Absolute Exercise Intensity Research Articles

Fat Oxidation Rates are Higher Over a Wide Range of Intensities in Rowing Compared to Cycling Ergometry

The relative contribution of carbohydrate and fat oxidation to whole body energy production during exercise is dependent on oxygen availability. Continuous incremental exercise is associated with a progressive increase in carbohydrate oxidation and a decrease in fat oxidation. The exercise modality, more specifically the muscle mass recruited, is also thought to be an important contributor to substrate selection. PURPOSE: The purpose of this study was to determine the rates of fat oxidation and the cross-over point for substrate utilisation over a wide range of intensities during incremental rowing and cycle ergometry. METHODS: Thirteen moderately trained male rowers [age, 23.2 ± 1.6 yrs; height, 1.82 ± 0.02 m; body mass, 77.0 ± 1.6 kg] performed a continuous incremental exercise test to exhaustion on an electronicaly braked cycle ergometer and an air braked rowing ergometer. The exercise intensity began at 95W and increased in 35W increments every 3-min. Rates of substrate oxidation and the relative contribution to energy expenditure were calculated for the same absolute (W) and relative (%VO2peak) intensity by indirect calorimetry during the last 2-min of each 3-min stage. RESULTS: Peak oxygen consumption was similar for the rowing (57.5 ± 1.5 ml kg min−1) and cycle (55.7 ± 1.6 ml kg min−1) ergometer tests. Peak fat oxidation was higher in rowing (0.72 ± 0.05 g.min−1) than cycling (0.51 ± 0.04 g.min−1, p=0.008) and occurred during the first stage. The rate of fat oxidation was greater during rowing at the same absolute (p=0.019) and relative (p=0.001) exercise intensities up to ∼93%VO2peak. The crossover point for substrate utilisation occurred at a higher relative exercise intensity for rowing than cycling (57.8 ± 2.1 vs. 42.1 ± 3.6 %VO2peak, p=0.003). CONCLUSION: The rate of fat oxidation is higher during rowing exercise than cycling, across a range of exercise intensities, despite similar oxygen uptake. It is possible that the greater muscle mass recruited during rowing may distribute the metabolic stress and facilitate fat oxidation. These results indicate that when prescribing exercise to optimise fat oxidation, the exercise modality should be such that it recruits a larger muscle mass.

Commentary on Point-Counterpoint

This letter is in response to the Point:Counterpoint series “Positive effects of intermittent hypoxia (live high:train low) on exercise performance are/are not mediated primarily by augmented red cell volume that appeared in the November issue (vol. 99: 2053–2058, 2005; doi: 10.1152/japplphysiol

Linear decrease in $$\dot V\hbox{O}_{2\max}$$ and performance with increasing altitude in endurance athletes

It has been hypothesized that one reason for decreased .VO(2max) in hypoxia could be the lower maximal exercise intensity achieved in incremental, time or distance trial tests. We hypothesized that (1).VO(2max) would be decreased at altitude even when exercising at the same absolute maximal exercise intensity as at sea level and; (2) the decline in .VO(2max) in endurance-trained athletes (ETA) would be linear across the range from sea level through moderate altitudes. Eight ETA performed combined .VO(2max) and performance tests running to exhaustion at the same speed in a randomized double blind fashion at simulated altitudes of 300, 800, 1,300, 1,800, 2,300 and 2,800 m above sea level using a hypobaric chamber. Douglas bag system was used for respiratory measurements and pulse oximetry was used to estimate arterial O(2) saturation. .VO(2max) declined linearly from 66+/-1.6 ml kg(-1) min(-1) at 300 m to 55+/-1.6 ml kg(-1) min(-1) at 2,800 m corresponding to a 6.3% decrease per 1,000 m increasing altitude (range 4.6-7.5%). Time to exhaustion (performance) at a constant velocity associated with 107% of sea level .VO(2max) decreased with 14.5% (P<0.001) per 1,000 m altitude between 300 and 2,800 m. Both .VO(2max) and performance decreased from 300 to 800 m (P<0.01; P<0.05). Arterial haemoglobin oxygen saturation at test cessation (SpO(2min)) declined from 89.0+/-2.9% at 300 m to 76.5+/-4.0% at 2,800 m (P=0.001). This study report that in ETA during acute exposure to altitude both performance and .VO(2max) decline from 300 to 800 m above sea level and continued to decrease linearly to 2,800 m.

Effect of exercise intensity and hypoxia on skeletal muscle AMPK signaling and substrate metabolism in humans

We compared in human skeletal muscle the effect of absolute vs. relative exercise intensity on AMP-activated protein kinase (AMPK) signaling and substrate metabolism under normoxic and hypoxic conditions. Eight untrained males cycled for 30 min under hypoxic conditions (11.5% O(2), 111 +/- 12 W, 72 +/- 3% hypoxia Vo(2 peak); 72% Hypoxia) or under normoxic conditions (20.9% O(2)) matched to the same absolute (111 +/- 12 W, 51 +/- 1% normoxia Vo(2 peak); 51% Normoxia) or relative (to Vo(2 peak)) intensity (171 +/- 18 W, 73 +/- 1% normoxia Vo(2 peak); 73% Normoxia). Increases (P < 0.05) in AMPK activity, AMPKalpha Thr(172) phosphorylation, ACCbeta Ser(221) phosphorylation, free AMP content, and glucose clearance were more influenced by the absolute than by the relative exercise intensity, being greatest in 73% Normoxia with no difference between 51% Normoxia and 72% Hypoxia. In contrast to this, increases in muscle glycogen use, muscle lactate content, and plasma catecholamine concentration were more influenced by the relative than by the absolute exercise intensity, being similar in 72% Hypoxia and 73% Normoxia, with both trials higher than in 51% Normoxia. In conclusion, increases in muscle AMPK signaling, free AMP content, and glucose disposal during exercise are largely determined by the absolute exercise intensity, whereas increases in plasma catecholamine levels, muscle glycogen use, and muscle lactate levels are more closely associated with the relative exercise intensity.

Exercise training increases electron and substrate shuttling proteins in muscle of overweight men and women with the metabolic syndrome

Aerobic conditioned muscle shows increased oxidative metabolism or glucose relative to untrained muscle at a given absolute exercise intensity. The studies of a targeted risk reduction intervention through defined exercise (STRRIDE) study is an aerobic exercise intervention in men and women with features of metabolic syndrome (Kraus WE, Torgan CE, Duscha BD, Norris J, Brown SA, Cobb FR, Bales CW, Annex BH, Samsa GP, Houmard JA, and Slentz CA, Med Sci Sports Exerc 33: 1774-1784, 2001), with four muscle biopsies taken during training and detraining time points. Here, we expanded a previous study (Hittel DS, Kraus WE, and Hoffman EP, J Physiol 548: 401-410, 2003) and used mRNA profiling to investigate gene transcripts associated with energy and substrate metabolism in STRRIDE participants. We found coordinate regulation of key metabolic enzymes with aerobic training in metabolic syndrome (aspartate aminotransferase 1, lactate dehydrogenase B, and pyruvate dehydrogenase-alpha(1)). All were also quickly downregulated by detraining, although the induction was not an acute response to activity. Protein and enzymatic assays were used to validate mRNA induction with aerobic training and loss with detraining (96 h to 2 wk) in 10 male and 10 female STRRIDE subjects. We propose that training coordinately increases the levels of aspartate aminotransferase 1, lactate dehydrogenase B, and pyruvate dehydrogenase-alpha(1) subunit, increasing glucose metabolism in muscle by liberating pyruvate for oxidative metabolism and, therefore, limiting lactate efflux. Serial measurement of fasting plasma lactate from 62 subjects from the same exercise group demonstrated a significant decrease of circulating lactate with training. We also found evidence for sex-specific molecular remodeling of muscle with ubiquinol-cytochrome c reductase core protein II, a component of mitochondrial respiratory complex III, which showed an increase after training that was specific to women. These biochemical adaptations complement existing molecular models for improved glucose tolerance with exercise intervention in prediabetic individuals.

Impaired leg vasodilation during dynamic exercise in healthy older women.

The purpose of the present study was to test the hypothesis that leg blood flow responses during leg cycle ergometry are reduced with age in healthy non-estrogen-replaced women. Thirteen younger (20-27 yr) and thirteen older (61-71 yr) normotensive, non-endurance-trained women performed both graded and constant-load bouts of leg cycling at the same absolute exercise intensities. Leg blood flow (femoral vein thermodilution), mean arterial pressure (MAP; radial artery), mean femoral venous pressure, cardiac output (acetylene rebreathing), and blood O2 contents were measured. Leg blood flow responses at light workloads (20-40 W) were similar in younger and older women. However, at moderate workloads (50-60 W), leg blood flow responses were significantly attenuated in older women. MAP was 20-25 mmHg higher (P < 0.01) in the older women across all work intensities, and calculated leg vascular conductance (leg blood flow/estimated leg perfusion pressure) was lower (P < 0.05). Exercise-induced increases in leg arteriovenous O2 difference and O2 extraction were identical between groups (P > 0.6). Leg O2 uptake was tightly correlated with leg blood flow across all workloads in both subject groups (r2 = 0.80). These results suggest the ability of healthy older women to undergo limb vasodilation in response to submaximal exercise is impaired and that the legs are a potentially important contributor to the augmented systemic vascular resistance seen during dynamic exercise in older women.

Physiological factors that regulate the use of endogenous fat and carbohydrate fuels during endurance exercise

Exercise causes a dramatic increase in energy requirements because of the metabolic needs of working muscles. Exercise-dependent factors regulate fuel use. Absolute exercise intensity determines the exercise-induced increase in energy demands, whereas exercise intensity relative to an individual's maximal aerobic capacity (VO2max) determines the proportional contribution of different fuel sources (i.e. plasma glucose, plasma fatty acids, muscle glycogen and intramuscular triacylglycerols). Endurance training increases aerobic capacity in muscle and the oxidation of fat during exercise. In addition, exercise-independent factors, such as diet composition, sex, age, and body composition also influence substrate use during exercise. The present review discusses the regulation of substrate use during exercise in human subjects, with a focus on the role of exercise-independent factors.

ENDURANCE EXERCISE INDUCED GLUTATHIONE ALTERATIONS ARE UNAFFECTED BY A MULTIVITAMIN-MULTIMINERAL SUPPLEMENTATION IN MALE SPORT STUDENTS

Purpose: After strenuous exercise, inducing a high oxidative stress, blood levels of reduced glutathione (GSH) are usually reduced and levels of oxidized glutathione (GSSG) are usually increased. It is not clear, whether exercise induced changes in glutathione system are affected by a multivitamin/multimineral supplementation in male sport students during the 1st semester. METHODS: 36 male sport students (age 19 ü 25 yrs) of the first semester were randomly devided into a verum group (V) and a placebo group (P), receiving a daily dosage of a multivitamin-multimineral supplementation (V) or a placebo (P), respectively. Prior to medication subjects took part in an incremental run field test (IRT) and a 2 hr endurance run (ER) (U1). Tests were repeated after 8 weeks of supplementation (U4). ER was started 24 hrs after IRT. Run velocity in ER remained constant in U4, corresponding to 60–70% of the individual 4 mmol/1 lactate threshold (v4) in U1. Venous blood samples were taken prior to and immediately after ER. GSH and GSSG were determined by HPLC. RESULTS: V4 increased significantly from U1 to U4 (3.90 ± 0.38 vs. 4.05 ± 0.38 m/s) without any significant differences between V and P. GSH, GSSG and GSH/GSSG in U1 and U4 before and after ER in V, P and the total group (T) are shown in the table. Exercise-induced changes were significant for GSH (decline), GSSG (increase) and GSH/GSSG (decline) (p < 0.01). There was a significant decline in GSH and GSSG, and a significant increase in GSH/GSSG (p < 0.01) from U1 to U4. Exercise induced decline in GSH was smaller in U4, increase in GSSG was higher in U4, and decline in GSH/GSSG was more pronounced in U4 compared to U1, respectively. There were no significant differences in resting values or exercise induced changes between V and P, respectively. CONCLUSIONS: In male sport students, a 2 hr run induces dramatic changes in blood glutathione system, indicating activation of antioxidant defense mechanisms. Although absolute exercise intensity remains the same, exercise induced decline in GSH is reduced and increase in GSSG is elevated, when aerobic fitness level gets better. Intake of a multivitamin-multimineral supplementation over serveral weeks does not have any further effect on glutathione system alterations.Table: No Caption Available

A MULTIVITAMIN-MULTIMINERAL SUPPLEMENTATION DOES NOT AFFECT ENDURANCE EXERCISE INDUCED GLUTATHIONE ALTERATIONS IN FEMALE SPORT STUDENTS

Purpose: After stremous exercise, inducing a high oxidative stress, blood levels of reduced glutathione (GSH) are usually reduced and levels of oxidized glutathione (GSSG) are usually increased. It is not clear, whether exercise induced changes in glutathione system are affected by a multivitamin/multimineral supplementation in female sport students during the 1st semester. METHODS: 36 female sport students, age (19 ü 25 yrs) of the first semester were randomly devided into a verum group (V) and a placebo group (P), receiving a daily dosage of a multivitamin-multimineral supplementation (V) or a placebo (P), respectively. Prior to medication subjects took part in an incremental run field test (IRT) and a 2 hr endurance run (ER) (U1). Tests were repeated after 8 weeks of supplementation (U4). ER was started 24 hrs after IRT. Run velocity in ER remained constant in U4, corresponding to 60–70% of the individual 4 mmol/1 lactate threshold (v4) in U1. Venous blood samples were taken prior to and immediately after ER. GSH and GSSG were determined by HPLC. RESULTS: V4 increased significantly from U1 to U4 (3.23 ± 0.43 m/s vs. 3.44 ± 0.33 m/s) without any significant differences between V and P. GSH, GSSG and GSH/GSSG in U1 and U4 before and after ER in V, P and the total group (T) are shown in the table. Exercise-induced changes were significant for GSH (decline), GSSG (increase) and GSH/GSSG (decline) (p < 0.01). There was a significant decline in GSH and GSSG, and a significant increase in GSH/GSSG (p < 0.01) from U1 to U4. Exercise induced decline in GSH was smaller in U4, increase in GSSG was smaller in U4, and decline in GSH/GSSG was less pronounced in U4 compared to U1, respectively. There were no significant differences in resting values or exercise induced changes between V and P, respectively. CONCLUSIONS: In female sport students, a 2 hr run induces dramatic changes in blood glutathione system, indicating activation of antioxidant defense mechanisms. Although absolute exercise intensity remains the same, exercise induced decline in GSH and increase in GSSG is reduced, when aerobic fitness level gets better. Intake of a multivitamin-multimineral supplementation over several weeks does not have any further effect on glutathione system alterations.Table: No Caption Available

Hypohydration Adversely Affects Lactate Threshold in Endurance Athletes

The purpose of this investigation was to observe the effect of hypohydration (-4% body mass) on lactate threshold (LAT) in 14 collegiate athletes (8 men and 6 women; age, 20.9 +/- 0.5 years; height, 171.1 +/- 2.4 cm; weight, 64.8 +/- 2.3 kg; V(O)2 max, 62.8 +/- 1.9 ml x kg(-1) x min(-1); percentage of fat, 11.4 +/- 1.5%). Subjects performed 2 randomized, discontinuous treadmill bouts at a dry bulb temperature (T(db)) of 22 degrees C to volitional exhaustion in 2 states of hydration, euhydrated and hypohydrated. The hypohydrated condition was achieved in a thermally neutral environment (T(db), 22 degrees C; humidity, 45%), with exercise conducted at a moderate intensity as defined by rating of perceived exertion (RPE, approximately 12) 12-16 hours before testing. On average, subjects decreased 3.9% of their body mass before the hypohydration test. Blood lactate, hematocrit, V(O)2, minute ventilation (VE), R value, heart rate (HR), and RPE were measured during each 4-minute stage of testing. In the hypohydrated condition, LAT occurred significantly earlier during exercise and at a lower absolute V(O)2, VE, respiratory exchange ratio, RPE, and blood lactate concentration. Also, the blood lactate concentration was significantly lower in the hypohydrated condition (6.7 +/- 0.8 mmol) compared with the euhydrated condition (10.2 +/- 0.9 mmol) at peak exercise. There were no differences in HR or percentage of maximum HR at LAT nor did plots of V(CO2):V(O)2 reveal differences in bicarbonate buffering during exercise between the 2 conditions. From these results, we speculate that hypohydration did not significantly alter cardiovascular function or buffering capacity but did cause LAT to occur at a lower absolute exercise intensity.

Skeletal muscle capillarity and angiogenic mRNA levels after exercise training in normoxia and chronic hypoxia.

Gene expression of vascular endothelial growth factor (VEGF), and to a lesser extent of transforming growth factor-beta(1) (TGF-beta(1)) and basic fibroblast growth factor (bFGF), has been found to increase in rat skeletal muscle after a single exercise bout. In addition, acute hypoxia augments the VEGF mRNA response to exercise, which suggests that, if VEGF is important in muscle angiogenesis, hypoxic training might produce greater capillary growth than normoxic training. Therefore, we examined the effects of exercise training (treadmill running at the same absolute intensity) in normoxia and hypoxia (inspired O(2) fraction = 0.12) on rat skeletal muscle capillarity and on resting and postexercise gene expression of VEGF, its major receptors (flt-1 and flk-1), TGF-beta(1), and bFGF. Normoxic training did not alter basal or exercise-induced VEGF mRNA levels but produced a modest twofold increase in bFGF mRNA (P < 0.05). Rats trained in hypoxia exhibited an attenuated VEGF mRNA response to exercise (1.8-fold compared 3.4-fold with normoxic training; P < 0.05), absent TGF-beta(1) and flt-1 mRNA responses to exercise, and an approximately threefold (P < 0.05) decrease in bFGF mRNA levels. flk-1 mRNA levels were not significantly altered by either normoxic or hypoxic training. An increase in skeletal muscle capillarity was observed only in hypoxically trained rats. These data show that, whereas training in hypoxia potentiates the adaptive angiogenic response of skeletal muscle to a given absolute intensity of exercise, this was not evident in the gene expression of VEGF or its receptors when assessed at the end of training.

PERCEIVED EXERTION IN FATIGUING ILLNESS

INTRODUCTION: It has been reported that ratings of perceived exertion (RPE) are elevated in chronic fatigue syndrome (CFS). However, methodological limitations have rendered this conclusion suspect. Additionally, it is unknown whether all fatiguing illness is associated with altered perceptions of exertion. Here we report on the RPE in 2 very different groups of individuals (female civilians and male Gulf Veterans (GVs)) with CFS. The primary purpose of the present investigation was to compare RPE in CFS among GVs and non-veterans. A second purpose was to provide recommendations for future research based on limitations in this and previous work. METHODS: 32 GVs (n = 18 healthy; n = 14 CFS) performed a maximal exercise test on a cycle ergometer. Following a 3-min warm-up, exercise intensity increased 30 watts/min until exhaustion. RPE (0–10) was obtained in the last 15 sec of each min. A second sample of 39 non-veterans (n = 20 healthy; n = 19 CFS) underwent max testing on a treadmill. Exercise began with a 3-min warm-up at 2.5 mph/0% incline. After the initial stage, treadmill speed was increased to 3.5 mph for 3 min and then incline was increased by 2% every 3 min until exhaustion. RPE (6–20) was obtained during the last 30 seconds of each 3-min stage. For both samples, HR, VO2, and VCO2 were measured continuously. RESULTS: For GVs, there were no significant differences in any peak exercise variable. GVs with CFS reported higher RPE at each absolute power output examined (F1,24 = 13, p = 0.001). Group differences in RPE remained significant when analyzed relative to peak VO2 (F1,30 = 6.2, p = 0.02). For the non-vets, there were no differences in peak VO2, RER, or RPE. Non-vet controls exercised 4 min longer (p = 0.037) and had higher peak HR (p = 0.03). Non-vets with CFS reported higher RPE at each exercise stage compared to controls (F1,33 = 5.4, p = 0.026). When RPE was expressed relative to peak VO2 there were no group differences (F1,35 = 2.4, p = 0.13). CONCLUSIONS: Our results show that RPE is greater in both GVs and non-vets with CFS in terms of absolute exercise intensity. However, when RPE is expressed relative to a common maximum the non-vets did not differ from controls. This finding is consistent with one other published study from our group. Contrary to our hypothesis, RPE in GVs with CFS remained higher than controls when expressed relative to peak VO2. These results suggest that GVs with CFS are unique compared to their civilian counterparts. Unfortunately, as is the problem with previous work with RPE in this population, different methodologies limit our ability to directly compare these groups. It is recommended that future research in fatiguing illness use standard scales and instructions, common modes of exercise, express data relative to a common max, and examine physiological correlates of RPE. Support: DVA NJ Ctr Environ Hazards Res 561-003; NIH u01 AI-32246

Free radicals in exhaustive physical exercise: mechanism of production, and protection by antioxidants.

Moderate exercise is a healthy practice. However, exhaustive exercise generates free radicals. This can be evidenced by increases in lipid peroxidation, glutathione oxidation, and oxidative protein damage. It is well known that activity of cytosolic enzymes in blood plasma is increased after exhaustive exercise. This may be taken as a sign of damage to muscle cells. The degree of oxidative stress and of muscle damage does not depend on the absolute intensity of exercise but on the degree of exhaustion of the person who performs exercise. Training partially prevents free radical-formation in exhaustive exercise. Treatment with antioxidants such as vitamins C or E protects in part against free radical-mediated damage in exercise. Xanthine oxidase is involved in free-radical formation in exercise in humans and inhibition of this enzyme with allopurinol decreases oxidative stress and muscle damage associated with exhaustive exercise. Knowledge of the mechanism of free-radical formation in exercise is important because it will be useful to prevent oxidative stress and damage associated with exhaustive physical activity.

Role of exercise stress testing and safety monitoring for older persons starting an exercise program.

While the benefits of physical activity and exercise among older persons are becoming increasingly clear, the role of exercise stress testing and safety monitoring for older persons who want to start an exercise program is unclear. Current guidelines regarding exercise stress testing likely are not applicable to the majority of persons aged 75 years or older who are interested in restoring or enhancing their physical function through a program of physical activity and exercise. In addition to being expensive and of unproven benefit, the current policy of routine exercise stress testing potentially could deter many older persons from participating in an exercise program. Research is needed to investigate current physician practices, evaluate the risk of adverse cardiac events, determine the role of pharmacological stress testing, and measure and compare absolute and relative exercise intensities. To assist clinicians, we offer a set of recommendations regarding precautions that can be taken to minimize the risk of adverse cardiac events among previously sedentary older persons who do not have symptomatic cardiovascular disease and are interested in starting an exercise program. JAMA. 2000;284:342-349

Endurance training increases gluconeogenesis during rest and exercise in men.

The hypothesis that endurance training increases gluconeogenesis (GNG) during rest and exercise was evaluated. We determined glucose turnover with [6,6-(2)H]glucose and lactate incorporation into glucose by use of [3-(13)C]lactate during 1 h of cycle ergometry at two intensities [45 and 65% peak O(2) consumption (VO(2 peak))] before and after training [65% pretraining VO(2 peak)], same absolute workload (ABT), and 65% posttraining VO(2 peak), same relative intensity (RLT). Nine males (178.1 +/- 2.5 cm, 81.8 +/- 3.3 kg, 27.4 +/- 2.0 yr) trained for 9 wk on a cycle ergometer 5 times/wk for 1 h at 75% VO(2 peak). The power output that elicited 66.0 +/- 1.1% of VO(2 peak) pretraining elicited 54.0 +/- 1.7% posttraining. Rest and exercise arterial glucose concentrations were similar before and after training, regardless of exercise intensity. Arterial lactate concentration during exercise was significantly greater than at rest before and after training. Compared with 65% pretraining, arterial lactate concentration decreased at ABT (4.75 +/- 0.4 mM, 65% pretraining; 2.78 +/- 0.3 mM, ABT) and RLT (3.76 +/- 0.46 mM) (P < 0.05). At rest after training, the percentage of glucose rate of appearance (R(a)) from GNG more than doubled (1.98 +/- 0.5% pretraining; 5.45 +/- 1.3% posttraining), as did the rate of GNG (0.11 +/- 0.03 mg x kg(-1) x min(-1) pretraining, 0.24 +/- 0.06 mg x kg(-1) x min(-1) posttraining). During exercise after training, %glucose R(a) from GNG increased significantly at ABT (2.3 +/- 0.8% at 65% pre- vs. 7.6 +/- 2.1% posttraining) and RLT (6.1 +/- 1.5%), whereas GNG increased almost threefold (P < 0.05) at ABT (0.24 +/- 0.08 mg x kg(-1) x min(-1) 65% pre-, and 0.71 +/- 0.18 mg x kg(-1) x min(-1) posttraining) and RLT (0.75 +/- 0.26 mg x kg(-1) x min(-1)). We conclude that endurance training increases gluconeogenesis twofold at rest and threefold during exercise at given absolute and relative exercise intensities.

The effect of endurance training on parameters of aerobic fitness.

Endurance exercise training results in profound adaptations of the cardiorespiratory and neuromuscular systems that enhance the delivery of oxygen from the atmosphere to the mitochondria and enable a tighter regulation of muscle metabolism. These adaptations effect an improvement in endurance performance that is manifest as a rightward shift in the 'velocity-time curve'. This shift enables athletes to exercise for longer at a given absolute exercise intensity, or to exercise at a higher exercise intensity for a given duration. There are 4 key parameters of aerobic fitness that affect the nature of the velocity-time curve that can be measured in the human athlete. These are the maximal oxygen uptake (VO2max), exercise economy, the lactate/ventilatory threshold and oxygen uptake kinetics. Other parameters that may help determine endurance performance, and that are related to the other 4 parameters, are the velocity at VO2max (V-VO2max) and the maximal lactate steady state or critical power. This review considers the effect of endurance training on the key parameters of aerobic (endurance) fitness and attempts to relate these changes to the adaptations seen in the body's physiological systems with training. The importance of improvements in the aerobic fitness parameters to the enhancement of endurance performance is highlighted, as are the training methods that may be considered optimal for facilitating such improvements.

EFFECTS OF OBESITY ON SUBSTRATE UTILIZATION DURING EXERCISE

1722 Skeletal muscle in obese individuals is characterized by reduced postabsorptive rates of fatty acid oxidation and a reduced oxidative capacity, thereby leading to an increased lipid accumulation within muscle. To further examine the influence of obesity on skeletal muscle fatty acid metabolism, this study determined whether fat oxidation is impaired in obese men during exercise. Seven obese (O) and 7 lean (L) sedentary otherwise healthy men (BMI = 33.7 ± 1.0 and 23.7 ± 1.0 kg/m2, respectively) of similar age participated in this study. O and L groups were matched for VO2max (48.0 ± 3.3 and 48.2 ± 3.0 ml/min/fat free mass (FFM), respectively) so that 60 min of cycle ergometry was performed at the same relative (50% VO2max) and absolute (1.53 ± 0.11 for O and 1.40 ± 0.11 l/min for L) exercise intensity. Plasma lactate levels were similar in O and L during exercise (2.5 ± 0.7 vs. 2.1 ± 0.7 mM). Total fatty acid oxidation determined with indirect calorimetry tended (p = 0.055) to be higher in the O group (18.7 ± 1.2 vs. 15.1 ± 1.2 μmol/FFM/min), and there was a trend (p = 0.08) for carbohydrate (CHO) oxidation to be higher in the L (122.2 ± 12.3 vs. 89.6 ± 12.3 μmol/FFM/min). The O group derived a significantly greater proportion of their energy from fatty acid oxidation than the L group (45 ± 4 vs. 31 ± 4%, p = 0.02). A strong association (r = 0.81, p = .0005) was observed between rates of CHO oxidation and work rate (W) for all subjects, but no association was observed between rates of fatty acid oxidation and work rate. These results suggest that during moderate intensity exercise, rates of total fatty acid oxidation determined with indirect calorimetry are not decreased in obese compared to lean men matched for aerobic fitness. In conclusion, contrary to the concept that fat oxidation is reduced in obesity, we find that sedentary obese men are not limited in their ability to oxidize fatty acids during exercise compared to lean sedentary men.

Norepinephrine response to exercise at the same relative intensity before and after endurance exercise training

It is well documented that endurance exercise training results in a blunted norepinephrine (NE) response to exercise of a given absolute exercise intensity. However, it is not clear what effect training has on the catecholamine response to exercise of the same relative intensity because previous studies have provided conflicting results. The purpose of the present study was, therefore, to determine the catecholamine response to exercise of the same relative exercise intensity before and after endurance exercise training. Six women and three men [age 28 +/- 8 (SD) yr] performed 10 wk of training. Maximal O2 uptake (VO2 max) was determined during treadmill exercise. Fifteen-minute treadmill exercise bouts were performed at 60, 65, 70, 75, 80, and 85% of VO2 max before and after training. VO2 max was increased by 20% (from 39.2 +/- 7.7 to 46.9 +/- 8.1 ml. kg-1. min-1; P < 0.05) in response to training. Plasma NE concentrations were higher (P < 0.05) during exercise at the same relative intensity after, compared with before, training at 65-85% of VO2 max. Differences between heart rates and plasma epinephrine concentrations after, compared with before, training were not statistically significant. These results provide evidence that the NE response to exercise is dependent on the absolute as well as the relative intensity of the exercise.

Effects of Training, Environment, and Host Factors on the Sweating Response to Exercise

Because metabolic heat production is proportional to the amount of work performed, the differences in core body temperature (Tcore) of humans exercising at similar absolute exercise intensities are due to differences in their efficiency of heat dissipation. The purpose of this paper is to delineate the effects of training status, heat acclimation, environmental conditions and host factors on the sweating response to exercise. These factors are reviewed in light of their effects on the biophysical enhancement or suppression of sweating, and modifications of the relationship between local sweat rate and Tcore (degrees C). Athletes are advised to optimize those factors that enhance, and eliminate those factors that diminish, the onset and responsiveness of sweating.

SYMPATHOADRENAL RESPONSES DURING EXERCISE AT HIGH ALTITUDE IN WOMEN

1515 We have previously documented an enhanced sympathoadrenal response during exercise to high altitude in men. The purpose of this investigation was to determine 1) if women respond in a similar manner as found previously in men, and 2) the extent to which menstrual cycle phase influences this response. Sixteen eumenorrheic women (23.6±1.2 yrs, 56.2±4.3 kgs) were studied at sea level and after 10 days of high altitude exposure (4,300 m) either in their follicular (F, n=11) or luteal (L, n=5) phase. While at sea level, subjects performed two 45 minute submaximal steady-state exercise tests(on separate days) on a bicycle ergometer at intensities which elicited 50& 65% VO2max. During day 10 of altitude exposure, an absolute exercise intensity similar to that of 50% sea level VO2max was chosen such that subjects were working at the same absolute VO2 which represented 65% of their VO2max at altitude. Compared to rest, plasma epinephrine levels increased 36% in response to exercise at 50% VO2max at sea level with no differences found between cycle phase. This increase was significantly greater (↑44%) during exercise at 65% VO2max. At altitude, the epinephrine response was identical to that found for 65% VO2max exercise at sea level (↑44%) with no differences found between phase assignments. The plasma norepinephrine response was similar to that found for epinephrine such that the increase with exercise at altitude(↑51%) was the same as 65% VO2max exercise at sea level (↑50%). Again, no phase differences were observed. It was concluded that the sympathoadrenal response to exercise: 1) did not differ between cycle phase across any condition; 2) was similar to that found previously in men and; 3) the relative exercise intensity is the primary factor responsible for the catecholamine response to exercise.