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

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

Endurance training of older men: responses to submaximal exercise.

The purpose of this study was to quantify the exercise response of older subjects on a time-to-fatigue (TTF) submaximal performance test before and after a training program. Eight older men (67.4 +/- 4.8 yr) performed two maximal treadmill tests to determine maximum oxygen uptake (VO2max) and ventilation threshold (TVE) and a constant-load submaximal exercise treadmill test that required an oxygen uptake (VO2) between TVE and VO2max. The submaximal test, performed at the same absolute work rate before and after the training program, was performed to volitional fatigue to measure endurance time. The men trained under supervision at an individualized pace representing approximately 70% of VO2max (80% maximum heart rate) for 1 h, four times per week for 9 wk. Significant increases were demonstrated for VO2max (ml.kg-1.min-1; 10.6%); maximal ventilation (VE, l/min; 11.6%), and TVE (l/min; 9.8%). Weight decreased 2.1%. Performance time on the TTF test increased by 180% (7.3 +/- 3.0 to 20.4 +/- 13.5 min). The similar end points for VO2, VE, and heart rate during the TTF and maximal treadmill tests established that the TTF test was stopped because of physiological limitations. The increase in performance time among the subjects was significantly correlated with improvements in VO2max and TVE, with the submaximal work rate representing a VO2 above TVE by 88% of the difference between TVE and VO2max pretraining and 73% of this difference on posttraining values.     

Effect of short-term sprint interval training on human skeletal muscle carbohydrate metabolism during exercise and time-trial performance.

Our laboratory recently showed that six sessions of sprint interval training (SIT) over 2 wk increased muscle oxidative potential and cycle endurance capacity (Burgomaster KA, Hughes SC, Heigenhauser GJF, Bradwell SN, and Gibala MJ. J Appl Physiol 98: 1895-1900, 2005). The present study tested the hypothesis that short-term SIT would reduce skeletal muscle glycogenolysis and lactate accumulation during exercise and increase the capacity for pyruvate oxidation via pyruvate dehydrogenase (PDH). Eight men [peak oxygen uptake (VO2 peak)=3.8+/-0.2 l/min] performed six sessions of SIT (4-7x30-s "all-out" cycling with 4 min of recovery) over 2 wk. Before and after SIT, biopsies (vastus lateralis) were obtained at rest and after each stage of a two-stage cycling test that consisted of 10 min at approximately 60% followed by 10 min at approximately 90% of VO2 peak. Subjects also performed a 250-kJ time trial (TT) before and after SIT to assess changes in cycling performance. SIT increased muscle glycogen content by approximately 50% (main effect, P=0.04) and the maximal activity of citrate synthase (posttraining: 7.8+/-0.4 vs. pretraining: 7.0+/-0.4 mol.kg protein -1.h-1; P=0.04), but the maximal activity of 3-hydroxyacyl-CoA dehydrogenase was unchanged (posttraining: 5.1+/-0.7 vs. pretraining: 4.9+/-0.6 mol.kg protein -1.h-1; P=0.76). The active form of PDH was higher after training (main effect, P=0.04), and net muscle glycogenolysis (posttraining: 100+/-16 vs. pretraining: 139+/-11 mmol/kg dry wt; P=0.03) and lactate accumulation (posttraining: 55+/-2 vs. pretraining: 63+/-1 mmol/kg dry wt; P=0.03) during exercise were reduced. TT performance improved by 9.6% after training (posttraining: 15.5+/-0.5 vs. pretraining: 17.2+/-1.0 min; P=0.006), and a control group (n=8, VO2 peak=3.9+/-0.2 l/min) showed no change in performance when tested 2 wk apart without SIT (posttraining: 18.8+/-1.2 vs. pretraining: 18.9+/-1.2 min; P=0.74). We conclude that short-term SIT improved cycling TT performance and resulted in a closer matching of glycogenolytic flux and pyruvate oxidation during submaximal exercise.     

Lactate and ventilatory thresholds: disparity in time course of adaptations to training

We tested the hypothesis that the lactate threshold (Tlac) during incremental exercise could be increased significantly during the first 3 wk of endurance training without any concomitant change in the ventilatory threshold (Tvent). Tvent is defined as O2 uptake (VO2) at which ventilatory equivalent for O2 [expired ventilation per VO2 (VE/VO2)] increased without a simultaneous increase in the ventilatory equivalent for CO2 (VE/VCO2). Weekly measurements of ventilatory gas exchange and blood lactate responses during incremental and steady-rate exercise were performed on six subjects (4 male; 2 female) who exercised 6 days/wk, 30 min/session at 70-80% of pretraining VO2max for 3 wk. Pretraining Tlac and Tvent were not significantly different. After 3 wk of training, significant increases (P less than 0.05) occurred for mean (+/- SE) VO2max (392 +/- 103 ml/min) and Tlac (482 +/- 135 ml/min). Tvent did not change during the 3 wk of training, despite significant (P less than 0.05) reductions in VE responses to both incremental and steady-rate exercise. Thus ventilatory adaptations to exercise during the first 3 wk of exercise training were not accompanied by a detectable alteration in the ventilatory "threshold" during a 1-min incremental exercise protocol. The mean absolute difference between pairs of Tlac and Tvent posttraining was 499 ml/min. Despite the significant training-induced dissociation between Tlac and Tvent a high correlation between the two parameters was obtained posttraining (r = 0.86, P less than 0.05). These results indicate a coincidental rather than causal relationship.(ABSTRACT TRUNCATED AT 250 WORDS)     

Cardiovascular responses of 70- to 79-yr-old men and women to exercise training

This study determined the effects of endurance or resistance exercise training on maximal O2 consumption (VO2max) and the cardiovascular responses to exercise of 70- to 79-yr-old men and women. Healthy untrained subjects were randomly assigned to a control group (n = 12) or to an endurance (n = 16) or resistance training group (n = 19). Training consisted of three sessions per week for 26 wk. Resistance training consisted of one set of 8-12 repetitions on 10 Nautilus machines. Endurance training consisted of 40 min at 50-70% VO2max and at 75-85% VO2max for the first and last 13 wk of training, respectively. The endurance training group increased its VO2max by 16% during the first 13 wk of training and by a total of 22% after 26 wk of training; this group also increased its maximal O2 pulse, systolic blood pressure, and ventilation, and decreased its heart rate and perceived exertion during submaximal exercise. The resistance training group did not elicit significant changes in VO2max or in other maximal or submaximal cardiovascular responses despite eliciting 9 and 18% increases in lower and upper body strength, respectively. Thus healthy men and women in their 70s can respond to prolonged endurance exercise training with adaptations similar to those of younger individuals. Resistance training in older individuals has no effect on cardiovascular responses to submaximal or maximal treadmill exercise.     

Training effects on regional blood flow response to maximal exercise in foxhounds

The effect of training on the regional blood flow response to maximal exercise was investigated in the foxhound. Training consisted of 8-12 wk of treadmill running at 80% of maximal heart rate 1 h/day for 5 days/wk and resulted in a 31% increase in maximal O2 consumption, a 28% increase in maximal cardiac output, and a 23% decrease in systemic vascular resistance during maximal exercise. Blood flow to the heart, diaphragm, brain, skin, and 9 of 10 muscles investigated was similar during maximal exercise pre- and posttraining; however, blood flow to the gastrocnemius muscle was greater posttraining than it was pretraining. Blood flow to the stomach, small intestine, and pancreas decreased during maximal exercise pre- and posttraining; however, blood flow to the large intestine, spleen, liver, adrenal glands, and kidneys decreased during maximal exercise only posttraining. In addition, a larger decrease in blood flow to the stomach during maximal exercise was found posttraining compared with pretraining. These results demonstrate that blood flow to skeletal muscle, the kidneys, and the splanchnic region of the foxhound during maximal exercise can be significantly altered by dynamic exercise training.     

Determinants of VO2max in rats after high-intensity sprint training

The hemodynamic response to maximal exercise was determined in rats that were subjected to high-intensity sprint training (HIST) and rats that served as sedentary controls. Training consisted of five 1-min bouts of treadmill running at work loads (15% grade, 97 m/min) in excess of the animals' maximal O2 uptake (VO2max) interspersed with 90 s of rest. Training was performed 6 days/wk for 6 wk. After the training regimen, all rats were acutely instrumented with catheters in the right carotid artery and right ventricle. O2 uptakes, hemodynamic parameters, arterial and mixed venous O2 concentrations, blood gases, and acid-base status were determined at rest and during submaximal and maximal exercise. Results demonstrated that VO2max of HIST rats was significantly greater than that found for sedentary control rats. This increase in VO2max was due to an increase in maximal cardiac output (Qmax), since maximal arteriovenous O2 difference was similar between trained and sedentary rats. The increase in Qmax was due to an increase in maximal stroke volume (SVmax), because maximal heart rate in trained rats was similar to that in sedentary control rats. Citrate synthase and phosphofructokinase activities measured in the white gastrocnemius, plantaris, and soleus muscles of trained and sedentary rats were similar. These results suggest that the increase in VO2max produced with HIST in rats is strongly linked to an increase in central cardiac function as indicated by an increase in Qmax and SVmax.     

Active muscle and whole body lactate kinetics after endurance training in men.

We evaluated the hypotheses that endurance training decreases arterial lactate concentration ([lactate](a)) during continuous exercise by decreasing net lactate release () and appearance rates (R(a)) and increasing metabolic clearance rate (MCR). Measurements were made at two intensities before [45 and 65% peak O(2) consumption (VO(2 peak))] and after training [65% pretraining VO(2 peak), same absolute workload (ABT), and 65% posttraining VO(2 peak), same relative intensity (RLT)]. Nine men (27.4 +/- 2.0 yr) trained for 9 wk on a cycle ergometer, 5 times/wk at 75% VO(2 peak). Compared with the 65% VO(2 peak) pretraining condition (4.75 +/- 0.4 mM), [lactate](a) decreased at ABT (41%) and RLT (21%) (P < 0.05). decreased at ABT but not at RLT. Leg lactate uptake and oxidation were unchanged at ABT but increased at RLT. MCR was unchanged at ABT but increased at RLT. We conclude that 1) active skeletal muscle is not solely responsible for elevated [lactate](a); and 2) training increases leg lactate clearance, decreases whole body and leg lactate production at a given moderate-intensity power output, and increases both whole body and leg lactate clearance at a high relative power output.     

Increases in maximal accumulated oxygen deficit after high-intensity interval training are not gender dependent.

Gender differences in maximal accumulated oxygen deficit (MAOD) were examined before and after 4 and 8 wk of high-intensity interval training. Untrained men (n = 7) and women (n = 7) cycled at 120% of pretraining peak oxygen uptake (VO2 peak) to exhaustion (MAOD test) pre-, mid-, and posttraining. A posttraining timed test was also completed at the MAOD test power output, but this test was stopped at the time to exhaustion achieved during the pretraining MAOD test. The 14.3 +/- 5.2% increase in MAOD observed in men after 4 wk of training was not different from the 14.0 +/- 3.0% increase seen in women (P > 0.05). MAOD increased by a further 6.6 +/- 1.9% in men, and this change was not different from the additional 5.1 +/- 2.3% increase observed in women after the final 4 wk of training. VO2 peak measured during incremental cycling increased significantly (P < 0.01) in male but not in female subjects after 8 wk of training. Moreover, the accumulated oxygen (AO2) uptake was higher in men during the posttraining timed test compared with the pretraining MAOD test (P < 0.01). In contrast, the AO2 uptake was unchanged from pre- to posttraining in female subjects. The increase in MAOD with training was not different between men and women, suggesting an enhanced ability to produce ATP anaerobically in both groups. However, the increase in VO2 peak and AO2 uptake obtained in male subjects after training indicates improved oxidative metabolism in men but not in women. We conclude that there are basic gender differences that may predispose men and women to specific metabolic adaptations after a period of intense interval training.     

Substrate utilization during endurance exercise in men and women after endurance training

We investigated the effect of endurance training on whole body substrate, glucose, and glycerol utilization during 90 min of exercise at 60% peak O2 consumption (VO2(peak)) in males and females. Substrate oxidation was determined before and after 7 wk of endurance training on a cycle ergometer, with posttesting performed at the same absolute (ABS, W) and relative (REL, VO2(peak)) intensities. [6,6-2H]glucose and [1,1,2,3,3-2H]glycerol tracers were used to calculate the respective substrate tracee flux. Endurance training resulted in an increase in VO2(peak) for both males and females of 17 and 22%, respectively (P < 0.001). Females demonstrated a lower respiratory exchange ratio (RER) both pretraining and posttraining compared with males during exercise (P < 0.001). Glucose rate of appearance (R(a)) and rate of disappearance (R(d)) were not different between males and females. Glucose metabolic clearance rate (MCR) was lower at 75 and 90 min of exercise for females compared with males (P < 0.05). Glucose R(a) and R(d) were lower during exercise at both ABS and REL posttraining exercise intensities compared with pretraining (P < 0.001). Females had a higher exercise glycerol R(a) and R(d) compared with males both pre- and posttraining (P < 0.001). Glycerol R(a) was not different at either the ABS or REL posttraining exercise intensities compared with pretraining. We concluded that females oxidize proportionately more lipid and less carbohydrate during exercise compared with males both pre- and posttraining, which was cotemporal with a higher glycerol R(a) in females. Furthermore, endurance training resulted in a decrease in glucose flux at both ABS and REL exercise intensities after endurance exercise training.     

The effects of training in hyperoxia vs. normoxia on skeletal muscle enzyme activities and exercise performance.

Inspiring a hyperoxic (H) gas permits subjects to exercise at higher power outputs while training, but there is controversy as to whether this improves skeletal muscle oxidative capacity, maximal O(2) consumption (Vo(2 max)), and endurance performance to a greater extent than training in normoxia (N). To determine whether the higher power output during H training leads to a greater increase in these parameters, nine recreationally active subjects were randomly assigned in a single-blind fashion to train in H (60% O(2)) or N for 6 wk (3 sessions/wk of 10 x 4 min at 90% Vo(2 max)). Training heart rate (HR) was maintained during the study by increasing power output. After at least 6 wk of detraining, a second 6-wk training protocol was completed with the other breathing condition. Vo(2 max) and cycle time to exhaustion at 90% of pretraining Vo(2 max) were tested in room air pre- and posttraining. Muscle biopsies were sampled pre- and posttraining for citrate synthase (CS), beta-hydroxyacyl-coenzyme A dehydrogenase (beta-HAD), and mitochondrial aspartate aminotransferase (m-AsAT) activity measurements. Training power outputs were 8% higher (17 W) in H vs. N. However, both conditions produced similar improvements in Vo(2 max) (11-12%); time to exhaustion (approximately 100%); and CS (H, 30%; N, 32%), beta-HAD (H, 23%; N, 21%), and m-AsAT (H, 21%; N, 26%) activities. We conclude that the additional training stimulus provided by training in H was not sufficient to produce greater increases in the aerobic capacity of skeletal muscle and whole body Vo(2 max) and exercise performance compared with training in N.     

Effects of sprint training on maximal stroke volume of rats with a chronic myocardial infarction.

The hemodynamic response to maximal exercise was determined in rats with a chronic myocardial infarction (MI) that were subjected to 6-8 wk of high-intensity sprint training (HIST) or limited exercise activity (sedentary control). Training was performed 6 days/wk and consisted of five 1-min bouts of treadmill running at work loads (15% grade, 97 m/min) in excess of the animal's maximal O2 uptake (VO2max). The left ventricular infarct size for the HIST and sedentary control rats was 35 +/- 4 and 34 +/- 3% of the total endocardial circumference, respectively. VO2max was significantly greater for MI rats subjected to the HIST paradigm than for sedentary control rats. This increase in VO2max was due to an increase in the maximal stroke volume that could be generated by the HIST rat during exercise, inasmuch as the maximal heart rate response and the ability to extract O2 from the blood were similar between the two groups of rats. Citrate synthase activities measured in the plantaris muscle of the HIST and sedentary control rats were similar. These results suggest that the increase in VO2max produced with HIST in MI rats may be linked to changes in central cardiac function, as indicated by the increase in maximal stroke volume that could be generated by the MI rat during maximal exercise conditions.     

Exercise training prevents decline in stroke volume during exercise in young healthy subjects.

Stroke volume (SV) increases above the resting level during exercise and then declines at higher intensities of exercise in sedentary subjects. The purpose of this study was to determine whether an attenuation of the decline in SV at higher exercise intensities contributes to the increase in maximal cardiac output (Qmax) that occurs in response to endurance training. We studied six men and six women, 25 +/- 1 (SE) yr old, before and after 12 wk of endurance training (3 days/wk running for 40 min, 3 days/wk interval training). Cardiac output was measured at rest and during exercise at 50 and 100% of maximal O2 uptake (Vo2max) by the C2H2-rebreathing method. VO2max was increased by 19% (from 2.7 +/- 0.2 to 3.2 +/- 0.3 l/min, P less than 0.001) in response to the training program. Qmax was increased by 12% (from 18.1 +/- 1 to 20.2 +/- 1 l/min, P less than 0.01), SV at maximal exercise was increased by 16% (from 97 +/- 6 to 113 +/- 8 ml/beat, P less than 0.001) and maximal heart rate was decreased by 3% (from 185 +/- 2 to 180 +/- 2 beats/min, P less than 0.01) after training. The calculated arteriovenous O2 content difference at maximal exercise was increased by 7% (14.4 +/- 0.4 to 15.4 +/- 0.4 ml O2/100 ml blood) after training. Before training, SV at VO2max was 9% lower than during exercise at 50% VO2max (P less than 0.05). In contrast, after training, the decline in SV between 50 and 100% VO2max was only 2% (P = NS). Furthermore, SV was significantly higher (P less than 0.01) at 50% VO2max after training than it was before. Left ventricular hypertrophy was evident, as determined by two-dimensional echocardiography at the completion of training. The results indicate that in young healthy subjects the training-induced increase in Qmax is due in part to attenuation of the decrease in SV as exercise intensity is increased.     

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)     

Angiotensin-converting enzyme ID polymorphism and fitness phenotype in the HERITAGE Family Study.

It has been suggested that genetic variation in the angiotensin-converting enzyme (ACE) gene is associated with physical performance. We studied the association between the ACE insertion (I)/deletion (D) polymorphism and several fitness phenotypes measured before and after 20 wk of a standardized endurance training program in sedentary Caucasian (n = 476) and black (n = 248) subjects. Phenotypes measured were oxygen uptake (VO(2)), work rate, heart rate, minute ventilation, tidal volume, and blood lactate levels during maximal and submaximal [50 W and at 60 and 80% of maximal VO(2) (VO(2 max))] exercise and stroke volume and cardiac output during submaximal exercise (50 W and at 60% VO(2 max)). The ACE ID polymorphism was typed with the three-primer PCR method. Out of 216 association tests performed on 54 phenotypes in 4 groups of participants, only 11 showed significant (P values from 0.042 to 0. 0001) associations with the ACE ID polymorphism. In contrast to previous claims, in Caucasian offspring, the DD homozygotes showed a 14-38% greater increase with training in VO(2 max), VO(2) at 80% of VO(2 max), and all work rate phenotypes and a 36% greater decrease in heart rate at 50 W than did the II homozygotes. No associations were evident in Caucasian parents or black parents or offspring. Thus these data do not support the hypothesis that the ACE ID polymorphism plays a major role in cardiorespiratory endurance.     

Frequency and duration of interval training programs and changes in aerobic power.

This study was designed to ascertain whether 7- and 13-wk interval training programs with training frequencies of 2 days/wk would produce improvement in maximal aerobic power (VO2max) comparable to that obtained from 7- and 13-wk programs of the same intensity consisting of 4 training days/wk. Sixty-nine young healthy college males were used as subjects. After training, there was a significant increase in VO2max (bicycle ergometer, open-circuit spirometry) that was independent of both training frequency and duration. However, there was a trend for greater gains after 13 wk. Maximal heart rate (direct lead ECG) was significantly decreased following training, being independent of both training frequency and duration. Submaximal VO2 did not change with training but submaximal heart rate decreased significantly with greater decreases the more frequent and longer the training. Within the limitations of this study, these results indicate that: 1) maximal stroke volume and/or maximal avO2 difference, principle determinants of VO2max, are not dependent on training frequency nor training duration, and 2) one benefit of more frequent and longer duration interval training is less circulatory stress as evidenced by decreased heart rate, during submaximal exercise.     

Response of ventilatory and lactate thresholds to continuous and interval training

The purpose of this study was to evaluate the effects of continuous and interval training on changes in lactate and ventilatory thresholds during incremental exercise. Seventeen males were assigned to one of three training groups: group 1:55 min continuous exercise at approximately 50% maximum O2 consumption (VO2max); group 2: 35 min continuous exercise at approximately 70% VO2max; and group 3: 10 X 2-min intervals at approximately 105% VO2max interspersed with rest intervals of 2 min. All of the subjects were tested and trained on a cycle ergometer 3 day/wk for 8 wk. Lactate threshold (LT) and ventilatory threshold (VT) (in addition to maximal exercise measures) were determined using a standard incremental exercise test before and after 4 and 8 wk of training. VO2max increased significantly in all groups with no statistically significant differences between the groups. Increases (+/- SE) in LT (ml O2 X min-1) for group 1 (569 +/- 158), group 2 (584 +/- 125), and group 3 (533 +/- 88) were significant (P less than 0.05) and of the same magnitude. VT also increased significantly (P less than 0.05) in each group. However, the increase in VT (ml O2 X min-1) for group 3 (699 +/- 85) was significantly greater (P less than 0.05) than the increases in VT for group 1 (224 +/- 52) and group 2 (404 +/- 85). For group 1, the posttraining increase in LT was significantly greater than the increase in VT (P less than 0.05). We conclude that both continuous and interval training were equally effective in augmenting LT, but interval training was more effective in elevating VT.(ABSTRACT TRUNCATED AT 250 WORDS)     

Muscle morphological and biochemical adaptations to training in obese Zucker rats

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

Day-to-day changes in oxygen uptake kinetics at the onset of exercise during strenuous endurance training.

The aim of this study was to assess the effect of strenuous endurance training on day-to-day changes in oxygen uptake (VO2) on-kinetics (time constant) at the onset of exercise. Four healthy men participated in strenuous training for 30 min.day-1, 6 days.week-1 for 3 weeks. The VO2 was measured breath-by-breath every day except Sunday at exercise intensities corresponding to the lactate threshold (LT) and the onset of blood lactate accumulation (OBLA) which were obtained before training. Furthermore, an incremental exercise test was performed to determine LT, OBLA and maximal oxygen uptake (VO2max) before and after the training period and every weekend. The 30-min heavy endurance training was performed on a cycle ergometer 5 days.week-1 for 3 weeks. Another six men served as the control group. After training, significant reductions of the VO2 time constant for exercise at the pretraining LT exercise intensity (P less than 0.05) and at OBLA exercise intensity (P less than 0.01) were observed, whereas the VO2 time constants in the control group did not change significantly. A high correlation between the decrease in the VO2 time constant and training day was observed in exercise at the pretraining LT exercise intensity (r = -0.76; P less than 0.001) as well as in the OBLA exercise intensity (r = -0.91; P less than 0.001). A significant reduction in the blood lactate concentration during submaximal exercise and in the heart rate on-kinetics was observed in the training group.(ABSTRACT TRUNCATED AT 250 WORDS)     

Endurance training in older men and women II. Blood lactate response to submaximal exercise

Seven men and four women (age 63 +/- 2 yr, mean +/- SD, range 61-67 yr) participated in a 12-mo endurance training program to determine the effects of low-intensity (LI) and high-intensity (HI) training on the blood lactate response to submaximal exercise in older individuals. Maximal oxygen uptake (VO2max), blood lactate, O2 uptake (VO2), heart rate (HR), ventilation (VE), and respiratory exchange ratio (R) during three submaximal exercise bouts (65-90% VO2max) were determined before training, after 6 mo of LI training, and after an additional 6 mo of HI training. VO2max (ml X kg-1 X min-1) was increased 12% after LI training (P less than 0.05), while HI training induced a further increase of 18% (P less than 0.01). Lactate, HR, VE, and R were significantly lower (P less than 0.05) at the same absolute work rates after LI training, while HI training induced further but smaller reductions in these parameters (P greater than 0.05). In general, at the same relative work rates (ie., % of VO2max) after training, lactate was lower or unchanged, HR and R were unchanged, and VO2 and VE were higher. These findings indicate that LI training in older individuals results in adaptations in the response to submaximal exercise that are similar to those observed in younger populations and that additional higher intensity training results in further but less-marked changes.