Soleus muscle stability in wild hibernating black bears.

Based on studies of fast skeletal muscles, hibernating black and brown bears resist skeletal muscle atrophy during months of reduced physical activity and not feeding. The present study examined atrophy sparing in the slow soleus muscle, known to be highly prone to disuse atrophy in humans and other mammals. We demonstrated histochemically that the black bear soleus is rich in slow fibers, averaging 84.0 ± 6.6%. The percentages of slow fibers in fall (87.3 ± 4.9%) and during hibernation (87.1 ± 5.6%) did not differ ( P = 0.3152) from summer. The average fiber cross-sectional area to body mass ratio (48.6 ± 11.7 µm2/kg) in winter hibernating bears was not significantly different from that of summer (54.1 ± 11.8 µm2/kg, P = 0.4186) and fall (47.0 ± 9.7 µm2/kg, P = 0.9410) animals. The percentage of single hybrid fibers containing both slow and fast myosin heavy chains, detected biochemically, increased from 2.6 ± 3.8% in summer to 24.4 ± 24.4% ( P = 0.0244) during hibernation. The shortening velocities of individual hybrid fibers remained unchanged from that of pure slow and fast fibers, indicating low content of the minority myosins. Slow and fast fibers in winter bears exhibited elevated specific tension (kN/m2; 22%, P = 0.0161 and 11%, P = 0.0404, respectively) and maintained normalized power. The relative stability of fiber type percentage and size, fiber size-to-body mass ratio, myosin heavy chain isoform content, shortening velocity, power output, and elevated specific tension during hibernation validates the ability of the black bear to preserve the biochemical and performance characteristics of the soleus muscle during prolonged hibernation.

Prolonged space flight-induced alterations in the structure and function of human skeletal muscle fibres.

The primary goal of this study was to determine the effects of prolonged space flight (180 days) on the structure and function of slow and fast fibres in human skeletal muscle. Biopsies were obtained from the gastrocnemius and soleus muscles of nine International Space Station crew members 45 days pre- and on landing day (R+0) post-flight. The main findings were that prolonged weightlessness produced substantial loss of fibre mass, force and power with the hierarchy of the effects being soleus type I > soleus type II > gastrocnemius type I > gastrocnemius type II. Structurally, the quantitatively most important adaptation was fibre atrophy, which averaged 20% in the soleus type I fibres (98 to 79 µm diameter). Atrophy was the main contributor to the loss of peak force (P(0)), which for the soleus type I fibre declined 35% from 0.86 to 0.56 mN. The percentage decrease in fibre diameter was correlated with the initial pre-flight fibre size (r = 0.87), inversely with the amount of treadmill running (r = 0.68), and was associated with an increase in thin filament density (r = 0.92). The latter correlated with reduced maximal velocity (V(0)) (r = 0.51), and is likely to have contributed to the 21 and 18% decline in V(0) in the soleus and gastrocnemius type I fibres. Peak power was depressed in all fibre types with the greatest loss (55%) in the soleus. An obvious conclusion is that the exercise countermeasures employed were incapable of providing the high intensity needed to adequately protect fibre and muscle mass, and that the crew's ability to perform strenuous exercise might be seriously compromised. Our results highlight the need to study new exercise programmes on the ISS that employ high resistance and contractions over a wide range of motion to mimic the range occurring in Earth's 1 g environment.

Training adaptations in skeletal muscle of juvenile diabetics.

Skeletal muscles from 12 male, juvenile-onset diabetics (JD) and 13 nondiabetics (ND) were studied to determine the effects of endurance training on mitochondrial enzyme activities, lipoprotein lipase (LPL) activity, and the oxidation of lipids (14C-palmityl CoA) in vitro. Ten weeks of endurance running (30 min/day, 5 days/wk) resulted in 11.0 and 12.9% gains in aerobic capacity for the JD and ND groups (P greater than 0.05), respectively. Both groups showed significant (P less than 0.05) increases in muscle LPL, carnitine palmityl transferase, succinate dehydrogenase, and hexokinase activities with training. Though the pretraining capacities for 14C-palmityl CoA oxidation were similar for both ND and JD groups, the diabetics showed a 41% greater improvement in the measurement of muscle lipid oxidation after training than did the ND group. The principal finding of this research was that skeletal muscle of juvenile diabetics who are in moderate insulin balance shows adaptations to endurance training that are similar to those of nondiabetic men.

Dietary potassium and heavy exercise: effects on muscle water and electrolytes.

Eight men were studied during two 4-day exercise-dietary regimens, once under a control diet (80 mEq K+/day) and again with a diet low in K+ (25 mEq/day). Muscle K+ increased 5 to 6% as a result of the two exercise-dietary regimens, while no change was observed for muscle Na+ or Mg++. Plasma volume increased throughout the 4 days of each exercise-diet sequence, with the low K+ regimen resulting in the largest plasma volume gain (+15%) and a marked reduction in urinary K+ excretion. Despite the losses of K+ in sweat and the low K+ intake, there was a relatively small decrease in total body K+ content (less than 2% of body content). Based on these measurements of extracellular (plasma) and tissue (muscle) water and electrolytes, we have concluded that in combination with 4 days of heavy exercise and sweating, a low K+ diet will not significantly diminish the total body K+ content.

The role of dietary carbohydrates in muscle glycogen resynthesis after strenuous running.

This study examined the effect of the type, amount, and the frequency of feeding of carbohydrates on muscle glycogen resynthesis after running. Trained male runners performed a 16.1 km run at 80% VO2 max to decrease gastrocnemius glycogen levels. A complex or simple carbohydrate diet (approximately 3000 kcal) resulted in similar muscle glycogen levels 24 h after exercise. Forty-eight hours after exercise the complex carbohydrate diet resulted in significantly higher (p less than 0.05) muscle glycogen levels. Consuming increasing amounts of carbohydrate, between 88 to 648 g carbohydrate/day, resulted in increasingly larger amounts of muscle glycogen resynthesis (24 h) after exercise. Frequent feedings of a high carbohydrate diet did not enhance muscle glycogen synthesis when compared to equal amounts of carbohydrates in two meals. It appears that muscle glycogen can be normalized between daily strenuous running activity.

Human vitamin B-6 pools estimated through muscle biopsies.

Previous estimates of total vitamin B-6 pools in humans based on extrapolations from tracer studies yielded values of 107-190 mumol when the tracer was administered orally and 345-725 mumol when the tracer was administered intravenously. To obtain a more direct estimate of vitamin B-6 pools, muscle biopsies from five female and seven male adults were analyzed by cation-exchange chromatography. Total muscle mass was estimated from creatinine excretion and the assumption that muscle is 40% of the body weight. The total muscle vitamin B-6 pool was estimated to be 917 +/- 319 mumol in the females and 850 +/- 216 mumol in the males. Because muscle accounts for approximately 80% of the vitamin B-6 in the body, the total body pool of vitamin B-6 in adult humans is probably approximately 1000 mumol.

Response of vitamin B-6 content of muscle to changes in vitamin B-6 intake in men.

Previous reports indicated that in growing rats the vitamin B-6 pool in muscle was relatively stable during deficiency but increased in response to increased vitamin B-6 intake. To determine whether human muscle would show a similar response 10 college-aged males received a low vitamin B-6 diet (1.76 mumol/d) for 6 wk followed by 6 wk on a self-selected diet supplemented with 0.98 mmol pyridoxine HCl/d. During depletion, excretion of pyridoxic acid rapidly adjusted to approximate the intake. Plasma pyridoxal phosphate concentrations at the end of the baseline, depletion, and supplementation periods were 81 +/- 51, 9 +/- 3, and 455 +/- 129 nmol/L, respectively, whereas muscle concentrations were 21 +/- 9, 20 +/- 4, and 25 +/- 7 nmol/g, respectively and total vitamin B-6 in muscle was 28 +/- 10, 27 +/- 4, and 35 +/- 10 nmol/g, respectively. These data provide further confirmation that the vitamin B-6 pools in skeletal muscle are resistant to depletion. They also demonstrate that in humans with constant body weight, vitamin B-6 supplementation is not associated with marked increases in vitamin B-6 in muscle.

Pyridoxic acid excretion during low vitamin B-6 intake, total fasting, and bed rest.

Vitamin B-6 metabolism in 10 volunteers during 21 d of total fasting was compared with results from 10 men consuming a diet low only in vitamin B-6 (1.76 mumol/d) and with men consuming a normal diet during bed rest. At the end of the fast mean plasma concentrations of vitamin B-6 metabolites and urinary excretion of 4-pyridoxic acid tended to be higher in the fasting subjects than in the low-vitamin B-6 group. The fasting subjects lost approximately 10% of their total vitamin B-6 pool and approximately 13% of their body weight. The low-vitamin B-6 group lost only approximately 4% of their vitamin B-6 pool. Compared with baseline, urinary excretion of pyridoxic acid was significantly increased during 17 wk of bed rest. There was no increase in pyridoxic acid excretion during a second 15-d bed rest study. These data suggest the possibility of complex interactions between diet and muscle metabolism that may influence indexes that are frequently used to assess vitamin B-6 status.

Submaximal and maximal working capacity of elite distance runners. Part II. Muscle fiber composition and enzyme activities.

The present study confirms earlier observations that the musculature of elite distance runners is characterized by a high predominance of ST fibers. Although the percent ST fibers effectively discriminates between good and elite distance runners, fiber composition alone is a poor predictor of distance running success within the group of elite runners. Muscle enzyme measurements suggest that the 11 to 20 miles (17.7 to 32.2 km) of daily training performed by the elite runners produced a significantly greater increase in muscle SDH activity than was observed in the good distance runners, who were running 7 to 11 miles (11.3 to 17.7 km) per day, Although such endurance training enhances the oxidative capacity of the muscle, it apparently has little influence on the enzymes of glycogenolysis.

Impaired muscle glycogen storage after muscle biopsy.

To assess the effects of repeated needle biopsies on the rate of muscle glycogen repletion, eight male subjects were studied immediately after and 2 days after an exhaustive cycling bout. A single biopsy was obtained from the right vastus lateralis muscle immediately after an exhaustive cycling bout. Two days later, a sample was taken 1 cm lateral or medial to sample A. In four of these subjects, additional biopsies were taken 3 cm distal and proximal. A control specimen was also taken from the left leg 2 days after the exercise. Ten days after the exercise, muscle was again sampled from each leg of these four subjects. Analysis of these samples revealed that the initial biopsy impaired glycogen storage in the muscle taken 1 cm medial or lateral to the previous site. This reduction in glycogen storage was most pronounced in the first 2 days after the exercise. Samples taken distal and proximal to the initial biopsy contained, on the average, less glycogen than the contralateral leg, but these differences were only significantly different in the distal muscle sample. Alteration in muscle glycogen storage was seen to persist for 10 days after the first biopsy, suggesting that care must be taken in selecting the site for repeated biopsies from the same muscle.

Effect of swim exercise training on human muscle fiber function.

This study examined the effect of a typical collegiate swim-training program and an intensified 10-day training period on the peak tension (Po), negative log molar Ca2+ concentration (pCa)-force, and maximal shortening speed (Vmax) of the slow-twitch type I and fast-twitch type II fibers of the deltoid muscle. Over a 10-wk period, the swimmers averaged 4,266 +/- 264 m/day swimming intermittent bouts of front crawl, kicking, or pulling. The training program induced an almost twofold increase in the mitochondrial marker enzyme citrate synthase. Po of the single fibers was not altered by either the training or 10-day intensive training programs, and no significant differences were observed in the Po (kg/cm2) of type I compared with the type II fibers. The type II fiber diameters were significantly larger than the type I fibers (94 +/- 4 vs. 80 +/- 2 microns), and although fiber diameters were unaffected by the training, the 10-day intensive training significantly reduced the type II fiber diameter. The type I fibers from the trained swimmers showed pCa-force curves shifted to the right such that higher free Ca2+ levels were required to elicit a given percent of Po (for values less than 0.5 Po). The activation threshold (pCa) for the onset of tension and the pCa required to elicit one-half maximal tension were not altered by the training in either fiber type. Fiber Vmax (measured by the slack test) was fivefold higher in type II compared with type I fibers (4.85 +/- 0.50 vs. 0.86 +/- 0.04 fiber lengths/s). The exercise-training program significantly increased and decreased the Vmax of the slow and fast fibers, respectively. The 10 days of intensified training produced a further significant decrease in the Vmax of the type II fibers. After a period of detraining, the Vmax of both fiber types returned to the control level. The force-velocity relation was not significantly altered in either fiber type by the swim training; however, the intensified training significantly depressed the velocity of the type II fiber at all loads studied. The Vmax changes with exercise training are likely explained by an exercise-induced expression of fast myosin in slow fibers and slow myosin in fast fibers.

Muscle metabolism during exercise in the heat in unacclimatized and acclimatized humans.

The effect of heat acclimatization on aerobic exercise tolerance in the heat and on subsequent sprint exercise performance was investigated. Before (UN) and after (ACC) 8 days of heat acclimatization, 10 male subjects performed a heat-exercise test (HET) consisting of 6 h of intermittent submaximal [50% of the maximal O2 uptake] exercise in the heat (39.7 degrees C dB, 31.0% relative humidity). A 45-s maximal cycle ride was performed before (sprint 1) and after (sprint 2) each HET. Mean muscle glycogen use during the HET was lower following acclimatization [ACC = 28.6 +/- 6.4 (SE) and UN = 57.4 +/- 5.1 mmol/kg; P less than 0.05]. No differences were noted between the UN and ACC trials with respect to blood glucose, lactate (LA), or respiratory exchange ratio. During the UN trial only, total work output during sprint 2 was reduced compared with sprint 1 (24.01 +/- 0.80 vs. 21.56 +/- 1.18 kJ; P less than 0.05). This reduction in sprint performance was associated with an attenuated fall in muscle pH following sprint 2 (6.86 vs. 6.67, P less than 0.05) and a reduced accumulation of LA in the blood. These data indicate that heat acclimatization produced a shift in fuel selection during submaximal exercise in the heat. The observed sparing of muscle glycogen may be associated with the enhanced ability to perform highly intense exercise following prolonged exertion in the heat.

Glucose feeding and exercise in trained rats: mechanisms for glycogen sparing.

This investigation studied the effect of an oral glucose feeding on glycogen sparing during exercise in non-glycogen-depleted and glycogen-depleted endurance-trained rats. The non-glycogen-depleted rats received via a stomach tube 2 ml of a 20% glucose solution labeled with [U-14C]glucose just prior to exercise (1 h at 25 m/min). Another group of rats ran for 40 min at higher intensity to deplete glycogen stores, after which they received the same glucose feeding and continued running for 1 h at 25 m/min. The initial 40-min run depleted glycogen in heart, skeletal muscle, and liver. In the non-glycogen-depleted rats the glucose feeding spared glycogen in the liver, primarily from the oxidation of blood-borne glucose in muscle. In the glycogen-depleted rats, muscle glycogen was repleted after the feeding, but sources other than the administered glucose also contributed to glycogen synthesis. The results suggest that glycogen depletion rather than the glucose feeding per se stimulates glycogen resynthesis in muscle during exercise in endurance-trained rats.

Threshold for muscle lactate accumulation during progressive exercise.

The purpose of this study was to investigate the relationship between muscle and blood lactate concentrations during progressive exercise. Seven endurance-trained male college students performed three incremental bicycle ergometer exercise tests. The first two tests (tests I and II) were identical and consisted of 3-min stage durations with 2-min rest intervals and increased by 50-W increments until exhaustion. During these tests, blood was sampled from a hyperemized earlobe for lactate and pH measurement (and from an antecubital vein during test I), and the exercise intensities corresponding to the lactate threshold (LT), individual anaerobic threshold (IAT), and onset of blood lactate accumulation (OBLA) were determined. The test III was performed at predetermined work loads (50 W below OBLA, at OBLA, and 50 W above OBLA), with the same stage and rest interval durations of tests I and II. Muscle biopsies for lactate and pH determination were taken at rest and immediately after the completion of the three exercise intensities. Blood samples were drawn simultaneously with each biopsy. Muscle lactate concentrations increased abruptly at exercise intensities greater than the "below-OBLA" stage [50.5% maximal O2 uptake (VO2 max)] and resembled a threshold. An increase in blood lactate and [H+] also occurred at the below-OBLA stage; however, no significant change in muscle [H+] was observed. Muscle lactate concentrations were highly correlated to blood lactate (r = 0.91), and muscle-to-blood lactate ratios at below-OBLA, at-OBLA, and above-OBLA stages were 0.74, 0.63, 0.96, and 0.95, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Aging among elite distance runners: a 22-yr longitudinal study.

The purpose of this study was to assess the physiological responses of former elite distance runners during submaximal and maximal exercise after a mean period of 22 yr. Fifty-three men were initially tested (T1) in the late 1960s and early 1970s when they were all highly trained and competitive. For the current evaluation (T2), these men were classified as highly trained (HT; n = 10), fitness trained (FT; n = 18), untrained (UT; n = 15), and fit older (FO; n = 10), depending on their continued level of training and age. The mean (+/- SE) age for the HT, FT, and UT men during T2 was similar (46.5 +/- 1.6 yr), whereas the FO men were significantly (P < 0.05) older (68.4 +/- 2.7 yr). All groups experienced a significant decrease (P < 0.05) in maximal O2 uptake (VO2 max) from T1 to T2. However, this decrease was related to the amount of training between evaluations. The HT men had the smallest reduction (6% per decade) in VO2 max (from 68.8 to 59.2 ml.g-1.min-1). The FT men's VO2 max was approximately 10% lower per decade (from 64.1 to 48.9 ml.kg-1.min-1), whereas an approximately 15% decrease per decade was observed for the UT (from 70.7 to 46.7 ml.kg-1.min-1) and FO (from 60.3 to 40.7 ml.kg-1.min-1) men, despite the continued training of the FO men. Energy requirements for a standardized run at 12 km/run were similar from T1 to T2 for the HT and FT men, whereas the UT men required an increased (P < 0.05) O2 uptake (40.3-41.8 l/min), ventilation (53.7-72.7 l/min), and heart rate (127-142 beats/min). The perceived effort and %VO2 max for this submaximal run were greater during T2 for all groups, which was related to the decline in VO2 max. These longitudinal data indicate that after more than two decades the physiological capacities of these aging runners are compromised, regardless of training. These data also confirm previous cross-sectional findings that aerobic capacity of highly trained middle-aged men declines approximately 5-7% per decade.

Skeletal muscle characteristics among distance runners: a 20-yr follow-up study.

The purpose of this investigation was to examine the histochemical and enzymatic characteristics of skeletal muscle after 20 yr of distance running training. Twenty-eight men were first studied between 1966 and 1974 when they were all highly trained distance runners. On the basis of their training regimens in the interim between testing, subjects were described as highly trained (HI; n = 11), fitness trained (FIT; n = 10), or untrained (UT; n = 7). Gastrocnemius muscle biopsy samples revealed a mean increase (P < 0.05) in the proportion of type I fibers of the FIT and UT groups, whereas the HI group, which was initially characterized by a high percentage (> 70%) of type I fibers, was unchanged. Although the mean fiber type change of the HI group was similar between evaluations, 6 of the 11 subjects did elicit an increase in the percentage of type I fibers. A subgroup of elite distance runners who had continued to train for competition experienced an approximately 25% reduction (P > 0.05) in muscle succinate dehydrogenase activity and decreases (P > 0.05) in types I and II muscle fiber areas. On the average, in 1993 the HI group had higher (P < 0.05) succinate dehydrogenase and citrate synthase activities than the FIT and UT groups, whereas phosphorylase activity did not differ among the three groups. These data suggest that the middle-aged men in this study had a significantly greater proportion of type I muscle fibers than when they were 20 yr younger.(ABSTRACT TRUNCATED AT 250 WORDS)

Progressive resistance training reduces myosin heavy chain coexpression in single muscle fibers from older men.

The purpose of this study was to examine myosin heavy chain (MHC) and myosin light chain (MLC) isoforms following 12 wk of progressive resistance training (PRT). A needle biopsy was taken from the vastus lateralis to determine fiber-type expression [ATPase (pH 4.54) and MHC/MLC] in seven healthy men (age = 74.0 +/- 1.8 yr). Subjects were also tested for 1-repetition maximum (1-RM), pre- and posttraining. The progressive knee extensor protocol consisted of three sets at 80% of 1-RM 3 days/wk for 12 wk. Freeze-dried, single muscle fibers were dissected for MHC and MLC analysis and then subjected to SDS-PAGE and silver staining, pre- and posttraining. MHC expression increased in the I (10.4%; P < 0.05) and decreased in I/IIa (9.0%; P < 0.05), I/IIa/x (0.9%; P < 0.05), and IIa/x (8.9%; P < 0.05) isoforms, with no change in the IIa and IIx isoforms, pre- vs. posttraining (total fibers = 3,059). The MLC(3f)-to-MLC(2) ratio did not change with the PRT in either the MHC I or MHC IIa isoforms (total fibers = 902), pre- to posttraining. ATPase fiber distribution did not significantly differ following training (I: 50. 4 +/- 6.7 vs. 51.9 +/- 7.9, IIa: 36.8 +/- 5.3 vs. 41.1 +/- 7.0, IIb: 12.8 +/- 5.6 vs. 7.0 +/- 4.0%; pre- vs. posttraining, respectively). 1-RM increased (51.9%; P < 0.05) from pre- to posttraining. The PRT provide a stimulus for alterations in MHC isoforms, which demonstrated a decrease in all hybrid isoforms and an increase in MHC I expression (not found in the ATPase results), unlike the MLC ratio (3:2), which was not altered with training.

Carbohydrate balance in competitive runners during successive days of intense training.

This study was designed to investigate the effect of intense training on muscle glycogen stores under conditions of controlled carbohydrate (CHO) intake. On two separate occasions, 10 highly trained distance runners increased their training load for 5 days (20 km/day, approximately 80% maximal O2 consumption) while eating a diet whose carbohydrate composition either equaled (EQ-CHO) or contained approximately 50% of the runner's estimated daily expenditure (LO-CHO). Total muscle glycogen levels were lower after the LO-CHO regimen. Photometric analysis of the glycogen content in individual fibers revealed that 27% type I and 17% type II fibers had optical densities less than 0.2 U after the LO-CHO regimen, whereas 7% type I and 0% type II were similarly depleted after the EQ-CHO diet. A linear relationship was observed between the histochemical and direct chemical analysis of muscle glycogen content. Treadmill O2 uptake measured at 185 and 238 m/min was higher during the LO-CHO than the EQ-CHO regimen. Ratings of perceived exertion were higher during the 238-m/min run for the LO-CHO regimen. After 3 days of rest, running economy and perception of effort returned to pretraining levels and muscle glycogen stores were approximately 85% of the pretraining values. Thus when CHO intake was only approximately 50% of the energy requirements there was a marked depletion of muscle glycogen stores, particularly in type I fibers, and a concomitant decrease in running economy and increased perception of fatigue.(ABSTRACT TRUNCATED AT 250 WORDS)

Improvements in exercise performance: effects of carbohydrate feedings and diet.

In an effort to determine the effects of carbohydrate (CHO) feedings immediately before exercise in both the fasted and fed state, 10 well-trained male cyclists [maximum O2 consumption (VO2 max), 4.35 +/- 0.11 l/min)] performed 45 min of cycling at 77% VO2 max followed by a 15-min performance ride on an isokinetic cycle ergometer. After a 12-h fast, subjects ingested 45 g of liquid carbohydrate (LCHO), solid carbohydrate confectionery bar (SCHO), or placebo (P) 5 min before exercise. An additional trial was performed in which a high-CHO meal (200 g) taken 4 h before exercise was combined with a confectionery bar feeding (M + SCHO) immediately before the activity. At 10 min of exercise, serum glucose values were elevated by 18 and 24% during SCHO and LCHO, respectively, compared with P. At 0 and 45 min no significant differences were observed in muscle glycogen concentration or total use between the four trials. Total work produced during the final 15 min of exercise was significantly greater (P less than 0.05) during M + SCHO (194,735 +/- 9,448 N X m), compared with all other trials and significantly greater (P less than 0.05) during LCHO and SCHO (175,204 +/- 11,780 and 176,013 +/- 10,465 N X m, respectively) than trial P (159,143 +/- 11,407 N X m). These results suggest that, under conditions when CHO stores are less than optimal, exercise performance is enhanced with the ingestion of 45 g of CHO 5 min before 1 h of intense cycling.(ABSTRACT TRUNCATED AT 250 WORDS)

Substrate utilization in leg muscle of men after heat acclimation.

Eight men were heat acclimated (39.6 degrees C and 29.2% rh) for 8 days to examine changes in substrate utilization. A heat exercise test (HET), (cycling for 60 min; 50% maximal O2 consumption) was performed before (UN-HET) and after (ACC-HET) the acclimation period. Muscle glycogen utilization (67.0 vs. 37.6 mmol/kg wet wt), respiratory exchange ratio (0.85 +/- 0.002 vs. 0.83 +/- 0.001), and calculated rate of carbohydrate oxidation (75.15 +/- 1.38 vs. 64.80 +/- 1.52 g/h) were significantly reduced (P less than 0.05) during the ACC-HET. Significantly lower (P less than 0.05) femoral venous glucose (15, 30, and 45 min) and lactate (15 min) levels were observed during the ACC-HET. No differences were observed in plasma free fatty acid (FFA) and glycerol concentrations or glucose, lactate and glycerol arteriovenous uptake/release between tests. A small but significant increase (P less than 0.05) above resting levels in FFA uptake was observed during the ACC-HET. Leg blood flow was slightly greater (P greater than 0.05) during the ACC-HET (4.64 +/- 0.13 vs. 4.80 +/- 0.13 l/min). These findings indicate a reduced use of muscle glycogen following heat acclimation. However, the decrease is not completely explained by a shift toward greater lipid oxidation or increased blood flow.