Influence of moderate cold exposure on blood lactate during incremental exercise

Summary This study examined the effect of exposure of the whole body to moderate cold on blood lactate produced during incremental exercise. Nine subjects were tested in a climatic chamber, the room temperature being controlled either at 30°C or at 10°C. The protocol consisted of exercise increasing in intensity in 35 W increments every 3 min until exhaustion. Oxygen consumption (VO₂) was measured during the last minute of each exercise intensity. Blood samples were collected at rest and at exhaustion for the measurement of blood glucose, free fatty acid (FFA), noradrenaline (NA) and adrenaline (A) concentrations and, during the last 15 s of each exercise intensity, for the determination of blood lactate concentration [la^–]_b. TheVO₂ was identical under both environments. At 10°C, as compared to 30°C, the lactate anaerobic threshold (Th_{an, la} ^–) occurred at an exercise intensity 15 W higher and [Th_{an, la} ^–]_b was lower for submaximal intensities above the Th_{an, la} ^– Regardless of ambient temperature, glycaemia, A and NA concentrations were higher at exhaustion while FFA was unchanged. At exhaustion the NA concentration was greater at 10°C [15.60 (SEM 3.15) nmol·l^–1] than at 30°C [8.64 (SEM 2.37) nmol·l^–1]. We concluded that exposure to moderate cold influences the blood lactate produced during incremental exercise. These results suggested that vasoconstriction was partly responsible for the lower [la^–]_b observed for submaximal high intensities during severe cold exposure.     

Maximal heart rates and plasma lactate concentrations observed in middle-aged men and women during a maximal cycle ergometer test

Summary The purpose of this study was to investigate criteria for maximal effort in middle-aged men and women undertaking a maximal exercise test until they were exhausted if no measurements of oxygen uptake are made. A large group of 2164 men and 975 women, all active in sports and aged between 40 and 65 years, volunteered for a medical examination including a progressive exercise test to exhaustion on a cycle ergometer. In the 3rd min of recovery a venous blood sample was taken to determine the plasma lactate concentration ([la^–]_{p, 3min}). Lactate concentration and maximal heart rate (f _{c, max}) were lower in the women than in the men (P<0.001). Multiple regression analyses were performed to assess the contribution of sex to [la^–]_{p, 3 min}, independent of age and f _c max, It was found that [la^–]_{p,3 min} was about 2.5 mmol·l^–1 lower in women than in men of the same age and f _{c, max}. In our population 88% of the men and 85% of the women met a combination of the following f _{c, max} and [la^–]_{p, 3min} criteria: f _{c, max} equal to or greater than 220 minus age beats·min^–1 and/or [la^–]_{p, 3min} equal to or greater than 8 mmol·l^–1 in the men and f _{c, max} equal to or greater than 220 minus age beats·min^–1 and/or [la^–]_{p, 3min} equal to or greater than 5.5 mmol·1^–1 in the women.     

Treadmill validation of an over-ground walking test to predict peak oxygen consumption

Summary The purpose of this study was to determine whether a test developed to predict maximal oxygen consumption (VO_2max) during over-ground walking, was similarly valid as a predictor of peak oxygen consumption (VO₂) when administered during a 1-mile (1.61 km) treadmill walk. Treadmill walk time, mean heart rate over the last 2 full min of the walk test, age, and body mass were entered into both generalized (GEN Eq.) and gender-specific (GSP Eq.) prediction equations. Overall results indicated a highly significant linear relationship between observed peakVO₂ and GEN Eq. predicted values (r=0.91), a total error (TE) of 5.26 ml · kg^–1 · min^–1 and no significant difference between observed and predicted peakVO₂ mean values. The peakVO₂ for women (n = 75) was predicted accurately by GSP Eq. (r = 0.85; TE = 4.5 ml · kg^–1 · min^–1), but was slightly overpredicted by GEN Eq. (overall mean difference = 1.4 ml · kg^–1 · min^–1;r=0.86; TE = 4.56 ml · kg^–1 · min^–1). No significant differences between observed peakVO₂ and either GEN Eq. (r=0.85; TE=4.3 ml · kg^–1 · min^–1) or GSP Eq. (r=0.85; TE = 4.8 ml · kg^–1 · min^–1)predicted values were noted for men (n=48) with peakVO₂ values less than or equal to 55 ml · kg^–1 · min^–1. However, both equations significantly underpredicted peakVO₂ for the remaining high peakVO₂ men (n = 22). In conclusion, the over-ground walking test, when administered on a treadmill, is a valid method of predicting peakVO₂ but underpredicts peakVO₂ of subjects with observed high peakVO₂ values. Present address: Human Performance Laboratory State University, Muncie, IN 47306, USA     

Peripheral and central inputs to the effort sense during cycling exercise

Summary The relationships between some physical and physiological events, and perceived effort were studied at several equivalent work outputs (V) at two pedalling rates (30 and 60 rev·min^–1). Subjects judged effort throughout a 4 min exercise bout. After 4 min at any sen it was always more effortful to pedal at 30 rev·min ^–1 even though there were no differences in V _E, VO₂ or integrated electromyography per minute (IEMG·min^–1) between pedalling rates. Effort was related to VO₂ and IEMG·min^–1 but it was more effortful to pedal at 30 rev·min^–1. Effort was also related to pedal resistance and IEMG of single contractions but was influenced by pedalling rate after 4 min of exercise. At any resistance it was more effortful to pedal at 60 rev·min ^–1, however, when effort was plotted as a function of resistance after 15 s, there was virtually no effect of pedalling rate. The rate effect grows with time from the onset of exercise and appears to be related to the central signal to the effort sense. The interaction of peripheral and central signals suggests a model of the effort sense during exercise.This research supported by NIH Training Grant No. ES00123     

The influence of a respiratory acidosis on the exercise blood lactate response

Summary The purpose of the present study was to examine the influence of a respiratory acidosis on the blood lactate (La) threshold and specific blood La concentrations measured during a progressive incremental exercise test. Seven males performed three step-incremental exercise tests (20 W · min^–1) breathing the following gas mixtures; 21% O₂ balance-nitrogen, and 21% O₂, 4% CO₂ balance-nitrogen or balance-helium. The log-log transformation of La oxygen consumption (VO₂) relationship and a 1 mmol ·1^–1 increase above resting values were used to determine a La threshold. Also, theVO₂ corresponding to a La value of 2 (La2) and 4 (La4) mmol · 1^–1 was determined. Breathing the hypercapnic gas mixtures significantly increased the resting partial pressure of carbon dioxide (PCO₂) from 5.6 kPa (42 mm Hg) to 6.1 kPa (46 mm Hg) and decreased pH from 7.395 to 7.366. During the incremental exercise test,PCO₂ increased significantly to 7.2 kPa (54 mm Hg) and 6.8 kPa (51 mm Hg) for the hypercapnic gas mixtures with nitrogen and helium, respectively, and pH decreased to 7.194 and 7.208. In contrast, bloodPCO₂ decreased to 4.9 kPa (37 mm Hg) at the end of the normocapnic exercise test and pH decreased to 7.291. A blood La threshold determined from a log-log transformation [1.20 (0.28) 1·min^–1] or as an increase of 1 mmol·1^–1[1.84 (0.46) 1·min^–1] was unaffected by the acid-base alterations. Similarly, theVO₂ corresponding to La2 and La4 was not affected by breathing the hypercapnic gas mixtures [2.12 (0.46) 1·min^–1 and 2.81 (0.52) 1·min^–1, respectively]. Blood La values were reduced significantly at maximal exercise while breathing the hypercapnic gas mixtures (5.72±1.34 mmol ·1^–1) compared with the normocapnic test (6.96±1.14 mmol·1^–1). It is concluded that respiratory-induced acid-base manipulations due to the inspiration of 4% CO₂ have a negligible influence on the blood La response during a progressive exercise test at low and moderate power outputs. Lower blood La values are observed at maximal exercise with an induced respiratory acidosis but this negative influence is less than what has been reported for an induced metabolic acidosis.     

Does the threshold of transcutaneous partial pressure of carbon dioxide represent the respiratory compensation point or anaerobic threshold?

On reaching the respiratory compensation point (RCP) during rapidly increasing incremental exercise, the ratio of minute ventilation (V_E) to CO₂ output (VCO₂) rises, which coincides with changes of arterial partial pressure of carbon dioxide (P _aCO₂). Since P _aCO₂ changes can be monitored by transcutaneous partial pressure of carbon dioxide (PCO_2,tc) RCP may be estimated by PCO_2,tc measurement. Few available studies, however, have dealt with comparisons between PCO_2,tc threshold (T _AT) and lactic, ventilatory or gas exchange threshold (V _AT), and the results have been conflicting. This study was designed to examine whether this threshold represents RCP rather than V _AT. A group of 11 male athletes performed incremental excercise (25 W · min^–1) on a cycle ergometer. The PCO_2,tc at (44°C) was continuously measured. Gas exchange was computed breath-by-breath, and hyperaemized capillary blood for lactate concentration ([la^–]_b) and P _aCO₂ measurements was sampled each 2 min. The T _AT was determined at the deflection point of PCO_2,tc curve where PCO_2,tc began to decrease continuously. The V _AT and RCP were evaluated with VCO₂ compared with oxygen uptake (VO₂) and V_E compared with the VCO₂ method, respectively. The PCO_2,tc correlated with P _aCO₂ and end-tidal PCO₂. At T _AT, power output [P, 294 (SD 40) W], VO₂ [4.18 (SD 0.57)l · min^–1] and [la^–] [4.40 (SD 0.64) mmol · l^–1] were significantly higher than those at V _AT[P 242 (SD 26) W, VO₂ 3.56 (SD 0.53) l · min^–1 and [la^–]_b 3.52 (SD 0.75), mmol · l^–1 respectively], but close to those at RCP [P 289 (SD 37) W; VO₂ 3.97 (SD 0.43) l · min^– and [la^–]_b 4.19 (SD 0.62) mmol · l^–1, respectively]. Accordingly, linear correlation and regression analyses showed that P, VO₂ and [la^–]_b at T _AT were closer to those at RCP than at V _AT. In conclusion, the T _AT reflected the RCP rather than V _AT during rapidly increasing incremental exercise.     

Effect of endurance training on excessive CO2 expiration due to lactate production in exercise

Summary We attempted to determine the change in total excess volume of CO₂ Output (CO₂ excess) due to bicarbonate buffering of lactic acid produced in exercise due to endurance training for approximately 2 months and to assess the relationship between the changes of CO₂ excess and distance-running performance. Six male endurance runners, aged 19–22 years, were subjects. Maximal oxygen uptake (VO_2max), oxygen uptake (VO₂) at anaerobic threshold (AT), CO₂ excess and blood lactate concentration were measured during incremental exercise on a cycle ergometer and 12-min exhausting running performance (12-min ERP) was also measured on the track before and after endurance training. The absolute magnitudes in the improvement due to training for C02 excess per unit of body mass per unit of blood lactate accumulation (Ala^–) in exercise (CO₂ excess·mass^–1·la^–), 12-min ERP, VO₂ at AT (AT-VO₂) and VO_2max on average were 0.8 ml·kg^–1·l^–1·mmol^–1, 97.8m, 4.4 ml·kg^–1· min^–1 and 7.3 ml·kg^–1·min^–1, respectively. The percentage change in CO₂ excess·mass^–1·la^– (15.7%) was almost same as those of VO_2max (13.7%) and AT-VO₂ (13.2%). It was found to be a high correlation between the absolute amount of change in CO₂ excess·mass^–1·la^– and the absolute amount of change in AT-VO₂ (r=0.94, P<0.01). Furthermore, the absolute amount of change in C02 excess·mass^–1·la^–, as well as that in AT-VO₂ (r=0.92, P<0.01), was significantly related to the absolute amount of change in 12-min ERP (r=0.81, P<0.05). It was concluded that a large CO₂ excess·mass^–1·la^–1 of endurance runners could be an important factor for success in performance related to comparatively intense endurance exercise such as 3000–4000 m races.     

Relationships between postcompetition blood lactate concentration and average running velocity over 100-m and 200-m races

The relationships between anaerobic glycolysis and average velocity () sustained during sprint running were studied in 12 national level male sprinters. A blood sample was obtained within 3 min of the completion of semi-finals and finals in the 100-m and 200-m Cameroon national championships and blood lactate concentration ([la^–]_b) was measured. The 35-m times were video-recorded. The 100-m and 200-m [la^–]_b were 8.5 (SD 0.8) and 10.3 (SD 0.8) mmol·l^–1, respectively. These were not correlated with the performances. Over 200 m [la^–]_b was correlated with the sustained over the last 165 m (r=0.65,P<0.05). In the 9 athletes who participated in both the 100-m and 200-m races, the difference between the [la^–]_b measured at the end of the two races was negatively correlated to the difference in v sustained over the two races (r=0.76,P>0.02). Energy expenditure during sprint running was estimated from the [la^–]_b values. This estimate was mainly based on the assumption that a 1 mmol·l^–1 increase in [la^–]_b corresponds to the energy produced by the utilization of 3.30 ml O₂·kg^–1. The energy cost of running was estimated at 0.275 (SD 0.02) ml O₂·kg^–1·m^–1 over 200-m and 0.433 (SD 0.03) ml O₂·kg^–1·m^–1 over 100-m races. These results would suggest that at the velocities studied anaerobic glycolysis contributes to at least 55% of the energy expenditure related to sprint running. However, the influence of both mechanical factors and the contribution of other energy processes obscure the relationship between [la^–]_b and performance.     

The oxygen uptake-power regression in cyclists and untrained men: implications for the accumulated oxygen deficit

The regression of oxygen uptake (O₂) on power output and the O₂ demand predicted for suprapeak oxygen uptake (O_2peak) exercise (power output = 432 W) were compared in ten male cyclists [C, mean O_2peak = 67.9 (SD 4.2) ml · kg^–1 · min^–1] and nine active, yet untrained men [UT, mean O_2peak = 54.1 (SD 6.5) ml · kg^–1 · min^–1]. The O₂-power regression was determined using a continuous incremental cycle test (CON4), performed twice, which comprised several 4-min exercise periods progressing in intensity from approximately 40%–85% O_2peak. Minute ventilation (_E), heart rate (HR), respiratory exchange ratio (R), blood lactate concentration ([1a^–]_b) and rectal temperature (T _re) were measured at rest and during CON4. The slope of the O₂-power regression was greater (P 0.05) in C [12.4 (SD 0.7) ml · min^–1. W^–1] compared to UT [11.7 (SD 0.4) ml · min^–1 W^–1]; as a result, the O₂ demand (at 432 W) was also higher (P 0.05) in C [5.97 (SD 0.23) l · min^–1] than UT [5.70 (SD 0.15) 1 · min^–1]. ExerciseR and [la^–]_b were lower (P 0.05) in C .in comparison to UT at all power outputs, whereas _E and HR were relatively lower (P 0.05) in C at power outputs approximating 180 W, 220 W and 270 W. Differences in fat metabolism estimated over the first three power outputs accounted for approximately 19% of the difference in O₂-power slopes between the groups and up to 46% of the difference in O₂ at a given intensity. Although the O₂-power regressions were linear for C [r = 0.997 (SD 0.001)] and UT [r = 0.997 (SD 0.001)], the O₂-power slope was higher at power outputs at or above the lactate threshold (13.2 ml · min^–1 · W^–1 than at lower intensities (11.6 ml · min^–1 · W^–1) in C, an effect which was less profound in UT. As a result, the exclusion of O₂ at the highest power outputs completely abolished the difference in O₂-power slopes between C and UT. Thus, the relatively higher O₂ during incremental exercise in C can be almost entirely attributed to the higher O₂ cost of cycling at higher power outputs. In addition, the presence of non-linear responses in O₂ at higher intensities also confirms the invalidity of describing the O₂ response across a wide range of power outputs using a linear function, and challenges the validity of predicting the O₂ demand of more intense exercise by a linear extrapolation of this same function.     

Maximal oxygen uptake,anaerobic threshold and running economy in women and men with similar performances level in marathons

Sex differences in running economy (gross oxygen cost of running, C_R), maximal oxygen uptake (VO_2max), anaerobic threshold (Th_an), percentage utilization of aerobic power (% VO_2max), and Th_an during running were investigated. There were six men and six women aged 20–30 years with a performance time of 2 h 40 min over the marathon distance. The VO_2max, Th_an, and CR were measured during controlled running on a treadmill at 1° and 3° gradient. From each subject's recorded time of running in the marathon, the average speed (v _M) was calculated and maintained during the treadmill running for 11 min. The VO_{2 max} was inversely related to body mass (m _b), there were no sex differences, and the mean values of the reduced exponent were 0.65 for women and 0.81 for men. These results indicate that for running the unit ml·kg^–0.75·min^–1 is convenient when comparing individuals with different m _b. The VO_2max was about 10% (23 ml·kg^–0.75·min^–1) higher in the men than in the women. The women had on the average 10–12 ml·kg^–0.75·min^–1 lower VO₂ than the men when running at comparable velocities. Disregarding sex, the mean value of C_R was 0.211 (SEM 0.005) ml·kg^–1·m^–1 (resting included), and was independent of treadmill speed. No sex differences in Th_an expressed as % VO_2max or percentage maximal heart rate were found, but Than expressed as VO₂ in ml·kg^–0.75·min^–1 was significantly higher in the men compared to the women. The percentage utilization of f _emax and concentration of blood lactate at v _M was higher for the female runners. The women ran 2 days more each week than the men over the first 4 months during the half year preceding the marathon race. It was concluded that the higher VO_2max and Th_an in the men was compensated for by more running, superior C_R, and a higher exercise intensity during the race in the performance-matched female marathon runners.     

Effect of previous supramaximal work on lacticaemia during supra-anaerobic threshold exercise

Summary Twelve male and female subjects (eight trained, four untrained) exercised for 30 min on a treadmill at an intensity of maximal O₂ consumption (% O_2max) 90.0%, SD 4.7 greater than the anaerobic threshold of 4 mmol ·1^–1 (Th_an =83.6% O_2max, SD 8.9). Time-dependent changes in blood lactate concentration ([la_b]) during exercise occurred in two phases: the oxygen uptake ( O₂) transient phase (from 0 to 4 min) and the O₂ steady-state phase (4–30 min). During the transient phase, [la_b] increased markedly (l.30 mmol · l ^–1 · min ^–1, SD 0.13). During the steady-state phase, [la_b] increased slightly (0.02 mmol · 1^–1 · min^–1, SD 0.06) and when individual values were considered, it was seen that there were no time-dependent increases in [la_b] in half of the subjects. Following hyperlacticaemia (8.8 mmol -l^–1, SD 2.0) induced by a previous 2 min of supramaximal exercise (120% O_2max), [la_b] decreased during the O₂ transient (–0.118 mmol · 1^–1 · min^–1, SD 0.209) and steady-state (–0.088 mmol · 1^–1 · min ^–1, SD 0.103) phases of 30 min exercise (91.4% O_2max, SD 4.8). In conclusion, it was not possible from the Th_an to determine the maximal [la_b] steady state for each subject. In addition, lactate accumulated during previous supramaximal exercise was eliminated during the O₂ transient phase of exercise performed at an intensity above the Th_an. This effect is probably largely explained by the reduction in oxygen deficit during the transient phase. Under these conditions, the time-course of changes in [la_b] during the O₂ steady state was also affected.     

Heart rate overshoot at the beginning of muscle exercise

Summary A characteristic notch in the heart rate (f _c) on-response at the beginning of square-wave exercise is described in 7 very fit marathon runners and 12 sedentary young men, during cycle tests at 30% and 60% of maximal oxygen consumption (VO_2max). The (f _c) notch revealed af _c overshoot with respect to the (f _c) values predicted from exponential beat-by-beat fitted models. While at 30% of (VO_2max). all subjects showed af _c over-shoot, at 60% of (VO_2max). it occurred in the marathon runners but not in the sedentary subjects. The mean time of occurrence of thef _c overshoot from the onset of the exercise was 16.7 (SD 4.7) s and 12.2 (SD 3.2) s at 30% of (VO_2max). in the runners and the sedentary subjects respectively, and 23.8 (SD 8.8) s at 60% of (VO_2max). in the runners. The amplitude of the overshoot, with respect to rest, was 41 (SD 12) beats·min^–1and 31 (SD 4) beats·min^–1 at 30% of (VO_2max). in the runners and the sedentary subjects respectively, and 46 (SD 19) beats·min^–1 at 60% of (VO_2max). in the runners. The existence and the amplitude of thef _c overshoot may have been related to central command and muscle heart reflex mechanisms and thus may have been indicators of changes in the balance between sympathetic and parasympathetic activity occurring in fit and unfit subjects.     

Lung diffusion capacity,oxygen uptake,cardiac output and oxygen transport during exercise before and after an Himalayan expedition

Studies were made of pulmonary diffusion capacity and oxygen transport before and after an expedition to altitudes at and above 4900 m. Maximum power (P _max) and maximal oxygen uptake (VO _2max) were measured in 11 mountaineers in an incremental cycle ergometer test (25W · min^–1) before and after return from basecamp (30 days at 4900 m or higher). In a second test, cardiac output (Q _c) and lung diffusion capacity of carbon monoxide (D _L,CO) were measured by acetylene and CO rebreathing at rest and during exercise at low, medium and submaximal intensities. After acclimatization, VO_2max and P _max decreased by 5.1% [from 61.0 (SD 6.2) to 57.9 (SD 10.2) ml·kg^–1, n.s.] and 9.9% [from 5.13 (SD 0.66) to 4.62 (SD 0.42) W·kg^–1, n.s.], respectively. The maximal cardiac index and DL,co decreased significantly by 15.6% [14.1 (SD 1.41) 1·min^–1 · m^–2 to 11.9 (SD 1.44)1·min^–1 m^–2, P<0.05] and 14.3% [85.9 (SD 4.36)ml·mmHg^–1 min^–t to 73.6 (SD 15.2) ml · mmHg^–1 -min^–1, P<0.05], respectively. The expedition to high altitude led to a decrease in maximal Q _c, oxygen uptake and D_L,CO. A decrease in muscle mass and capillarity may have been responsible for the decrease in maximal Q_c which may have resulted in a decrease of D _L,CO and an increase in alveolar-arterial oxygen difference. The decrease in D _L,CO especially at lower exercise intensities after the expedition may have been due to a ventilation-perfusion mismatch and changes in blood capacitance. At higher exercise intensities diffusion limitation due to reduced pulmonary capillary contact time may also have occurred.     

Effect of acute sodium bicarbonate ingestion on excess C02 output during incremental exercise

Summary The effect of bicarbonate ingestion on total excess volume of CO₂ Output (CO₂ excess), due to bicaronate buffering of lactic acid in exercise, was studied in eight healthy male volunteers during incremental exercise on a cycle ergometer performed after ingestion (0.3 g · kg^–1 body mass) of CaCO₃ (control) and NaHCO₃ (alkalosis). The resting arterialized venous blood pH (P<0.05) and bicarbonate concentration ([HCO₃ ^–]_b;P<0.01) were significantly higher in acute metabolic alkalosis [AMA; pH, 7.44 (SD 0.03); [HCO₃ ^–]_b; 29.4 (SD 1.5) mmol·1^-1] than in the control [pH, 7.39 (SD 0.03); [HCO₃ ^–]_b, 25.5 (SD 1.0) mmol·1^–1]. The blood lactate concentrations ([la^–]_b) during exercise below the anaerobic threshold (AT) were not affected by AMA, while significantly higher [la^–]_b at exhaustion [12.29 (SD 1.87) vs 9.57 (SD 2.14) mmol·1^–1,P < 0.05] and at 3 min after exercise [14.41 (SD 1.75) vs 12.26 (SD 1.40) mmol · l^–1,P < 0.05] were found in AMA compared with the control. The CO₂ excess increased significantly from the control [3177 (SD 506) ml] to AMA [3897 (SD 381) ml;P < 0.05]. The CO₂ excess per body mass was found to be significantly correlated with both the increase of [la^–]_b from rest to 3 min after exercise ( [la^–]_b;r=0.926,P < 0.001) and with the decrease of [HCO₃ ^–]_b from rest to 3 min after exercise ( [HCO₃ ^–]_b;_r=0.872,P<0.001), indicating that CO₂ excess per body mass increased linearly with both [la^– _b and [HCO₃ ^–]_b. As a consequence, CO₂ excess per body mass per unit increase of [la^–]_b (CO₂ excess·mass^–1· [la^–]_b) was similar for the two conditions. The present results would suggest that the relationship between CO₂ excess and blood lactate accumulation was unaffected by acute metabolic alkalosis, because the relative contribution of bicarbonate buffering of lactic acid was the same as in the control.     

Training effects of cross-country skiing and running on maximal aerobic cycle performance and on blood lipids

Summary Two experiments were carried out to compare the cardiorespiratory and metabolic effects of cross-country skiing and running training during two successive winters. Forty-year-old men were randomly assigned into skiing (n = 15 in study 1,n = 16 in study 2), running (n = 16 in study 1 andn = 16 in study 2) and control (n = 17 in study 1 andn = 16 in study 2) groups. Three subjects dropped out of the programme. The training lasted 9–10 weeks with 40-min exercise sessions three times each week. The training intensity was controlled at 75%–85% of the maximal oxygen consumption (VO_2max) using portable heart rate metres and the mean heart rate was 156–157 beats·min^–1 in the training groups. In the pooled data of the two studies the mean increase in theVO_2max (in ml·min^–1·kg^–1) on a cycle ergometer was 17% for the skiing group, 13% for the running group and 2% for the control group. The increase inVO_2max was highly significant in the combined exercise group compared to the control group but did not differ significantly between the skiing and running groups. The fasting serum concentrations of lipoproteins and insulin did not change significantly in any of the groups. These results suggested that training by cross-country skiing and running of the same duration and intensity at each session for 9–10 weeks improved equally the cardiorespiratory fitness of untrained middle-aged men.     

The effects of intensity of exercise on excess postexercise oxygen consumption and energy expenditure in moderately trained men and women

Summary This experiment investigated the effects of intensity of exercise on excess postexercise oxygen consumption (EPOC) in eight trained men and eight women. Three exercise intensities were employed 40%, 50%, and 70% of the predetermined maximal oxygen consumption (VO_2max). All ventilation measured was undertaken with a standard, calibrated, open circuit spirometry system. No differences in the 40%, 50% and 70% VO_2max trials were observed among resting levels of oxygen consumption (V0₂) for either the men or the women. The men had significantly higher resting VO₂ values being 0.31 (SEM 0.01) 1·min^–1 than did the women, 0.26 (SEM 0.01) 1·min^–1 (P < 0.05). The results indicated that there were highly significant EPOC for both the men and the women during the 3-h postexercise period when compared with resting levels and that these were dependent upon the exercise intensity employed. The duration of EPOC differed between the men and the women but increased with exercise intensity: for the men 40% – 31.2 min; 50% – 42.1 min; and 70% – 47.6 min and for the women, 40% – 26.9 min; 50% – 35.6 min; and 70% – 39.1 min. The highest EPOC, in terms of both time and energy utilised was at 70% VO_2max. The regression equation for the men, where y=O₂ in litres, and x=exercise intensity as a percentage of maximum was y=0.380x + 1.9 (r ²=0.968) and for the women is y=0.374x–0.857 (r ²=0.825). These findings would indicate that the men and the women had to exercise at the same percentage of their VO_2max to achieve the maximal benefits in terms of energy expenditure and hence body mass loss. However, it was shown that a significant EPOC can be achieved at moderate to low exercise intensities but without the same body mass loss and energy expenditure.     

The relationship between anaerobic threshold and electromyographic fatigue threshold in college women

Summary The purpose of this study was to investigate the relationship between anaerobic threshold (Th_an) and muscle fatigue threshold (EMG_FT) as estimated from electromyographic (EMG) data taken from the quadriceps muscles (vastus lateralis) during exercise on a cycle ergometer. The subjects in this study were 20 female college students, including highly trained endurance athletes and untrained sedentary individuals, whose fitness levels derived from their maximal oxygen consumption ranged from 24.9 to 62.2 ml · kg^–1·min^–1. The rate of increase in integrated EMG (iEMG) activity as a function of time (iEMG slope) was calculated at each of four constant power outputs (350, 300, 250, 200 W), sufficiently high to bring about muscle fatigue. The iEMG slopes so obtained were plotted against the exercise intensities imposed, resulting in linear plots which were extrapolated to zero slope to give an intercept on the power axis which was in turn interpreted as the highest exercise intensity sustainable without electromyographic evidence of neuromuscular fatigue (EMGF_FT). The Th_an was estimated from gas exchange parameters during an incremental exercise test on the same cycle ergometer. The mean results indicated that oxygen uptake (VO₂) at Th_an was 1.391·min^–1, SD 0.44 andVO₂ at EMG_FT was 1.33 1·min^–1, SD 0.57. There was no significant difference between these mean values (P>0.05) and there was a highly significant correlation betweenVO₂ at Th_an andVO₂ at EMG_FT (r=0.823,P<0.01). These data supported the concept of Th_an on the basis that Than was associated with the highest exercise intensity that could be sustained without evidence of neuromuscular fatigue and thus suggested that EMG_FT may provide an attractive alternative to the measurement of Th_an.     

V O 2 kinetics in subjects differing in aerobic capacity: investigation by spectral analysis

Summary The power-V _{O 2} transfer functions of 38 subjects differing in aerobic capacity have been determined on the basis of breath-by-breath total oxygen uptake (V _{O 2.1}) measurements during light cycle ergometer exercise (lactic acid concentrations below 2 mmol · l^–1). At constant pedalling frequency (1 Hz) pseudorandom binary sequences (PRBS) of workload were used as the testing signal. TheV _{O 2.1} response was analysed by autocorrelating the ergometer power input and crosscorrelating the power input andV _{O 2.1} output. From the spectra of these functions the amplitude ratios and phase relationships were computed for the first six harmonics of the PRBS fundamental (14 mrad · s^–1). We found that differences in aerobic capacity are associated with significant differences in the amplitude plots of theV _{O 2} transfer function.     

Metabolic cost of exercise and physical performance in children with some observations on external loading

Summary The metabolic cost (VO₂) of running was studied on a motor-driven treadmill in nine athletic boys, five athletic girls, and nine active boys aged 11–13 years and the results compared with their performance times during racing out of doors. On 15 of the children, additional observations of the effects of external loading on aerobic power output were made. The results showed that VO₂ was proportional to body weight in children but when expressed in ml·kg^–1·min^–1, VO₂ for a given speed of running was significantly higher in children than expected from previously collected data on adults. There were no significant differences between aerobic cost of running of the athletic boys, girls, or the active boys. The increased VO₂ ml·kg^–1·min^–1 in children appeared to be independent of stride length and frequency but external loading equivalent to 5% of body weight reduced VO₂ (ml·kg^–1·min^–1), particularly at the higher speeds. It was suggested in young active and athletic children due to their relatively light body weights and highly developed aerobic power outputs, that the required frequency of leg movement was not optimally matched to the force necessary to produce the most economic conversion of aerobic energy into mechanical work. Thus, in competitive events their performance times were related to their maximal aerobic power output (r=–0.75) but their times were always inferior to those which one might have expected from previous aerobic power weight data collected on adult male and female athletes.     

Effects of prolonged cycle ergometer exercise on maximal muscle power and oxygen uptake in humans

Summary The mechanical power (W_tot, W·kg^–1) developed during ten revolutions of all-out periods of cycle ergometer exercise (4–9 s) was measured every 5–6 min in six subjects from rest or from a baseline of constant aerobic exercise [50%–80% of maximal oxygen uptake (VO_2max)] of 20–40 min duration. The oxygen uptake [VO₂ (W·kg^–1, 1 ml O₂ = 20.9 J)] and venous blood lactate concentration ([la]_b, mM) were also measured every 15 s and 2 min, respectively. During the first all-out period, W_tot decreased linearly with the intensity of the priming exercise (W_tot = 11.9–0.25·VO₂). After the first all-out period (i greater than 5–6 min), and if the exercise intensity was less than 60% VO_2max, W_tot, VO₂ and [la]_b remained constant until the end of the exercise. For exercise intensities greater than 60% VO_2max, VO₂ and [la]_b showed continuous upward drifts and W_tot continued decreasing. Under these conditions, the rate of decrease of W_tot was linearly related to the rate of increase of V [(d W_tot/dt) (W·kg^–1·s^–1) = 5.0·10^–5 –0.20·(d VO₂/dt) (W·kg^–1·s^–1)] and this was linearly related to the rate of increase of [la]_b [(d VO₂/dt) (W·kg^–1·s^–1) = 2.310^–4 + 5.910^–5·(d [la]_b/dt) (mM·s^–1)]. These findings would suggest that the decrease of W_tot during the first all-out period was due to the decay of phosphocreatine concentration in the exercising muscles occurring at the onset of exercise and the slow drifts of VO₂ (upwards) and of W_tot (downwards) during intense exercise at constant W_tot could be attributed to the continuous accumulation of lactate in the blood (and in the working muscles).