The International Physical Activity Questionnaire-long form overestimates self-reported physical activity of Brazilian adults.

OBJECTIVE: To explore issues associated with measuring physical activity using the International Physical Activity Questionnaire (IPAQ)-long form in adults living in a mid-sized Brazilian city. METHODS: A stratified random sampling procedure was used to select a representative sample of adults living in Rio Claro. This yielded 1572 participants who were interviewed using the IPAQ-long form. The data were analysed using standard statistical procedures. RESULTS: Overall, 83% of men and 89% of women reported at least 150 min of combined moderate and/or vigorous physical activity per week. Reliable values of leisure and transportation-related physical activity were observed for both males and females. With regard to the household and work-related physical activity domains, both males and females reported unusually high levels of participation. CONCLUSION: The IPAQ-long form appears to overestimate levels of physical activity for both males and females, suggesting that the instrument has problems in measuring levels of physical activity in Brazilian adults. Accordingly, caution is warranted before using IPAQ data to support public policy decisions related to physical activity.

Predicting MAOD using only a supramaximal exhaustive test.

The objective of this study was to propose an alternative method (MAOD(ALT)) to estimate the maximal accumulated oxygen deficit (MAOD) using only one supramaximal exhaustive test. Nine participants performed the following tests: (a) a maximal incremental exercise test, (b) six submaximal constant workload tests, and (c) a supramaximal constant workload test. Traditional MAOD was determined by calculating the difference between predicted O(2) demand and accumulated O(2) uptake during the supramaximal test. MAOD(ALT) was established by summing the fast component of excess post-exercise oxygen consumption and the O(2) equivalent for energy provided by blood lactate accumulation, both of which were measured during the supramaximal test. There was no significant difference between MAOD (2.82+/-0.45 L) and MAOD(ALT) (2.77+/-0.37 L) (P=0.60). The correlation between MAOD and MAOD(ALT) was also high (r=0.78; P=0.014). These data indicate that the MAOD(ALT) can be used to estimate the MAOD.

Manipulation of rest period length induces different causes of fatigue in vertical jumping.

The aim of this study was to directly compare the causes of fatigue after a short- and a long-rest interval between consecutive stretch-shortening cycle exercises. Eleven healthy males jumped with different resting period lengths (short=6.1+/-1 s, long=8.6+/-0.9 s), performing countermovement jumps at 95% of their maximal jump height until they were unable to sustain the target height. After short- and long-rest, the maximal voluntary isometric contraction knee extension torque decreased (-7%; p=0.04), comparing to values obtained before exercise protocols. No change was seen from pre- to post-exercise, for either short- or long-rest, in biceps femoris coactivation (-1%; p=0.95), peak-to-peak amplitude (1%; p=0.95) and duration (-8%; p=0.92) of the compound muscle action potential of the vastus lateralis. Evoked peak twitch torque reduced after both exercise protocols (short=-26%, long=-32%; p=0.003) indicating peripheral fatigue. However, central fatigue occurred only after short-rest evidenced by a reduction in voluntary activation of the quadriceps muscle (-14%; p=0.013) measured using the interpolated twitch technique. In conclusion, after stretch-shortening cycle exercise using short rest period length, the cause of fatigue was central and peripheral, while after using long rest period length, the cause of fatigue was peripheral.

Evaluation of an innovative critical power model in intermittent vertical jump.

The aim of this study was to test if the critical power model can be used to determine the critical rest interval (CRI) between vertical jumps. Ten males performed intermittent countermovement jumps on a force platform with different resting periods (4.1+/-0.3 s, 5.0+/-0.4 s, 5.9+/-0.6 s). Jump trials were interrupted when participants could no longer maintain 95% of their maximal jump height. After interruption, number of jumps, total exercise duration and total external work were computed. Time to exhaustion (s) and total external work (J) were used to solve the equation Work=a+b x time. The CRI (corresponding to the shortest resting interval that allowed jump height to be maintained for a long time without fatigue) was determined dividing the average external work needed to jump at a fixed height (J) by b parameter (J/s). In the final session, participants jumped at their calculated CRI. A high coefficient of determination (0.995+/-0.007) and the CRI (7.5+/-1.6 s) were obtained. In addition, the longer the resting period, the greater the number of jumps (44+/-13, 71+/-28, 105+/-30, 169+/-53 jumps; p<0.0001), time to exhaustion (179+/-50, 351+/-120, 610+/-141, 1,282+/-417s; p<0.0001) and total external work (28.0+/-8.3, 45.0+/-16.6, 67.6+/-17.8, 111.9+/-34.6kJ; p<0.0001). Therefore, the critical power model may be an alternative approach to determine the CRI during intermittent vertical jumps.

5-aminolevulinic acid-induced alterations of oxidative metabolism in sedentary and exercise-trained rats.

5-Aminolevulinic acid (ALA), a heme precursor that accumulates in acute intermittent porphyria patients and lead-exposed individuals, has previously been shown to autoxidize with generation of reactive oxygen species and to cause in vitro oxidative damage to rat liver mitochondria. We now demonstrate that chronically ALA-treated rats (40 mg/kg body wt every 2 days for 15 days) exhibit decreased mitochondrial enzymatic activities (superoxide dismutase, citrate synthase) in liver and soleus (type I, red) and gastrocnemius (type IIb, white) muscle fibers. Previous adaptation of rats to endurance exercise, indicated by augmented (cytosolic) CuZn-superoxide dismutase (SOD) and (mitochondrial) Mn-SOD activities in several organs, does not protect the animals against liver and soleus mitochondrial damage promoted by intraperitoneal injections of ALA. This is suggested by loss of citrate synthase and Mn-SOD activities and elevation of serum lactate levels, concomitant to decreased glycogen content in soleus and the red portion of gastrocnemius (type IIa) fibers of both sedentary and swimming-trained ALA-treated rats. In parallel, the type IIb gastrocnemius fibers, which are known to obtain energy mainly by glycolysis, do not undergo these biochemical changes. Consistently, ALA-treated rats under swimming training reach fatigue significantly earlier than the control group. These results indicate that ALA may be an important prooxidant in vivo.

Regulatory mechanisms of blood lactate production during exercise in man.

During cycloergometric exercise at progressively increasing loads, blood lactate concentration increased about 12-fold. Pyruvate concentration decreased initially (for loads of 50-75 W), increased with loads of 75 to 125 W and then decreased again until the end of exercise. The malate concentration increased abruptly between 50 and 75 W, followed by a slow decline; citrate increased about nine-fold as the exercise load was increased to 125 W and then fell sharply. Thus, the production of lactate during low-intensity exercise seems to occur by the "mass-action effect" caused by enhanced glycolysis, whereas with moderate loads the glycolysis rate is very much reduced and most of the lactate production seems to involve the action of the malate-aspartate shuttle. For high-intensity exercise, both mechanisms appear to participate in lactate production.

Blood glucose responses in humans mirror lactate responses for individual anaerobic threshold and for lactate minimum in track tests.

The equilibrium point between blood lactate production and removal (La-(min)) and the individual anaerobic threshold (IAT) protocols have been used to evaluate exercise. During progressive exercise, blood lactate [La-]b, catecholamine and cortisol concentrations, show exponential increases at upper anaerobic threshold intensities. Since these hormones enhance blood glucose concentrations [Glc]b, this study investigated the [Glc] and [La-]b responses during incremental tests and the possibility of considering the individual glucose threshold (IGT) and glucose minimum (Glc(min)) in addition to IAT and La-(min) in evaluating exercise. A group of 15 male endurance runners ran in four tests on the track 3000 m run (v3km); IAT and IGT - 8 x 800 m runs at velocities between 84% and 102% of v3km; La-(min) and Glc(min) - after lactic acidosis induced by a 500-m sprint, the subjects ran 6 x 800 m at intensities between 87% and 97% of v3km; endurance test (ET) - 30 min at the velocity of IAT. Capillary blood (25 microl) was collected for [La-]b and [Glc]b measurements. The IAT and IGT were determined by [La-]b and [Glc]b kinetics during the second test. The La-(min) and Glc(min) were determined considering the lowest [La-] and [Glc]b during the third test. No differences were observed (P < 0.05) and high correlations were obtained between the velocities at IAT [283 (SD 19) and IGT 281 (SD 21) m. x min(-1); r = 0.096; P < 0.001] and between La-(min) [285 (SD 21)] and Glc(min) [287 (SD 20) m. x min(-1) r = 0.77; P < 0.05]. During ET, the [La-]b reached 5.0 (SD 1.1) and 5.3 (SD 1.0) mmol x l(-1) at 20 and 30 min, respectively (P > 0.05). We concluded that for these subjects it was possible to evaluate the aerobic capacity by IGT and Glc(min) as well as by IAT and La-(min).

Maximal lactate steady state in rats submitted to swimming exercise.

The higher concentration during exercise at which lactate entry in blood equals its removal is known as 'maximal lactate steady state' (MLSS) and is considered an important indicator of endurance exercise capacity. The aim of the present study was to determine MLSS in rats during swimming exercise. Adult male Wistar rats, which were adapted to water for 3 weeks, were used. After this, the animals were separated at random into groups and submitted once a week to swimming sessions of 20 min, supporting loads of 5, 6, 7, 8, 9 or 10% of body wt. for 6 consecutive weeks. Blood lactate was determined every 5 min to find the MLSS. Sedentary animals presented MLSS with overloads of 5 and 6% at 5.5 mmol/l blood lactate. There was a significant (P<0.05) increase in blood lactate with the other loads. In another set of experiments, rats of the same strain, sex and age were submitted daily to 60 min of swimming with an 8% body wt. overload, 5 days/week, for 9 weeks. The rats were then submitted to a swimming session of 20 min with an 8% body wt. overload and blood lactate was determined before the beginning of the session and after 10 and 20 min of exercise. Sedentary rats submitted to the same acute exercise protocol were used as a control. Physical training did not alter the MLSS value (P<0.05) but shifted it to a higher exercise intensity (8% body wt. overload). Taken together these results indicate that MLSS measured in rats in the conditions of the present study was reproducible and seemed to be independent of the physical condition of the animals.

Regulatory mechanisms of blood lactate production during exercise in man

During cycloergometric exercise at progressively increasing loads, blood lactate concentration increased about 12-fold. Pyruvate concentration decreased initially(for loads of 50-75 W), increased with loads of 75 to 125 W and then decreased again until the end of exercise. the malate concentration increased abruptly between 50 and 75 W, followed by a slow decline; citrate increased about nine-fold as the exercise load was increased to 125 W and then fell sharply. Thus, the production of lactate during low-intensity exercise seems to occur by the "mass-action effect" caused by enhanced glycolysis, whereas with moderate loads the glycolysis rate is very much reduced and most of the lactate production seems to involve the action of the malate-aspartate shuttle. For high-intensity exercise, both mechanisms appear to participate in lactate production