Lipid oxidation in fit young adults during postexercise recovery.

To evaluate the hypothesis that lipid oxidation predominates in postexercise recovery, we examined healthy men (n = 6; age = 21.2 +/- 0.6 yr) and women (n = 6; age = 22.8 +/- 2.1 yr) during and after two exercise tasks [89 min at 45% and 60 min at 65% of peak rate of oxygen consumption (V(O2 peak))] as well as a time-matched resting control trial (Con). Exercise bouts were matched for energy expenditure. Respiratory exchange ratios (RER) during exercise at 65% V(O2 peak) for both men and women (0.95 +/- 0.01 and 0.93 +/- 0.02) were significantly higher than 45% V(O2 peak) (0.89 +/- 0.01 and 0.86 +/- 0.02) and Con trials (0.86 +/- 0.01 and 0.86 +/- 0.02, respectively). During recovery, for men RER values were 0.78 +/- 0.01 and 0.76 +/- 0.01 after 45% and 65% exercise, respectively. For women, values were 0.79 +/- 0.01 and 0.78 +/- 0.01. These were significantly lower than during both the preexercise resting period and the corresponding no-exercise Con period (0.82 +/- 0.01 and 0.83 +/- 0.01, mean RER for men and women, respectively). Hence, the contribution of lipid oxidation to energy supply increased significantly during recovery compared with preexercise levels, and it was greater after exercise than during the time-matched, no-exercise Con period. It is concluded that, although carbohydrate is the major fuel source during moderate- to high-intensity exercise, 1) there is substantial postexercise lipid oxidation; and 2) lipid oxidation is the same during postexercise recovery whether the relative power output is 45% or 65% of V(O2 peak) when energy expenditure of exercise is matched.     

Effect of naloxone on perceived exertion and exercise capacity during maximal cycle ergometry.

We assessed the effects of naloxone, an opioid antagonist, on exercise capacity in 13 men and 5 women (mean age = 30.1 yr, range = 21-35 yr) during a 25 W/min incremental cycle ergometer test to exhaustion on different days during familiarization trial and then after 30 mg (iv bolus) of naloxone or placebo (Pl) in a double-blind, crossover design. Minute ventilation (Ve), O(2) consumption (Vo(2)), CO(2) production, and heart rate (HR) were monitored. Perceived exertion rating (0-10 scale) and venous samples for lactate were obtained each minute. Lactate and ventilatory thresholds were derived from lactate and gas-exchange data. Blood pressure was obtained before exercise, 5 min postinfusion, at maximum exercise, and 5 min postexercise. There were no control-Pl differences. The naloxone trial demonstrated decreased exercise time (96% Pl; P < 0.01), total cumulative work (96% Pl; P < 0.002), peak Vo(2) (94% Pl; P < 0.02), and HR (96% Pl; P < 0.01). Other variables were unchanged. HR and Ve were the same at the final common workload, but perceived exertion was higher (8.1 +/- 0.5 vs. 7.1 +/- 0.5) after naloxone than Pl (P < 0.01). The threshold for effort perception amplification occurred at approximately 60 +/- 4% of Pl peak Vo(2). Thus we conclude that peak work capacity was limited by perceived exertion, which can be attenuated by endogenous opioids rather than by physiological limits.     

The role of exercise intensity in the bone metabolic response to an acute bout of weight-bearing exercise

We compared the effects of exercise intensity (EI) on bone metabolism during and for 4 days after acute, weight-bearing endurance exercise. Ten males [mean ± SD maximum oxygen uptake (Vo(2max)): 56.2 ± 8.1 ml·min(-1)·kg(-1)] completed three counterbalanced 8-day trials. Following three control days, on day 4, subjects completed 60 min of running at 55%, 65%, and 75% Vo(2max). Markers of bone resorption [COOH-terminal telopeptide region of collagen type 1 (β-CTX)] and formation [NH(2)-terminal propeptides of procollagen type 1 (P1NP), osteocalcin (OC), bone-alkaline phosphatase (ALP)], osteoprotegerin (OPG), parathyroid hormone (PTH), albumin-adjusted calcium (ACa), phosphate (PO(4)), and cortisol were measured during and for 3 h after exercise and on four follow-up days (FU1-FU4). At 75% Vo(2max), β-CTX was not significantly increased from baseline by exercise but was higher compared with 55% (17-19%, P < 0.01) and 65% (11-13%, P < 0.05) Vo(2max) in the first hour postexercise. Concentrations were decreased from baseline in all three groups by 39-42% (P < 0.001) at 3 h postexercise but not thereafter. P1NP increased (P < 0.001) during exercise only, while bone-ALP was increased (P < 0.01) at FU3 and FU4, but neither were affected by EI. PTH and cortisol increased (P < 0.001) with exercise at 75% Vo(2max) only and were higher (P < 0.05) than at 55% and 65% Vo(2max) during and immediately after exercise. The increases (P < 0.001) in OPG, ACa, and PO(4) with exercise were not affected by EI. Increasing EI from 55% to 75% Vo(2max) during 60 min of running resulted in higher β-CTX concentrations in the first hour postexercise but had no effect on bone formation markers. Increased bone-ALP concentrations at 3 and 4 days postexercise suggest a beneficial effect of this type of exercise on bone mineralization. The increase in OPG was not influenced by exercise intensity, whereas PTH was increased at 75% Vo(2max) only, which cannot be fully explained by changes in serum calcium or PO(4) concentrations.     

Menstrual cycle phase and oral contraceptive effects on triglyceride mobilization during exercise.

We examined the effects of menstrual cycle phase and oral contraceptive (OC) use on triglyceride mobilization during 90 min of rest and 60 min of leg ergometry exercise at 45 and 65% peak O(2) uptake (Vo(2 peak)) in eight moderately physically active, eumenorrheic women (24.8 +/- 1.2 yr). Subjects were tested during the follicular phase (FP) and the luteal phase (LP) before OC use and during the inactive phase (IP) and high-dose phase (HP) after 4 complete mo of OC use. Glycerol rate of appearance (R(a)), a measure of triglyceride mobilization, was determined in a 3-h postabsorptive state using a primed constant infusion of [1,1,2,3,3-(2)H]glycerol. Before OC use (BOC), there were no significant differences between FP and LP in any of the variables studied. Dietary composition, exercise patterns, plasma glycerol concentrations, growth hormone concentrations, and exercise respiratory exchange ratio did not change with OC use. However, 4 mo of OC use significantly (P < 0.05) increased glycerol R(a) in HP during exercise at 45% Vo(2 peak) (6.2 +/- 0.2, 6.5 +/- 0.4, and 7.7 +/- 1.1 micromol.kg(-1).min(-1) for BOC, IP, and HP, respectively) and in IP and HP at 65% Vo(2 peak) (6.6 +/- 0.1, 8.2 +/- 0.6, and 8.1 +/- 0.7 micromol.kg(-1).min(-1) for BOC, IP, and HP, respectively). Plasma cortisol concentrations were significantly higher with OC use at rest and during exercise at 45 and 65% Vo(2 peak). In summary, although fluctuations of endogenous ovarian steroids have little effect on triglyceride mobilization, the synthetic ovarian steroids found in OCs increase triglyceride mobilization and plasma cortisol concentrations in exercising women. We conclude that the hierarchy of effects of ovarian steroids and their analogs on triglyceride mobilization in exercising women is as follows: energy flux > OC use > recent carbohydrate nutrition, menstrual cycle effects.     

Contributions of working muscle to whole body lipid metabolism are altered by exercise intensity and training

To evaluate the contribution of working muscle to whole body lipid oxidation, we examined the effects of exercise intensity and endurance training (9 wk, 5 days/wk, 1 h, 75% Vo(2 peak)) on whole body and leg free fatty acid (FFA) kinetics in eight male subjects (26 +/- 1 yr, means +/- SE). Two pretraining trials [45 and 65% Vo(2 max) (45UT, 65UT)] and two posttraining trials [65% of pretraining Vo(2 peak) (ABT), and 65% of posttraining Vo(2 peak) (RLT)] were performed using [1-(13)C]palmitate infusion and femoral arteriovenous sampling. Training increased Vo(2 peak) by 15% (45.2 +/- 1.2 to 52.0 +/- 1.8 ml.kg(-1).min(-1), P < 0.05). Muscle FFA fractional extraction was lower during exercise (EX) compared with rest regardless of workload or training status ( approximately 20 vs. 48%, P < 0.05). Two-leg net FFA balance increased from net release at rest ( approximately -36 micromol/min) to net uptake during EX for 45UT (179 +/- 75), ABT (236 +/- 63), and RLT (136 +/- 110) (P < 0.05), but not 65UT (51 +/- 127). Leg FFA tracer measured uptake was higher during EX than rest for all trials and greater during posttraining in RLT (716 +/- 173 micromol/min) compared with pretraining (45UT 450 +/- 80, 65UT 461 +/- 72, P < 0.05). Leg muscle lipid oxidation increased with training in ABT (730 +/- 163 micromol/min) vs. 65UT (187 +/- 94, P < 0.05). Leg muscle lipid oxidation represented approximately 62 and 30% of whole body lipid oxidation at lower and higher relative intensities, respectively. In summary, training can increase working muscle tracer measured FFA uptake and lipid oxidation for a given power output, but both before and after training the association between whole body and leg lipid metabolism is reduced as exercise intensity increases.     

Effects of the menstrual cycle and sex on postexercise hemodynamics

Factors associated with the menstrual cycle, such as the endogenous hormones estrogen and progesterone, have dramatic effects on cardiovascular regulation. It is unknown how this affects postexercise hemodynamics. Therefore, we examined the effects of the menstrual cycle and sex on postexercise hemodynamics. We studied 14 normally menstruating women [24.0 (4.2) yr; SD] and 14 men [22.5 (3.5) yr] before and through 90 min after cycling at 60% .VO2(peak) for 60 min. Women were studied during their early follicular, ovulatory, and mid-luteal phases; men were studied once. In men and women during all phases studied, mean arterial pressure was decreased after exercise throughout 60 min (P < 0.001) postexercise and returned to preexercise values at 90 min (P = 0.089) postexercise. Systemic vascular conductance was increased following exercise in both sexes throughout 60 min (P = 0.005) postexercise and tended to be elevated at 90 min postexercise (P = 0.052), and femoral vascular conductance was increased following exercise throughout 90 min (P < 0.001) postexercise. Menstrual phase and sex had no effect on the percent reduction in arterial pressure (P = 0.360), the percent rise in systemic vascular conductance (P = 0.573), and the percent rise in femoral vascular conductance (P = 0.828) from before to after exercise, nor did the pattern of these responses differ across recovery with phase or sex. This suggests that postexercise hemodynamics are largely unaffected by sex or factors associated with the menstrual cycle.     

Substantial working muscle glycerol turnover during two-legged cycle ergometry

We combined tracer and arteriovenous (a-v) balance techniques to evaluate the effects of exercise and endurance training on leg triacylglyceride turnover as assessed by glycerol exchange. Measurements on an exercising leg were taken to be a surrogate for working skeletal muscle. Eight men completed 9 wk of endurance training [5 days/wk, 1 h/day, 75% peak oxygen consumption (Vo(2peak))], with leg glycerol turnover determined during two pretraining trials [45 and 65% Vo(2peak) (45% Pre and 65% Pre, respectively)] and two posttraining trials [65% of pretraining Vo(2peak) (ABT) and 65% of posttraining Vo(2peak) (RLT)] using [(2)H(5)]glycerol infusion, femoral a-v sampling, and measurement of leg blood flow. Endurance training increased Vo(2peak) by 15% (45.2 +/- 1.2 to 52.0 +/- 1.8 mlxkg(-1)xmin(-1), P < 0.05). At rest, there was tracer-measured leg glycerol uptake (41 +/- 8 and 52 +/- 15 micromol/min for pre- and posttraining, respectively) even in the presence of small, but significant, net leg glycerol release (-68 +/- 19 and -50 +/- 13 micromol/min, respectively; P < 0.05 vs. zero). Furthermore, while there was no significant net leg glycerol exchange during any of the exercise bouts, there was substantial tracer-measured leg glycerol turnover during exercise (i.e., simultaneous leg muscle uptake and leg release) (uptake, release: 45% Pre, 194 +/- 41, 214 +/- 33; 65% Pre, 217 +/- 79, 201 +/- 84; ABT, 275 +/- 76, 312 +/- 87; RLT, 282 +/- 83, 424 +/- 75 micromol/min; all P < 0.05 vs. corresponding rest). Leg glycerol turnover was unaffected by exercise intensity or endurance training. In summary, simultaneous leg glycerol uptake and release (indicative of leg triacylglyceride turnover) occurs despite small or negligible net leg glycerol exchange, and furthermore, leg glycerol turnover can be substantially augmented during exercise.     

Untrained females: effects of submaximal exercise and heat on body fluids.

Five untrained females having no history of heat exposure worked in a cool (16-20 degrees C db, 28% rh) environment on day 1 and a warm environment on day 2 (45 degrees C db, 28% rh). Exercise level (bicycle ergometer) was 30% of individual Vo2 max values and work time on both days was 45 min. Venous blood samples were obtained at rest, after 40 min of exercise and 25 min after exercise ceased. Analysis of blood samples indicated an 8.3% increase in Hct during exercise on day 1 and a plasma volume reduction of 12.8% though total circulating protein increased 11.5%. Except for K+ all parameters approximated control values within 25 min postexercise. On day 2, exercise in heat caused a 12% increase in Hct and a plasma volume reduction of 17.7%. Mean total protein did not significantly change from resting values. These data indicated that for a given % Vo2 max, untrained females suffer considerably greater reductions in plasma volumes than do exercised males. Similar to males, dilatation of the cutaneous vascular bed in unacclimatized females resulted in loss of protein from the vascular volume.     

Effects of intravenous N-acetylcysteine infusion on time to fatigue and potassium regulation during prolonged cycling exercise.

The production of reactive oxygen species in skeletal muscle is linked with muscle fatigue. This study investigated whether the antioxidant compound N-acetylcysteine (NAC) augments time to fatigue during prolonged, submaximal cycling exercise. Seven men completed a double-blind, crossover study, receiving NAC or placebo before and during cycling exercise, comprising 45 min at 70% of peak oxygen consumption (Vo2 peak) and then to fatigue at 90% Vo2 peak. NAC was intravenously infused at 125 mg.kg-1.h-1 for 15 min and then 25 mg.kg-1.h-1 for 20 min before and throughout exercise, which was continued until fatigue. Arterialized venous blood was analyzed for NAC concentration, hematology, and plasma electrolytes. NAC induced no serious adverse reactions and did not affect hematology, acid-base status, or plasma electrolytes. Time to fatigue was reproducible in preliminary trials (coefficient of variation 7.4 +/- 1.2%) and was not augmented by NAC (NAC 14.6 +/- 4.5 min; control 12.8 +/- 5.4 min). However, time to fatigue during NAC trials was correlated with Vo2 peak (r = 0.78; P < 0.05), suggesting that NAC effects on performance may be dependent on training status. The rise in plasma K+ concentration at fatigue was attenuated by NAC (P < 0.05). The ratio of rise in K+ concentration to work and the percentage change in time to fatigue tended to be inversely related (r = -0.71; P < 0.07). Further research is required to clarify a possible training status-dependent effect of NAC on muscle performance and K+ regulation.     

IMCL area density, but not IMCL utilization, is higher in women during moderate-intensity endurance exercise, compared with men

Women use more fat during endurance exercise as evidenced by a lower respiratory exchange ratio (RER). The contribution of intramyocellular lipid (IMCL) to lipid oxidation during endurance exercise is controversial, and studies investigating sex differences in IMCL utilization have found conflicting results. We determined the effect of sex on net IMCL use during an endurance exercise bout using an ultrastructural evaluation. Men (n = 17) and women (n = 19) completed 90-min cycling at 63% Vo(2peak). Biopsies were taken before and after exercise and fixed for electron microscopy to determine IMCL size, # IMCL/area, IMCL area density, and the % IMCL touching mitochondria. Women had a lower RER and carbohydrate oxidation rate and a higher lipid oxidation rate during exercise (P < 0.05), compared with men. Women had a higher # IMCL/area and IMCL area density (P < 0.05), compared with men. Women, but not men, had a higher % IMCL touching mitochondria postexercise (P = 0.03). Exercise decreased IMCL area density (P = 0.01), due to a decrease in the # IMCL/area (P = 0.02). There was no sex difference in IMCL size or net use. In conclusion, women have higher IMCL area density compared with men, due to an increased # IMCL and not an increased IMCL size, as well as an increased % IMCL touching mitochondria postexercise. Endurance exercise resulted in a net decrease in IMCL density due to decreased number of IMCL, not decreased IMCL size, in both sexes.     

Glucose kinetics differ between women and men, during and after exercise.

As exercise can improve the regulation of glucose and carbohydrate metabolism, it is important to establish biological factors, such as sex, that may influence these outcomes. Glucose kinetics, therefore, were compared between women and men at rest, during exercise, and postexercise. It was hypothesized that glucose flux would be significantly lower in women than men during both the exercise and postexercise periods. Subjects included normal weight, healthy, eumenorrehic women and men, matched for habitual activity level and maximal oxygen uptake per kilogram lean body mass. Testing occurred following 3 days of diet control, with no exercise the day before. Subjects were tested in the overnight-fasted condition with women studied in the midluteal phase of the menstrual cycle. Resting (120 min), exercise (85% lactate threshold, 90 min), and postexercise (180 min) measurements of glucose flux and substrate metabolism were made. During exercise, women had a significantly lower rate of glucose appearance (Ra) (P<0.001) and disappearance (Rd) (P<0.002) compared with men. Maximal values were achieved at 90 min of exercise for both glucose Ra (mean+/-SE: 22.8+/-1.12 micromol.kg body wt-1.min-1 women and 33.6+/-1.79 micromol.kg body wt-1.min-1 men) and glucose Rd (23.2+/-1.26 and 34.1+/-1.71 micromol.kg body wt-1.min-1, respectively). Exercise epinephrine concentration was significantly lower in women compared with men (P<0.02), as was the increment in glucagon from rest to exercise (P<0.04). During the postexercise period, glucose Ra and Rd were also significantly lower in women vs. men (P<0.001), with differences diminishing over time. In conclusion, circulating blood glucose flux was significantly lower during 90 min of moderate exercise, and immediately postexercise, in women compared with men. Sex differences in the glucagon increase to exercise, and/or the epinephrine levels during exercise, may play a role in determining these sex differences in exercise glucose turnover.     

H1 and H2 receptors mediate postexercise hyperemia in sedentary and endurance exercise-trained men and women.

In sedentary individuals, H(1) receptors mediate the early portion of postexercise skeletal muscle hyperemia, whereas H(2) receptors mediate the later portion. It is not known whether postexercise hyperemia also presents in endurance-trained individuals. We hypothesized that the postexercise skeletal muscle hyperemia would also exist in endurance-trained individuals and that combined blockade of H(1) and H(2) receptors would abolish the long-lasting postexercise hyperemia in trained and sedentary individuals. We studied 28 sedentary and endurance trained men and women before and through 90 min after a 60-min bout of cycling at 60% peak O(2) uptake on control and combined H(1)- and H(2)-receptor antagonist days (fexofenadine and ranitidine). We measured arterial pressure (brachial auscultation) and femoral blood flow (Doppler ultrasound). On the control day, femoral vascular conductance (calculated as flow/pressure) was elevated in all groups 60 min after exercise (sedentary men: Delta86 +/- 35%, trained men, Delta65 +/- 18%; sedentary women, Delta61 +/- 19%, trained women: Delta59 +/- 23%, where Delta is change; all P < 0.05 vs. preexercise). In contrast, on the histamine antagonist day, femoral vascular conductance was not elevated in any of the groups after exercise (sedentary men: Delta21 +/- 17%, trained men: Delta9 +/- 5%, sedentary women: Delta19 +/- 4%, trained women: Delta11 +/- 11%; all P > 0.16 vs. preexercise; all P < 0.05 vs. control day). These data suggest postexercise skeletal muscle hyperemia exists in endurance trained men and women. Furthermore, histaminergic mechanisms produce the long-lasting hyperemia in sedentary and endurance-trained individuals.     

Left ventricular function during arm exercise: influence of leg cycling and lower body positive pressure.

The purpose of this study was to characterize left ventricular (LV) diastolic filling and systolic performance during graded arm exercise and to examine the effects of lower body positive pressure (LBPP) or concomitant leg exercise as means to enhance LV preload in aerobically trained individuals. Subjects were eight men with a mean age (+/-SE) of 26.8 +/- 1.2 yr. Peak exercise testing was first performed for both legs [maximal oxygen uptake (Vo(2)) = 4.21 +/- 0.19 l/min] and arms (2.56 +/- 0.16 l/min). On a separate occasion, LV filling and ejection parameters were acquired using non-imaging scintography using in vivo red blood cell labeling with technetium 99(m) first during leg exercise performed in succession for 2 min at increasing grades to peak effort. Graded arm exercise (at 30, 60, 80, and 100% peak Vo(2)) was performed during three randomly assigned conditions: control (no intervention), with concurrent leg cycling (at a constant 15% leg maximal Vo(2)) or with 60 mmHg of LBPP using an Anti G suit. Peak leg exercise LV ejection fraction was higher than arm exercise (60.9 +/- 1.7% vs. 55.9 +/- 2.7%; P < 0.05) as was peak LV end-diastolic volume was reported as % of resting value (110.3 +/- 4.4% vs. 97 +/- 3.7%; P < 0.05) and peak filling rate (end-diastolic volume/s; 6.4 +/- 0.28% vs. 5.2 +/- 0.25%). Concomitant use of either low-intensity leg exercise or LBPP during arm exercise failed to significantly increase LV filling or ejection parameters. These observations suggest that perturbations in preload fail to overcome the inherent hemodynamic conditions present during arm exercise that attenuate LV performance.     

Effects of oral contraceptives on glucose flux and substrate oxidation rates during rest and exercise.

We examined the effects of oral contraceptives (OC) on glucose flux and whole body substrate oxidation rates during rest (90 min) and two exercise intensities [60-min leg ergometer cycling at 45 and 65% peak O(2) uptake (Vo(2 peak))]. Eight healthy, eumenorrheic women were studied during the follicular and luteal phases before OC and the inactive and high-dose phases after 4 mo of a low-dose, triphasic OC. Subjects were studied in the morning 3 h after a standardized (308 kcal) breakfast. There were significant reductions in glucose rates of appearance and disappearance during exercise of both intensities with OC but not rest. There were no phase effects on substrate oxidation during rest or exercise. These results are interpreted to mean that, in women fed several hours before study, 1) OC decreases glucose flux, but not overall carbohydrate and lipid oxidation rates during moderate-intensity exercise; and 2) synthetic ovarian hormone analogs in the doses contained in OC have greater metabolic effects on glucose metabolism during exercise than do endogenous ovarian hormones.     

Regional hemodynamics during postexercise hypotension. II. Cutaneous circulation.

After an acute bout of exercise, there is an unexplained elevation in systemic vascular conductance that is not completely offset by an increase in cardiac output, resulting in a postexercise hypotension. The contributions of the splanchnic and renal circulations are examined in a companion paper (Pricher MP, Holowatz LA, Williams JT, Lockwood JM, and Halliwill JR. J Appl Physiol 97: 2065-2070, 2004). The purpose of this study was to determine the contribution of the cutaneous circulation in postexercise hypotension under thermoneutral conditions (approximately 23 degrees C). Arterial blood pressure was measured via an automated sphygmomanometer, internal temperature was measured via an ingestible pill, and skin temperature was measured with eight thermocouples. Red blood cell flux (laser-Doppler flowmetry) was monitored at four skin sites (chest, forearm, thigh, and leg), and cutaneous vascular conductance (CVC) was calculated (red blood cell flux/mean arterial pressure) and scaled as percent maximal CVC (local heating to 43 degrees C). Ten subjects [6 men and 4 women; age 23 +/- 1 yr; peak O(2) uptake (Vo(2 peak)) 45.8 +/- 2.0 ml.kg(-1).min(-1)] volunteered for this study. After supine rest (30 min), subjects exercised on a bicycle ergometer for 1 h at 60% of their Vo(2 peak) and were then positioned supine for 90 min. Exercise elicited a postexercise hypotension reaching a nadir at 46.0 +/- 4.5 min postexercise (77 +/- 1 vs. 82 +/- 2 mmHg preexercise; P < 0.05). Internal temperature increased (38.0 +/- 0.1 vs. 36.7 +/- 0.1 degrees C preexercise; P < 0.05), remaining elevated at 90 min postexercise (36.9 +/- 0.1 degrees C vs. preexercise; P < 0.05). CVC at all four skin sites was elevated by the exercise bout (P < 0.05), returning to preexercise values within 50 min postexercise (P > 0.05). Therefore, although transient changes in CVC occur postexercise, they do not appear to play an obligatory role in mediating postexercise hypotension under thermoneutral conditions.     

Relation of heart rate to percent VO2 peak during submaximal exercise in the heat.

We tested the hypothesis that elevation in heart rate (HR) during submaximal exercise in the heat is related, in part, to increased percentage of maximal O(2) uptake (%Vo(2 max)) utilized due to reduced maximal O(2) uptake (Vo(2 max)) measured after exercise under the same thermal conditions. Peak O(2) uptake (Vo(2 peak)), O(2) uptake, and HR during submaximal exercise were measured in 22 male and female runners under four environmental conditions designed to manipulate HR during submaximal exercise and Vo(2 peak). The conditions involved walking for 20 min at approximately 33% of control Vo(2 max) in 25, 35, 40, and 45 degrees C followed immediately by measurement of Vo(2 peak) in the same thermal environment. Vo(2 peak) decreased progressively (3.77 +/- 0.19, 3.61 +/- 0.18, 3.44 +/- 0.17, and 3.13 +/- 0.16 l/min) and HR at the end of the submaximal exercise increased progressively (107 +/- 2, 112 +/- 2, 120 +/- 2, and 137 +/- 2 beats/min) with increasing ambient temperature (T(a)). HR and %Vo(2 peak) increased in an identical fashion with increasing T(a). We conclude that elevation in HR during submaximal exercise in the heat is related, in part, to the increase in %Vo(2 peak) utilized, which is caused by reduced Vo(2 peak) measured during exercise in the heat. At high T(a), the dissociation of HR from %Vo(2 peak) measured after sustained submaximal exercise is less than if Vo(2 max) is assumed to be unchanged during exercise in the heat.     

Short-term training attenuates muscle TCA cycle expansion during exercise in women.

Muscle glycogenolytic flux and lactate accumulation during exercise are lower after 3-7 days of "short-term" aerobic training (STT) in men (e.g., Green HJ, Helyar R, Ball-Burnett M, Kowalchuk N, Symon S, and Farrance B. J Appl Physiol 72: 484-491, 1992). We hypothesized that 5 days of STT would attenuate pyruvate production and the increase in muscle tricarboxylic acid cycle intermediates (TCAI) during exercise, because of reduced flux through the reaction catalyzed by alanine aminotransferase (AAT; pyruvate + glutamate <--> 2-oxoglutarate + alanine). Eight women [22 +/- 1 yr, peak oxygen uptake (Vo2 peak) = 40.3 +/- 4.6 ml. kg-1. min-1] performed seven 45-min bouts of cycle exercise at 70% Vo2 peak over 9 days (1 bout/day; rest only on days 2 and 8). During the first and last bouts, biopsies (vastus lateralis) were obtained at rest and after 5 and 45 min of exercise. Muscle glycogen concentration was approximately 50% higher at rest after STT (493 +/- 38 vs. 330 +/- 20 mmol/kg dry wt; P 相似文献   

Gender differences in cardiovascular regulation during recovery from exercise.

Are women more susceptible to acute postexercise orthostatic hypotension compared with men? We hypothesized that decreases in arterial pressure during recovery from dynamic exercise are greater in women compared with men. We studied 8 men and 11 women during inactive and active recovery from cycling exercise. Heart rate, stroke volume (SV), cardiac output, mean arterial pressure (MAP), and total peripheral resistance (TPR) were measured during and after 3 min of exercise at 60% of calculated maximum heart rate. At 1 min after exercise, MAP decreased less (P < 0.05) during inactive recovery in men (-18 +/- 2 mmHg) compared with women (-30 +/- 2 mmHg). This difference was due to greater decreases in SV and less increase in TPR during inactive recovery from exercise in women compared with men. These differences persisted for 5 min after exercise. MAP decreased less during active recovery in men compared with women. These findings suggest that women may have increased risk of postexercise orthostatic hypotension and that active recovery from exercise may reduce this risk.     

Measurement of gluconeogenesis in exercising men by mass isotopomer distribution analysis.

We evaluated the hypothesis that coordinated adjustments in absolute rates of gluconeogenesis (GNG(ab)) and hepatic glycogenolysis (Gly) would maintain euglycemia and match glucose production (GP) to peripheral utilization during rest and exercise. Specifically, we evaluated the extent to which gradations in exercise power output would affect the contribution of GNG(ab) to GP. For these purposes, we employed mass isotopomer distribution analysis (MIDA) and isotope-dilution techniques on eight postabsorptive (PA) endurance-trained men during 90 min of leg cycle ergometry at 45 and 65% peak O(2) consumption (VO(2 peak); moderate and hard intensities, respectively) and the preceding rest period. GP was constant in resting subjects, whereas the fraction from GNG (f(GNG)) increased over time during rest (22.3 +/- 0.9% at 11.25 h PA vs. 25.6 +/- 0.9% at 12.0 h PA, P < 0.05). In the transition from rest to exercise, GP increased in an intensity-dependent manner (rest, 2.0 +/- 0.1; 45%, 4.0 +/- 0.4; 65%, 5.84 +/- 0.64 mg. kg(-1). min(-1), P < 0.05), although glucose rate of disappearance exceeded rate of appearance during the last 30 min of exercise at 65% VO(2 peak). Compared with rest, increases in GP were sustained by 92 and 135% increments in GNG(ab) during moderate- and hard-intensity exercises, respectively. Correspondingly, Gly (calculated as the difference between GP and MIDA-measured GNG(ab)) increased 100 and 203% over rest during the two exercise intensities. During moderate-intensity exercise, f(GNG) was the same as at rest; however, during the harder exercise f(GNG) decreased significantly to account for only 21% of GP. The highest sustained GNG(ab) observed in these trials on PA men was 1.24 +/- 0.3 mg. kg(-1). min(-1). We conclude that, after an overnight fast, 1) absolute GNG rates increased with intensity of effort despite a reduced f(GNG) at 65% VO(2 peak), 2) during exercise Gly is more responsible than GNG(ab) for maintaining GP, and 3) in 12-h fasted men, neither increased Gly or GNG(ab) nor was their combination able to maintain euglycemia during prolonged hard (65% VO(2 peak)) exercise.     

Effects of progressive exercise and hypoxia on human muscle sarcoplasmic reticulum function.

This study examined the effects of progressive exercise to fatigue in normoxia (N) on muscle sarcoplasmic reticulum (SR) Ca(2+) cycling and whether alterations in SR Ca(2+) cycling are related to the blunted peak mechanical power output (PO(peak)) and peak oxygen consumption (Vo(2 peak)) observed during progressive exercise in hypoxia (H). Nine untrained men (20.7 +/- 0.42 yr) performed progressive cycle exercise to fatigue on two occasions, namely during N (inspired oxygen fraction = 0.21) and during H (inspired oxygen fraction = 0.14). Tissue extracted from the vastus lateralis before exercise and at power output corresponding to 50 and 70% of Vo(2 peak) (as determined during N) and at fatigue was used to investigate changes in homogenate SR Ca(2+)-cycling properties. Exercise in H compared with N resulted in a 19 and 21% lower (P < 0.05) PO(peak) and Vo(2 peak), respectively. During progressive exercise in N, Ca(2+)-ATPase kinetics, as determined by maximal activity, the Hill coefficient, and the Ca(2+) concentration at one-half maximal activity were not altered. However, reductions with exercise in N were noted in Ca(2+) uptake (before exercise = 357 +/- 29 micromol x min(-1) x g protein(-1); at fatigue = 306 +/- 26 micromol x min(-1) x g protein(-1); P < 0.05) when measured at free Ca(2+) concentration of 2 microM and in phase 2 Ca(2+) release (before exercise = 716 +/- 33 micromol x min(-1) x g protein(-1); at fatigue = 500 +/- 53 micromol x min(-1) x g protein(-1); P < 0.05) when measured in vitro in whole muscle homogenates. No differences were noted between N and H conditions at comparable power output or at fatigue. It is concluded that, although structural changes in SR Ca(2+)-cycling proteins may explain fatigue during progressive exercise in N, they cannot explain the lower PO(peak) and Vo(2 peak) observed during H.