Exercise intensity and erythrocyte 2,3-diphosphoglycerate concentration

The present study examines the acute effects of two different exercise intensities on erythrocyte 2,3-diphosphoglycerate (2,3-DPG) concentration. Thirty-one females (X +/- SD age = 23.7 +/- 3.37 yr; VO2max = 44.3 +/- 5.40 ml X kg-1 X min-1) completed 2 separate 15-min constant load cycling tests at exercise intensities representing 35 and 75% of VO2max. Venous blood was obtained pre-exercise (PRE), immediately post-exercise (POST), 15 min post-exercise (POST15), and 30 min post-exercise (POST30) to determine lactic acid, 2,3-DPG, and hemoglobin concentrations and hematocrit. Significant increases (P less than 0.01) in lactic acid concentration (1.1 +/- 0.14 at PRE to 6.2 +/- 0.48 m X mol-1 X l-1 at POST), 2,3-DPG concentration (1.9 +/- 0.06 at PRE to 2.1 +/- 0.06 mumol X ml-1 at POST), and 2,3-DPG corrected for plasma volume shift (PVC 2,3-DPG) (1.9 +/- 0.06 at PRE to 2.4 +/- 0.07 mumol X ml-1 at POST15) were observed only following the 75% submaximal exercise. At POST30 (75% VO2max) PVC 2,3-DPG and lactic acid remained 5.3 and 97% (P less than 0.05) above baseline, respectively. An exercise intensity effect was observed only in lactic acid response (P less than 0.05) but not in 2,3-DPG (mumol X ml-1 and mumol X g-1 hemoglobin or PVC 2,3-DPG. A significant time-intensity interaction (P less than 0.05) for PVC 2,3-DPG suggests that PVC 2,3-DPG response over time was different between the two exercise intensity levels, with the 75% intensity eliciting a greater increase in PVC 2,3-DPG.(ABSTRACT TRUNCATED AT 250 WORDS)     

Exercise intensity-related responses of beta-endorphin and catecholamines

Ten men and 10 women exercised on a bicycle ergometer for 20 min at 40, 60, and 80% maximal oxygen uptake (VO2max) to determine the relationship between plasma beta-endorphin, catecholamines, and exercise intensity. Compared to rest, plasma beta-endorphins were not significantly elevated during the 40 and 60% workloads (4.8 +/- 1.0 pmol.l-1 vs 3.8 +/- 0.7 and 6.3 +/- 0.9, respectively). In contrast, the 80% exercise significantly elevated endorphins to 16.1 +/- 4.0 pmol.l-1. Plasma norepinephrine concentrations were 0.30 +/- 0.04 ng.ml-1 at rest and increased with exercise intensity (40% = 0.60 +/- 0.05, 60% = 0.93 +/- 0.07, 80% = 2.00 +/- 0.14, VO2max = 2.55 +/- 0.14 ng.ml-1). Plasma epinephrine followed the same trend (rest = 0.07 +/- 0.01, 40% = 0.33 +/- 0.03, 60% = 0.49 +/- 0.02, 80% = 0.88 +/- 0.07, VO2max = 0.95 +/- 0.06 ng.ml-1). Norepinephrine was found to significantly correlate to endorphins (r = 0.499; P less than 0.02). Conversely, epinephrine was not correlated with beta-endorphin (r = 0.309; P greater than 0.05). The low correlation suggests a weak relationship between beta-endorphin and catecholamine responses during exercise. The results of this investigation suggest that the relationship between beta-endorphin and exercise intensity is curvilinear, with anaerobic activity producing the most significant endorphin response. It was also noted that the beta-endorphin response was not related to gender, but the amine response to exercise was gender-related, being greater for the men.     

Maximal oxygen uptake as a parametric measure of cardiorespiratory capacity

INTRODUCTION: Maximal oxygen uptake (.VO2max) was defined by Hill and Lupton in 1923 as the oxygen uptake attained during maximal exercise intensity that could not be increased despite further increases in exercise workload, thereby defining the limits of the cardiorespiratory system. This concept has recently been disputed because of the lack of published data reporting an unequivocal plateau in .VO2 during incremental exercise. PURPOSE: The purpose of this investigation was to test the hypothesis that there is no significant difference between the .VO2max obtained during incremental exercise and a subsequent supramaximal exercise test in competitive middle-distance runners. We sought to determine conclusively whether .VO2 attains a maximal value that subsequently plateaus or decreases with further increases in exercise intensity. METHODS: Fifty-two subjects (36 men, 16 women) performed three series of incremental exercise tests while measuring .VO2 using the Douglas bag method. On the day after each incremental test, the subjects returned for a supramaximal test, during which they ran at 8% grade with the speed chosen individually to exhaust the subject between 2 and 4 min. .VO2 at supramaximal exercise intensities (30% above incremental .VO2max) was measured continuously. RESULTS: .VO2max measured during the incremental test (63.3 +/- 6.3 mL.kg(-1).min(-1); mean +/- SD) was indistinguishable from the .VO2max during the supramaximal test (62.9 +/- 6.2, N = 156; P = 0.77) despite a sufficient duration of exercise to demonstrate a plateau in .VO2 during continuous supramaximal exercise. These data provide strong support for the hypothesis that there is indeed a peak and subsequent plateau in .VO2 during maximal exercise intensity. CONCLUSIONS: .VO2max is a valid index measuring the limits of the cardiorespiratory systems' ability to transport oxygen from the air to the tissues at a given level of physical conditioning and oxygen availability.     

Maximal fat oxidation during exercise in trained men

Fat oxidation increases from low to moderate exercise intensities and decreases from moderate to high exercise intensities. Recently, a protocol has been developed to determine the exercise intensity, which elicits maximal fat oxidation rates (Fat(max)). The main aim of the present study was to establish the reliability of the estimation of Fat(max) using this protocol (n = 10). An additional aim was to determine Fat(max) in a large group of endurance-trained individuals (n = 55). For the assessment of reliability, subjects performed three graded exercise tests to exhaustion on a cycle ergometer. Tests were performed after an overnight fast and diet and exercise regime on the day before all tests were similar. Fifty-five male subjects performed the graded exercise test on one occasion. The typical error (root mean square error and CV) for Fat(max) and Fat(min) was 0.23 and 0.33 l O(2) x min(-1) and 9.6 and 9.4 % respectively. Maximal fat oxidation rates of 0.52 +/- 0.15 g x min(-1) were reached at 62.5 +/- 9.8 % VO(2)max, while Fat(min) was located at 86.1 +/- 6.8 % VO(2)max. When the subjects were divided in two groups according to their VO(2)max, the large spread in Fat(max) and maximal fat oxidation rates remained present. The CV of the estimation of Fat(max) and Fa(min) is 9.0 - 9.5 %. In the present study the average intensity of maximal fat oxidation was located at 63 % VO(2)max. Even within a homogeneous group of subjects, there was a relatively large inter-individual variation in Fat(max) and the rate of maximal fat oxidation.     

Effect of exercise intensity on relationship between VO2max and cardiac output

PURPOSE: The purpose of this study was to determine whether the maximal oxygen uptake (VO2max) is attained with the same central and peripheral factors according to the exercise intensity. METHODS: Nine well-trained males performed an incremental exercise test on a cycle ergometer to determine the maximal power associated with VO2max (pVO2max) and maximal cardiac output (Qmax). Two days later, they performed two continuous cycling exercises at 100% (tlim100 = 5 min 12 s +/- 2 min 25 s) and at an intermediate work rate between the lactate threshold and pVO2max (tlimDelta50 +/- 12 min 6 s +/- 3 min 5 s). Heart rate and stroke volume (SV) were measured (by impedance) continuously during all tests. Cardiac output (Q) and arterial-venous O2 difference (a-vO2 diff) were calculated using standard equations. RESULTS: Repeated measures ANOVA indicated that: 1) maximal heart rate, VE, blood lactate, and VO2 (VO2max) were not different between the three exercises but Q was lower in tlimDelta50 than in the incremental test (24.4 +/- 3.6 L x min(-1) vs 28.4 +/- 4.1 L x min(-1); P < 0.05) due to a lower SV (143 +/- 27 mL x beat(-1) vs 179 +/- 34 mL x beat(-1); P < 0.05), and 2) maximal values of a-vO2 diff were not significantly different between all the exercise protocols but reduced later in tlimDelta50 compared with tlim100 (6 min 58 s +/- 4 min 29 s vs 3 min 6 s +/- 1 min 3 s, P = 0.05). This reduction in a-vO2 diff was correlated with the arterial oxygen desaturation (SaO2 = -15.3 +/- 3.9%) in tlimDelta50 (r = -0.74, P = 0.05). CONCLUSION: VO2max was not attained with the same central and peripheral factors in exhaustive exercises, and tlimDelta50 did not elicit the maximal Q. This might be taken into account if the training aim is to enhance the central factors of VO2max using exercise intensities eliciting VO2max but not necessarily Qmax.     

Thermoregulatory and metabolic responses to jogging prior to and during pregnancy

Ten joggers were serially studied prior to and during pregnancy at their individual training intensity levels to estimate their thermal and metabolic response to exercise in the field. Prior to conception, a 20-min run at 74% of VO2max (range = 62 to 90%) increased the respiratory exchange ratio to 0.90 +/- 0.01 (range = 0.87 to 0.96) with a rise in whole blood glucose (5.19 +/- 0.14 to 6.63 +/- 0.23 mM X l-1), lactate (0.61 +/- 0.06 to 2.62 +/- 0.74 mM X l-1), and rectal temperature (37.5 +/- 0.1 to 39.0 +/- 0.1 degree C). Despite a spontaneous decrease in exercise intensity to 57 +/- 5% of VO2max (range = 34 to 79%) at 20 and to 47 +/- 2% of VO2max (range = 36 to 59%) at 32 wk gestation, the rise in respiratory exchange ratio with exercise was maintained at 0.92 +/- 0.02 (range = 0.88 to 0.97) and 0.93 +/- 0.01 (range = 0.88 to 0.97), respectively, suggesting a shift to the left in the relationship between exercise intensity and fractional carbohydrate utilization by muscle during exercise in pregnancy. The concomitant changes in whole blood glucose before and after exercise at 20 (4.46 +/- 0.16 to 4.45 +/- 0.08 mM X l-1) and 32 (5.30 +/- 0.19 to 4.55 +/- 0.15 mM X l-1) wk further strengthen this view. Post-exercise, whole blood lactate levels at 20 (0.53 +/- 0.06 to 1.59 +/- 0.30 mM X l-1) and 32 (0.77 +/- 0.07 to 0.89 +/- 0.11 mM X l-1) wk were lower than those observed prior to pregnancy.(ABSTRACT TRUNCATED AT 250 WORDS)     

Enkephalins, catecholamines, and psychological mood alterations: effects of prolonged exercise

Seven healthy trained men were studied to determine if running at various relative intensities [percent maximal oxygen consumption (VO2max)] alters peripheral venous levels of leucine enkephalin-like material. Enkephalins were measured using a radio-receptor assay (Leu-Enk RRA). Subjects ran for 80 min at 40 and 60% VO2max and for 40 min at 80% VO2max. Each session was separated by at least 1 wk. Heart rate, blood pressure, lactic acid, and rectal temperature responses increased in an intensity-dependent manner. Epinephrine increased from resting values of 38.2 +/- 6.8 pg X ml-1, mean +/- SE to 75.0 +/- 13.3 pg X ml-1 during the 40% VO2max run, from 60.2 +/- 15 to 186 +/- 45 pg X ml-1 during the 60% run, and from 33.4 +/- 7.6 to 311 +/- 52 pg X ml-1 at the 40th min of the highest workload (80% VO2max). These increases were significant (P less than 0.05). Plasma Leu-Enk RRA was between 3.8 and 6.2 pmol X ml-1 prior to each run and did not change significantly as a result of exercise. Levels of Leu-Enk RRA also did not change during 30 min of supine recovery. Perception of effort increased (P less than 0.05) with increases in exercise intensity, and effort sense was unrelated to plasma Leu-Enk RRA. Psychological tension decreased significantly (P less than 0.05) following exercise at 60 and 80% of VO2max, but the decrease following the 40% run was not significant (P greater than 0.05). Reduced tension following exercise was not related to Leu-Enk RRA.(ABSTRACT TRUNCATED AT 250 WORDS)     

Cardiovascular drift is related to reduced maximal oxygen uptake during heat stress

INTRODUCTION/PURPOSE: This study investigated whether the progressive rise in heart rate (HR) and fall in stroke volume (SV) during prolonged, constant-rate, moderate-intensity exercise (cardiovascular drift, CVdrift) in a hot environment is associated with a reduction in VO(2max). METHODS: CVdrift was measured in nine male cyclists between 15 and 45 min of cycling at 60% VO(2max) in 35 degrees C that was immediately followed by measurement of VO(2max). VO(2max) also was measured after 15 min of cycling on a separate day, so that any change in VO(2max) between 15 and 45 min could be associated with the CVdrift that occurred during that time interval. This protocol was performed under one condition in which fluid was ingested and there was no significant body weight change (0.3 +/- 0.4%), and under another in which no fluid was ingested and dehydration occurred (2.5 +/- 1%, P < 0.05). RESULTS: Fluid ingestion did not affect CVdrift or change in VO(2max). A 12% increase in HR (151 +/- 9 vs 169 +/- 10 bpm, P < 0.05) and 16% decrease in SV (120 +/- 12 vs 101 +/- 10 mL.beat(-1), P < 0.05) between 15 and 45 min was accompanied by a 19% decrease in VO(2max) (4.4 +/- 0.6 vs 3.6 +/- 0.4 L.min(-1), P < 0.05) despite attainment of a higher maximal HR (P < 0.05) at 45 min (194 +/- 5 bpm) vs 15 min (191 +/- 5 bpm). Submaximal VO(2) increased only slightly over time, but VO(2max) increased from 63 +/- 5% at 15 min to 78 +/- 8% at 45 min (P < 0.05). CONCLUSION: We conclude CVdrift during 45 min of exercise in the heat is associated with decreased VO(2max) and increased relative metabolic intensity. The results support the validity of using changes in HR to reflect changes in relative metabolic intensity during prolonged exercise in a hot environment in which CVdrift occurs.     

Oxygen consumption in nonexercising muscle after exercise

Little is known about the effect of exercise intensity on post-exercise oxygen consumption in nonexercising muscle. This study examined the effect of exercise intensity on muscle oxygen consumption (VO2mus) in nonexercising forearm flexor muscles (nonexVO2mus) after cycling exercise. Eight healthy male subjects performed 20 min of cycling exercise at 30%, 50%, and 70% of maximal oxygen consumption (%VO2max) on separate days. The nonexVO2mus values at rest, at the end of exercise, and during recovery after exercise were measured by near-infrared spectroscopy. VO2mus was determined using the rate of decrease in oxygenated hemoglobin during arterial occlusion. The nonexVO2mus at the end of exercise significantly increased by 1.3 +/- 0.1, 2.0 +/- 0.3, and 2.2 +/- 0.3-fold over resting values at 30%, 50%, and 70% VO2max, respectively. NonexVO2mus returned to the resting value after 3 - 5 min of recovery and then showed no significant change for 120 min after exercise at all exercise intensities. NonexVO2mus at the end of exercise at 70% VO2max was significantly higher than that after exercise at 30% VO2max. These results show that 20 min of cycling exercise induced an increase in nonexVO2mus and that higher intensity exercise produces a larger increase in nonexVO2mus after exercise.     

Incremental test protocol, recovery mode and the individual anaerobic threshold

The individual anaerobic threshold (IAT) is defined as the highest metabolic rate at which blood lactate (LA) concentrations are maintained at a steady-state during prolonged exercise. The purpose of this study was to compare the effects of active and passive recovery on the determination of IAT following both a submaximal or maximal incremental exercise test. Seven males (VO2max = 57.6 +/- 5.8 ml.kg-1.min -1) did two submaximal, incremental cycle exercise tests (30 W and 4 min per step) and two maximal incremental tests. Blood was sampled repeatedly during exercise and for 12 min during the subsequent recovery period, which was passive for one submaximal and one maximal test and active (approximately 35% VO2max) during the other tests. An IAT metabolic rate and power output were calculated for the submax-passive (IATsp, LA = 1.85 +/- 0.42 mmol.l-1), max-passive (IATmp, LA = 3.41 +/- 1.14 mmol.l-1), submax-active (IATsa, LA = 2.13 +/- 0.45 mmol.l-1) and max-active (IATma, LA = 3.44 +/- 0.73 mmol.l-1) protocols. At weekly intervals, the subjects exercised for 30 min at one of the four IAT metabolic rates. Active recovery did not affect the calculation of IAT, but following the maximal incremental tests, IAT occurred at a higher (p less than 0.05) power output, absolute VO2 and %VO2max (71% VO2max) compared with the IAT determined with the submaximal incremental tests (61% VO2max).(ABSTRACT TRUNCATED AT 250 WORDS)     

Effect of a prior intermittent run at vVO2max on oxygen kinetics during an all-out severe run in humans

BACKGROUND: The purpose of this study was to examine the influence of prior intermittent running at VO2max on oxygen kinetics during a continuous severe intensity run and the time spent at VO2max. METHODS: Eight long-distance runners performed three maximal tests on a synthetic track (400 m) whilst breathing through the COSMED K4 portable telemetric metabolic analyser: i) an incremental test which determined velocity at the lactate threshold (vLT), VO2max and velocity associated with VO2max (vVO2max), ii) a continuous severe intensity run at vLT+50% (vdelta50) of the difference between vLT and vVO2max (91.3+/-1.6% VO2max)preceded by a light continuous 20 minute run at 50% of vVO2max (light warm-up), iii) the same continuous severe intensity run at vdelta50 with a prior interval training exercise (hard warm-up) of repeated hard running bouts performed at 100% of vVO2max and light running at 50% of vVO2max (of 30 seconds each) performed until exhaustion (on average 19+/-5 min with 19+/-5 interval repetitions). This hard warm-up speeded the VO2 kinetics: the time constant was reduced by 45% (28+/-7 sec vs 51+/-37 sec) and the slow component of VO2 (deltaVO2 6-3 min) was deleted (-143+/-271 ml x min(-1) vs 291+/-153 ml x min(-1)). In conclusion, despite a significantly lower total run time at vdelta50 (6 min 19+/-0) min 17 vs 8 min 20+/-1 min 45, p=0.02) after the intermittent warm-up at VO2max, the time spent specifically at VO2max in the severe continuous run at vdelta50 was not significantly different.     

A comparison of heart rate methods for predicting endurance training intensity.

Comparing results of various training studies is often confounded by use of different indices of exercise intensity. Two frequently used indices are: 1) the % HR max method (exercise at a HR corresponding to a chosen percentage of maximal HR), and 2) this study, % net VO2max was employed as the criterion measure of exercise intensity and a comparison was made between the prediction of % net VO2-MAXby the above two methods. Experiments were performed on nine males (M +/- SD age = 23.7 +/- 2.6 yrs) and consisted of double determinations of resting VO2 and multiple measurements of resting HR under five different conditions. Duplicate determinations of maximal VO2 and HR preceded a third treadmill test consisting of four, 5-minute workloads representing approx 25, 45, 65, and 85% net VO2max. The results demonstrated that the KM's prediction of exercise intensity was not significantly different (P greater than 0.05) from measured intensity at any of the four workloads. Additionally, the % HR max procedure yielded large, significant overpredictions of exercise intensity (29, 22, 16 and 8% overpredictions for the four submaximal intensities, respectively. These results suggest that the KM yields a training HR that reflects exercise intensity within reasonable limits of accuracy.     

Short-arm (1.9 m) +2.2 Gz acceleration: isotonic exercise load-O2 uptake relationship

BACKGROUND: The deconditioning syndrome from prolonged bed rest (BR) or spaceflight includes decreases in maximal oxygen uptake (VO2max), muscular strength and endurance, and orthostatic tolerance. In addition to exercise training as a countermeasure, +Gz (head-to-foot) acceleration training on 1.8-2.0 m centrifuges can ameliorate the orthostatic and acceleration intolerances induced by BR and immersion deconditioning. PURPOSE: Study A was designed to determine the magnitude and linearity of the heart rate (HR) response to human-powered centrifuge (HPC) acceleration with supine exercise vs. passive (no exercise) acceleration. Study B was designed to test the hypothesis that moderate +Gz acceleration during exercise will not affect the respective normal linear relationships between exercise load and VO2max, HR, and pulmonary ventilation (VEBTPS). Study C: To determine if these physiological responses from the HPC runs (exercise + on-platform acceleration) will be similar to those from the exercise + off-platform acceleration responses. METHODS: In Study A, four men and two women (31-62 yr) were tested supine during exercise + acceleration and only passive acceleration at 100% [maximal acceleration (rpm) = Amax] and at 25%, 50%, and 75% of Amax. In Studies B and C, seven men (33+/-SD 7 yr) exercised supine on the HPC that has two opposing on-platform exercise stations. A VO2max test and submaximal exercise runs occurred under three conditions: (EX) exercise (on-platform cycle at 42%, 61%, 89% and 100% VO2max) with no acceleration; (HPC) exercise + acceleration via the chain drive at 25%,50%, and 100% Gzmax (35%, 72% and 100% VO2max); and (EXA) exercise (on-platform cycle at 42%, 61%, 89%, and 100% VO2max) with acceleration performed via the off-platform cycle operator at +2.2+/-0.2 Gz [50% of max (rpm) G]. RESULTS: Study A: Mean (+/-SE) Amax was 43.7+/-1.3 rpm (mean = +3.9+/-0.2, range = 3.3 to 4.9 Gz). Amax run time for exercise +acceleration was 50-70 s, and 40-70 s for passive acceleration. Regression of X HR on Gz levels indicated explained variances (r2) of 0.88 (exercise) and 0.96 (passive). The mean exercise HR of 107+/-4 (25%), to 189+/-13 (100%) bpm were 43-50 bpm higher (p < 0.05) than comparable passive HR of 64+/-2 to 142+/-22 bpm, respectively. Study B: There were no significant differences in VO2, HR or VEBTPS at the submaximal or maximal levels between the EX and EXA runs. Mean (+/-SE) VO2max for EX was 2.86+/-0.12 L x min(-1)(35+/-2 ml x min(-1) x kg(-1)) and for EXA was 3.09+/-0.14 L x min(-1) (37+/-2 ml-min(-1) x kg(-1)). Study C: There were no significant differences in the essentially linear relationships between the HPC and EXA data for VO2 (p = 0.45), HR (p < 0.08), VEBTPS (p = 0.28), or the RE (p = 0.15) when the exercise load was % VO2max. CONCLUSION: Addition of + 2.2 Gz acceleration does not significantly influence levels of oxygen uptake, heart rate, or pulmonary ventilation during submaximal or maximal cycle ergometer leg exercise on a short-arm centrifuge.     

Plasma beta-endorphin concentration: response to intensity and duration of exercise

Twelve college-age men exercised on a bicycle ergometer to VO2max and at 60, 70, and 80% VO2max for 30 min to determine the effects of exercise intensity on plasma beta-endorphin (B-EP). The time course for alterations in B-EP and the relationship to lactate were also examined. Following the VO2max test, the three submaximal intensities were completed on separate days using a counter-balanced design. Blood was sampled from an indwelling venous catheter at rest during exercise and recovery to assess the time course response. B-EP content was determined by radioimmunoassay (Immunonuclear) with less than 5% cross-reactivity to B-LPH. At rest, B-EP content was similar across visits, 4.34 +/- 0.36 pmol.l-1. The 60% intensity did not elevate B-EP at any time measured. B-EP content increased by 15 min at 70% VO2max with a further increase at 30 min. B-EP remained elevated during the 20 min recovery. At 80% VO2max B-EP content increased by 5 min. B-EP continued to increase during the exercise and peaked at 21.91 +/- 2.03 pmol.l-1 5 min into the recovery. Lactate showed a mild correlation with B-EP (r = 0.43) at 80% VO2max. A significant correlation (r = 0.78) between lactate and B-EP did occur with the VO2max test. It is concluded that an exercise intensity of at least 70% VO2max for 15 min is needed to increase plasma B-EP. Furthermore, the higher the exercise intensity the more rapid the onset for increases in plasma B-EP.     

Is determination of exercise intensities as percentages of VO2max or HRmax adequate?

Often exercise intensities are defined as percentages of maximal oxygen uptake (VO2max) or heart rate (HRmax). PURPOSE: The purpose of this investigation was to test the applicability of these criteria in comparison with the individual anaerobic threshold. METHODS: One progressive cycling test to exhaustion (initial stage 100 W, increment 50 W every 3 min) was analyzed in a group of 36 male cyclists and triathletes (24.9 +/- 5.5 yr; 71.6 +/- 5.7 kg; VO2max: 62.2 +/- 5.0 mL x min(-1) x kg(-1); individual anaerobic threshold = IAT: 3.64 +/- 0.41 W x kg(-1); HRmax: 188 +/- 8 min). Power output and lactate concentrations for 60 and 75% of VO2max as well as for 70 and 85% of HRmax were related to the IAT. RESULTS: There was no significant difference between the mean value of IAT (261 +/- 34 W, 2.92 +/- 0.65 mmol x L(-1)), 75% of VO2max (257 +/- 24 W, 2.84 +/-0.92 mmol x L(-1)), and 85% of HRmax (259 +/- 30 W, 2.98 +/- 0.87 mmol L(-1)). However, the percentages of the IAT ranged between 86 and 118% for 75% VO2max and 87 and 116% for 85% HRmax (corresponding lactate concentrations: 1.41-4.57 mmol x L(-1) and 1.25-4.93 mmol x L(-1), respectively). The mean values at 60% of VO2max (198 +/- 19 W, 1.55 +/- 0.67 mmol x L(-1)) and 70% of HRmax (180 +/- 27 W, 1.45 +/- 0.57 mmol x L(-1)) differed significantly (P < 0.0001) from the IAT and represented a wide range of intensities (66-91% and 53-85% of the IAT, 0.70-3.16 and 0.70-2.91 mmol x L(-1), respectively). CONCLUSIONS: In a moderately to highly endurance-trained group, the percentages of VO2max and HRmax vary considerably in relation to the IAT. As most physiological responses to exercise are intensity dependent, reliance on these parameters alone without considering the IAT is not sufficient.     

Exercise training below and above the lactate threshold in the elderly

In this study we report the effects of training at intensities below and above the lactate threshold on parameters of aerobic function in elderly subjects (age range 65-75 yr). The subjects were randomized into high-intensity (HI, N = 8; 75% of heart rate reserve = approximately 82% VO2max = approximately 121% of lactate threshold) and low-intensity (LI, N = 9; 35% of heart rate reserve = approximately 53% VO2max = approximately 72% of lactate threshold) training groups which trained 4 d.wk-1 for 30 min.session-1 for 8 wk. Before and after the training, subjects performed an incremental exercise test for determination of maximal aerobic power (VO2max) and lactate threshold (LT). In addition, the subjects performed a 6-min single-stage exercise test at greater than 75% of pre-training VO2max (SST-High) during which cardiorespiratory responses were evaluated each minute of the test. After training, the improvements in VO2max (7%) for LI and HI were not different from one another (delta VO2max for LI = 1.8 +/- 0.7 ml.kg-1.min-1; delta VO2max for HI = 1.8 +/- 1.0 ml.kg-1.min-1) but were significantly greater (P = 0.02) than the post-testing change observed in the control group (N = 8). Training improved the LT significantly (10-12%; P less than 0.01) and equally for both LI and HI (delta LT for for LI = 2.3 +/- 0.6 ml O2.kg-1.min-1; delta LT for HI = 1.8 +/- 0.8 ml O2.kg-1.min-1).(ABSTRACT TRUNCATED AT 250 WORDS)     

Exercise mode affects the time to achieve VO2max without influencing maximal exercise time at the intensity associated with VO2max in triathletes

The objective of this study was to analyze, in triathletes, the possible influence of the exercise mode (running x cycling) on time to exhaustion (TTE) and oxygen uptake (VO2) response during exercise performed at the intensity associated with the achievement of maximal oxygen uptake (IVO2max). Eleven male triathletes (21.8 +/- 3.8 yr) performed the following tests on different days on a motorized treadmill and on a cycle ergometer: 1) incremental tests in order to determine VO2max and IVO2max and, 2) constant work rate tests to exhaustion at IVO2max to determine TTE and to describe VO2 response (time to achieve VO2max - TAVO2max, and time maintained at VO2max-TMVO2max). No differences were found in VO2max, TTE and TMVO2max obtained on the treadmill tests (63.7 +/- 4.7 ml . kg (-1) . min (-1); 324.6 +/- 109.1 s; 178.9 +/- 93.6 s) and cycle ergometer tests (61.4 +/- 4.5 ml . kg (- 1) . min (-1); 390.4 +/- 114.4 s; 213.5 +/- 102.4 s). However, TAVO2max was influenced by exercise mode (145.7 +/- 25.3 vs. 176.8 +/- 20.1 s; in treadmill and cycle ergometer, respectively; p = 0.006). It is concluded that exercise modality affects the TAVO2max, without influencing TTE and TMVO2max during exercise at IVO2max in triathletes.     

Whole‐body fat oxidation determined by graded exercise and indirect calorimetry: a role for muscle oxidative capacity?

During whole-body exercise, peak fat oxidation occurs at a moderate intensity. This study investigated whole-body peak fat oxidation in untrained and trained subjects, and the presence of a relation between skeletal muscle oxidative enzyme activity and whole-body peak fat oxidation. Healthy male subjects were recruited and categorized into an untrained (N=8, VO(2max) 3.5+/-0.1 L/min) and a trained (N=8, VO(2max) 4.6+/-0.2 L/min) group. Subjects performed a graded exercise test commencing at 60 W for 8 min followed by 35 W increments every 3 min. On a separate day, muscle biopsies were obtained from vastus lateralis and a 3 h bicycle exercise test was performed at 58% of VO(2max). Whole-body fat oxidation was calculated during prolonged and graded exercise from the respiratory exchange ratio using standard indirect calorimetry equations. Based on the graded exercise test, whole-body peak fat oxidation was determined. The body composition was determined by DEXA. Whole-body peak fat oxidation (250+/-25 and 462+/-33 mg/min) was higher (P<0.05) and occurred at a higher (P<0.05) relative workload (43.5+/-1.8% and 49.9+/-1.2% VO(2max)) in trained compared with untrained subjects, respectively. Muscle citrate synthase activity and beta-hydroxy-acyl-CoA-dehydrogenase activity were higher (49% and 35%, respectively, P<0.05) in trained compared with untrained subjects. Both lean body mass and maximal oxygen uptake were significantly correlated to whole-body peak fat oxidation (r(2)=0.57, P<0.001), but leg muscle oxidative capacity was not correlated to whole-body peak fat oxidation. In conclusion, whole-body peak fat oxidation occurred at a higher relative exercise load in trained compared with untrained subjects. Whole-body peak fat oxidation was not significantly related to leg muscle oxidative capacity, but was related to lean body mass and maximal oxygen uptake. This may suggest that leg muscle oxidative activity is not the main determinant of whole-body peak fat oxidation.     

Relationship between %HRmax, %HR reserve, %VO2max, and %VO2 reserve in elite cyclists

PURPOSE: To evaluate the relations between %HRmax, %HRR, %VO2max, and %VO2R in elite cyclists and to check whether the intensity scale recommended by ACSM in its 1998 position stand is also applicable to this specific population. METHODS: Twenty-six male elite road cyclists (25.1 +/- 0.7 yr, 71.0 +/- 1.2 kg, 70.9 +/- 1.2 mL x kg(-1) x min(-1), 433.9 +/- 9.8 W) performed an incremental maximal exercise test (50 W x 3 min(-1)). Individual linear regressions based on HR and VO2 values measured at rest, end of each stage, and maximum, were used to calculate slopes and intercepts, and to predict %HRmax, %HRR, %VO2max, or %VO2R for a given exercise intensity. RESULTS: Below 85% VO2max or VO2R, predicted %HRmax values were significantly higher (P < 0.001) than the ACSM intensity scale (58, 65, 73, and 87% vs 55, 62, 70, and 85% HRmax at 40, 50, 60, and 80% VO2max, and 48, 61, 74% vs 35, 55, and 70% HRmax at 20, 40, and 60% VO2R). The %HRR versus %VO2max regression mean slope (1.069 +/- 0.01) and intercept (-5.747 +/- 0.80) were significantly different (P < 0.0001) from 1 and 0, respectively. Conversely, the %HRR versus %VO2R regression was indistinguishable from the line of identity (mean slope = 1.003 +/- 0.01; mean intercept = 0.756 +/- 0.7). Predicted %VO2R values were equivalent to %HRR in the 35-95%HRR range. %VO2max was equivalent to %HRR at and above 75%HRR, and it was significantly higher at (P < 0.05) and below 65%HRR (P < 0.001). CONCLUSION: The intensity scale recommended by ACSM underestimates exercise intensity in elite cyclists. Prediction of %HRR by %VO2R is better than by %VO2max. Thus, elite cyclists should use %HRR in relation to %VO2R rather than in relation to %VO2max.     

The effect of exercise training on salivary immunoglobulin A and cortisol responses to maximal exercise.

The salivary immunoglobulin A (s-IgA) and cortisol responses to maximal exercise were examined in 24 adult males (X +/- SD; 22.1 +/- 3.0 yrs) before and after 10 weeks of run training. The subjects performed an incremental treadmill test to exhaustion and were randomly assigned to one of three groups: control (CON; n = 5), low intensity training (LO; n = 8), or high intensity training (HI; n = 11). Following the ten weeks of training, the subjects performed a second maximal treadmill test. Saliva samples were collected before, as well as immediately and 1 hr following each of the maximal treadmill tests and were analyzed for s-IgA and salivary cortisol. Maximal oxygen consumption (VO2max) increased significantly (p < 0.05) in the LO and HI groups but remained unchanged in the CON group. The s-IgA levels decreased significantly (p < 0.05) immediately post-exercise but returned to pre-exercise levels by one hour recovery. In addition, s-IgA and cortisol levels were not significantly (p > 0.05) correlated at any of the sampling times. These findings indicated that the s-IgA response to maximal exercise was unaffected by moderate (70% of VO2 max) to heavy (86% of VO2max) training (designed to develop cardiorespiratory fitness in healthy non-athletic adults) and independent of salivary cortisol.