J mice which had been on a high‐fat diet for 3 months. Four hours after administration of acipimox, plasma FFA levels were reduced to 0.46 ± 0.06 mmol L^?1 compared with 0.88 ± 0.10 mmol L^?1 in controls (P < 0.001). At this point, the glucose elimination rate after an intravenous glucose load (1 g kg^?1) was markedly improved. Thus, the elimination constant (K_G) for the glucose disposal between 1 and 50 min after the glucose challenge was increased from 0.54 ± 0.01% min^?1 in controls to 0.66 ± 0.01% min^?1 by acipimox (P < 0.001). In contrast, the acute insulin response to glucose (1–5 min) was not significantly different between the groups, although the area under the insulin for the entire 50‐min period after glucose administration was significantly reduced by acipimox from 32.1 ± 2.9 to 23.9 ± 1.2 nmol L^?1 × 50 min (P=0.036). This, however, was mainly because of lower insulin levels at 20 and 50 min because of the lowered glucose levels. In contrast, administration of acipimox to mice fed a normal diet did not affect plasma levels of FFA or the glucose elimination or insulin levels after the glucose load. It is concluded that reducing FFA levels by acipimox in glucose intolerant high‐fat fed mice improves glucose tolerance mainly by improving insulin sensitivity making the ambient islet function adequate, suggesting that increased FFA levels are of pathophysiological importance in this model of glucose intolerance.     

The acute effect of 30 min of moderate exercise on high density lipoprotein cholesterol in untrained middle-aged men

Summary Fifteen middle-aged, untrained (defined as no regular exercise) men (mean age 49.9 years, range 42–67) cycled on a cycle ergometer at 50 rpm for 30 min at an intensity producing 60% predicted maximum heart rate [(f _c,max), wheref _{c, max} = 220 - age]. Total cholesterol (TC), high-density lipoprotein cholesterol (HDL-C), low-density lipoprotein cholesterol (LDL-C) and triglyceride (Tg) concentrations were measured from fasting fingertip capillary blood samples collected at rest, after 15 and 30 min of exercise, and at 15 min post-exercise. The mean HDL-C level increased significantly from the resting level of 0.85 mmol · l^–1 to 0.97 mmol · 1^–1 (P<0.05) after 15 min of exercise, increased further to 1.08 mmol · 1^–1 (P<0.01) after 30 min of exercise and remained elevated at 1.07 mmol · 1^–1 (P<0.01) at 15 min post-exercise. These increases represented changes above the mean resting level of 14.1%, 27.1% and 25.9% respectively. The HDL-C/LDL-C ratio increased significantly from a resting ratio of 0.20 to 0.26 after 30 min of exercise (P < 0.01) and to 0.24 at 15 min post-exercise (P<0.05). The mean Tg level increased significantly from a resting level of 0.88 mmol · 1^–1 to 1.05 mmol · 1^–1 after 15 min, and to 1.06 mmol · I^–1 after 30 min of exercise (P<0.05 at each time). The TC/HDL-C ratio decreased significantly (P=0.05) after 30 min of exercise and at 15 min post-exercise by 18.8% and 14%, respectively. No significant changes were observed in the levels of TC or LDL-C over time. These results indicate that 30 min of moderate exercise elicits significant changes in HDL-C concentration during and up to 15 min after the exercise in untrained middle-aged men with low mean resting levels of HDL-C (0.85 mmol · 1^–1).     

Characterization of sports by the Vo2 dynamics of athletes in response to sinusoidal work load

The purpose of this study was to evaluate the specificity of maximal oxygen uptake (Vo_2max) and the dynamic response of oxygen uptake (Vo₂) to sinusoidal work load in distance runners and in American-football players. Sinusoidal work load during ergometer cycling was carried from 30 W to 60% to Vo_2max(60% Vo_2max) for a 2 min period. Vo₂ was measured by the breath-by-breath method. The subjects were 10 distance runners (DRs), 10 American-football players (AFPs), and 11 untrained men (UTM). Mean Vo_2max was 64.4 mL kg^-1 min^-1 in the DRs, 53.1 mL kg^-1 min^-1 in the AFPs and 47.3 mL kg^-1 min^-1 in the UTM. The fundamental amplitudes ofthe Vo₂ response, nomalized by dividing by steady state Vo₂ at 60% Vo_2max were similar in the AFPs (20.3%) and the UTM (19.5%), and both were significantly less than in the DRs (25.5%). Phase shift to work load expressed in degrees was similar in the AFPs (87.7d?) and UTM (88.0d?), but significantly greater than in the DRs (80.4d?). HR dynamics in all three groups were similar to a dynamic Vo₂ response. These findings suggest that development of the dynamic Vo₂ response and higher Vo_2max in the AFPs there is no improvement in the dynamic Vo₂ response. The results of the present study demonstrate that athletes participating in different sports have characteristic dynamic Vo₂ responses during cycling exercise.     

Effects of acute carbohydrate supplementation during sessions of high-intensity intermittent exercise

Abs tract The present study evaluated the acute effects of carbohydrate supplementation on heart rate (HR), rate of perceived exertion (RPE), metabolic and hormonal responses during and after sessions of high-intensity intermittent running exercise. Fifteen endurance runners (26 ± 5 years, 64.5 ± 4.9 kg) performed two sessions of intermittent exercise under carbohydrate (CHO) and placebo (PLA) ingestion. The sessions consisted of 12 × 800 m separated by intervals of 1 min 30 s at a mean velocity corresponding to the previously performed 3-km time trial. Both the CHO and PLA sessions were concluded within ∼28 min. Blood glucose was significantly elevated in both sessions (123.9 ± 13.2 mg dl⁻¹ on CHO and 147.2 ± 16.3 mg dl⁻¹ on PLA) and mean blood lactate was significantly higher in the CHO (11.4 ± 4.9 mmol l⁻¹) than in the PLA condition (8.4 ± 5.1 mmol l⁻¹) (P < 0.05). The metabolic stress induced by the exercise model used was confirmed by the elevated HR (∼182 bpm) and RPE (∼18 on the 15-point Borg scale) for both conditions. No significant differences in plasma insulin, cortisol or free fatty acids were observed during exercise between the two trials. During the recovery period, free fatty acid and insulin concentrations were significantly lower in the CHO trial. Supplementation with CHO resulted in higher lactate associated with lipolytic suppression, but did not attenuate the cortisol, RPE or HR responses.     

Contribution of pH,diprotonated phosphate and potassium for the reflex increase in blood pressure during handgrip

The relative importance of pH, diprotonated phosphate (H₂PO₄^?) and potassium (K⁺) for the reflex increase in mean arterial pressure (MAP) during exercise was evaluated in seven subjects during rhythmic handgrip at 15 and 30% maximal voluntary contraction (MVC), followed by post-exercise muscle ischaemia (PEMI). During 15% MVC, MAP rose from 92 ± 1 to 103 ± 2 mmHg, [K⁺] from 4.1 ± 0.1 to 5.1 ± 0.1 mmol L^?1, while the intracellular (7.00 ± 0.01 to 6.80 ± 0.06) and venous pH fell (7.39 ± 0.01 to 7.30 ± 0.01) (P < 0.05). The intracellular [H₂PO₄^?] increased 8.4 ± 2 mmol kg^?1 and the venous [H₂PO₄^?] from 0.14 ± 0.01 to 0.16 ± 0.01 mmol L^?1 (P < 0.05). During PEMI, MAP remained elevated along with the intracellular [H₂PO₄^?] as well as a low intracellular and venous pH. However, venous [K⁺] and [H₂PO₄^?] returned to the level at rest. During 30% MVC handgrip, MAP rose to 130 ± 3 mmHg, [K⁺] to 5.8 ± 0.2 mmol L^?1, the intracellular and extracellular [H₂PO₄^?] by 20 ± 5 mmol kg^?1 and to 0.20 ± 0.02 mmol L^?1, respectively, while the intracellular (6.33 ± 0.06) and venous pH fell (7.23 ± 0.02) (P < 0.05). During post-exercise muscle ischaemia all variables remained close to the exercise levels. Analysis of each variable as a predictor of blood pressure indicated that only the intracellular pH and diprotonated phosphate were linked to the reflex elevation of blood pressure during handgrip.     

Exercise‐induced changes in brain glucose and serotonin revealed by microdialysis in rat hippocampus: effect of glucose supplementation

The aim of this study was to assess extracellular glucose changes in hippocampus in response to physical exercise and to determine the influence of glucose supplementation. In the same time, we have observed the changes in serotonin, in order to study the relationship between glucose and serotonin during exercise. Both glucose and serotonin were assessed using microdialysis. Exercise induced an increase in extracellular glucose levels over baseline during exercise to 121.1 ± 3.0% (P < 0.001), then a decrease to baseline during recovery. The serotonin followed glucose changes during the first 90 min of exercise, but followed a different pattern during recovery, increasing to a maximum of 129.9 ± 7.0% after 30 min of recovery (P < 0.001). When a 15% glucose solution was infused (10 μL min^–1) during exercise and recovery, blood glucose concentration was increased, but extracellular brain glucose decreased to reach a minimum of 73.3 ± 4.6% after 90 min of recovery (P < 0.001). Serotonin was always the mirror‐reflect of cerebral glucose, with a maximum increase of 142.0 ± 6.9% after 90 min of recovery (P < 0.001). These results show that exercise induces changes in brain glucose and 5‐hydroxytryptamine (5‐HT) levels, which were dramatically modified by glucose infusion. Taking into account the implication of brain 5‐HT in central fatigue, they suggest that if glucose supplementation, before and during exercise, undoubtedly increase performance because of its peripheral positive action, it would have a negative impact on the quality of recovery after the end of the exercise.     

Endogenous opioids may modulate catecholamine secretion during high intensity exercise

To determine the effect of endogenous opioids on catecholamine response during intense exercise [80% maximal oxygen uptake ( O_2max)], nine fit men [mean (SE) ( O_2max, 63.9 (1.7) ml · kg^–1 · min^–1; age 27.6 (1.6) years] were studied during two treadmill exercise trials. A double-blind experimental design was used with subjects undertaking the two exercise trials in counterbalanced order. Exercise trials were 20 min in duration and were conducted 7 days apart. One exercise trial was undertaken following administration of naloxone (N; 1.2 mmol · l^–1; 3 ml) and the other after receiving a placebo (P; 0.9% saline; 3 ml). Prior to each experimental trial a flexible catheter was placed into an antecubital vein and baseline blood samples were collected. Immediately afterwards, each subject received bolus injection of either N or P. Blood samples were also collected after 20 min of continuous exercise while running. Epinephrine and norepinephrine were higher (P < 0.05) in the N than P exercise trial with mean (SE) values of 1679 (196) versus 1196 (155) pmol · l^–1 and 24 (2.2) versus 20 (1.7) nmol · · l^–1 respectively. Glucose and lactate were higher (P < 0.05) in the N than P exercise trial with values of 7 (0.37) versus 5.9 (0.31) mmol · l^–1 and 6.9 (1.1) versus 5.3 (0.9) mmol · l^–1 respectively. These data suggest an opioid inhibition in the release of catecholamines during intense exercise.     

Effects of anaemia and stepwise-induced polycythaemia on maximal aerobic power in individuals with high and low haemoglobin concentrations

Increasing the haemoglobin concentration ([Hb]) improves the oxygen transport capacity but it also increases the viscosity of the blood. The influence of changes in [Hb] and viscosity on submaximal exercise capacity and maximal aerobic power was investigated in eight healthy males in varying states of training and with a normal resting [Hb] ([Hb]_r), ranging from 123 to 178 g]^-1. The subjects were venesected five times (450 ml per unit) and exercise tests were performed in the anaemic state. After 5–7 weeks, when [Hb] had returned to the ‘normal’ value, a stepwise re-transfusion of three to five units of blood was performed with exercise tests after each transfusion. The [Hb]_r was 137 ± 15 g l^-1 in the anaemic state (A) and 170 ± 16 g l^-1 after the last re-transfusion (LT). The V_o2max rose from 3.94 ± 0.35 in A to 4.68 ± 0.30 1 min^-1 after LT. Individual regression lines for [Hb] and V_o2max revealed a mean increase in V_o2max of 19 ± 6 ml min^-1 per g l^-1 change in [Hb]. This value did not differ between individuals with high and low normal [Hb]. Furthermore, in intra-individual comparisons the relationship between [Hb] and V_o2max in high and low individual [Hb] ranges was not found to be statistically different despite a 40% increase in the in vitro viscosity from the anaemic to the polycythaemic state. The average individual correlation (based on five to seven measurements) between [Hb] at rest and after exercise and V_o2max was r= 0.89 (P > 0.01) in the former case and r= 0.92 (P > 0.01) in the latter. The running velocity corresponding to a blood lactate concentration of 4 mM (V_Hla4.0) increased from 15.3 ± 2.3 in the control state to 15.6±2.3 km h¹ after the last transfusion (P > 0.01). A leftward shift of the blood lactate curve, expressed as a percentage of V_o2max, was found. In conclusion, the results obtained indicate a close relationship between V_o2max and [Hb] up to at least 170 g l^-1. Furthermore, both inter-and intra-individual comparisons suggest that the influence of viscosity as such on V_o2max does not differ at high and low [Hb] levels.     

Effect of age and combined sprint and strength training on plasma catecholamine responses to a Wingate-test

Purpose

The purpose of this research is to study the effects of aging and combined training (sprint and strength) on catecholamine responses [adrenaline (A) and noradrenaline (NA)].

Methods

Thirty-two male subjects voluntarily participated in this study. They were randomly divided into four groups: A young trained group (age 21.4 ± 1.2 years, YT, n = 8), a young control group (age 21.9 ± 1.9 years, YC, n = 8), a middle-aged trained group (age 40.8 ± 2.8 years, AT, n = 8) and a middle-aged control group (age 40.4 ± 2.0 years, AC, n = 8). YT and AT participated in a high intensity sprint and strength training program (HISST) for 13 weeks. All the participants realized the Wingate-test before (P1) and after (P2) HISST. Plasma A and NA concentrations were determined at rest (A ₀, NA₀) and at the end of exercise (A _max, NA_max).

Results

At P1, a significant difference (p < 0.05) in terms of age was observed for NA₀ and A ₀ between YT and AT and between control groups YC and AC. This age effect disappeared after training when compared YT and AT. After HISST, A _max increased significantly (p < 0.05) in YT and AT (from 3.08 ± 0.17 to 3.23 ± 0.34 nmol l^?1 in YT and from 3.23 ± 0.52 to 4.59 ± 0.10 nmol l^?1 in AT). However, NA_max increased significantly (p < 0.05) in AT only (from 3.34 ± 0.31 to 3.75 ± 0.60 nmol l^?1). A _max was highly increased in AT compared to YT (4.59 ± 0.10 vs. 3.23 ± 0.34 nmol l^?1), respectively.

Conclusion

The combined training (sprint and strength) appeared to reduce the age effect of the catecholamine response both at rest and in response to exercise.