Anaerobic threshold which describes the onset of systematic increase in blood lactate concentration is a widely used concept in clinical and sports medicine. A deflection point between heart rate-work rate has been introduced to determine the anaerobic threshold non-invasively. However, some researchers have consistently reported a heart rate deflection at higher work rates, while others have not. The present study was designed to investigate whether the heart rate deflection point accurately predicts the anaerobic threshold under the condition of acute hypoxia. Eight untrained males performed two incremental exercise tests using an electromagnetically braked cycle ergometer: one breathing room air and one breathing 12 % O2. The anaerobic threshold was estimated using the V-slope method and determined from the increase in blood lactate and the decrease in standard bicarbonate concentration. This threshold was also estimated by in the heart rate-work rate relationship. Not all subjects exhibited a heart rate deflection. Only two subjects in the control and four subjects in the hypoxia groups showed a heart rate deflection. Additionally, the heart rate deflection point overestimated the anaerobic threshold. In conclusion, the heart rate deflection point was not an accurate predictor of anaerobic threshold and acute hypoxia did not systematically affect the heart rate-work rate relationships.
The purpose of this study was to investigate the validity of non-invasive lactate threshold estimation using ventilatory and pulmonary gas exchange indices under condition of acute hypoxia. Seven untrained males (21.41.2 years) performed two incremental exercise tests using an electromagnetically braked cycle ergometer: one breathing room air and other breathing 12 % O2. The lactate threshold was estimated using the following parameters: increase of ventilatory equivalent for O2 (VE/VO2) without increase of ventilatory equivalent for CO2 (VE/VCO2). It was also determined from the increase in blood lactate and decrease in standard bicarbonate. The VE/VO2 and lactate increase methods yielded the respective values for lactate threshold: 1.910.10 l/min (for the VE/VO2) vs. 1.890.1 l/min (for the lactate). However, in hypoxic condition, VE/VO2 started to increase prior to the actual threshold as determined from blood lactate response: 1.670.1 l/min (for the lactate) vs. 1.370.09 l/min (for the VE/VO2) (P=0.0001), i.e. resulted in pseudo-threshold behavior. In conclusion, the ventilatory and gas exchange indices provide an accurate lactate threshold. Although the potential for pseudo-threshold behavior of the standard ventilatory and gas exchange indices of the lactate threshold must be concerned if an incremental test is performed under hypoxic conditions in which carotid body chemosensitivity is increased.
The aim of this study was to investigate the relationship between cardiopulmonary fitness as indicated by maximal work rate (Wmax) production and aerobic capacities (WAT), body mass index (BMI) and heart rate reserve. A total of 60 sedentary subjects (30 males, 30 females, aged 18-25 years) were enrolled in the study. Each subject performed an incremental exercise test (15 W/min) to the limit of tolerance on an electromagnetically-braked cycle ergometer. There was a negative correlation between increased BMI to Wmax capacity per kilogram body weight in male (r=–0.846, P=0.0001) and in female (r=–0.896, P=0.0001) subjects. In addition, WAT for each kilogram body weight also negatively correlated with increased BMI in male (r=–0.870, P=0.0001) and in females (r=–0.807, P=0.0001). The heart rate reserve correlated negatively with increasing BMI: r=–0.699, P=0.0001 (males) and r=–0.655, P=0.0001 (females). The results of the present study have suggested that, due to the inverse correlation between BMI, Wmax capacity, aerobic fitness and heart rate reserve, it may be useful to consider BMI in establishing cardiopulmonary fitness in various subjects.
We investigated the effects of different weight loss protocols on leptin levels in obese females with the aim of addressing the leptin resistance which has been found to be an aggravating factor in obesity. Twenty-four obese females enrolled to one of three 12-week weight loss protocols: orlistat-induced weight loss (OWL, n=8), exercise-induced weight loss (EWL, n=8) and orlistat plus exercise-induced weight loss (OEWL, n=8). Serum leptin levels were measured in duplicate by radioimmunoassay. There were significant reductions (P<0.01) in body weight and fat mass after the 12 week period in all groups: -11.4±0.5 kg and -9.8
±0.5 kg (OEWL), -8.3±0.8 kg and -5.7±0.9 kg (OWL), -8.9±1.2 kg and -7.4±1.2 kg (EWL), respectively. Serum leptin levels were also decreased markedly in all groups: -59.2 %(OEWL1), -37.8 % (OWL) and -48.6 % (EWL) (P<0.01 all). In addition, there were marked decreases in leptin levels for each kilogram of fat mass after the 12 week period: -48.2
±7.2 % (OEWL), -27.8±4.8 % (OWL) and -39.3±4.3% (EWL) (P<0.01 all). Decreases in serum leptin levels expressed per kilogram of fat mass were significantly higher in the OEWL group compared to the OWL group (P=0.03). Consequently, an exercise training program in adjunct to
pharmacotherapy provides higher weight reduction and fat mass loss in obesity treatment. It also seems to have further beneficial effects on leptin re
sistance, as indicated by decreases in leptin levels expressed per kilogram of fat mass.
We examined the effects of weight loss induced by diet-orlistat (DO) and diet-orlistat combined with exercise (DOE) on maximal work rate production (Wmax) capacity in obese patients. Total of 24 obese patients were involved in this study. Twelve of them were subjected to DO therapy only and the remaining 12 patients participated in a regular aerobic exercise-training program in addition to DO therapy (DOE). Each patient performed two incremental ramp exercise tests up to exhaustion using an electromagnetically-braked cycle ergometer: one at the onset and one at the end of the 4th week. DOE therapy caused a significant decrease in total body weight: 101.5±17.4 kg (basal) vs 96.3±17.3 kg (4 wk) associated with a significant decrease in body fat mass: 45.0±10.5 kg (basal) vs 40.9±9.8 kg (4 wk). DO therapy also resulted in a significant decrease of total body weight 94.9±14.9 kg (basal) vs 91.6±13.5 kg (4 wk) associated with small but significant decreases in body fat mass: 37.7±5.6 kg (basal) to 36.0±6.2 kg (4 wk). Weight reduction achieved during DO therapy was not associated with increased Wmax capacity: 106±32 W (basal) vs 106±33 W (4 wk), while DOE therapy resulted in a markedly increased Wmax capacity: 109±39 W (basal) vs 138±30 W (4 wk). DO therapy combined with aerobic exercise training resulted in a significant reduction of fat mass tissue and markedly improved the aerobic fitness and Wmax capacities of obese patients. Considering this improvement within such a short period, physicians should consider applying an aerobic exercise-training program to sedentary obese patients for improving their physical fitness and thereby reduce the negative outcomes of obesity.