Comparison between voluntary and stimulated contractions of the quadriceps femoris for growth hormone response and muscle damage.

This study aimed to compare voluntary and stimulated exercise for changes in muscle strength, growth hormone (GH), blood lactate, and markers of muscle damage. Nine healthy men had two leg press exercise bouts separated by 2 wk. In the first bout, the quadriceps muscles were stimulated by biphasic rectangular pulses (75 Hz, duration 400 mus, on-off ratio 6.25-20 s) with current amplitude being consistently increased throughout 40 contractions at maximal tolerable level. In the second bout, 40 voluntary isometric contractions were performed at the same leg press force output as the first bout. Maximal voluntary isometric strength was measured before and after the bouts, and serum GH and blood lactate concentrations were measured before, during, and after exercise. Serum creatine kinase (CK) activity and muscle soreness were assessed before, immediately after, and 24, 48, and 72 h after exercise. Maximal voluntary strength decreased significantly (P < 0.05) after both bouts, but the magnitude of the decrease was significantly (P < 0.05) greater for the stimulated contractions (-22%) compared with the voluntary contractions (-9%). Increases in serum GH and lactate concentrations were significantly (P < 0.05) larger after the stimulation compared with the voluntary exercise. Increases in serum CK activity and muscle soreness were also significantly (P < 0.05) greater for the stimulation than voluntary exercise. It was concluded that a single bout of electrical stimulation exercise resulted in greater GH response and muscle damage than voluntary exercise.     

Substrate utilization by the inactive leg during one-leg or arm exercise.

Substrate utilization by the nonexercising leg was studied in healthy subjects during one-leg exercise at an average work load of 105 W for 40 min (n equals 8) or during arm exercise at 65 W for 20 min (n equals 5). During one-leg exercise both the blood flow and the A-FV difference of oxygen for the non exercising leg rose, resulting in an approximately five fold increment in oxygen uptake. EMG activity of the leg was increased above basal. Despite unchanged or falling arterial levels of insulin, the A-FV difference for glucose across the nonexercising leg rose during exercise and the estimated glucose uptake increased approximately fourfold. Release of lactate in the basal state reverted to a significant net uptake of lactate by the nonexercising leg. During arm exercise there was a 20-70% rise in leg blood flow and the leg oxygen uptake rose 25-45% in spite of minimal EMG activity from the thigh muscles. There was a large uptake of lactate by the legs during arm exercise. We conclude that several important metabolic alterations take place in the nonexercising leg tissues during physical exertion: 1) blood flow and oxygen uptake rise, partly as a consequence of motor activation; 2) substrate utilization shifts from a predominant FFA uptake in the basal state to a greater utilization of carbohydrate; 3) nonexercising muscle, and possibly adipose tissue, play an important role in the removal of lactate during exercise.     

Influence of moderate cold exposure on blood lactate during incremental exercise.

This study examined the effect of exposure of the whole body to moderate cold on blood lactate produced during incremental exercise. Nine subjects were tested in a climatic chamber, the room temperature being controlled either at 30 degrees C or at 10 degrees C. The protocol consisted of exercise increasing in intensity in 35 W increments every 3 min until exhaustion. Oxygen consumption (VO2) was measured during the last minute of each exercise intensity. Blood samples were collected at rest and at exhaustion for the measurement of blood glucose, free fatty acid (FFA), noradrenaline (NA) and adrenaline (A) concentrations and, during the last 15 s of each exercise intensity, for the determination of blood lactate concentration [la-]b. The VO2 was identical under both environments. At 10 degrees C, as compared to 30 degrees C, the lactate anaerobic threshold (Than,la-) occurred at an exercise intensity 15 W higher and [la-]b was lower for submaximal intensities above the Than,la-. Regardless of ambient temperature, glycaemia, A and NA concentrations were higher at exhaustion while FFA was unchanged. At exhaustion the NA concentration was greater at 10 degrees C [15.60 (SEM 3.15) nmol.l-1] than at 30 degrees C [8.64 (SEM 2.37) nmol.l-1]. We concluded that exposure to moderate cold influences the blood lactate produced during incremental exercise. These results suggested that vasoconstriction was partly responsible for the lower [la-]b observed for submaximal high intensities during severe cold exposure.     

Blood lactate accumulation during arm exercise in world class kayak paddlers and strength trained athletes

Blood lactate accumulation was studied during progressive arm exercise in male and female world class kayak paddlers (K male, K female, n = 11), weight-/power-lifters (WL/PL, n = 6), bodybuilders (BB, n = 8) and non-athletes (NA, n = 6). The heavy resistance trained athletes exhibited greater upper-body muscle volume than the other subject groups. During low submaximal exercise intensities, blood lactate concentrations were significantly lower both in male and female kayakers compared with WL/PL, BB, and NA. Mean values at 120 W were 1.9 (K male), 2.1 (K female), 4.8 (WL/PL), 4.5 (BB), and 5.1 (NA) mmol X l-1. At higher power outputs the difference between females and non-kayakers diminished, while the difference between K male and all other groups increased. Exercise tolerance was greatest in K male and was equal among the other groups. Our results suggest that factors other than the muscle mass per se involved in exercise are responsible for the blood lactate response during this kind of work. Moreover, the physiological response observed in kayakers probably represents the upper limit of man's ability to perform continuous progressive arm-cranking exercise.     

The growth hormone response to repeated bouts of sprint exercise with and without suppression of lipolysis in men.

A single 30-s sprint is a potent physiological stimulus for growth hormone (GH) release. However, repeated bouts of sprinting attenuate the GH response, possibly due to negative feedback via elevated systemic free fatty acids (FFA). The aim of the study was to use nicotinic acid (NA) to suppress lipolysis to investigate whether serum FFA can modulate the GH response to exercise. Seven nonobese, healthy men performed two trials, consisting of two maximal 30-s cycle ergometer sprints separated by 4 h of recovery. In one trial (NA), participants ingested NA (1 g 60 min before, and 0.5 g 60 and 180 min after sprint 1); the other was a control (Con) trial. Serum FFA was not significantly different between trials before sprint 1 but was significantly lower in the NA trial immediately before sprint 2 [NA vs. Con: mean (SD); 0.08 (0.05) vs. 0.75 (0.34) mmol/l, P < 0.05]. Peak and integrated GH were significantly greater following sprint 2 compared with sprint 1 in the NA trial [peak GH: 23.3 (7.0) vs. 7.7 (11.9) microg/l, P < 0.05; integrated GH: 1,076 (350) vs. 316 (527) microg.l(-1).60 min(-1), P < 0.05] and compared with sprint 2 in the Con trial [peak GH: 23.3 (7.0) vs. 5.2 (2.3) microg/l, P < 0.05; integrated GH: 1,076 (350) vs. 206 (118) microg.l(-1).60 min(-1), P < 0.05]. In conclusion, suppressing lipolysis resulted in a significantly greater GH response to the second of two sprints, suggesting a potential role for serum FFA in negative feedback control of the GH response to repeated exercise.     

Metabolic responses to light arm and leg exercise when sitting

Seven male subjects performed progressive exercises with a light work load on an upper limb or bicycle ergometer in the sitting position. At any comparable work load above zero, arm exercise induced higher oxygen uptake, ventilation, heart rate, oxygen pulse, respiratory rate and tidal volume than leg exercise. At similar levels of VO2 above 0.45 1 X min-1, heart rate and ventilation were higher during arm exercise. A close linear relationship between carbon dioxide output and oxygen uptake was observed during both arm and leg exercises, the slope for arm work being steeper. The ventilatory equivalent for VCO2 (VE/VCO2) gradually decreased during both types of exercise. The ventilatory equivalent for VO2(VE/VO2) remained constant (arm) while it rose (leg) to a peak at 9.8 W and then gradually decreased. Ventilation in relation to tidal volume had a linear relationship with leg exercise, but became curvilinear with arm exercise after tidal volume exceeded 1100 ml. The observed differences in response between arm and leg exercises at a given work load appear to be influenced by differences in sympathetic outflow due to the greater level of static contraction of the relatively small muscle groups required by arm exercise.     

Effects of three-day bed rest on metabolic, hormonal and circulatory responses to an oral glucose load in endurance or strength trained athletes and untrained subjects.

The study was designed to find out (1) whether the effect of 3-day bed rest on blood glucose (BG) and plasma insulin (IRI) responses to glucose ingestion depends on preceding physical activity and (2) whether plasma adrenaline (A), noradrenaline (NA) and cardiovascular changes following a glucose load are modified by bed rest. Eleven sedentary students (22.5+/-0.3 yrs), 8 long distance runners (18.6+/-0.3 yrs) and 10 strength trained athletes (21.2+/-2.1 yrs) were examined before and after bed rest. Plasma IRI, BG, NA, A, heart rate (HR), and blood pressure (BP) were measured during 2 hrs following glucose (75 g) ingestion. The responses of BG and IRI to glucose load were calculated as incremental areas under the curves (auc). Both in athletes and untrained subjects bed rest markedly increased IRIauc, while BGauc was elevated only in sedentary subjects (p<0.05). The greatest increases in IRIauc and IRI/BG ratios were found in the endurance athletes. The data from all subjects (n = 29) revealed that the initial plasma NA and glucose-induced increases in NA and A were lowered after bed rest (p < 0.01). These effects were most pronounced in the endurance athletes. Bed rest did not influence HR or BP in any group. It is concluded that (1) the athletes have more adequate compensation for the bed-rest-induced decrement in insulin sensitivity than sedentary men; (2) three-day bed rest diminishes basal sympathetic activity and attenuates sympathoadrenal response to oral glucose; (3) endurance athletes have greater sympathetic inhibition than strength athletes or sedentary men.     

Effects of short-term oral salbutamol administration on exercise endurance and metabolism.

The present study examined whether oral short-term administration of salbutamol (Sal) modifies performance and selected hormonal and metabolic variables during submaximal exercise. Eight recreational male athletes completed two cycling trials at 80-85% peak O(2) consumption until exhaustion after either gelatin placebo (Pla) or oral Sal (12 mg/day for 3 wk) treatment, according to a double-blind and randomized protocol. Blood samples were collected at rest, after 5, 10, and 15 min, and at exhaustion to determine growth hormone (GH), cortisol, testosterone, triiodothyronine (T(3)), C peptide, free fatty acid (FFA), blood glucose, lactate, and blood urea values. Time of cycling was significantly increased after chronic Sal intake (Sal: 30.5 +/- 3.1 vs. Pla: 23.7 +/- 1.6 min, P < 0.05). No change in any variable was found before cycling except a decrease in blood urea concentration and an increase in T(3) after Sal that remained significant throughout the exercise test (P < 0.05). Compared with rest, exercise resulted in a significant increase in GH, cortisol, testosterone, T(3), FFAs, and lactate and a decrease in C peptide after both treatments with higher exercise FFA levels and exhaustion GH concentrations after Sal (P < 0.05). Sal but not Pla significantly decreased exercise blood glucose levels. From these data, short-term Sal intake did appear to improve performance during intense submaximal exercise with concomitant increase in substrate availability and utilization, but the exact mechanisms involved need further investigation.     

Effect of thyroxine treatment on metabolic responses to a single insulin injection

Metabolic responses to a single i.v. injection of cristalline insulin (0.2 i.u./kg b.w.) were compared in control and T4-treated dogs both at rest and after prolonged physical exercise. The post-insulin decrease in blood glucose was significantly correlated with the pre-insulin BG concentration. Thus, the insulin-induced fall of BG was greatest in T4-treated dogs at rest, in which significantly higher BG levels were found in comparison with controls, and smallest in the same dogs after exercise, i.e. at the lowest initial BG concentrations. The post-insulin hypoglycaemia caused marked increases in the plasma FFA level in control dogs, both at rest and after physical effort, and in T4-treated dogs at rest. They were accompanied by elevations in the plasma adrenaline levels. In T4-treated dogs given insulin after exercise decreases both in the plasma FFA and A concentrations were found. In the majority of the control and T4-treated dogs insulin injected at rest caused an increase in blood LA levels, being more pronounced in the latter. Insulin injected after physical exercise did not change blood LA level in T4 treated dogs, and it caused its decrease in the control animals. The results of these investigations show that both T4-treatment and physical exercise, performed prior to insulin injection, modify the metabolic response to insulin and post-insulin hypoglycaemia.     

Studies of growth hormone secretion in juvenile diabetes.

To further investigate the GH secretion in juvenile diabetics, blood glucose (BG) and plasma growth hormone (GH) were determined during controlled exercise performed in basal condition and under glucose infusion, in 7 controls and 22 juvenile diabetics aged 12--35 years, 10 of them with fundal vascular lesions. In controls, glucose infusion significantly lowered the exercise induced GH rise observed under basal conditions. In diabetics, under basal conditions, diabetics with low basal BG (BG less than 100 mg/100ml) had higher GH secretion than those with high basal BG (BG greater than 140 mg/100 ml; p less than 0.05). Under glucose infusion, diabetics with normal BG peak values (not different from controls: BG = 284 +/- (SK) 45 mg/100 ml) had significantly higher plasma GH levels than controls (p less than 0.01). In contrast, in diabetics with BG peak value higher than controls (BG greater than 374 ng/100 ml), plasma GH levels were not different from control values. This study indicates that exercise induced GH secretion in diabetics is mainly related to actual BG levels. Furthermore, we found no relation between the magnitude of GH secretion and the presence of retinopathy in diabetics.     

Influence of cold exposure on blood lactate response during incremental exercise

This study examined the effect of acute exposure of the whole body to cold on blood lactate response during incremental exercise. Eight subjects were tested with a cycle ergometer in a climatic chamber, room temperature being controlled either at 24 degrees C (MT) or at -2 degrees C (CT). The protocol consisted of a step increment in exercise intensity of 30 W every 2 min until exhaustion. Oxygen consumption (VO2) was measured at rest and during the last minute of each exercise intensity. Blood samples were collected at rest and at exhaustion for estimations of plasma norepinephrine (NE), epinephrine (E), free fatty acid (FFA) and glucose concentrations, during the last 15 s of each exercise step and also during the 1st, 4th, 7th, and the 10th min following exercise for the determination of blood lactate (LA) concentration. The VO2 was higher during CT than during MT at rest and during nearly every exercise intensity. At CT, lactate anaerobic threshold (LAT), determined from a marked increase of LA above resting level, increased significantly by 49% expressed as absolute VO2, and 27% expressed as exercise intensity as compared with MT. The LA tended to be higher for light exercise intensities and lower for heavy exercise intensities during CT than during MT. The E and NE concentrations increased during exercise, regardless of ambient temperature. Furthermore, at rest and at exhaustion E concentrations did not differ between both conditions, while NE concentrations were greater during CT than during MT. Moreover, an increase off FFA was found only during CT.(ABSTRACT TRUNCATED AT 250 WORDS)     

Fatty acid kinetics and carbohydrate metabolism during electrical exercise in spinal cord-injured humans

Motor center activity and reflexes from contracting muscle have been shown to be important for mobilization of free fatty acids (FFA) during exercise. We studied FFA metabolism in the absence of these mechanisms: during involuntary, electrically induced leg cycling in individuals with complete spinal cord injury (SCI). Healthy subjects performing voluntary cycling served as controls (C). Ten SCI (level of injury: C5-T7) and six C exercised for 30 min at comparable oxygen uptake rates (approximately 1 l/min), and [1-14C]palmitate was infused continuously to estimate FFA turnover. From femoral arteriovenous differences, blood flow, muscle biopsies, and indirect calorimetry, leg substrate balances as well as concentrations of intramuscular substrates were determined. Leg oxygen uptake was similar in the two groups during exercise. In SCI, but not in C, plasma FFA and FFA appearance rate fell during exercise, and plasma glycerol increased less than in C (P < 0.05). Fractional uptake of FFA across the working legs decreased from rest to exercise in all individuals (P < 0.05) but was always lower in SCI than in C (P < 0.05). From rest to exercise, leg FFA uptake increased less in SCI than in C subjects (14 +/- 3 to 57 +/- 20 vs. 41 +/- 13 to 170 +/- 57 micromol x min(-1) x leg(-1); P < 0.05). Muscle glycogen breakdown, leg glucose uptake, carbohydrate oxidation, and lactate release were higher (P < 0.05) in SCI than in C during exercise. Counterregulatory hormonal changes were more pronounced in SCI vs. C, whereas insulin decreased only in C. In conclusion, FFA mobilization, delivery, and fractional uptake are lower and muscle glycogen breakdown and glucose uptake are higher in SCI patients during electrically induced leg exercise compared with healthy subjects performing voluntary exercise. Apparently, blood-borne mechanisms are not sufficient to elicit a normal increase in fatty acid mobilization during exercise. Furthermore, in exercising muscle, FFA delivery enhances FFA uptake and inhibits carbohydrate metabolism, while carbohydrate metabolism inhibits FFA uptake.     

Cardiac output and leg and arm blood flow during incremental exercise to exhaustion on the cycle ergometer.

To determine central and peripheral hemodynamic responses to upright leg cycling exercise, nine physically active men underwent measurements of arterial blood pressure and gases, as well as femoral and subclavian vein blood flows and gases during incremental exercise to exhaustion (Wmax). Cardiac output (CO) and leg blood flow (BF) increased in parallel with exercise intensity. In contrast, arm BF remained at 0.8 l/min during submaximal exercise, increasing to 1.2 +/- 0.2 l/min at maximal exercise (P < 0.05) when arm O(2) extraction reached 73 +/- 3%. The leg received a greater percentage of the CO with exercise intensity, reaching a value close to 70% at 64% of Wmax, which was maintained until exhaustion. The percentage of CO perfusing the trunk decreased with exercise intensity to 21% at Wmax, i.e., to approximately 5.5 l/min. For a given local Vo(2), leg vascular conductance (VC) was five- to sixfold higher than arm VC, despite marked hemoglobin deoxygenation in the subclavian vein. At peak exercise, arm VC was not significantly different than at rest. Leg Vo(2) represented approximately 84% of the whole body Vo(2) at intensities ranging from 38 to 100% of Wmax. Arm Vo(2) contributed between 7 and 10% to the whole body Vo(2). From 20 to 100% of Wmax, the trunk Vo(2) (including the gluteus muscles) represented between 14 and 15% of the whole body Vo(2). In summary, vasoconstrictor signals efficiently oppose the vasodilatory metabolites in the arms, suggesting that during whole body exercise in the upright position blood flow is differentially regulated in the upper and lower extremities.     

Effects of low-intensity resistance exercise under acute systemic hypoxia on hormonal responses

Previous studies have shown that low-intensity resistance exercises with vascular occlusion and slow movement effectively increase muscular size and strength. Researchers have speculated that local hypoxia by occlusion and slow movement may contribute to such adaptations via promoting anabolic hormone secretions by the local accumulation of metabolites. In this study, we determined the effects of low-intensity resistance exercise under acute systemic hypoxia on metabolic and hormonal responses. Eight male subjects participated in 2 experimental trials: (a) low-intensity resistance exercise while breathing normoxic air (normoxic resistance exercise [NR]), (b) low-intensity resistance exercise while breathing 13% oxygen (hypoxic resistance exercise [HR]). The resistance exercises (bench press and leg press) consisted of 14 repetitions for 5 sets at 50% of maximum strength with 1 minute of rest between sets. Blood lactate (LA), serum growth hormone (GH), norepinephrine (NE), testosterone, and cortisol concentrations were measured before normoxia and hypoxia exposures; 15 minutes after the exposures; and at 0, 15, and 30 minutes after the exercises. The LA levels significantly increased after exercises in both trials (p ≤ 0.05). The area under the curve for LA after exercises was significantly higher in the HR trial than in the NR trial (p ≤ 0.05). The GH significantly increased only after the HR trial (p ≤ 0.05). The NE and testosterone significantly increased after the exercises in both trials (p ≤ 0.05). Cortisol did not significantly change in both trials. These results suggest that low-intensity resistance exercise in the hypoxic condition caused greater metabolic and hormonal responses than that in the normoxic condition. Coaches may consider low-intensity resistance exercise under systemic hypoxia as a potential training method for athletes who need to maintain muscle mass and strength during the long in-season.     

Gentle exercise with a previously inactive muscle group hastens the decline of blood lactate concentration after strenuous exercise

The aim of this study was to elucidate the mechanism by which the disappearance of blood lactate following severe exercise is enhanced during active recovery in comparison with recovery at rest. Rates of decline of arterialised venous blood lactate concentrations in man after maximal one-leg exercise were compared during four different modes of recovery: passive (PR), exercise of the muscles involved in the initial exercise (SL), exercise of the corresponding muscles in the hitherto-inactive leg (OL), or exercise of one arm (RA). Recovery exercise workloads were each 40% of the onset of blood lactate accumulation (OBLA) for the limb used. In comparison with PR, SL and OL accelerated the fall in blood lactate to similar extents whereas RA was without effect. The first-order rate constant (min-1) for decline of arterialised venous blood lactate concentration after the intense exercise was 0.027 (0.003) in PR, 0.058 (0.025) in SL, 0.034 (0.002) in OL, and in RA was 0.028 (0.002) [mean (SEM), n = 6 subjects]. Preliminary studies had shown that RA in isolation elevated blood lactate whereas SL and OL did not. Thus, with appropriate workloads, exercise of either hitherto active or passive muscles enhanced blood lactate decline during recovery from intense exercise. This suggests that the effect resulted principally from the uptake and utilisation of lactate in the circulation by those exercising muscles rather than from increased transport of lactate to other sites of clearance by sustained high blood flow through the previously active muscles.     

Increase by somatostatin of the arginine induced rise in blood glucose in untreated insulin requiring diabetics.

We have demonstrated previously that cyclic somatostatin (GH-RIH) exerts a diabetogenic action in healthy subjects. To further examine the impact of this phenomenon studies of blood glucose (BG), immunoreactive insulin (IRI), glucagon (IRG) and growth hormone (GH) were performed in insulin requiring diabetics (n = 6) receiving i.v. arginine (0.5 g/kg) both in the absence and presence of i.v. GH-RIH (500 microgram/h). The infusion of GH-RIH-resulted in a persistent diminution in plasma IRI, IRG and GH. BG fell during i.v. GH-RIH during the initial 30 min and was below control values up to 45 min after initiation of i.v. arginine, but subsequently exceeded control levels (p less than 0.05 - less than 0.025). The excess rise in BG occurred in spite of suppression by somatostatin of the ariginine induced release of IRG, IRI and GH. A fall in BG was seen following cessation of i.v. GH-RIH and during a rebound of insulin release with glucagon levels remaining in the basal range. These findings indicate a diabetogenic action of somatostatin also in insulin requiring diabetics as long as some residual capacity for insulin release is retained.     

Acute exposure to GH during exercise stimulates the turnover of free fatty acids in GH-deficient men.

The secretion of growth hormone (GH) increases acutely during exercise, but whether this is associated with the concomitant alterations in substrate metabolism has not previously been studied. We examined the effects of acute GH administration on palmitate, glucose, and protein metabolism before, during, and after 45 min of moderate-intensity aerobic exercise in eight GH-deficient men (mean age = 40.8 +/- 2.9 yr) on two occasions, with (+GH; 0.4 IU GH) and without GH administered (-GH). A group of healthy controls (n = 8, mean age = 40.4 +/- 4.2 yr) were studied without GH. The GH replacement during exercise on the +GH study mimicked the endogenous GH profile seen in healthy controls. No significant difference in resting free fatty acid (FFA) flux was found between study days, but during exercise a greater FFA flux was found when GH was administered (211 +/- 26 vs. 168 +/- 28 micromol/min, P < 0.05) and remained elevated throughout recovery (P < 0.05). With GH administered, the exercise FFA flux was not significantly different from that observed in control subjects (188 +/- 14 micromol/min), but the recovery flux was greater on the +GH day than in the controls (169 +/- 17 vs. 119 +/- 11 micromol/min, respectively, P < 0.01). A significant time effect (P < 0.01) for glucose rate of appearance from rest to exercise and recovery occurred in the GH-deficient adults and the controls, whereas there were no differences in glucose rate of disappearance. No significant effect across time was found for protein muscle balance. In conclusion, 1) acute exposure to GH during exercise stimulates the FFA release and turnover in GH-deficient adults, 2) GH does not significantly impact glucose or protein metabolism during exercise, and 3) the exercise-induced secretion of GH plays a significant role in the regulation of fatty acid metabolism.     

Arm blood flow at rest and during arm exercise

To test the applicability of a dye-dilution method to quantitate total arm blood flow at rest and during arm exercise, indocyanine green was infused at a constant rate into the brachial artery. Eight subjects performed continuous 30-min arm exercises with an increase in intensity every 10 min (30, 60, and 90 W). The loads corresponded to 29 +/- 1, 48 +/- 2, and 78 +/- 4% (means +/- SE) of the maximal O2 uptake (VO2max 2.13 +/- 0.08 l/min) during arm exercise. VO2max during arm exercise was 61 +/- 1.7% of that during leg exercise. The dye concentration was analyzed in blood samples from three arm veins, two ipsi- and one contralateral, at shoulder level. Corresponding dye concentrations in both ipsilateral veins and a stable concentration difference between ipsi- and contralateral veins were achieved. Total arm blood flow was calculated to be 0.21 +/- 0.04 l/min at rest and 2.43 +/- 0.14 l/min at 90 W. Arm O2 uptake rose from 9 +/- 2 to 323 +/- 21 ml/min. Arm blood flow and O2 uptake each correlated linearly with both work load (r = 0.98) and pulmonary O2 uptake (r greater than or equal to 0.98). Mechanical efficiency for the arm and body was 34-44 and 16-19%, respectively. We conclude that arm blood flow can be determined by continuous infusion of indocyanine green.     

Muscle metabolism, blood lactate and oxygen uptake in steady state exercise at aerobic and anaerobic thresholds

Muscle metabolites and blood lactate concentration were studied in five male subjects during five constant-load cycling exercises. The power outputs were below, equal to and above aerobic (AerT) and anaerobic (AnT) threshold as determined during an incremental leg cycling test. At AerT, muscle lactate had increased significantly (p less than 0.05) from the rest value of 2.31 to 5.56 mmol X kg-1 wet wt. This was accompanied by a significant reduction in CP by 28% (p less than 0.05), whereas only a minor change (9%) was observed for ATP. At AnT muscle lactate had further increased and CP decreased although not significantly as compared with values at AerT. At the highest power outputs (greater than AnT) muscle lactate had increased (p less than 0.01) and CP decreased (p less than 0.01) significantly from the values observed at AnT. Furthermore, a significant reduction (p less than 0.05) in ATP over resting values was recorded. Blood lactate decreased significantly (p less than 0.01) during the last half of the lowest 5 min exercise, remained unchanged at AerT and increased significantly (p less than 0.05-0.01) at power outputs greater than or equal to AnT. It is concluded that anaerobic muscle metabolism is increased above resting values at AerT: at low power outputs (less than or equal to AerT) this could be related to the transient oxygen deficit during the onset of exercise or the increase in power output. At high power outputs (greater than AnT) anaerobic energy production is accelerated and it is suggested that AnT represents the upper limit of power output where lactate production and removal may attain equilibrium during constant load exercise.     

Effects of reduced free fatty acid availability on skeletal muscle PDH activation during aerobic exercise. Pyruvate dehydrogenase

This study investigated the effect of reduced free fatty acid (FFA) availability on pyruvate dehydrogenase activation (PDHa) and carbohydrate metabolism during moderate aerobic exercise. Eight active male subjects cycled for 40 min at 55% Vo(2 peak) on two occasions. During one trial, subjects ingested 20 mg/kg body mass of the antilipolytic drug nicotinic acid (NA) during the hour before exercise to reduce FFA. Nothing was ingested in the control trial (CON). Blood and expired gas measurements were obtained throughout the trials, and muscle biopsy samples were obtained immediately before exercise and at 5, 20, and 40 min of exercise. Plasma FFA were lower in the NA trial (0.13 +/- 0.01 vs. 0.48 +/- 0.03 mM, P < 0.05), and the respiratory exchange ratio (RER) was increased with NA (0.93 +/- 0.01 vs. 0.89 +/- 0.01, P < 0.05), resulting in a 14.5 +/- 1.8% increase in carbohydrate oxidation compared with CON. PDHa increased rapidly in both trials at exercise onset but was approximately 15% higher (P < 0.05) throughout exercise in the NA trial (2.44 +/- 0.19 and 2.07 +/- 0.12 mmol x kg wet muscle(-1) x min(-1) for NA and CON at 40 min). Muscle glycogenolysis was 15.3 +/- 9.6% greater in the NA trial vs. the CON trial but did not reach statistical significance. Glucose 6-phosphate contents were elevated (P < 0.05) in the NA trial at 30 and 40 min of exercise, but pyruvate and lactate contents were unaffected. These data demonstrate that the reduction of exogenous FFA availability increased the activation of PDH and carbohydrate oxidation during moderate aerobic exercise in men. The increased activation of PDH was not explained by changes in muscle pyruvate or the ATP/ADP ratio but may be related to a decrease in the NADH/NAD(+) ratio or an epinephrine-induced increase in calcium concentration.