Effect of carbohydrate feedings during high-intensity exercise

To determine the upper limits of steady-state exercise performance and carbohydrate oxidation late in exercise, seven trained men were studied on two occasions during prolonged cycling that alternated every 15 min between approximately 60% and approximately 85% of VO2max. When fed a sweet placebo throughout exercise, plasma glucose and respiratory exchange ratio (R) declined (P less than 0.05) from 5.0 +/- 0.1 mM and 0.91 +/- 0.01 after 30 min (i.e., at 85% VO2max) to 3.7 +/- 0.3 mM and 0.79 +/- 0.01 at fatigue (i.e., when the subjects were unable to continue exercise at 60% VO2max). Carbohydrate feeding throughout exercise (1 g/kg at 10 min, then 0.6 g/kg every 30 min) increased plasma glucose to approximately 6 mM and partially prevented this decline in carbohydrate oxidation, allowing the men to perform 19% more work (2.74 +/- 0.13 vs. 2.29 +/- 0.09 MJ, P less than 0.05) before fatiguing. Even when fed carbohydrate, however, by the 3rd h of exercise, R had fallen from 0.92 to 0.87, accompanied by a reduction in exercise intensity from approximately 85% to approximately 75% VO2max (both P less than 0.05). These data indicate that carbohydrate feedings enable trained cyclists to exercise at up to 75% VO2max and to oxidize carbohydrate at up to 2 g/min during the later stages of prolonged intense exercise.     

Disposal of blood [1-13C]lactate in humans during rest and exercise

Lactate irreversible disposal (RiLa) and oxidation (RoxLa) rates were studied in six male subjects during rest (Re), easy exercise [EE, 140 min of cycling at 50% of maximum O2 consumption (VO2max)] and hard exercise (HE, 65 min at 75% VO2max). Twenty minutes into each condition, subjects received a Na+-L(+)-[1-13C]lactate intravenous bolus injection. Blood was sampled intermittently from the contralateral arm for metabolite levels, acid-base status, and enrichment of 13C in lactate. Expired air was monitored continuously for determination of respiratory parameters, and aliquots were collected for determination of 13C enrichment in CO2. Steady-rate values for O2 consumption (VO2) were 0.33 +/- 0.01, 2.11 +/- 0.03, and 3.10 +/- 0.03 l/min for Re, EE, and HE, respectively. Corresponding values of blood lactate levels were 0.84 +/- 0.01, 1.33 +/- 0.05, and 4.75 +/- 0.28 mM in the three conditions. Blood lactate disposal rates were significantly correlated to VO2 (r = 0.78), averaging 123.4 +/- 20.7, 245.5 +/- 40.3, and 316.2 +/- 53.7 mg X kg-1 X h-1 during Re, EE, and HE, respectively. Lactate oxidation rate was also linearly related to VO2 (r = 0.81), and the percentage of RiLa oxidized increased from 49.3% at rest to 87.0% during exercise. A curvilinear relationship was found between RiLa and blood lactate concentration. It was concluded that, in humans, 1) lactate disposal (turnover) rate is directly related to the metabolic rate, 2) oxidation is the major fate of lactate removal during exercise, and 3) blood lactate concentration is not an accurate indicator of lactate disposal and oxidation.     

Exercise intensity: effect on postexercise O2 uptake in trained and untrained women

Despite many reports of long-lasting elevation of metabolism after exercise, little is known regarding the effects of exercise intensity and duration on this phenomenon. This study examined the effect of a constant duration (30 min) of cycle ergometer exercise at varied intensity levels [50 and 70% of maximal O2 consumption (VO2max)] on 3-h recovery of oxygen uptake (VO2). VO2 and respiratory exchange ratios were measured by open-circuit spirometry in five trained female cyclists (age 25 +/- 1.7 yr) and five untrained females (age 27 +/- 0.8 yr). Postexercise VO2 measured at intervals for 3 h after exercise was greater (P less than 0.01) after exercise at 50% VO2max in trained (0.40 +/- 0.01 l/min) and untrained subjects (0.39 +/- 0.01 l/min) than after 70% VO2max in (0.31 +/- 0.02 l/min) and untrained subjects (0.29 +/- 0.02 l/min). The lower respiratory exchange ratio values (P less than 0.01) after 50% VO2max in trained (0.78 +/- 0.01) and untrained subjects (0.80 +/- 0.01) compared with 70% VO2max in trained (0.81 +/- 0.01) and untrained subjects (0.83 +/- 0.01) suggest that an increase in fat metabolism may be implicated in the long-term elevation of metabolism after exercise. This was supported by the greater estimated fatty acid oxidation (P less than 0.05) after 50% VO2max in trained (147 +/- 4 mg/min) and untrained subjects (133 +/- 9 mg/min) compared with 70% VO2max in trained (101 +/- 6 mg/min) and untrained subjects (85 +/- 7 mg/min).     

Muscle morphological and biochemical adaptations to training in obese Zucker rats

The purposes of the present study were to characterize the histochemical and enzymatic profiles of various hindlimb skeletal muscles, as well as to determine maximal O2 consumption (VO2max) and respiratory exchange ratios (R) during steady-state exercise in the obese Zucker rat. The changes that occurred in these parameters in response to a 6-wk training program were then assessed. Obese rats were randomly assigned to a sedentary or training group. Lean littermates served as a second control. Training consisted of treadmill running at 18 m/min up an 8% grade, 1.5 h/day, 5 day/wk for 6 wk. During week 6, VO2max and R during a steady-state run (74% max) were determined. After 2 days of inactivity, hindlimb muscles were excised, stained for fiber type and capillaries, and assayed for hexokinase, citrate synthase, cytochrome oxidase, and beta-hydroxyacetyl-CoA dehydrogenase. The obese sedentary rats demonstrated greater oxidative enzyme activities per gram of muscle tissue than their lean littermates, greater R values during submaximal exercise of the same relative intensity, and greater absolute VO2max values. Training resulted in a 20-56% increase in oxidative enzymes, a 10% increase in VO2max, and an increase in capillary density in the soleus and plantaris. There was no alteration in R values during exercise at 74% VO2max or in fiber type composition in response to exercise training. Results suggest that the muscle of the obese Zucker rat manifests a greater oxidative capacity than the muscle of its lean littermates. The apparent inability of the obese rat to increase its use of fat during submaximal exercise of the same relative intensity in response to training remains to be elucidated.     

Effects of prolonged exercise at a similar percentage of maximal oxygen consumption in trained and untrained subjects

Six trained male cyclists and six untrained but physically active men participated in this study to test the hypothesis that the use of percentage maximal oxygen consumption (%VO2max) as a normalising independent variable is valid despite significant differences in the absolute VO2max of trained and untrained subjects. The subjects underwent an exercise test to exhaustion on a cycle ergometer to determine VO2max and lactate threshold. The subjects were grouped as trained (T) if their VO2max exceeded 60 ml.kg-1.min-1, and untrained (UT) if their VO2max was less than 50 ml.kg-1.min-1. The subjects were required to exercise on the ergometer for up to 40 min at power outputs that corresponded to approximately 50% and 70% VO2max. The allocation of each exercise session (50% or 70% VO2max) was random and each session was separated by at least 5 days. During these tests venous blood was taken 10 min before exercise (- 10 min), just prior to the commencement of exercise (0 min), after 20 min of exercise (20 min), at the end of exercise and 10 min postexercise (+ 10 min) and analysed for concentrations of cortisol, [Na+], [K+], [Cl-], glucose, free fatty acid, lactate [la-], [NH3], haemoglobin [Hb] and for packed cell volume. The oxygen consumption (VO2) and related variables were measured at two time intervals (14-15 and 34-35 min) during the prolonged exercise tests. Rectal temperature was measured throughout both exercise sessions. There was a significant interaction effect between the level of training and exercise time at 50% VO2max for heart rate (fc) and venous [la-].(ABSTRACT TRUNCATED AT 250 WORDS)     

Exercise and nasal patency

Nasal airflow resistances were studied in 20 healthy subjects at rest, with exercise, and during recovery from exercise. Resistances were first measured under resting conditions. As a basis for comparison 0.1% xylometazoline was applied by insufflation; it reduced nasal resistance by an average of 49%. On a subsequent occasion, the degree and time course of changes in resistance were measured 1) during 5-min exercise bouts at rest 25, 50, and 75% of predicted maximum O2 intake (VO2max), 2) during 5-, 10-, and 15-min exercise bouts at 50% of VO2max, and 3) during recovery from exercise. Resistance decreased with intensity but not duration of exercise; an initial sudden decrease was followed by a more gradual but progressive decrease, which continued for several minutes following vigorous short duration exercise. Thus following 5 min of effort at 75% of VO2max, resistance reached a nadir (46% fall) 5 min after cessation of exercise. Recovery of preexercise values required 5 min after 5 min of exercise at 25% of VO2max and 10 min after 5 min of exercise at 50% of VO2max. Some decrease persisted 15 min after 5 min of exercise at 75% of VO2max.     

Effects of training on lactate production and removal during progressive exercise in humans.

To determine whether the reduced blood lactate concentrations [La] during submaximal exercise in humans after endurance training result from a decreased rate of lactate appearance (Ra) or an increased rate of lactate metabolic clearance (MCR), interrelationships among blood [La], lactate Ra, and lactate MCR were investigated in eight untrained men during progressive exercise before and after a 9-wk endurance training program. Radioisotope dilution measurements of L-[U-14C]lactate revealed that the slower rise in blood [La] with increasing O2 uptake (VO2) after training was due to a reduced lactate Ra at the lower work rates [VO2 less than 2.27 l/min, less than 60% maximum VO2 (VO2max); P less than 0.01]. At power outputs closer to maximum, peak lactate Ra values before (215 +/- 28 mumol.min-1.kg-1) and after training (244 +/- 12 mumol.min-1.kg-1) became similar. In contrast, submaximal (less than 75% VO2max) and peak lactate MCR values were higher after than before training (40 +/- 3 vs. 31 +/- 4 ml.min-1.kg-1, P less than 0.05). Thus the lower blood [La] values during exercise after training in this study were caused by a diminished lactate Ra at low absolute and relative work rates and an elevated MCR at higher absolute and all relative work rates during exercise.     

Effect of previous supramaximal work on lacticaemia during supra-anaerobic threshold exercise

Twelve male and female subjects (eight trained, four untrained) exercised for 30 min on a treadmill at an intensity of maximal O2 consumption (% VO2max) 90.0%, SD 4.7 greater than the anaerobic threshold of 4 mmol.l-1 (Than = 83.6% VO2max, SD 8.9). Time-dependent changes in blood lactate concentration [( lab]) during exercise occurred in two phases: the oxygen uptake (VO2) transient phase (from 0 to 4 min) and the VO2 steady-state phase (4-30 min). During the transient phase, [lab] increased markedly (1.30 mmol.l-1.min-1, SD (0.13). During the steady-state phase, [lab] increased slightly (0.02 mmol.l-1.min-1, SD 0.06) and when individual values were considered, it was seen that there were no time-dependent increases in [lab] in half of the subjects. Following hyperlacticaemia (8.8 mmol.l-1, SD 2.0) induced by a previous 2 min of supramaximal exercise (120% VO2max), [lab] decreased during the VO2 transient (-0.118 mmol.l-1.min-1, SD 0.209) and steady-state (-0.088 mmol.l-1.min-1, SD 0.103) phases of 30 min exercise (91.4% VO2max, SD 4.8). In conclusion, it was not possible from the Than to determine the maximal [lab] steady state for each subject. In addition, lactate accumulated during previous supramaximal exercise was eliminated during the VO2 transient phase of exercise performed at an intensity above the Than. This effect is probably largely explained by the reduction in oxygen deficit during the transient phase. Under these conditions, the time-course of changes in [lab] during the VO2 steady state was also affected.     

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 (VO2). 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 VO(2) (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 < 0.05). Energy expenditure was constant (22.5-90 min of exercise) and was not different in intermittent intense [0.81 (0.01) kJ x min(-1). kg(-1)] and continuous submaximal [0.85 (0.01) kJ x min(-1) x kg(-1)] exercise. Overall exercise intensity, represented as a proportion of peak aerobic power (VO2(peak)), was 68.1 (2.5)% VO2(peak) and 71.8 (1.8)% VO2(peak) for intermittent and continuous exercise protocols, respectively. Fat oxidation was almost 3 times lower (P < 0.05) and carbohydrate oxidation was approximately 1.2 times higher (P < 0.05) during intermittent compared to continuous exercise, despite the same overall energy expenditure. Capillary plasma lactate was constant from 15 to 90 min of exercise, and pyruvate was constant from 15 to 75 min, although both were higher (P < 0.0001, lactate; P < 0.001, pyruvate) during intermittent [5.05 (0.28) mM, 200 (7) microM, respectively] compared to continuous exercise [2.41 (0.10) mM, 114 (4) microM, respectively]. There was no difference between protocols for either plasma glycerol or non-esterified fatty acids. The decrease in muscle oxygenation during work periods of intermittent exercise resulted in a lower nadir oxygenation [54.62 (0.41)%] compared to continuous exercise [58.82 (0.21)%, P < 0.001]. The decline in oxygenation was correlated with treadmill speed (r = 0.72; P < 0.05). These results show a difference in substrate utilisation and muscle oxygen availability during sustained intermittent intense and continuous submaximal exercise, despite a similar overall VO(2) and identical energy expenditure.     

Effect of endurance training on possible determinants of VO2 during heavy exercise

When moderate exercise begins, O2 uptake (VO2) reaches a steady state within 3 min. However, with heavy exercise, VO2 continues to rise beyond 3 min (VO2 drift). We sought to identify factors contributing to VO2 drift. Ten young subjects performed cycle ergometer tests of 15 min duration for each of four constant work rates, corresponding to 90% of the anaerobic threshold (AT) and 25, 50, and 75% of the difference between maximum VO2 (VO2 max) and AT for that subject. Time courses of VO2, minute ventilation (VE), and rectal temperature were recorded. Blood lactate, norepinephrine, and epinephrine were measured at the end of exercise. Eight weeks of cycle ergometer endurance training improved average VO2 max by 15%. Subjects then performed four tests identical to pretraining studies. For the above AT tests, training reduced VO2 drift substantially; reduction in each of the possible mediators we measured was also demonstrated. The training-induced decrease in VO2 drift was well correlated with decreases in end exercise lactate and less well correlated with the drift in VE seen at above AT work rates. The training-induced reduction in VO2 drift was not significantly correlated with attenuation of rectal temperature rise or decrease in end-exercise level of the catecholamines. Thus the slow rise in VO2 during heavy exercise seems linked to lactate, though a component dictated by the work of breathing cannot be ruled out.     

Effect of induced metabolic alkalosis on human skeletal muscle metabolism during exercise

The purpose of the study was to examine the roles of active pyruvate dehydrogenase (PDH(a)), glycogen phosphorylase (Phos), and their regulators in lactate (Lac(-)) metabolism during incremental exercise after ingestion of 0.3 g/kg of either NaHCO(3) [metabolic alkalosis (ALK)] or CaCO(3) [control (CON)]. Subjects (n = 8) were studied at rest, rest postingestion, and during constant rate cycling at three stages (15 min each): 30, 60, 75% of maximal O(2) uptake (VO(2 max)). Radial artery and femoral venous blood samples, leg blood flow, and biopsies of the vastus lateralis were obtained during each power output. ALK resulted in significantly (P < 0.05) higher intramuscular Lac(-) concentration ([Lac(-)]; ALK 72.8 vs. CON 65.2 mmol/kg dry wt), arterial whole blood [Lac(-)] (ALK 8.7 vs. CON 7.0 mmol/l), and leg Lac(-) efflux (ALK 10.0 vs. CON 4.2 mmol/min) at 75% VO(2 max). The increased intramuscular [Lac(-)] resulted from increased pyruvate production due to stimulation of glycogenolysis at the level of Phos a and phosphofructokinase due to allosteric regulation mediated by increased free ADP (ADP(f)), free AMP (AMP(f)), and free P(i) concentrations. PDH(a) increased with ALK at 60% VO(2 max) but was similar to CON at 75% VO(2 max). The increased PDH(a) may have resulted from alterations in the acetyl-CoA, ADP(f), pyruvate, NADH, and H(+) concentrations leading to a lower relative activity of PDH kinase, whereas the similar values at 75% VO(2 max) may have reflected maximal activation. The results demonstrate that imposed metabolic alkalosis in skeletal muscle results in acceleration of glycogenolysis at the level of Phos relative to maximal PDH activation, resulting in a mismatch between the rates of pyruvate production and oxidation resulting in an increase in Lac(-) production.     

NADH content in type I and type II human muscle fibres after dynamic exercise.

The effect of dynamic exercise on the NADH content of human type I (slow-twitch) and II (fast-twitch) muscle fibres was investigated. Muscle biopsy samples were obtained from the quadriceps femoris of seven healthy subjects at rest and after bicycle exercise at 40, 75 and 100% of the maximal oxygen uptake [VO2(max.)]. At rest and after exercise at 100% VO2(max.), muscle NADH content was significantly higher (P less than 0.05) in type I than in type II fibres. After exercise at 40% VO2(max.), muscle NADH decreased in type I fibres (P less than 0.01), but was not significantly changed in type II fibres. After exercise at 75 and 100% VO2(max.), muscle NADH increased above the value at rest in both type I and II fibres (P less than 0.05). Muscle lactate was unchanged at 40% VO2(max.), but increased 20- and 60-fold after exercise at 75 and 100% VO2(max.) respectively. The finding that NADH decreased only in type I fibres at 40% VO2(max.) supports the idea that type I is the fibre type predominantly recruited during low-intensity exercise. The increase of NADH in both fibre types after exercise at 75% and 100% VO2(max.) suggests that the availability of oxygen relative to the demand is decreased in both fibre types at high exercise intensities.     

Leukocyte, lymphocyte and platelet response to dynamic exercise. Duration or intensity effect?

The influence of work intensity and duration on the white blood cell (WBC), lymphocyte (L) and platelet (P) count response to exercise was studied in 16 trained subjects (22 +/- 5.4 years, means +/- SD). They performed three cyclo-ergospirometric protocols: A) 10 min at 150 W followed by a progressive test (30 W/3 min) till exhaustion; B) constant maximal work (VO2max); C) a 45 min Square-Wave Endurance Exercise Test (SWEET), (n = 5). Arterial blood samples were taken: at rest, submaximal and maximal exercise in A; maximal exercise in B; 15th, 30th and 45th min in the SWEET. Lactate, [H+], PaCO2, PaO2, [Hct], Hb, cortisol, ACTH, total platelet volume (TPV), total blood red cell (RBC), WBC, L and P were measured. At 150 W, WBC, L, P, and TPV increased. VO2max did not differ between A and B, but a difference was found in total exercise time (A = 25 +/- 3 min; B = 7 +/- 2 min, p less than 0.001). In A, at VO2max, the increase was very small for Hct, [Hb], and RBC (10%), in contrast with large changes for WBC (+93%), L (+137%), P (+32%), TPV (+35%), [H+] (+39%), lactate (+715%), and ACTH (+95%). At VO2max there were no differences in these variables between A and B. During the SWEET: WBC, L, P, TPV and ACTH increased at the 15th min as much as in VO2max, but no difference was observed between the 15th, 30th and 45th min, except for ACTH which continued to rise; the lactate increase during the SWEET was about half (+341%) the value observed at VO2max, and [H+] did not vary with respect to values at rest.(ABSTRACT TRUNCATED AT 250 WORDS)     

Effects of short-term training using powercranks on cardiovascular fitness and cycling efficiency

Powercranks use a specially designed clutch to promote independent pedal work by each leg during cycling. We examined the effects of 6 wk of training on cyclists using Powercranks (n=6) or normal cranks (n=6) on maximal oxygen consumption (VO2max) and anaerobic threshold (AT) during a graded exercise test (GXT), and heart rate (HR), oxygen consumption (VO2), respiratory exchange ration (RER), and gross efficiency (GE) during a 1-hour submaximal ride at a constant load. Subjects trained at 70% of VO2max for 1 h.d(-1), 3 d.wk(-1), for 6 weeks. The GXT and 1-hour submaximal ride were performed using normal cranks pretraining and posttraining. The 1-hour submaximal ride was performed at an intensity equal to approximately 69% of pretraining VO2max with VO2, RER, GE, and HR determined at 15-minute intervals during the ride. No differences were observed between or within groups for VO2max or AT during the GXT. The Powercranks group had significantly higher GE values than the normal cranks group (23.6 +/- 1.3% versus 21.3 +/- 1.7%, and 23.9 +/- 1.4% versus 21.0 +/- 1.9% at 45 and 60 min, respectively), and significantly lower HR at 30, 45, and 60 minutes and VO2 at 45 and 60 minutes during the 1-hour submaximal ride posttraining. It appears that 6 weeks of training with Powercranks induced physiological adaptations that reduced energy expenditure during a 1-hour submaximal ride.     

Effect of exercise to rest ratio on plasma lactate concentration at work rates above and below maximum oxygen uptake

The metabolic and physiological responses to different exercise to rest ratios (E:R) (2:1, 1:1, 1:2) of eight subjects exercising at work rates approximately 10% above and below maximum oxygen uptake (VO2max) were assessed. Each of the six protocols consisted of 15 1-min-long E:R intervals. Total work (kJ), oxygen uptake (VO2), heart rate (fc) and plasma lactate concentrations were monitored. With increases in either E:R or work rate, VO2 and fc increased (P < 0.05). The average (15 min) VO2 and fc ranged from 40 to 81%, and from 62 to 91% of maximum, respectively. Plasma lactate concentrations nearly doubled at each E:R when work rate was increased from 90 to 110% of VO2max and ranged from a low of 1.8 mmol.l-1 (1:2-90) to a high of 10.7 mmol.l-1 (2:1-110). The 2:1-110 protocol elicited plasma lactate concentrations which were approximately 15 times greater than that of rest. These data suggest that plasma lactate concentrations during intermittent exercise are very sensitive to both work rate and exercise duration.     

Anemia causes a relative decrease in blood lactate concentration during exercise

The purpose of the present study was to examine to what degree a reduction in systemic oxygen transport capacity influences the absolute and relative levels (% of maximal oxygen uptake) of submaximal blood lactate accumulation. Anemia was induced by repeated venesections in eight healthy males. After 9-10 weeks of anemia, hemoglobin concentration [Hb] was restored by retransfusion of packed erythrocytes. The [Hb] values obtained were, before venesections, in control (C) = 145 +/- 10, in the anemic state (A) = 110 +/- 8, and after retransfusion (R) = 143 +/- 8 g X l-1 respectively. In all states, muscle biopsies were taken and measurements made of VO2max and VO2 at a running velocity corresponding to a blood lactate concentration of 4 mM (upsilon Hla 4.0). In the A condition Vo2max decreased by 19% as compared to C (P less than 0.01). upsilon Hla 4.0 was 14% lower in A as compared to C and R (p less than 0.01). VO2 at upsilon Hla 4.0 was 13% lower in A as compared to C (P less than 0.01). However, VO2 at upsilon Hla 4.0 expressed as a percentage of VO2max was increased (P less than 0.01) in the anemic state, the values obtained being C = 83.3%, A = 89.8% and R = 84.8%. Ventilation at upsilon Hla 4.0 was higher in A as compared to C and R (P less than 0.05). R and C values were not significantly different for any of the values presented above. The maximal activity of citrate synthase in muscle did not differ between the three different conditions.(ABSTRACT TRUNCATED AT 250 WORDS)     

Effects of exercise in normoxia and acute hypoxia on respiratory muscle metabolites

We determined changes in rat plantaris, diaphragm, and intercostal muscle metabolites following exercise of various intensities and durations, in normoxia and hypoxia (FIO2 = 0.12). Marked alveolar hyperventilation occurred during all exercise conditions, suggesting that respiratory muscle motor activity was high. [ATP] was maintained at rest levels in all muscles during all normoxic and hypoxic exercise bouts, but at the expense of creatine phosphate (CP) in plantaris muscle and diaphragm muscle following brief exercise at maximum O2 uptake (VO2max) in normoxia. In normoxic exercise plantaris [glycogen] fell as exercise exceeded 60% VO2max, and was reduced to less than 50% control during exhaustive endurance exercise (68% VO2max for 54 min and 84% for 38 min). Respiratory muscle [glycogen] was unchanged at VO2max as well as during either type of endurance exercise. Glucose 6-phosphate (G6P) rose consistently during heavy exercise in diaphragm but not in plantaris. With all types of exercise greater than 84% VO2max, lactate concentration ([LA]) in all three muscles rose to the same extent as arterial [LA], except at VO2max, where respiratory muscle [LA] rose to less than half that in arterial blood or plantaris. Exhaustive exercise in hypoxia caused marked hyperventilation and reduced arterial O2 content; glycogen fell in plantaris (20% of control) and in diaphragm (58%) and intercostals (44%). We conclude that respiratory muscle glycogen stores are spared during exhaustive exercise in the face of substantial glycogen utilization in plantaris, even under conditions of extreme hyperventilation and reduced O2 transport. This sparing effect is due primarily to G6P inhibition of glycogen phosphorylase in diaphragm muscle. The presence of elevated [LA] in the absence of glycogen utilization suggests that increased lactate uptake, rather than lactate production, occurred in the respiratory muscles during exhaustive exercise.     

Oxygen consumption following exercise of moderate intensity and duration.

To study the effects of exercise intensity and duration on excess postexercise oxygen consumption (EPOC), 8 men [age = 27.6 (SD 3.8) years, VO2max = 46.1 (SD 8.5) ml min-1 kg-1] performed four randomly assigned cycle-ergometer tests (20 min at 60% VO2max, 40 min at 60% VO2max, 20 min at 70% VO2max, and 40 min at 70% VO2max). O2 uptake, heart rate and rectal temperature were measured before, during, and for 1 h following the exercise tests. Blood for plasma lactate measurements was obtained via cannulae before, and at selected times, during and following exercise. VO2 rapidly declined to preexercise levels following each of the four testing sessions, and there were no differences in EPOC between the sessions. Blood lactate and rectal temperature increased (P < 0.05) with exercise, but had returned to preexercise levels by 40 min of recovery. The results indicate that VO2 returned to resting levels within 40 min after the end of exercise, regardless of the intensity (60% and 70% VO2max) or duration (20 min and 40 min) of the exercise, in men with a moderate aerobic fitness level.     

Effects of exercise on maximal instantaneous muscular power of humans

The maximal instantaneous anaerobic power (w), as determined during a high jump off both feet on a force platform, was measured on eight subjects starting from a resting base line; a base line of steady-state cycloergometric exercise requiring 30, 50, and 70% of individual maximum O2 consumption (VO2max); and a base line of maximal and supramaximal exercise (100 and 120% of VO2max). In addition, w was also measured during the VO2 transients from rest to each of the above work loads. Blood lactate concentration ([Lab]) was determined before and 8 min after the end of each priming load. After the onset of any priming load, w decreases with time reaching in 2 min a steady level that is lower the higher the VO2. For the three lowest work rates, the steady w level is unchanged by increasing the duration of the priming exercise up to 30 min. For low work levels, the decrease of w as a function of VO2 is essentially parallel to that of estimated muscle concentration of ATP ([ATP]). For work levels greater than 60% of VO2max involving a substantial accumulation of lactate, the decrease of w becomes smaller than the estimated drop of muscle [ATP]. This finding is tentatively attributed to an increase of either the mechanical equivalent or of the velocity constant of ATP splitting brought about by the lowering of intracellular muscle pH after lactate accumulation.(ABSTRACT TRUNCATED AT 250 WORDS)     

Effect of exercise training at different intensities on fat metabolism of obese men.

The present study investigated the effect of exercise training at different intensities on fat oxidation in obese men. Twenty-four healthy male obese subjects were randomly divided in either a low- [40% maximal oxygen consumption (VO(2 max))] or high-intensity exercise training program (70% VO(2 max)) for 12 wk, or a non-exercising control group. Before and after the intervention, measurements of fat metabolism at rest and during exercise were performed by using indirect calorimetry, [U-(13)C]palmitate, and [1,2-(13)C]acetate. Furthermore, body composition and maximal aerobic capacity were measured. Total fat oxidation did not change at rest in any group. During exercise, after low-intensity exercise training, fat oxidation was increased by 40% (P < 0.05) because of an increased non-plasma fatty acid oxidation (P < 0.05). High-intensity exercise training did not affect total fat oxidation during exercise. Changes in fat oxidation were not significantly different among groups. It was concluded that low-intensity exercise training in obese subjects seemed to increase fat oxidation during exercise but not at rest. No effect of high-intensity exercise training on fat oxidation could be shown.