Effects of exercise training on thermoregulatory responses and blood volume in older men.

We assessed the effects of aerobic and/or resistance training on thermoregulatory responses in older men and analyzed the results in relation to the changes in peak oxygen consumption rate (VO(2 peak)) and blood volume (BV). Twenty-three older men [age, 64 +/- 1 (SE) yr; VO(2 peak), 32.7 +/- 1.1 ml. kg(-1). min(-1)] were divided into three training regimens for 18 wk: control (C; n = 7), aerobic training (AT; n = 8), and resistance training (RT; n = 8). Subjects in C were allowed to perform walking of ~10,000 steps/day, 6-7 days/wk. Subjects in AT exercised on a cycle ergometer at 50-80% VO(2 peak) for 60 min/day, 3 days/wk, in addition to the walking. Subjects in RT performed a resistance exercise, including knee extension and flexion at 60-80% of one repetition maximum, two to three sets of eight repetitions per day, 3 days/wk, in addition to the walking. After 18 wk of training, VO(2 peak) increased by 5.2 +/- 3.4% in C (P > 0.07), 20.0 +/- 2.5% in AT (P < 0.0001), and 9.7 +/- 5.1% in RT (P < 0.003), but BV remained unchanged in all trials. In addition, the esophageal temperature (T(es)) thresholds for forearm skin vasodilation and sweating, determined during 30-min exercise of 60% VO(2 peak) at 30 degrees C, decreased in AT (P < 0.02) and RT (P < 0.02) but not in C (P > 0.2). In contrast, the slopes of forearm skin vascular conductance/T(es) and sweat rate/T(es) remained unchanged in all trials, but both increased in subjects with increased BV irrespective of trials with significant correlations between the changes in the slopes and BV (P < 0.005 and P < 0.0005, respectively). Thus aerobic and/or resistance training in older men increased VO(2 peak) and lowered T(es) thresholds for forearm skin vasodilation and sweating but did not increase BV. Furthermore, the sensitivity of the increase in skin vasodilation and sweating at a given increase in T(es) was more associated with BV than with VO(2 peak).     

Effects of hypohydration on thermoregulation during exercise before and after 5-day aerobic training in a warm environment in young men

We examined whether enhanced cardiovascular and thermoregulatory responses during exercise after short-term aerobic training in a warm environment were reversed when plasma volume (PV) expansion was reversed by acute isotonic hypohydration. Seven young men performed aerobic training at the 70% peak oxygen consumption rate (Vo(?peak)) at 30°C atmospheric temperature and 50% relative humidity, 30 min/day for 5 days. Before and after training, we performed the thermoregulatory response test while measuring esophageal temperature (T(es)), forearm skin vascular conductance, sweat rate (SR), and PV during 30 min exercise at the metabolic rate equivalent to pretraining 65% Vo(?peak) in euhydration under the same environment as during training in four trials (euhydration and hypohydration, respectively). Hypohydration targeting 3% body mass was attained by combined treatment with low-salt meals to subjects from ~48 h before the test and administration of a diuretic ~4 h before the test. After training, the T(es) thresholds for cutaneous vasodilation and sweating decreased by 0.3 and 0.2°C (P = 0.008 and 0.012, respectively) when PV increased by ~10%. When PV before and after training was reduced to a similar level, ~10% reduction from that in euhydration before training, the training-induced reduction in the threshold for cutaneous vasodilation increased to a level similar to hypohydration before training (P = 0.093) while that for sweating remained significantly lower than that before training (P = 0.004). Thus the enhanced cutaneous vasodilation response after aerobic training in a warm environment was reversed when PV expansion was reversed while the enhanced SR response remained partially.     

Reduced hyperthermia-induced cutaneous vasodilation and enhanced exercise-induced plasma water loss at simulated high altitude (3,200 m) in humans

We examined whether less convective heat loss during exercise at high altitude than at sea level was partially caused by reduced cutaneous vasodilation due to enhanced plasma water loss into contracting muscles and whether it was caused by hypoxia rather than by hypobaria. Seven young men performed cycling exercise for 40 min at 50% peak aerobic power in normoxia at (710 mmHg) 610 m, determined before the experiments, in three trials: 1) normobaric normoxia at 610 m (CNT), 2) hypobaric hypoxia [low pressure and low oxygen (LPLO)] at 3,200 m (510 mmHg), 3) normobaric hypoxia [normal pressure and low oxygen (NPLO)] at 610 m, in an artificial climate chamber where atmospheric temperature and relative humidity were maintained at 30°C and 50%, respectively. Subjects in CNT and LPLO breathed room air, whereas those in NPLO breathed a mixed gas of 14% O? balanced N?, equivalent to the gas composition in LPLO. We measured change in PV (ΔPV), oxygen consumption rate (Vo?), mean arterial blood pressure (MBP), esophageal temperature (T(es)), mean skin temperature (T(sk)), forearm skin blood flow (FBF), and sweat rate (SR) during exercise. Although Vo?, MBP, T(sk), and SR responses during exercise were similar between trials (P > 0.05), the sensitivity of forearm vascular conductance (FBF/MBP) in response to increased T(es) was lower in LPLO and NPLO than in CNT (P < 0.05), whereas that of SR was not, resulting in a greater increase in T(es) from minute 5 to 40 of exercise in LPLO and NPLO than in CNT (P = 0.026 and P = 0.011, respectively). ΔPV during exercise was twofold greater in LPLO and NPLO than in CNT. These variables were not significantly different between LPLO and NPLO. Thus reduced convective heat loss during exercise at 3,200 m was partially caused by reduced cutaneous vasodilation due to enhanced PV loss. Moreover, this may be caused by hypoxia rather than by hypobaria.     

Operation Everest III: role of plasma volume expansion on VO(2)(max) during prolonged high-altitude exposure.

We hypothesize that plasma volume decrease (DeltaPV) induced by high-altitude (HA) exposure and intense exercise is involved in the limitation of maximal O(2) uptake (VO(2)(max)) at HA. Eight male subjects were decompressed for 31 days in a hypobaric chamber to the barometric equivalent of Mt. Everest (8,848 m). Maximal exercise was performed with and without plasma volume expansion (PVX, 219-292 ml) during exercise, at sea level (SL), at HA (370 mmHg, equivalent to 6, 000 m after 10-12 days) and after return to SL (RSL, 1-3 days). Plasma volume (PV) was determined at rest at SL, HA, and RSL by Evans blue dilution. PV was decreased by 26% (P < 0.01) at HA and was 10% higher at RSL than at SL. Exercise-induced DeltaPV was reduced both by PVX and HA (P < 0.05). Compared with SL, VO(2)(max) was decreased by 58 and 11% at HA and RSL, respectively. VO(2)(max) was enhanced by PVX at HA (+9%, P < 0.05) but not at SL or RSL. The more PV was decreased at HA, the more VO(2)(max) was improved by PVX (P < 0.05). At exhaustion, plasma renin and aldosterone were not modified at HA compared with SL but were higher at RSL, whereas plasma atrial natriuretic factor was lower at HA. The present results suggest that PV contributes to the limitation of VO(2)(max) during acclimatization to HA. RSL-induced PVX, which may be due to increased activity of the renin-aldosterone system, could also influence the recovery of VO(2)(max).     

Acute hypoosmolality attenuates the suppression of cutaneous vasodilation with increased exercise intensity.

We examined the hypothesis that elevation of the body core temperature threshold for forearm skin vasodilation (TH(FVC)) with increased exercise intensity is partially caused by concomitantly increased plasma osmolality (P(osmol)). Eight young male subjects, wearing a body suit perfused with warm water to maintain the mean skin temperature at 34 +/- 1 degree C (ranges), performed 20-min cycle-ergometer exercise at 30% peak aerobic power (VO2(peak)) under isoosmotic conditions (C), and at 65% VO2(peak) under isoosmotic (H(EX)I(OS)) and hypoosmotic (H(EX)L(OS)) conditions. In H(EX)L(OS), hypoosmolality was attained by hypotonic saline infusion with DDAVP, a V2 agonist, before exercise. P(osmol) (mosmol/kg H2O) increased after the start of exercise in both H(EX) trials (P < 0.01) but not in C. The average P(osmol) at 5 and 10 min in H(EX)I(OS) was higher than in C (P < 0.01), whereas that in H(EX)L(OS) was lower than in H(EX)I(OS) (P < 0.01). The change in TH(FVC) was proportional to that in P(osmol) in every subject for three trials. The change in TH(FVC) per unit change in P(osmol) (deltaTH(FVC)/deltaP(osmol), degrees C x mosmol(-1) x kg H2O(-1)) was 0.064 +/- 0.012 when exercise intensity increased from C to H(EX)I(OS), similar to 0.086 +/- 0.020 when P(osmol) decreased from H(EX)I(OS) to H(EX)L(OS) (P > 0.1). Moreover, there were no significant differences in plasma volume, heart rate, mean arterial pressure, and plasma lactate concentration around TH(FVC) between H(EX)I(OS) and H(EX)L(OS) (P > 0.1). Thus the increase in TH(FVC) due to increased exercise intensity was at least partially explained by the concomitantly increased P(osmol).     

Ten-day endurance training attenuates the hyperosmotic suppression of cutaneous vasodilation during exercise but not sweating.

It is well known that hyperosmolality suppresses thermoregulatory responses and that plasma osmolality (P(osmol)) increases with exercise intensity. We examined whether the decreased esophageal temperature thresholds for cutaneous vasodilation (TH(FVC)) and sweating (TH(SR)) after 10-day endurance training (ET) are caused by either attenuated increase in P(osmol) at a given exercise intensity or blunted sensitivity of hyperosmotic suppression. Nine young male volunteers exercised on a cycle ergometer at 60% peak oxygen consumption rate (V(O2 peak)) for 1 h/day for 10 days at 30 degrees C. Before and after ET, thermoregulatory responses were measured during 20-min exercise at pretraining 70% V(O2 peak) in the same environment as during ET under isoosmotic or hyperosmotic conditions. Hyperosmolality by approximately 10 mosmol/kgH2O was attained by acute hypertonic saline infusion. After ET, V(O2 peak) and blood volume (BV) both increased by approximately 4% (P < 0.05), followed by a decrease in TH(FVC) (P < 0.05) but not by that in TH(SR). Although there was no significant decrease in P(osmol) at the thresholds after ET, the sensitivity of increase in TH(FVC) at a given increase in P(osmol) [deltaTH(FVC)/deltaP(osmol), degrees C x (mosmol/kgH2O)(-1)], determined by hypertonic infusion, was reduced to 0.021 +/- 0.005 from 0.039 +/- 0.004 before ET (P < 0.05). The individual reductions in deltaTH(FVC)/deltaP(osmol) after ET were highly correlated with their increases in BV around TH(FVC) (r = -0.89, P < 0.005). In contrast, there was no alteration in the sensitivity of the hyperosmotic suppression of sweating after ET. Thus the downward shift of TH(FVC) after ET was partially explained by the blunted sensitivity to hyperosmolality, which occurred in proportion to the increase in BV.     

Effect of high-intensity endurance training on isokinetic muscle power

The purpose of this study was to determine the effects of high-intensity endurance training on isokinetic muscle power. Six male students majoring in physical-education participated in high intensity endurance training on a cycle ergometer at 90% of maximal oxygen uptake (VO2max) for 7 weeks. The duration of the daily exercise session was set so that the energy expenditure equalled 42 kJ.kg-1 of lean body mass. Peak knee extension power was measured at six different speeds (30 degrees, 60 degrees, 120 degrees, 180 degrees, 240 degrees, and 300 degrees.s-1) with an isokinetic dynamometer. After training, VO2max increased significantly from mean values of 51.2 ml.kg-1.min-1, SD 6.5 to 56.3 ml.kg-1.min-1, SD 5.3 (P less than 0.05). Isokinetic peak power at the lower test speeds (30 degrees, 60 degrees and 120 degrees.s-1) increased significantly (P less than 0.05). However, no significant differences in muscle peak power were found at the faster velocities of 180 degrees, 240 degrees, and 300 degrees.s-1. The percentage improvement was dependent on the initial muscle peak power of each subject and the training stimulus (intensity of cycle ergometer exercise).     

Early adaptations in gas exchange, cardiac function and haematology to prolonged exercise training in man

In order to determine the effect of short-term training on central adaptations, gas exchange and cardiac function were measured during a prolonged submaximal exercise challenge prior to and following 10-12 consecutive days of exercise. In addition, vascular volumes and selected haematological properties were also examined. The subjects, healthy males between the ages of 19 and 30 years of age, cycled for 2 h per day at approximately 59% of pre-training peak oxygen consumption (VO2) i.e., maximal oxygen consumption (VO2max). Following the training, VO2max (l.min-1) increased (P less than 0.05) by 4.3% (3.94, 0.11 vs 4.11, 0.11; mean, SE) whereas maximal exercise ventilation (VE,max) and maximal heart rate (fc,max) were unchanged. During submaximal exercise, VO2 was unaltered by the training whereas carbon dioxide production (VE) and respiratory exchange ratio were all reduced (P less than 0.05). The altered activity pattern failed to elicit adaptations in either submaximal exercise cardiac output or arteriovenous O2 difference. fc was reduced (P less than 0.05). Plasma volume (PV) as measured by 125I human serum albumin increased by 365 ml or 11.8%, while red cell volume (RCV) as measured by 51chromium-labelled red blood cells (RBC) was unaltered. The increase in PV was accompanied by reductions (P less than 0.05) in haematocrit, haemoglobin concentration (g.100 ml-1), and RBCs (10(6) mm-3). Collectively these changes suggest only minimal adaptations in maximal oxygen transport during the early period of prolonged exercise training. However, as evidenced by the changes during submaximal exercise, both the ventilatory and the cardiodynamic response were altered.(ABSTRACT TRUNCATED AT 250 WORDS)     

Endurance exercise training attenuates leucine oxidation and BCOAD activation during exercise in humans

We studied the effects of a 38-day endurance exercise training program on leucine turnover and substrate metabolism during a 90-min exercise bout at 60% peak O(2) consumption (VO(2 peak)) in 6 males and 6 females. Subjects were studied at both the same absolute (ABS) and relative (REL) exercise intensities posttraining. Training resulted in a significant increase in whole body VO(2 peak) and skeletal muscle citrate synthase (CS; P < 0.001), complex I-III (P < 0.05), and total branched-chain 2-oxoacid dehydrogenase (BCOAD; P < 0.001) activities. Leucine oxidation increased during exercise for the pretraining trial (PRE, P < 0.001); however, there was no increase for either the ABS or REL posttraining trial. Leucine oxidation was significantly lower for females at all time points during rest and exercise (P < 0.01). The percentage of BCOAD in the activated state was significantly increased after exercise for both the PRE and REL exercise trials, with the increase in PRE being greater (P < 0.001) compared with REL (P < 0.05). Females oxidized proportionately more lipid and less carbohydrate during exercise compared with males. In conclusion, we found that 38 days of endurance exercise training significantly attenuated both leucine oxidation and BCOAD activation during 90 min of endurance exercise at 60% VO(2 peak) for both ABS and REL exercise intensities. Furthermore, females oxidize proportionately more lipid and less carbohydrate compared with males during endurance exercise.     

Thermogenic responses of high-altitude adapted rats on low temperatures and low pressures

The male rats were raised in two groups, one at Mt. Yatsugatake (2,100 m above sea level, the average ambient temperature 12.5 degrees C) for 30 days, and the other at a laboratory of Matsumoto (610 m above sea level, the average temperature 20 degrees C). The steady-state oxygen consumptions (VO2) and the rectal temperatures (TR) were measured under exposure conditions of various temperatures combined with different simulated altitudes. The values of VO2 and TR for a control group at 610 m-20 degrees C were regarded as 100% and the relative changes to the control values were obtained at various temperatures in the respective low-pressure condition. When measured at a simulated altitude of 2,000 m on the 2nd day after the rats raised at Mt. Yatsugatake were translocated to Matsumoto, the values at 0 degrees C and 10 degrees C room temperatures, VO2 and TR, were still significantly increased as compared with those of rats raised at Matsumoto. On the 40th day after the translocation from Mt. Yatsugatake, however, the values turned out to exhibit no significant difference in both groups. These results indicated that the greater thermogenesis of high-altitude adapted rats had been established by combined stimuli of low temperatures and low pressures as compared with those of Matsumoto-level adapted rats, but the responses returned to the control level by deadaptation process at 40 days after the translocation.     

Exercise training increases branched-chain oxoacid dehydrogenase kinase content in human skeletal muscle

The branched-chain oxoacid dehydrogenase complex (BCOAD) is rate determining for the oxidation of branched-chain amino acids (BCAAs) in skeletal muscle. Exercise training blunts the acute exercise-induced activation of BCOAD (BCOADa) in human skeletal muscle (McKenzie S, Phillips SM, Carter SL, Lowther S, Gibala MJ, Tarnopolsky MA. Am J Physiol Endocrinol Metab 278: E580-E587, 2000); however, the mechanism is unknown. We hypothesized that training would increase the muscle protein content of BCOAD kinase, the enzyme responsible for inactivation of BCOAD by phosphorylation. Twenty subjects [23 +/- 1 yr; peak oxygen uptake (.VO(2peak)) = 41 +/- 2 ml.kg(-1).min(-1)] performed 6 wk of either high-intensity interval or continuous moderate-intensity training on a cycle ergometer (n = 10/group). Before and after training, subjects performed 60 min of cycling at 65% of pretraining .VO(2peak), and needle biopsy samples (vastus lateralis) were obtained before and immediately after exercise. The effect of training was demonstrated by an increased .VO(2peak), increased citrate synthase maximal activity, and reduced muscle glycogenolysis during exercise, with no difference between groups (main effects, P < 0.05). BCOADa was lower after training (main effect, P < 0.05), and this was associated with a approximately 30% increase in BCOAD kinase protein content (main effect, P < 0.05). We conclude that the increased protein content of BCOAD kinase may be involved in the mechanism for reduced BCOADa after exercise training in human skeletal muscle. These data also highlight differences in models used to study the regulation of skeletal muscle BCAA metabolism, since exercise training was previously reported to increase BCOADa during exercise and decrease BCOAD kinase content in rats (Fujii H, Shimomura Y, Murakami T, Nakai N, Sato T, Suzuki M, Harris RA. Biochem Mol Biol Int 44: 1211-1216, 1998).     

Response of red cell and plasma volume to prolonged training in humans

To clarify the role of progressive heavy training on vascular volumes and hematologic status, seven untrained males [maximal O2 uptake (VO2max) = 45.1 +/- 1.1 (SE) ml.kg-1.min-1] cycled 2 h/day at an estimated 62% of VO2max. Training was conducted five to six times per week for approximately 8 wk. During this time, VO2max increased (P less than 0.05) by 17.2%. Plasma volume (PV) measured by 125I increased (P less than 0.05) from 3,068 +/- 104 ml at 0 wk to 3,490 +/- 126 ml at 4 wk and then plateaued during the remaining four wk (3,362 +/- 113 ml). Red cell (RBC) mass (RCM) measured by 51Cr-labeled RBC did not change during the initial 4 wk of training (2,247 +/- 66 vs. 2,309 +/- 128 ml). As well, no apparent change occurred in RCM during the final 4 wk of training when RCM was estimated using PV and hematocrit (Hct). Collectively, PV plus RCM, expressed as total blood volume (TBV), increased (P less than 0.05) by 10% at 4 wk and then stabilized for the final 4 wk. During the initial phase of training, reductions (P less than 0.05) were also noted in Hct (4.6%), hemoglobin (Hb, 4.0%), and RBC count (6.3%). In contrast, an increase in mean cell volume (MCV, 1.7%) and mean cell Hb (2.3%) was observed (P less than 0.05). From 4 to 8 wk, no further changes (P greater than 0.05) in Hb, RBC, and MCV were found, whereas both mean cell Hb and Hct returned to pretraining levels.(ABSTRACT TRUNCATED AT 250 WORDS)     

Prolonged exercise following diuretic-induced hypohydration: effects on cardiovascular and thermal strain

To examine the role of a reduction in plasma volume (PV) on the cardiovascular and thermoregulatory responses to submaximal exercise, ten untrained males (VO2 peak = 3.96 +/- 0.14 L x min(-1); mean +/- SE) performed 60 min of cycle exercise at -61% of VO2 peak while on a diuretic (DIU) and under control (CON) conditions. Participants consumed either Novotriamazide (100 mg triameterene + 50 mg hydrochlorothiazide, a diuretic) or a placebo, in random order, for 4 days prior to the exercise. Diuretic resulted in a calculated 14.6% reduction (P < 0.05) in resting PV. Heart rate was higher (P < 0.05) at rest and throughout exercise for DIU compared with CON. No differences were observed for cardiac output (Qc) and stroke volume (SV) at rest for the two conditions, but during exercise both Qc and SV were lower (P < 0.05) with DIU. Exercise VO2 (L x min(-1)) for CON and DIU at 30 min (2.39 +/- 0.09 vs 2.43 +/- 0.08) and 60 min (2.56 +/- 0.08 vs 2.53 +/- 0.12) were similar between conditions. Whole body a-vO2 difference was significantly greater (P < 0.05) for DIU both at rest and during exercise as compared with CON. Rectal temperature (Tre) was significantly higher (P < 0.05) during DIU from 15 min to the end of exercise. Blood concentrations of norepinephrine were higher (P < 0.05) with DIU compared to CON at 15 min of exercise and beyond. For blood epinephrine, no differences were observed between DIU and CON. These results suggest that reductions in PV led to greater circulating concentrations of norepinephrine which likely resulted from increased cardiac and thermoregulatory stresses. In addition, reductions in PV do not appear to increase cardiovascular instability during prolonged dynamic exercise.     

Dietary carbohydrate, muscle glycogen, and power output during rowing training

The belief that high-carbohydrate diets enhance training capacity (mean power output) has been extrapolated from studies that have varied dietary carbohydrate over a few days and measured muscle glycogen but did not assess power output during training. We hypothesized that a high-carbohydrate (HI) diet (10 g.kg body mass-1.day-1) would promote greater muscle glycogen content and greater mean power output during training than a moderate-carbohydrate (MOD) diet (5 g.kg body mass-1.day-1) over 4 wk of intense twice-daily rowing training. Dietary protein intake was 2 g.kg body mass-1.day-1, and fat intake was adjusted to maintain body mass. Twelve male and 10 female collegiate rowers were randomly assigned to the treatment groups. Training was 40 min at 70% peak O2 consumption (VO2) (A.M.) and either three 2,500-m time trials to assess power output or interval training at 70-90% peak VO2 (P.M.). Mean daily training was 65 min at 70% peak VO2 and 38 min at greater than or equal to 90% peak VO2. Mean muscle glycogen content increased 65% in the HI group (P less than 0.05) but remained constant at 119 mmol/kg in the MOD group over the 4 wk. Mean power output in time trials increased 10.7 and 1.6% after 4 wk in the HI and MOD groups, respectively (P less than 0.05). We conclude that a diet with 10 g carbohydrate.kg body mass-1.day-1 promotes greater muscle glycogen content and greater power output during training than a diet containing 5 g carbohydrate.kg body mass-1.day-1 over 4 wk of intense twice-daily rowing training.(ABSTRACT TRUNCATED AT 250 WORDS)     

Acute plasma volume expansion in the untrained alters the hormonal response to prolonged moderate-intensity exercise.

To investigate the role of an increase in plasma volume (PV), characteristically observed with short-term endurance training, on the endocrine response to prolonged moderate intensity exercise, eight untrained males (VO2 peak = 3.52 +/- 0.12 l x min(-1)) performed 90 min of cycle ergometry at approximately 60% VO2peak both before (CON) and following (PVX) PV expansion. Acute PV expansion, which was accomplished using a solution of Dextran (6%) or Pentispan (10%) (6.7 ml kg(-1)), resulted in a calculated 15.8+/-2.2% increase (p<0.05) in PV. The prolonged exercise resulted in increases (p<0.05) in plasma vasopressin (AVP), plasma rennin activity (PRA), aldosterone (ALD), atrial naturetic peptide (alpha-ANP), and the catecholamines norepinephrine (NE) and epinephrine (EPI). PVX blunted the increases (p<0.05) in AVP, PRA, ALD, NE and EPI, during the exercise itself. The concentration of alpha-ANP was also lower (p<0.05) during exercise following PVX, an effect that could be attributed to the lower resting levels. No differences in osmolality was observed between conditions. These results demonstrate that PVX alters the fluid regulatory hormonal response in untrained subjects to moderate intensity dynamic exercise in a manner similar to that observed following short-term training induced alterations in PV. The specific mechanisms responsible for these alterations remain unclear, but appear to be related directly to the increase in PV.     

Cold exposure increases running VO(2max) and cost of transport in goats

We inadvertently subjected a group of goats to 5 mo of cold exposure (mean minimum temperature less than -13 degrees C) during an experiment designed to examine the effects of training by daily running on one member of each sibling pair. During the three coldest months, the sedentary but cold-exposed goats experienced a 34% increase in maximal oxygen uptake (VO(2 max), P < 0.01) and a 29% increase in running speed at maximal (P < 0.05). When temperatures increased in the spring, both oxygen uptake and running speed decreased. We interpret these findings as evidence that cold is a sufficient stimulus to invoke the development of aerobic structures in muscle and that these structures subsequently can be utilized for the novel task of running. When the experiment was subsequently repeated without the cold exposure, running speed and VO(2 max) of trained animals increased less than in either group of cold-exposed animals. However, the cost of transport of these warm runners was lower than either group of cold-exposed animals (from 13-19%, P < 0. 0001). Thus, although aerobic capacity was increased with acclimation to severe winter weather, cold-acclimated goats operated with lower efficiency during locomotion.     

Endurance training increases fatty acid turnover, but not fat oxidation, in young men.

We examined the effects of exercise intensity and a 10-wk cycle ergometer training program [5 days/wk, 1 h, 75% peak oxygen consumption (VO2 peak)] on plasma free fatty acid (FFA) flux, total fat oxidation, and whole body lipolysis in healthy male subjects (n = 10; age = 25.6 +/- 1.0 yr). Two pretraining trials (45 and 65% of VO2 peak) and two posttraining trials (same absolute workload, 65% of old VO2 peak; and same relative workload, 65% of new VO2 peak) were performed by using an infusion of [1-13C]palmitate and [1,1,2,3, 3-2H]glycerol. An additional nine subjects (age 25.4 +/- 0.8 yr) were treated similarly but were infused with [1,1,2,3,3-2H]glycerol and not [1-13C]palmitate. Subjects were studied postabsorptive for 90 min of rest and 1 h of cycling exercise. After training, subjects increased VO2 peak by 9.4 +/- 1.4%. Pretraining, plasma FFA kinetics were inversely related to exercise intensity with rates of appearance (Ra) and disappearance (Rd) being significantly higher at 45 than at 65% VO2 peak (Ra: 8.14 +/- 1.28 vs. 6.64 +/- 0.46, Rd: 8. 03 +/- 1.28 vs. 6.42 +/- 0.41 mol. kg-1. min-1) (P 相似文献   

Adrenergic regulation of HSL serine phosphorylation and activity in human skeletal muscle during the onset of exercise

Skeletal muscle hormone-sensitive lipase (HSL) activity is increased by contractions and increases in blood epinephrine (EPI) concentrations and cyclic AMP activation of the adrenergic pathway during prolonged exercise. To determine the importance of hormonal stimulation of HSL activity during the onset of moderate- and high-intensity exercise, nine men [age 24.3 +/- 1.2 yr, 80.8 +/- 5.0 kg, peak oxygen consumption (VO2 peak) 43.9 +/- 3.6 ml x kg(-1) x min(-1)] cycled for 1 min at approximately 65% VO2 peak, rested for 60 min, and cycled at approximately 90% VO2 peak for 1 min. Skeletal muscle biopsies were taken pre- and postexercise, and arterial blood was sampled throughout exercise. Arterial EPI increased (P < 0.05) postexercise at 65% (0.45 +/- 0.10 to 0.78 +/- 0.27 nM) and 90% VO2 peak (0.57 +/- 0.34 to 1.09 +/- 0.50 nM). HSL activity increased (P < 0.05) following 1 min of exercise at 65% VO2 peak [1.05 +/- 0.39 to 1.78 +/- 0.54 mmol x min(-1) x kg dry muscle (dm)(-1)] and 90% VO2 peak (1.07 +/- 0.24 to 1.91 +/- 0.62 mmol x min(-1) x kg dm(-1)). Cyclic AMP content also increased (P < 0.05) at both exercise intensities (65%: 1.52 +/- 0.67 to 2.75 +/- 1.12, 90%: 1.85 +/- 0.65 to 2.64 +/- 0.93 micromol/kg dm). HSL Ser660 phosphorylation (approximately 55% increase) and ERK1/2 phosphorylation ( approximately 33% increase) were augmented following exercise at both intensities, whereas HSL Ser563 and Ser565 phosphorylation were not different from rest. The results indicate that increases in arterial EPI concentration during the onset of moderate- and high-intensity exercise increase cyclic AMP content, which results in the phosphorylation of HSL Ser660. This adrenergic stimulation contributes to the increase in HSL activity that occurs in human skeletal muscle in the first minute of exercise at 65% and 90% VO2 peak.     

Endurance training amplifies the pulsatile release of growth hormone: effects of training intensity.

The effects of intensity of run training on the pulsatile release of growth hormone (GH) were investigated in 21 eumenorrheic untrained women. The O2 consumption (VO2) at the lactate threshold (LT); fixed blood lactate concentrations (FBLC) of 2.0, 2.5, and 4.0 mM; peak VO2; maximal VO2; body composition; and pulsatile release of GH were measured. Subjects in both the at-lactate threshold (/LT, n = 9) and above-lactate threshold (greater than LT, n = 7) training groups increased VO2 at LT and FBLC of 2.0, 2.5, and 4.0 mM and VO2max after 1 yr of run training. However, the increase observed in the greater than LT group was greater than that in the /LT group (P less than 0.05). No change was observed for the control group (n = 5). No among- or within-group differences were observed for body weight, although trends for reductions in percent body fat (P less than 0.06) and fat weight (P less than 0.15) were observed in the greater than LT group, and both training groups significantly increased fat-free weight (P less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)     

Sex differences in postexercise esophageal and muscle tissue temperature response

Factors associated with blood pressure regulation during recovery from exercise dramatically influence core temperature regulation. However, it is unknown whether sex-related differences in postexercise hemodynamics affect core and muscle temperature response. Sixteen participants (8 males, 8 females) completed an incremental isotonic test on a Kin-Com isokinetic apparatus to determine their activity-specific peak oxygen consumption during bilateral knee extensions (Vo(2)(sp)). On a separate day, participants performed 15 min of isolated bilateral knee extensions at a moderate (60% Vo(2)(sp)) exercise intensity followed by a 90-min recovery. Esophageal temperature (T(es)), mean arterial pressure (MAP), muscle temperature at four depths in the active vastus medialis (T(VM)) and three depths in the inactive triceps brachii (T(TB)) were measured concurrently with sweat rate and cutaneous vascular conductance (CVC). Relative to the preexercise resting T(es) of 36.7 degrees C (SD 0.1), between 10 and 50-min of recovery T(es) was 0.19 degrees C (SD 0.02) higher for females than males (P = 0.037). All measurements of T(VM) (0.036 > P > 0.014) and T(TB) (0.048 > P > 0.008) were higher for females during the initial 30 min of recovery by between 0.46 degrees C and 0.64 degrees C for T(VM) and by between 0.53 degrees C and 0.70 degrees C for T(TB). In parallel, females showed a 5 to 7 mmHg greater reduction in MAP during recovery relative to males (P = 0.002) and a significantly lower CVC (P = 0.020) and sweat rate (P = 0.034). Therefore, it is concluded that females demonstrate a greater and more prolonged elevation in postexercise esophageal temperature and active and inactive muscle temperatures, which is paralleled by a greater postexercise hypotensive response.