Changes in cardiorespiratory fitness and coronary heart disease risk factors following 24 wk of moderate- or high-intensity exercise of equal energy cost.

This study was designed to investigate the effect of exercise intensity on cardiorespiratory fitness and coronary heart disease risk factors. Maximum oxygen consumption (Vo(2 max)), lipid, lipoprotein, and fibrinogen concentrations were measured in 64 previously sedentary men before random allocation to a nonexercise control group, a moderate-intensity exercise group (three 400-kcal sessions per week at 60% of Vo(2 max)), or a high-intensity exercise group (three 400-kcal sessions per week at 80% of Vo(2 max)). Subjects were instructed to maintain their normal dietary habits, and training heart rates were represcribed after monthly fitness tests. Forty-two men finished the study. After 24 wk, Vo(2 max) increased by 0.38 +/- 0.14 l/min in the moderate-intensity group and by 0.55 +/- 0.27 l/min in the high-intensity group. Repeated-measures analysis of variance identified a significant interaction between monthly Vo(2 max) score and exercise group (F = 3.37, P < 0.05), indicating that Vo(2 max) responded differently to moderate- and high-intensity exercise. Trend analysis showed that total cholesterol, low-density lipoprotein cholesterol, non-high-density lipoprotein cholesterol, and fibrinogen concentrations changed favorably across control, moderate-intensity, and high-intensity groups. However, significant changes in total cholesterol (-0.55 +/- 0.81 mmol/l), low-density lipoprotein cholesterol (-0.52 +/- 0.80 mmol/l), and non-high-density lipoprotein cholesterol (-0.54 +/- 0.86 mmol/l) were only observed in the high-intensity group (all P < 0.05 vs. controls). These data suggest that high-intensity training is more effective in improving cardiorespiratory fitness than moderate-intensity training of equal energy cost. These data also suggest that changes in coronary heart disease risk factors are influenced by exercise intensity.     

Effects of exercise training on acclimatization to hypoxia: systemic O2 transport during maximal exercise.

Acclimatization to hypoxia has minimal effect on maximal O2 uptake (Vo2 max). Prolonged hypoxia shows reductions in cardiac output (Q), maximal heart rate (HR-max), myocardial beta-adrenoceptor (beta-AR) density, and chronotropic response to isoproterenol. This study tested the hypothesis that exercise training (ET), which attenuates beta-AR downregulation, would increase HRmax and Q of acclimatization and result in higher Vo2 max. After 3 wk of ET, rats lived at an inspired Po2 of 70 Torr for 10 days (acclimatized trained rats) or remained in normoxia, while both groups continued to train in normoxia. Controls were sedentary acclimatized and nonacclimatized rats. All rats exercised maximally in normoxia and hypoxia (inspired Po2 of 70 Torr). Myocardial beta-AR density and the chronotropic response to isoproterenol were reduced, and myocardial cholinergic receptor density was increased after acclimatization; all of these receptor changes were reversed by ET. Normoxic Vo2 max (in ml.min-1.kg-1) was 95.8 +/- 1.0 in acclimatized trained (n = 6), 87.7 +/- 1.7 in nonacclimatized trained (P < 0.05, n = 6), 74.2 +/- 1.4 in acclimatized sedentary (n = 6, P < 0.05), and 72.5 +/- 1.2 in nonacclimatized sedentary (n = 8; P > 0.05 acclimatized sedentary vs. nonacclimatized sedentary). A similar distribution of Vo2 max values occurred in hypoxic exercise. Q was highest in trained acclimatized and nonacclimatized, intermediate in nonacclimatized sedentary, and lowest in acclimatized sedentary groups. ET preserved Q in acclimatized rats thanks to maintenance of HRmax as well as of maximal stroke volume. Q preservation, coupled with a higher arterial O2 content, resulted in the acclimatized trained rats having the highest convective O2 transport and Vo2 max. These results show that ET attenuates beta-AR downregulation and preserves Q and Vo2 max after acclimatization, and support the idea that beta-AR downregulation partially contributes to the limitation of Vo2 max after acclimatization in rats.     

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.     

Cardiac parasympathetic regulation: respective associations with cardiorespiratory fitness and training load

The objective of this study was to establish the separate associations between parasympathetic modulations of the heart [evaluated through heart rate (HR) variability (HRV) indexes and postexercise HR recovery (HRR) indexes] with cardiorespiratory fitness and training load. We have measured cardiorespiratory fitness through peak oxygen consumption (Vo2 max) and estimated weekly training load with the Baecke sport score in 55 middle-aged individuals (30.8 +/- 1.8 yr, body mass index 24.5 +/- 0.4 kg/m2). HRV indexes were analyzed at rest under controlled breathing, and HRR was estimated from HR curve fitting after maximal exercise or from measurements of the number of beats recovered at 60 s after exercise. Multiple linear regressions were used to investigate the separate relationships between vagal-related HRV indexes and Vo2 max and Baecke scores. On the basis of their Vo2 max and Baecke scores, subjects were classified as fit or unfit and as low trained (LT) or moderately trained (MT), which yielded four groups: UnfitLT, UnfitMT, FitLT, and FitMT. Vagal-related HRV indexes were positively correlated with Vo2 max (P < 0.05) but not with Baecke scores. In contrast, HRR indexes were related to Baecke scores (P < 0.05) but not with Vo2 max. FitLT and FitMT had significantly higher (P < 0.05) normalized vagal-related HRV indexes than UnfitLT and UnfitMT, but HRR did not change. Moderate training was associated with significantly lower HRR indexes both in UnfitMT and FitMT compared with UnfitLT and FitLT, but there was no difference in vagal-related HRV indexes. These results indicate that vagal-related HRV indexes are related more to cardiorespiratory fitness, whereas HRR appears to be better associated with training load.     

Aging attenuates vascular and metabolic plasticity but does not limit improvement in muscle VO(2) max

The interactions between exercise, vascular and metabolic plasticity, and aging have provided insight into the prevention and restoration of declining whole body and small muscle mass exercise performance known to occur with age. Metabolic and vascular adaptations to normoxic knee-extensor exercise training (1 h 3 times a week for 8 wk) were compared between six sedentary young (20 +/- 1 yr) and six sedentary old (67 +/- 2 yr) subjects. Arterial and venous blood samples, in conjunction with a thermodilution technique facilitated the measurement of quadriceps muscle blood flow and hematologic variables during incremental knee-extensor exercise. Pretraining, young and old subjects attained a similar maximal work rate (WR(max)) (young = 27 +/- 3, old = 24 +/- 4 W) and similar maximal quadriceps O(2) consumption (muscle Vo(2 max)) (young = 0.52 +/- 0.03, old = 0.42 +/- 0.05 l/min), which increased equally in both groups posttraining (WR(max), young = 38 +/- 1, old = 36 +/- 4 W, Muscle Vo(2 max), young = 0.71 +/- 0.1, old = 0.63 +/- 0.1 l/min). Before training, muscle blood flow was approximately 500 ml lower in the old compared with the young throughout incremental knee-extensor exercise. After 8 wk of knee-extensor exercise training, the young reduced muscle blood flow approximately 700 ml/min, elevated arteriovenous O(2) difference approximately 1.3 ml/dl, and increased leg vascular resistance approximately 17 mmHg x ml(-1) x min(-1), whereas the old subjects revealed no training-induced changes in these variables. Together, these findings indicate that after 8 wk of small muscle mass exercise training, young and old subjects of equal initial metabolic capacity have a similar ability to increase quadriceps muscle WR(max) and muscle Vo(2 max), despite an attenuated vascular and/or metabolic adaptation to submaximal exercise in the old.     

Exercise training increases intramyocellular lipid and oxidative capacity in older adults

Intramyocellular lipid (IMCL) has been associated with insulin resistance. However, an association between IMCL and insulin resistance might be modulated by oxidative capacity in skeletal muscle. We examined the hypothesis that 12 wk of exercise training would increase both IMCL and the oxidative capacity of skeletal muscle in older (67.3 +/- 0.7 yr), previously sedentary subjects (n = 13; 5 men and 8 women). Maximal aerobic capacity (Vo(2 max)) increased from 1.65 +/- 0.20 to 1.85 +/- 0.14 l/min (P < 0.05), and systemic fat oxidation induced by 1 h of cycle exercise at 45% of Vo(2 max) increased (P < 0.05) from 15.03 +/- 40 to 19.29 +/- 0.80 (micromol.min(-1).kg fat-free mass(-1)). IMCL, determined by quantitative histological staining in vastus lateralis biopsies, increased (P < 0.05) from 22.9 +/- 1.9 to 25.9 +/- 2.6 arbitrary units (AU). The oxidative capacity of muscle, determined by succinate dehydrogenase staining intensity, significantly increased (P < 0.05) from 75.2 +/- 5.2 to 83.9 +/- 3.6 AU. The percentage of type I fibers significantly increased (P < 0.05) from 35.4 +/- 2.1 to 40.1 +/- 2.3%. In conclusion, exercise training increases IMCL in older persons in parallel with an enhanced capacity for fat oxidation.     

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.     

Greater rate of decline in maximal aerobic capacity with age in endurance-trained than in sedentary men.

To determine the relation between habitual endurance exercise status and the age-associated decline in maximal aerobic capacity [i.e., maximal O(2) consumption (Vo(2 max))] in men, we performed a well-controlled cross-sectional laboratory study on 153 healthy men aged 20-75 yr: 64 sedentary and 89 endurance trained. Vo(2 max) (ml. kg(-1). min(-1)), measured by maximal treadmill exercise, was inversely related to age in the endurance-trained (r = -0.80) and sedentary (r = -0.74) men but was higher in the endurance-trained men at any age. The rate of decline in Vo(2 max) with age (ml. kg(-1). min(-1)) was greater (P < 0.001) in the endurance-trained than in the sedentary men. Whereas the relative rate of decline in Vo(2 max) (percent decrease per decade from baseline levels in young adulthood) was similar in the two groups, the absolute rate of decline in Vo(2 max) was -5.4 and -3.9 ml. kg(-1). min(-). decade(-1) in the endurance-trained and sedentary men, respectively. Vo(2 max) declined linearly across the age range in the sedentary men but was maintained in the endurance-trained men until approximately 50 yr of age. The accelerated decline in Vo(2 max) after 50 yr of age in the endurance-trained men was related to a decline in training volume (r = 0.46, P < 0.0001) and was associated with an increase in 10-km running time (r = -0.84, P < 0.0001). We conclude that the rate of decline in maximal aerobic capacity during middle and older age is greater in endurance-trained men than in their sedentary peers and is associated with a marked decline in O(2) pulse.     

The respiratory Vco2/Vo2 exchange ratio during maximum exercise and its use as a predictor of maximum oxygen uptake

The purpose of this study was to define carefully the dynamic relationship between oxygen uptake (as % Vo2max) and the respiratory Vco2/Vo2 exchange ratio (R) during maximum progressive treadmill exercise in trained and untrained men, and to determine if this relationship could be used to predict Vo2max. Respiratory gases were continuously monitored and the %Vo2max/R time profile calculated at 15 sec intervals over the final 5 min of each test. Young sedentary men (controls, n = 122) and over-60y sedentary men (n = 30) shared the same %Vo2max/R relationship but the latter group had lower R values at Vo2max (1.06 +/- 0.03 vs 1.08 +/- 0.03, p less than 0.01) than controls. Endurance trained men (n = 45) had a lower %Vo2max/R relationship and higher R at Vo2max (1.11 +/- 0.02, p less than 0.001), team athletes (n = 98) had a lower %Vo2max/R relationship but lower R at Vo2max (1.06 +/- 0.03, p less than 0.001) and the weight trained (n = 19) had a higher %Vo2max/R relationship and lower R at Vo2max (1.01 +/- 0.02, p less than 0.001) all compared to controls. From the %Vo2max/R time profile, the following formulae were devised for the estimation of Vo2max (Vo2maxR): Young Sedentary, Vo2maxR = Vo2R (3.000-1.874 R); Over-60y Sedentary, Vo2maxR = Vo2R (3.457-2.345 R); Endurance Trained, Vo2max = Vo2R (1.980-0.912 R); Team Athletes, Vo2maxR = Vo2R (2.805-1.726 R); Weight Trained, Vo2maxR = Vo2R (4.236-3.191 R).(ABSTRACT TRUNCATED AT 250 WORDS)     

Prolonged electrical muscle stimulation exercise improves strength and aerobic capacity in healthy sedentary adults.

This investigation evaluated training responses to prolonged electrical muscle stimulation (EMS) in sedentary adults. Fifteen healthy subjects (10 men, 5 women) with a sedentary lifestyle completed a 6-wk training program during which they completed an average of 29 1-h EMS sessions. The form of EMS used by the subjects was capable of eliciting a cardiovascular exercise response without loading the limbs or joints. It achieved this by means of inducing rapid, rhythmical contractions in the large leg muscles. A crossover study design was employed with subjects undergoing their habitual activity levels during the nontraining phase of the study. The training effect was evaluated by means of a treadmill test to determine peak aerobic capacity [peak oxygen consumption (Vo(2))], a 6-min walking distance test, and measurement of body mass index (BMI) and quadriceps muscle strength. At baseline, the mean values for peak Vo(2), 6-min walking distance, quadriceps strength, and BMI were 2.46 +/- 0.57 l/min, 493.3 +/- 36.8 m, 360.8 +/- 108.7 N, and 26.9 +/- 3.4 kg/m(2), respectively. After training, subjects demonstrated statistically significant improvements in all variables except BMI. Peak Vo(2) increased by an average of 0.24 +/- 0.16 l/min (P < 0.05), walking distance increased by 36.6 +/- 19.7 m (P < 0.005), and quadriceps strength increased by 87.5 +/- 55.9 N (P < 0.005); we did not observe a significant effect due to training on BMI (P > 0.05). These results suggest that EMS can be used in sedentary adults to improve physical fitness. It may provide a viable alternative to more conventional forms of exercise in this population.     

Exercise and diet enhance fat oxidation and reduce insulin resistance in older obese adults.

Older, obese, and sedentary individuals are at high risk of developing diabetes and cardiovascular disease. Exercise training improves metabolic anomalies associated with such diseases, but the effects of caloric restriction in addition to exercise in such a high-risk group are not known. Changes in body composition and metabolism during a lifestyle intervention were investigated in 23 older, obese men and women (aged 66 +/- 1 yr, body mass index 33.2 +/- 1.4 kg/m(2)) with impaired glucose tolerance. All volunteers undertook 12 wk of aerobic exercise training [5 days/wk for 60 min at 75% maximal oxygen consumption (Vo(2max))] with either normal caloric intake (eucaloric group, 1,901 +/- 277 kcal/day, n = 12) or a reduced-calorie diet (hypocaloric group, 1,307 +/- 70 kcal/day, n = 11), as dictated by nutritional counseling. Body composition (decreased fat mass; maintained fat-free mass), aerobic fitness (Vo(2max)), leptinemia, insulin sensitivity, and intramyocellular lipid accumulation (IMCL) in skeletal muscle improved in both groups (P < 0.05). Improvements in body composition, leptin, and basal fat oxidation were greater in the hypocaloric group. Following the intervention, there was a correlation between the increase in basal fat oxidation and the decrease in IMCL (r = -0.53, P = 0.04). In addition, basal fat oxidation was associated with circulating leptin after (r = 0.65, P = 0.0007) but not before the intervention (r = 0.05, P = 0.84). In conclusion, these data show that exercise training improves resting substrate oxidation and creates a metabolic milieu that appears to promote lipid utilization in skeletal muscle, thus facilitating a reversal of insulin resistance. We also demonstrate that leptin sensitivity is improved but that such a trend may rely on reducing caloric intake in addition to exercise training.     

Training at high exercise intensity promotes qualitative adaptations of mitochondrial function in human skeletal muscle

This study explored mitochondrial capacities to oxidize carbohydrate and fatty acids and functional optimization of mitochondrial respiratory chain complexes in athletes who regularly train at high exercise intensity (ATH, n = 7) compared with sedentary (SED, n = 7). Peak O(2) uptake (Vo(2max)) was measured, and muscle biopsies of vastus lateralis were collected. Maximal O(2) uptake of saponin-skinned myofibers was evaluated with several metabolic substrates [glutamate-malate (V(GM)), pyruvate (V(Pyr)), palmitoyl carnitine (V(PC))], and the activity of the mitochondrial respiratory complexes II and IV were assessed using succinate (V(s)) and N,N,N',N'-tetramethyl-p-phenylenediamine dihydrochloride (V(TMPD)), respectively. Vo(2max) was higher in ATH than in SED (57.8 +/- 2.2 vs. 31.4 +/- 1.3 ml.min(-1).kg(-1), P < 0.001). V(GM) was higher in ATH than in SED (8.6 +/- 0.5 vs. 3.3 +/- 0.3 micromol O(2).min(-1).g dry wt(-1), P < 0.001). V(Pyr) was higher in ATH than in SED (8.7 +/- 1.0 vs. 5.5 +/- 0.2 micromol O(2).min(-1).g dry wt(-1), P < 0.05), whereas V(PC) was not significantly different (5.3 +/- 0.9 vs. 4.4 +/- 0.5 micromol O(2).min(-1).g dry wt(-1)). V(S) was higher in ATH than in SED (11.0 +/- 0.6 vs. 6.0 +/- 0.3 micromol O(2).min(-1).g dry wt(-1), P < 0.001), as well as V(TMPD) (20.1 +/- 1.0 vs. 16.2 +/- 3.4 micromol O(2).min(-1).g dry wt(-1), P < 0.05). The ratios V(S)/V(GM) (1.3 +/- 0.1 vs. 2.0 +/- 0.1, P < 0.001) and V(TMPD)/V(GM) (2.4 +/- 1.0 vs. 5.2 +/- 1.8, P < 0.01) were lower in ATH than in SED. In conclusion, comparison of ATH vs. SED subjects suggests that regular endurance training at high intensity promotes the enhancement of maximal mitochondrial capacities to oxidize carbohydrate rather than fatty acid and induce specific adaptations of the mitochondrial respiratory chain at the level of complex I.     

Regulation of fuel metabolism by preexercise muscle glycogen content and exercise intensity.

To date, the results of studies that have examined the effects of altering preexercise muscle glycogen content and exercise intensity on endogenous carbohydrate oxidation are equivocal. Differences in the training status of subjects between investigations may, in part, explain these inconsistent findings. Accordingly, we determined the relative effects of exercise intensity and carbohydrate availability on patterns of fuel utilization in the same subjects who performed a random order of four 60-min rides, two at 45% and two at 70% of peak O(2) uptake (Vo(2 peak)), after exercise-diet intervention to manipulate muscle glycogen content. Preexercise muscle glycogen content was 596 +/- 43 and 202 +/- 21 mmol/kg dry mass (P < 0.001) for high-glycogen (HG) and low-glycogen (LG) conditions, respectively. Respiratory exchange ratio was higher for HG than LG during exercise at both 45% (0.85 +/- 0.01 vs. 0.74 +/- 0.01; P < 0.001) and 70% (0.90 +/- 0.01 vs. 0.79 +/- 0.01; P < 0.001) of Vo(2 peak). The contribution of whole body muscle glycogen oxidation to energy expenditure differed between LG and HG for exercise at both 45% (5 +/- 2 vs. 45 +/- 5%; P < 0.001) and 70% (25 +/- 3 vs. 60 +/- 3%; P < 0.001) of Vo(2 peak). Yet, despite marked differences in preexercise muscle glycogen content and its subsequent utilization, rates of plasma glucose disappearance were similar under all conditions. We conclude that, in moderately trained individuals, muscle glycogen availability (low vs. high) does not influence rates of plasma glucose disposal during either low- or moderate-intensity exercise.     

V(O2) max is unaffected by altering the temporal pattern of stimulation frequency in rat hindlimb in situ.

It might be anticipated that fatiguing contractions would impair the aerobic metabolic response in skeletal muscle if significant fatigue developed before full activation of aerobic metabolism. On the basis of this premise, we examined two groups of rats to test the hypothesis that a gradual increase in stimulation frequency would yield a higher maximal O2 uptake (Vo2 max) than beginning immediately with an intense stimulation frequency because of a slower progression of fatigue under the former conditions. In one group of animals, the distal hindlimb muscles were electrically stimulated at a frequency of 60 tetani/min for 4 min (F60; n = 6 rats); in the other group, the muscles were incrementally stimulated for 1 min at each of 7.5, 15, 30, and 60 tetani/min and for 2 min at 90 tetani/min (FInc; n = 5 rats). Despite large differences in rate of fatigue [time to 60% of initial force was 47 +/- 3 (SE) vs. 188 +/- 1 s in F60 and FInc, respectively] and the time at which Vo2 max occurred (120 +/- 15 vs. 264 +/- 6 s), Vo2 max was not different (419 +/- 24 vs. 381 +/- 44 micromol x min-1. 100 g-1). Furthermore, time x tension integral at Vo2 max (3.82 +/- 0.41 vs. 4.07 +/- 0.31 N. s) and peak lactate efflux (910 +/- 45 vs. 800 +/- 98 micromol x min-1. 100 g-1) were not different between groups. Thus our results show that the more rapid progression of fatigue in F60 did not compromise the aerobic metabolic response in electrically stimulated rat hindlimb muscles. However, in both groups, O2 uptake and lactate efflux declined after Vo2 max was attained in similar proportion to a further fall in force, suggesting that ongoing fatigue with intense contractions reduced ATP demand below that requiring maximal aerobic and glycolytic metabolic responses once Vo2 max was reached.     

Decline in VO2max with aging in master athletes and sedentary men

Fifteen well-trained master endurance athletes [62.0 +/- 2.3 (SE) yr] and 14 sedentary control subjects (61.4 +/- 1.4 yr) were reevaluated after an average follow-up period of approximately 8 yr to obtain information regarding the effects of physical activity on the age-related decline in maximal O2 uptake capacity (VO2max). The master athletes had been training for 10.2 +/- 2.9 yr before initial testing and continued to train during the follow-up period. The sedentary subjects' VO2max declined by an average of 3.3 ml.kg-1.min-1 (33.9 +/- 1.7 vs. 30.6 +/- 1.6, P less than 0.001) over the course of the study, a decline of 12% per decade. In these subjects maximal heart rate declined 8 beats/min (171 vs. 163) and maximal O2 pulse decreased from 0.20 to 0.18 ml.kg-1.beat (P less than 0.05). The master athletes' VO2 max decreased by an average of 2.2 ml.kg-1.min-1 (54.0 +/- 1.7 vs. 51.8 +/- 1.8, P less than 0.05), a 5.5% decline per decade. The master athletes' maximal heart rate was unchanged (171 +/- 3 beats/min) and their maximal O2 pulse decreased from 0.32 to 0.30 ml.kg-1.beat (P less than 0.05). These findings provide evidence that the age-related decrease in VO2max of master athletes who continue to engage in regular vigorous endurance exercise training is approximately one-half the rate of decline seen in age-matched sedentary subjects. Furthermore our results suggest that endurance exercise training may reduce the rate of decline in maximal heart rate that typically occurs as an individual ages.     

Downhill treadmill running trains the rat spinotrapezius muscle.

There are currently no models of exercise that recruit and train muscles, such as the rat spinotrapezius, that are suitable for transmission intravital microscopic investigation of the microcirculation. Recent experimental evidence supports the concept that running downhill on a motorized treadmill recruits the spinotrapezius muscle of the rat. Based on these results, we tested the hypothesis that 6 wk of downhill running (-14 degrees grade) for 1 h/day, 5 days/wk, at a speed of up to 35 m/min, would 1) increase whole body peak oxygen uptake (Vo(2 peak)), 2) increase spinotrapezius citrate synthase activity, and 3) reduce the fatigability of the spinotrapezius during electrically induced 1-Hz submaximal tetanic contractions. Trained rats (n = 6) elicited a 24% higher Vo(2 peak) (in ml.min(-1).kg(-1): sedentary 58.5 +/- 2.0, trained 72.7 +/- 2.0; P < 0.001) and a 41% greater spinotrapezius citrate synthase activity (in mumol.min(-1).g(-1): sedentary 14.1 +/- 0.7, trained 19.9 +/- 0.9; P < 0.001) compared with sedentary controls (n = 6). In addition, at the end of 15 min of electrical stimulation, trained rats sustained a greater percentage of the initial tension than their sedentary counterparts (control 34.3 +/- 3.1%, trained 59.0 +/- 7.2%; P < 0.05). These results demonstrate that downhill running is successful in promoting training adaptations in the spinotrapezius muscle, including increased oxidative capacity and resistance to fatigue. Since the spinotrapezius muscle is commonly used in studies using intravital microscopy to examine microcirculatory function at rest and during contractions, our results suggest that downhill running is an effective training paradigm that can be used to investigate the mechanisms for improved microcirculatory function following exercise training in health and disease.     

Kinetics of muscle deoxygenation are accelerated at the onset of heavy-intensity exercise in patients with COPD: relationship to central cardiovascular dynamics.

Patients with chronic obstructive pulmonary disease (COPD) have slowed pulmonary O(2) uptake (Vo(2)(p)) kinetics during exercise, which may stem from inadequate muscle O(2) delivery. However, it is currently unknown how COPD impacts the dynamic relationship between systemic and microvascular O(2) delivery to uptake during exercise. We tested the hypothesis that, along with slowed Vo(2)(p) kinetics, COPD patients have faster dynamics of muscle deoxygenation, but slower kinetics of cardiac output (Qt) following the onset of heavy-intensity exercise. We measured Vo(2)(p), Qt (impedance cardiography), and muscle deoxygenation (near-infrared spectroscopy) during heavy-intensity exercise performed to the limit of tolerance by 10 patients with moderate-to-severe COPD and 11 age-matched sedentary controls. Variables were analyzed by standard nonlinear regression equations. Time to exercise intolerance was significantly (P < 0.05) lower in patients and related to the kinetics of Vo(2)(p) (r = -0.70; P < 0.05). Compared with controls, COPD patients displayed slower kinetics of Vo(2)(p) (42 +/- 13 vs. 73 +/- 24 s) and Qt (67 +/- 11 vs. 96 +/- 32 s), and faster overall kinetics of muscle deoxy-Hb (19.9 +/- 2.4 vs. 16.5 +/- 3.4 s). Consequently, the time constant ratio of O(2) uptake to mean response time of deoxy-Hb concentration was significantly greater in patients, suggesting a slower kinetics of microvascular O(2) delivery. In conclusion, our data show that patients with moderate-to-severe COPD have impaired central and peripheral cardiovascular adjustments following the onset of heavy-intensity exercise. These cardiocirculatory disturbances negatively impact the dynamic matching of O(2) delivery and utilization and may contribute to the slower Vo(2)(p) kinetics compared with age-matched controls.     

Six sessions of sprint interval training increases muscle oxidative potential and cycle endurance capacity in humans.

Parra et al. (Acta Physiol. Scand 169: 157-165, 2000) showed that 2 wk of daily sprint interval training (SIT) increased citrate synthase (CS) maximal activity but did not change "anaerobic" work capacity, possibly because of chronic fatigue induced by daily training. The effect of fewer SIT sessions on muscle oxidative potential is unknown, and aside from changes in peak oxygen uptake (Vo(2 peak)), no study has examined the effect of SIT on "aerobic" exercise capacity. We tested the hypothesis that six sessions of SIT, performed over 2 wk with 1-2 days rest between sessions to promote recovery, would increase CS maximal activity and endurance capacity during cycling at approximately 80% Vo(2 peak). Eight recreationally active subjects [age = 22 +/- 1 yr; Vo(2 peak) = 45 +/- 3 ml.kg(-1).min(-1) (mean +/- SE)] were studied before and 3 days after SIT. Each training session consisted of four to seven "all-out" 30-s Wingate tests with 4 min of recovery. After SIT, CS maximal activity increased by 38% (5.5 +/- 1.0 vs. 4.0 +/- 0.7 mmol.kg protein(-1).h(-1)) and resting muscle glycogen content increased by 26% (614 +/- 39 vs. 489 +/- 57 mmol/kg dry wt) (both P < 0.05). Most strikingly, cycle endurance capacity increased by 100% after SIT (51 +/- 11 vs. 26 +/- 5 min; P < 0.05), despite no change in Vo(2 peak). The coefficient of variation for the cycle test was 12.0%, and a control group (n = 8) showed no change in performance when tested approximately 2 wk apart without SIT. We conclude that short sprint interval training (approximately 15 min of intense exercise over 2 wk) increased muscle oxidative potential and doubled endurance capacity during intense aerobic cycling in recreationally active individuals.     

Effects of exercise training on contractile function in myocardial trabeculae after ischemia-reperfusion.

Potential protective effects of aerobic exercise training on the myocardium, before an ischemic event, are not completely understood. The purpose of the study was to investigate the effects of exercise training on contractile function after ischemia-reperfusion (Langendorff preparation with 15-min global ischemia/30-min reperfusion). Trabeculae were isolated from the left ventricles of both sedentary control and 10- to 12-wk treadmill exercise-trained rats. The maximal normalized isometric force (force/cross-sectional area; Po/CSA) and shortening velocity (Vo) in isolated, skinned ventricular trabeculae were measured using the slack test. Ischemia-reperfusion induced significant contractile dysfunction in hearts from both sedentary and trained animals; left ventricular developed pressure (LVDP) and maximal rates of pressure development and relaxation (+/-dP/dtmax) decreased, whereas end-diastolic pressure (EDP) increased. However, this dysfunction (as expressed as percent change from the last 5 min before ischemia) was attenuated in trained myocardium [LVDP: sedentary -60.8 +/- 6.4% (32.0 +/- 5.5 mmHg) vs. trained -15.6 +/- 8.6% (64.9 +/- 6.6 mmHg); +dP/dtmax: sedentary -54.1 +/- 4.7% (1,058.7 +/- 124.2 mmHg/s) vs. trained -16.7 +/- 8.4% (1,931.9 +/- 188.3 mmHg/s); -dP/dtmax: sedentary -44.4 +/- 2.5% (-829.3 +/- 52.0 mmHg/s) vs. trained -17.9 +/- 7.2% (-1,341.3 +/- 142.8 mmHg/s); EDP: sedentary 539.5 +/- 147.6%; (41.3 +/- 6.0 mmHg) vs. trained 71.6 +/- 30.6%; 11.4 +/- 1.2 mmHg]. There was an average 26% increase in Po/CSA in trained trabeculae compared with sedentary controls, and this increase was not affected by ischemia-reperfusion. Ischemia-reperfusion reduced Vo by 39% in both control and trained trabeculae. The relative amount of the beta-isoform of myosin heavy chain (MHC-beta) was twofold greater in trained trabeculae as well as in the ventricular free walls. Despite a possible increase in the economy in the trained heart, presumed from a greater amount of MHC-beta, ischemia-reperfusion reduced Vo, to a similar extent in both control and trained animals. Nevertheless, the trained myocardium appears to have a greater maximum force-generating ability that may, at least partially, compensate for reduced contractile function induced by a brief period of ischemia.     

Changes in maximal aerobic capacity with age in endurance-trained women: 7-yr follow-up.

On the basis of cross-sectional data, we previously reported that the absolute, but not the relative (%), rate of decline in maximal oxygen consumption (VO(2 max)) with age is greater in endurance-trained compared with healthy sedentary women. We tested this hypothesis by using a longitudinal approach. Eight sedentary (63 +/- 2 yr at follow-up) and 16 endurance-trained (57 +/- 2) women were reevaluated after a mean follow-up period of 7 yr. At baseline, VO(2 max) was ~70% higher in endurance-trained women (48.1 +/- 1.7 vs. 28.1 +/- 0.8 ml. kg(-1). min(-1). yr(-1)). At follow-up, body mass, fat-free mass, maximal respiratory exchange ratio, and maximal rating of perceived exertion were not different from baseline in either group. The absolute rate of decline in VO(2 max) was twice as great (P < 0.01) in the endurance-trained (-0.84 +/- 0.15 ml. kg(-1). min(-1). yr(-1)) vs. sedentary (-0.40 +/- 0.12 ml. kg(-1). min(-1). yr(-1)) group, but the relative rates of decline were not different (-1.8 +/- 0.3 vs. -1.5 +/- 0.4% per year). Differences in rates of decline in VO(2 max) were not related to changes in body mass or maximal heart rate. However, among endurance-trained women, the relative rate of decline in VO(2 max) was positively related to reductions in training volume (r = 0.63). Consistent with this, the age-related reduction in VO(2 max) in a subgroup of endurance-trained women who maintained or increased training volume was not different from that of sedentary women. These longitudinal data indicate that the greater decrease in maximal aerobic capacity with advancing age observed in middle-aged and older endurance-trained women in general compared with their sedentary peers is due to declines in habitual exercise in some endurance-trained women. Endurance-trained women who maintain or increase training volume demonstrated age-associated declines in maximal aerobic capacity not different from healthy sedentary women.