Additive effects of training and high-fat diet on energy metabolism during exercise

This study was conducted to obtain additional information about the adaptations after 12 wk of high-fat diet (HFD) per se or HFD combined with endurance training in the rat using a two [diet: carbohydrate (CHO) or HFD] by two (training: sedentary or trained) by two (condition at death: rested or exercised) factorial design. Adaptation to prolonged HFD increases maximal O2 uptake (VO2max; 13%, P less than 0.05) and submaximal running endurance (+64%, P less than 0.05). This enhancement in exercise capacity could be attributed to 1) an increase in skeletal muscle aerobic enzyme activities (3-hydroxyacyl-CoA dehydrogenase and citrate synthase in soleus and red quadriceps) or 2) a decrease in liver glycogen breakdown in response to 1 h exercise at 80% VO2max. When training is superimposed to HFD, the most prominent finding provided by this study is that the diet-induced effects are cumulative with the well-known training effect on VO2max, exercise endurance, oxidative capacity of red muscle, and metabolic responses to exercise, with a further reduction in liver glycogen breakdown.     

Chronic cold exposure increases skeletal muscle oxidative structure and function in Monodelphis domestica, a marsupial lacking brown adipose tissue

Monodelphis domestica (Marsupialia: Didelphidae) was used as a model animal to investigate and compare muscle adaptation to exercise training and cold exposure. The experimental treatment consisted of four groups of animals: either warm or cold acclimation temperature and with or without endurance exercise training. Maximal aerobic capacity during a running VO2max test in the warm-exercised or cold-exposed (with or without exercise) groups was about 130 mL O(2)/kg/min, significantly higher than the warm-acclimated controls at 113.5 mL O(2)/kg/min. Similarly, during an acute cold challenge (VO2summit), maximal aerobic capacity was higher in these three experimental groups at approximately 95 mL O(2)/kg/min compared with 80.4 mL O(2)/kg/min in warm-acclimated controls. Respiratory exchange ratio was significantly lower (0.89-0.68), whereas relative heart mass (0.52%-0.73%) and whole-body muscle mitochondrial volume density (2.59 to 3.04 cm(3)) were significantly higher following cold exposure. Chronic cold exposure was a stronger stimulus than endurance exercise training for tissue-specific adaptations. Although chronic cold exposure and endurance exercise are distinct challenges, physiological adaptations to each overlap such that the capacities for aerobic performance in response to both cold exposure and running are increased by either or both treatments.     

Exercise training in normobaric hypoxia in endurance runners. I. Improvement in aerobic performance capacity.

This study investigates whether a 6-wk intermittent hypoxia training (IHT), designed to avoid reductions in training loads and intensities, improves the endurance performance capacity of competitive distance runners. Eighteen athletes were randomly assigned to train in normoxia [Nor group; n = 9; maximal oxygen uptake (VO2 max) = 61.5 +/- 1.1 ml x kg(-1) x min(-1)] or intermittently in hypoxia (Hyp group; n = 9; VO2 max = 64.2 +/- 1.2 ml x kg(-1) x min(-1)). Into their usual normoxic training schedule, athletes included two weekly high-intensity (second ventilatory threshold) and moderate-duration (24-40 min) training sessions, performed either in normoxia [inspired O2 fraction (FiO2) = 20.9%] or in normobaric hypoxia (FiO2) = 14.5%). Before and after training, all athletes realized 1) a normoxic and hypoxic incremental test to determine VO2 max and ventilatory thresholds (first and second ventilatory threshold), and 2) an all-out test at the pretraining minimal velocity eliciting VO2 max to determine their time to exhaustion (T(lim)) and the parameters of O2 uptake (VO2) kinetics. Only the Hyp group significantly improved VO2 max (+5% at both FiO2, P < 0.05), without changes in blood O2-carrying capacity. Moreover, T(lim) lengthened in the Hyp group only (+35%, P < 0.001), without significant modifications of VO2 kinetics. Despite similar training load, the Nor group displayed no such improvements, with unchanged VO2 max (+1%, nonsignificant), T(lim) (+10%, nonsignificant), and VO2 kinetics. In addition, T(lim) improvements in the Hyp group were not correlated with concomitant modifications of other parameters, including VO2 max or VO2 kinetics. The present IHT model, involving specific high-intensity and moderate-duration hypoxic sessions, may potentialize the metabolic stimuli of training in already trained athletes and elicit peripheral muscle adaptations, resulting in increased endurance performance capacity.     

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.     

Endurance training in humans: aerobic capacity and structure of skeletal muscle

The adaptation of muscle structure, power output, and mass-specific rate of maximal O2 consumption (VO2max/Mb) with endurance training on bicycle ergometers was studied for five male and five female subjects. Biopsies of vastus lateralis muscle and VO2max determinations were made at the start and end of 6 wk of training. The power output maintained on the ergometer daily for 30 min was adjusted to achieve a heart rate exceeding 85% of the maximum for two-thirds of the training session. It is proposed that the observed preferential proliferation of subsarcolemmal vs. interfibrillar mitochondria and the increase in intracellular lipid deposits are two possible mechanisms by which muscle cells adapt to an increased use of fat as a fuel. The relative increase of VO2max/Mb (14%) with training was found to be smaller by more than twofold than the relative increase in maximal maintained power (33%) and the relative change in the volume density of total mitochondria (+40%). However, the calculated VO2 required at an efficiency of 0.25 to produce the observed mass-specific increase in maximal maintained power matched the actual increase in VO2max/Mb (8.0 and 6.5 ml O2 X min-1 X kg-1, respectively). These results indicate that despite disparate relative changes the absolute change in aerobic capacity at the local level (maintained power) can account for the increase in aerobic capacity observed at the general level (VO2max).     

Reduced training intensities and loss of aerobic power, endurance, and cardiac growth

Twelve subjects participated in an exercise program of cycling and running 40 min/day, 6 days/wk. After 10 wk, they continued to train with either a one-third or two-thirds reduction in work rates for an additional 15 wk. Frequency and duration for the additional training remained the same as during the 10 wk of training. The average increases in maximum O2 uptake (VO2 max) were between 11 and 20% when measured during cycling and treadmill running after 10 wk of training. VO2 max was not maintained at the 6-day/wk training levels with a one-third reduction in training intensity but was still higher than pretraining levels. With a two-thirds reduction in intensity, VO2 max declined to an even greater extent than with the one-third reduction. Short-term endurance (approximately 5 min) was maintained in the one-third reduced group but was markedly reduced in the two-thirds reduced group. Long-term endurance was decreased significantly from training by 21% in the one-third reduced group (184-145 min) and by 30% in the two-thirds reduced group (202-141 min). Calculated left ventricular mass, obtained from echocardiographic measurements, increased approximately 15% after training but returned to control levels after reduced training in both groups. These results demonstrate that training intensity is an essential requirement for maintaining the increased aerobic power and cardiac enlargement with reduced training.(ABSTRACT TRUNCATED AT 250 WORDS)     

Intermittent locomotion increases endurance in a gecko

Nocturnal geckos can actively forage at low temperatures. A low minimum cost of locomotion allows greater sustainable speeds by partially offsetting the decrease in maximal oxygen consumption (VO2max) associated with low nocturnal temperatures. The nocturnality hypothesis (Autumn et al. 1997) proposes that the reduced cost of continuous locomotion is a shared, derived characteristic that increases the capacity to sustain locomotion at low temperatures. Yet many lizards move intermittently at speeds exceeding those that elicit VO2max. We exercised the frog-eyed gecko, Teratoscincus przewalskii, continuously and intermittently on a treadmill. At an exercise speed of 0.90 km h-1 (270% maximum aerobic speed), lizards alternating a 15-s exercise period with a 30-s pause period exhibited a 1.7-fold increase in distance capacity (total distance traveled before fatigue) compared with lizards exercised continuously at the same average speed (0.30 km h-1). The average aerobic cost of intermittent exercise was not significantly different from VO2max. Locomoting intermittently could augment the increase in endurance resulting from the low minimum cost of continuous locomotion in nocturnal geckos. Intermittent behavior could increase the endurance of lizard movement in general.     

Metabolic adaptations to training precede changes in muscle mitochondrial capacity.

To determine whether increases in muscle mitochondrial capacity are necessary for the characteristic lower exercise glycogen loss and lactate concentration observed during exercise in the trained state, we have employed a short-term training model involving 2 h of cycling per day at 67% maximal O2 uptake (VO2max) for 5-7 consecutive days. Before and after training, biopsies were extracted from the vastus lateralis of nine male subjects during a continuous exercise challenge consisting of 30 min of work at 67% VO2max followed by 30 min at 76% VO2max. Analysis of samples at 0, 15, 20, and 60 min indicated a pronounced reduction (P less than 0.05) in glycogen utilization after training. Reductions in glycogen utilization were accompanied by reductions (P less than 0.05) in muscle lactate concentration (mmol/kg dry wt) at 15 min [37.4 +/- 9.3 (SE) vs. 20.2 +/- 5.3], 30 min (30.5 +/- 6.9 vs. 17.6 +/- 3.8), and 60 min (26.5 +/- 5.8 vs. 17.8 +/- 3.5) of exercise. Maximal aerobic power, VO2max (l/min) was unaffected by the training (3.99 +/- 0.21 vs. 4.05 +/- 0.26). Measurements of maximal activities of enzymes representative of the citric acid cycle (succinic dehydrogenase and citrate synthase) were similar before and after the training. It is concluded that, in the voluntary exercising human, altered metabolic events are an early adaptive response to training and need not be accompanied by changes in muscle mitochondrial capacity.     

Intensity-controlled treadmill running in rats: VO(2 max) and cardiac hypertrophy

Physiological studies of long-term cardiovascular adaptation to exercise require training regimens that give robust conditioning effects and adequate testing procedures to quantify the outcome. We developed a valid and reproducible protocol for measuring maximal oxygen uptake (VO(2 max)), which was reached at a 25 degrees inclination with a respiratory exchange ratio > 1.05 and blood lactate > 6 mmol/l. The effect of intensity-controlled aerobic endurance training was studied in adult female and male rats that ran 2 h/day, 5 days/wk, in intervals of 8 min at 85-90% of VO(2 max) and 2 min at 50-60% of VO(2 max), with adjustment of exercise level according to VO(2 max) every week. After 7 wk, the increase in VO(2 max) plateaued at 60-70% above sedentary controls. Ventricular weights and myocyte length were up 25-30% and 6-12%, respectively. Work economy, oxygen pulse, and heart rate were sufficiently changed to indicate substantial cardiovascular adaptation. The model mimics important human responses to training and could be used in future studies on cellular, molecular, and integrative mechanisms of improved cardiovascular function.     

Training-induced skeletal muscle adaptations are independent of systemic adaptations

To isolate the peripheral adaptations to training, five normal subjects exercised the nondominant (ND) wrist flexors for 41 +/- 11 days, maintaining an exercise intensity below the threshold required for cardiovascular adaptations. Before and after training, intracellular pH and the ratio of inorganic phosphate to phosphocreatine (Pi/PCr) were measured by 31P magnetic resonance spectroscopy. Also maximal O2 consumption (VO2 max), muscle mass, and forearm blood flow were determined by graded systemic exercise, magnetic resonance imaging, and venous occlusion plethysmography, respectively. Blood flow, Pi/PCr, and pH were measured in both forearms at rest and during submaximal wrist flexion at 5, 23, and 46 J/min. Training did not affect VO2 max, exercise blood flow, or muscle mass. Resting pH, Pi/PCr, and blood flow were also unchanged. After training, the ND forearm demonstrated significantly lower Pi/PCr at 23 and 46 J/min. Endurance, measured as the number of contractions to exhaustion, also was increased significantly (63%) after training in the ND forearm. We conclude that 1) forearm training results in a lower Pi/PCr at identical submaximal work loads; 2) this improvement is independent of changes in VO2 max, muscle mass, or limb blood flow; and 3) these differences are associated with improved endurance and may reflect improved oxidative capacity of skeletal muscle.     

Interactive effects of anemia and muscle oxidative capacity on exercise endurance

We used endurance training and acute anemia to assess the interactions among maximal oxygen consumption (VO2max), muscle oxidative capacity, and exercise endurance in rats. Animals were evaluated under four conditions: untrained and endurance-trained with each group subdivided into anemic (animals with reduced hemoglobin concentrations) and control (animals with unchanged hemoglobin concentrations). Anemia was induced by isovolemic plasma exchange transfusion. Hemoglobin concentration and hematocrit were decreased by 38 and 41%, respectively. Whole body VO2max was decreased by 18% by anemia regardless of training condition. Anemia significantly reduced endurance by 78% in untrained rats but only 39% in trained animals. Endurance training resulted in a 10% increase in VO2max, a 75% increase in the distance run to exhaustion, and 35, 45, and 58% increases in skeletal muscle pyruvate-malate, alpha-ketoglutarate, and palmitylcarnitine oxidase activities, respectively. We conclude that endurance is related to the interactive effects of whole body VO2max and muscle oxidative capacities for the following reasons: 1) anemic untrained and trained animals had similar VO2max but trained rats had higher muscle oxidative capacities and greater endurance; 2) regardless of training status, the effect of acute anemia was to decrease VO2max and endurance; and 3) trained anemic rats had lower VO2max but had greater muscle oxidative capacity and greater endurance than untrained controls.     

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)     

Training does not protect against exhaustive exercise-induced lactate transport capacity alterations

The effects of endurance training on lactate transport capacity remain controversial. This study examined whether endurance training 1) alters lactate transport capacity, 2) can protect against exhaustive exercise-induced lactate transport alteration, and 3) can modify heart and oxidative muscle monocarboxylate transporter 1 (MCT1) content. Forty male Wistar rats were divided into control (C), trained (T), exhaustively exercised (E), and trained and exercised (TE) groups. Rats in the T and TE groups ran on a treadmill (1 h/day, 5 days/wk at 25 m/min, 10% incline) for 5 wk; C and E were familiarized with the exercise task for 5 min/day. Before being killed, E and TE rats underwent exhaustive exercise (25 m/min, 10% grade), which lasted 80 and 204 min, respectively (P < 0.05). Although lactate transport measurements (zero-trans) did not differ between groups C and T, both E and TE groups presented an apparent loss of protein saturation properties. In the trained groups, MCT1 content increased in soleus (+28% for T and +26% for TE; P < 0.05) and heart muscle (+36% for T and +33% for TE; P < 0.05). Moreover, despite the metabolic adaptations typically observed after endurance training, we also noted increased lipid peroxidation byproducts after exhaustive exercise. We concluded that 1) endurance training does not alter lactate transport capacity, 2) exhaustive exercise-induced lactate transport alteration is not prevented by training despite increased MCT1 content, and 3) exercise-induced oxidative stress may enhance the passive diffusion responsible for the apparent loss of saturation properties, possibly masking lactate transport regulation.     

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.     

Acute exercise and training alter blood lipid and lipoprotein profiles differently in overweight and obese men and women

Our purpose was to elucidate effects of acute exercise and training on blood lipids-lipoproteins, and high-sensitivity C-reactive protein (hsCRP) in overweight/obese men (n = 10) and women (n = 8); age, BMI, body fat percentage, and VO(2)max were (mean ± SEM): 45 ± 2.5 years, 31.9 ± 1.4 kg·m(-2), 41.1 ± 1.5%, and 25.2 ± 1.3 mlO(2)·kg(-1)·min(-1). Before exercise training subjects performed an acute exercise session on a treadmill (70% VO(2)max, 400 kcal energy expenditure), followed by 12 weeks of endurance exercise training (land-based or aquatic-based treadmill): 3 sessions·week(-1), progressing to 500 kcal·session(-1) during which subjects maintained accustomed dietary habits. After training, the acute exercise session was repeated. Blood samples, obtained immediately before and 24 h after acute exercise sessions, were analyzed for serum lipids, lipoproteins, and hsCRP adjusted for plasma volume shifts. Exercise training increased VO(2)max (+3.67 mlO(2)·kg(-1)·min(-1), P < 0.001) and reduced body weight (-2.7 kg, P < 0.01). Training increased high-density lipoprotein (HDL) and HDL(2b)-cholesterol (HDL-C) concentrations (+3.7 and +2.4 mg·dl(-1), P < 0.05) and particle numbers (+588 and +206 nmol·l(-1), P < 0.05) in men. In women despite no change in total HDL-C, subfractions shifted from HDL(3)-C (-3.2, P < 0.01) to HDL(2b)-C (+3.5, P < 0.05) and HDL(2a)-C (+2.2 mg·dl(-1), P < 0.05), with increased HDL(2b) particle number (+313 nmol·l(-1), P < 0.05). Training reduced LDL(3) concentration and particle number in women (-1.6 mg·dl(-1) and -16 nmol·l(-1), P < 0.05). Acute exercise reduced the total cholesterol (TC): HDL-C ratio in men (-0.16, P < 0.01) and increased hsCRP in all subjects (+0.05 mg·dl(-1), P < 0.05), regardless of training. Training did not affect acute exercise responses. Our data support the efficacy of endurance training, without dietary intervention, to elicit beneficial changes in blood lipids-lipoproteins in obese men and women.     

Changes in isometric function following rhythmic exercise

Seven male subjects exercised for 1, 3, 10 and 20 min on a cycle ergometer at 20, 60 and 80% VO2max, and then held to fatigue a sustained contraction of the quadriceps at 40% maximal voluntary contraction in order to determine what influence various levels of dynamic exercise would have on isometric function of the same group of muscles. Muscle temperature was measured before and within 15 s of the completion of the cycling to determine whether changes in muscle temperature might influence the subsequent isometric performance. Isometric endurance was shorter as the severity of the cycling increased beyond 20% VO2max, and as the duration of cycling increased up to 10 min. There were discrete linear relationships between muscle temperature and isometric endurance associated with cycling at 60% and 80% VO2max. There was a direct inverse relationship between quadriceps strength after cycling and muscle temperature, yet a significant reduction in strength occurred only after cycling at 80% VO2max. These results suggest that the encroachment on endurance and strength are controlled by different mechanisms. The heart rates during the isometric contractions were dependent on the preceding rhythmic exercise and decreased after exercise at 60 or 80% VO2max. In contrast, the blood pressure always increased during the isometric contractions, reaching similar values at the point of fatigue, regardless of the severity of the previous rhythmic exercise. These data provide additional evidence that separate mechanisms control changes in heart rate and blood pressure.     

Effects of training on the physiological responses to one- and two-leg work.

The effects of training resulting from one-leg exercise on a stationary bicycle ergometer have been studied. Seven subjects were habituated to one- and two-leg progressive exercise tests on 11 successive days and were then trained for 60 min-day-1 (30 min each leg) 3 times per wk for 5-6 wk at approximately 80% of their one-leg VO2 max. VE max increased (P less than 0.05) by approximately 14 1-min-1 and VO2 max by approximately 0.34 1-min-1 (+14%; P less than 0.05) in one-leg exercise. This latter increase was not, however, reflected in the two-leg VO2 max which only increased 145 ml-min-1 (4.7%). It was concluded that training is specific and in one-leg work the phenomenon is mainly peripheral in origin, but in two-leg work the limitation to maximal exercise is still provided by the capacity of the central cardiovascular system to transport oxygen to a given effective muscle mass.     

Growth hormone treatment in growth hormone-deficient adults. II. Effects on exercise performance

Growth hormone (GH) treatment in adults with GH deficiency increases lean body mass and thigh muscle cross-sectional area. The functional significance of this was examined by incremental cycle ergometry in 24 GH-deficient adults treated in a double-blind placebo-controlled trial with recombinant DNA human GH (rhGH) for 6 mo (0.07 U/kg body wt daily). Compared with placebo, the rhGH group increased mean maximal O2 uptake (VO2max) (+406 +/- 71 vs. +133 +/- 84 ml/min; P = 0.016) and maximal power output (+24.6 +/- 4.3 vs. +9.7 +/- 4.8 W; P = 0.047), without differences in maximal heart rate or ventilation. Forced expiratory volume in 1 s, vital capacity, and corrected CO gas transfer were within normal limits and did not change with treatment. Mean predicted VO2max, based on height and age, increased from 78.9 to 96.0% in the rhGH group (compared with 78.5 and 85.0% for placebo; P = 0.036). The anaerobic ventilatory threshold increased in the rhGH group (+159 +/- 39 vs. +1 +/- 51 ml/min; P = 0.02). The improvement in VO2max was noted when expressed per kilogram body weight but not lean body mass or thigh muscle area. We conclude that rhGH treatment in adults with GH deficiency improves and normalizes maximal exercise performance and improves submaximal exercise performance and that these changes are related to increases in lean body mass and muscle mass. Improved cardiac output may also contribute to the effect of rhGH on exercise performance.