36 resultados para 1-min average

em Deakin Research Online - Australia


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The purpose of this study was to examine the relationship between skeletal muscle monocarboxylate transporters 1 and 4 (MCT1 and MCT4) expression, skeletal muscle oxidative capacity and endurance performance in trained cyclists. Ten well-trained cyclists (mean ± SD; age 24.4 ± 2.8 years, body mass 73.2 ± 8.3 kg, VO2max 58 ± 7 ml kg−1 min−1) completed three endurance performance tasks [incremental exercise test to exhaustion, 2 and 10 min time trial (TT)]. In addition, a muscle biopsy sample from the vastus lateralis muscle was analysed for MCT1 and MCT4 expression levels together with the activity of citrate synthase (CS) and 3-hydroxyacyl-CoA dehydrogenase (HAD). There was a tendency for VO2max and peak power output obtained in the incremental exercise test to be correlated with MCT1 (r = −0.71 to −0.74; P < 0.06), but not MCT4. The average power output (P average) in the 2 min TT was significantly correlated with MCT4 (r = −0.74; P < 0.05) and HAD (r = −0.92; P < 0.01). The P average in the 10 min TT was only correlated with CS activity (r = 0.68; P < 0.05). These results indicate the relationship between MCT1 and MCT4 as well as cycle TT performance may be influenced by the length and intensity of the task.

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Understanding potential determinants of change in television (TV) viewing among children may enhance the effectiveness of programs targeting this behaviour. This study aimed to investigate the contribution of individual, social and home environment factors among 10-year-old Australian children to change in TV viewing over a 21-month period. A total of 164 children (49% boys) completed a 19-lesson (9-month) intervention program to reduce TV viewing time. Children completed self-administered surveys four times over 21 months (pre- and post-intervention, 6- and 12-month follow-up). Baseline factors associated with change in TV viewing during the intervention and follow-up periods were: ‘asking parents ≥once/week to switch off the TV and play with them’ (21.6 min/day more than those reporting <once/week, p = 0.007); being able to ‘watch just 1 h of TV per day’ (26.1 min/day less than those who could not, p = 0.010); ‘watching TV no matter what was on’ (36.6 min/day more than those who did not, p < 0.001); and ‘continuing to watch TV after their program was over’ (33.0 min/day more than those who did not, p = 0.006). With every unit increase in baseline frequency of TV viewing with family and friends, children spent on average 4.0 min/day more watching TV over the 21-month period (p = 0.047). Baseline number and placement of TVs at home did not predict change in children's TV viewing over the 21 months. Greater understanding of the family dynamics and circumstances, as well as the individual and social determinants of TV viewing, will be required if we are to develop effective strategies for reducing TV viewing in children.

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In an attempt to improve automated gene prediction in the untranslated region of a gene, we completed an in-depth analysis of the minimum free energy for 8,689 sub-genetic DNA sequences. We expanded Zhang's classification model and classified each sub-genetic sequence into one of 27 possible motifs. We calculated the minimum free energy for each motif to explore statistical features that correlate to biologically relevant sub-genetic sequences. If biologically relevant sub-genetic sequences fall into distinct free energy quanta it may be possible to characterize a motif based on its minimum free energy. Proper characterization of motifs can lead to greater understanding in automated genefinding, gene variability and the role DNA structure plays in gene network regulation.

Our analysis determined: (1) the average free energy value for exons, introns and other biologically relevant sub-genetic sequences, (2) that these subsequences do not exist in distinct energy quanta, (3) that introns exist however in a tightly coupled average minimum free energy quantum compared to all other biologically relevant sub-genetic sequence types, (4) that single exon genes demonstrate a higher stability than exons which span the entire coding sequence as part of a multi-exon gene and (5) that all motif types contain a free energy global minimum at approximately nucleotide position 1,000 before reaching a plateau. These results should be relevant to the biochemist and bioinformatician seeking to understand the relationship between sub-genetic sequences and the information behind them.

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The metabolism of 52–73-day old Antarctic fur seal pups from Bird Island, South Georgia, was investigated during fasting periods of normal duration while their mothers were at sea foraging. Body mass decreased exponentially with pups losing 3.5–3.8% of body mass per day. Resting metabolic rate also decreased exponentially from 172–197 ml (O2)·min−1 at the beginning of the fast and scaled to Mb0.74 at 2.3 times the level predicted for adult terrestrial mammals of similar size. While there was no significant sex difference in RMR, female pups had significantly higher (F1,18=6.614, P<0.019) mass-specific RMR than male pups throughout the fasting period. Fasting FMR was also significantly (t15=2.37, P<0.035) greater in females (823 kJ·kg−1·d−1) than males (686 kJ·kg−1·d−1). Average protein turnover during the study period was 19.3 g·d−1 and contributed to 5.4% of total energy expenditure, indicating the adoption of a protein-sparing strategy with a reliance on primarily lipid catabolism for metabolic energy. This is supported by observed decreases in plasma BUN, U/C, glucose and triglyceride concentrations, and an increase in β-HBA concentration, indicating that Antarctic fur seals pups adopt this strategy within 2–3 days of fasting. Mean RQ also decreased from 0.77 to 0.72 within 3 days of fasting, further supporting a rapid commencement of protein-sparing. However, RQ gradually increased thereafter to 0.77, suggesting a resumption of protein catabolism which was not substantiated by changes in plasma metabolites. Female pups had higher TBL (%) than males for any given mass, which is consistent with previous findings in this and other fur seal species, and suggests sex differences in metabolic fuel use. The observed changes in plasma metabolites and protein turnover, however, do not support this.

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Discharging the nutrient rich aquaculture effluents into inland water bodies and oceans is becoming a serious concern due to the adverse effect that brings in the form of eutrophication and subsequent damages to those waters. A laboratory scale biological reactor consisting of a denitrifying compartment followed by a submerged membrane bioreactor (SMBR) compartment was used to treat 40 L d−1 of aquaculture effluent with an average concentration of 74 mg L−1 nitrate (NO3 − ). Sugar was added to the aquaculture effluent in order that to enter into the denitrifying compartment at a carbon: nitrogen ratio (C:N) of 2:1 and 4:1. A hollow fibre membrane with a pore size of 0.4 μm and a filtration area of 0.20 m2 was used in the SMBR and was operated at an average flux of 0.20 m3 m−2 d−1. An intermittent suction period of 12 min followed by a relaxation period of 3 min was maintained in the SMBR throughout the experiment. Different aeration rates of 1, 3, 5 and 10 Lpm were applied to the SMBR to determine the rate of membrane fouling and 5 Lpm aeration rate was found to be optimum with respect to the rate of fouling of membrane at a C:N ratio of 4:1. The average rate of fouling at 1, 3, 5 and 10 Lpm were 1.17, 0.70, 0.48 and 0.52 kPa d−1, respectively. The increase in the rate of fouling when the aeration was increased from 5 to 10 Lpm may be due to the breakage of suspended particles into finer particles which could have increased the fouling of membrane. It was also found that increasing the C:N ratio from 2:1 to 4:1 resulted in more cake being formed on the membrane surface as well as an increase in the reduction of NO3 − from 64% to 78%. Preliminary calculations show that 2.4 to 3.2 g of suspended solids could be accumulated per square meter of membrane surface before physical cleaning of membrane is required (at a transmembrane pressure of 20 kPa).

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Purpose
As impaired glucose metabolism may arise progressively during childhood, we sought to determine whether the introduction of specialist-taught school physical education (PE) based on sound educational principles could improve insulin resistance (IR) in elementary school children.

Methods
In this 4-yr cluster-randomized intervention study, participants were 367 boys and 341 girls (mean age = 8.1 yr, SD = 0.35) initially in grade 2 in 29 elementary schools situated in suburbs of similar socioeconomic status. In 13 schools, 100 min·wk−1 of PE, usually conducted by general classroom teachers, was replaced with two classes per week taught by visiting specialist PE teachers; the remaining schools formed the control group. Teacher and pupil behavior were recorded, and measurements in grades 2, 4, and 6 included fasting blood glucose and insulin to calculate the homeostatic model of IR, percent body fat, physical activity, fitness, and pubertal development.

Results
On average, the intervention PE classes included more fitness work than the control PE classes (7 vs 1 min, P < 0.001) and more moderate physical activity (17 vs 10 min, P < 0.001). With no differences at baseline, by grade 6, the intervention had lowered IR by 14% (95% confidence interval = 1%–31%) in the boys and by 9% (95% confidence interval = 5%–26%) in the girls, and the percentage of children with IR greater than 3, a cutoff point for metabolic risk, was lower in the intervention than the control group (combined, 22% vs 31%, P = 0.03; boys, 12% vs 21%, P = 0.06; girls, 32% vs 40%, P = 0.05).

Conclusions
Specialist-taught primary school PE improved IR in community-based children, thereby offering a primordial preventative strategy that could be coordinated widely although a school-based approach.

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PURPOSE: To assess the impact of very hot (45°C) conditions on the performance of, and physiological responses to, a simulated firefighting manual-handling task compared to the same work in a temperate environment (18°C). METHODS: Ten male volunteer firefighters performed a 3-h protocol in both 18°C (CON) and 45°C (VH). Participants intermittently performed 12 × 1-min bouts of raking, 6 × 8-min bouts of low-intensity stepping, and 6 × 20-min rest periods. The area cleared during the raking task determined work performance. Core temperature, skin temperature, and heart rate were measured continuously. Participants also periodically rated their perceived exertion (RPE) and thermal sensation. Firefighters consumed water ad libitum. Urine specific gravity (USG) and changes in body mass determined hydration status. RESULTS: Firefighters raked 19% less debris during the VH condition. Core and skin temperature were 0.99 ± 0.20 and 5.45 ± 0.53°C higher, respectively, during the VH trial, and heart rate was 14-36 beats.min(-1) higher in the VH trial. Firefighters consumed 2950 ± 1034 mL of water in the VH condition, compared to 1290 ± 525 in the CON trial. Sweat losses were higher in the VH (1886 ± 474 mL) compared to the CON trial (462 ± 392 mL), though both groups were hydrated upon protocol completion (USG < 1.020). Participants' average RPE was higher in the VH (15.6 ± 0.9) compared to the CON trial (12.6 ± 0.9). Similarly, the firefighers' thermal sensation scores were significantly higher in the VH (6.4 ± 0.5) compared to the CON trial (4.4 ± 0.4). CONCLUSIONS: Despite the decreased work output and aggressive fluid replacement observed in the VH trial, firefighters' experienced increases in thermal stress, and exertion. Fire agencies should prioritize the health and safety of fire personnel in very hot temperatures, and consider the impact of reduced productivity on fire suppression efforts.

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Purpose. Glabridin is a major active constituent of Glycyrrhiza glabra which is commonly used in the treatment of cardiovascular and central nervous system (CNS) diseases. Recently, we have found that glabridin is a substrate of P-glycoprotein (PgP/MDR1). This study aimed to investigate the role of PgP in glabridin penetration across the blood–brain barrier (BBB) using several in vitro and in vivo models.
Materials and Methods. Cultured primary rat brain microvascular endothelial cells (RBMVECs) were used in the uptake, efflux and transcellular transport studies. A rat bilateral in situ brain perfusion model was used to investigate the brain distribution of glabridin. The brain and tissue distribution of glabridin in rats with or without coadministered verapamil or quinidine were examined with correction for the tissue residual blood. In addition, the brain distribution of glabridin in mdr1a(-/-) mice was compared with the wild-type mice. Glabridin in various biological matrices was determined by a validated liquid chromatography mass spectrometric method.
Results. The uptake and efflux of glabridin in cultured RBMVECs were ATP-dependent and significantly altered in the presence of a PgP or multi-drug resistance protein (Mrp1/2) inhibitor (e.g. verapamil or MK-571). A polarized transport of glabridin was found in RBMVEC monolayers with
facilitated efflux from the abluminal (BL) to luminal (AP) side. Addition of a PgP or Mrp1/2 inhibitor in both luminal and abluminal sides attenuated the polarized transport across RBMVECs. In a bilateral in situ brain perfusion model, the uptake of glabridin into the cerebrum increased from 0.42 T 0.09% at 1 min to 9.27 T 1.69% (ml/100 g tissue) at 30 min and was significantly greater than that for sucrose. Coperfusion of a PgP or Mrp1/2 inhibitor significantly increased the brain distribution of glabridin by 33.6j142.9%. The rat brain levels of glabridin were only about 27% of plasma levels when corrected by tissue residual blood and it was increased to up to 44% when verapamil or quinidine was coadministered. The area under the brain concentration-time curve (AUC) of glabridin in mdr1a(-/-) mice was 6.0-fold higher than the wild-type mice.
Conclusions. These findings indicate that PgP limits the brain penetration of glabridin through the BBB and PgP may cause drug resistance to glabridin (licorice) therapy for CNS diseases and potential drugglabridin interactions. However, further studies are needed to explore the role of other drug transporters (e.g. Mrp1-4) in restricting the brain penetration of glabridin.

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Cryptotanshinone (CTS), a major constituent from the roots of Salvia miltiorrhiza (Danshen), is widely used in the treatment of coronary heart disease, stroke and less commonly Alzheimer's disease. Our recent study indicates that CTS is a substrate for Pglycoprotein (PgP/MDR1/ABCB1). This study has investigated the nature of the brain distribution of CTS across the brain-blood barrier (BBB) using several in vitro and in vivo rodent models. A polarized transport of CTS was found in rat primary microvascular endothelial cell (RBMVEC) monolayers, with facilitated efflux from the abluminal side to luminal side. Addition of a PgP (e.g. verapamil and quinidine) or multi-drug resistance protein 1/2 (MRP1/2) inhibitor (e.g. probenecid and MK-571) in both luminal and abluminal sides attenuated the polarized transport. In a bilateral in situ brain perfusion model, the uptake of CTS into the cerebrum increased from 0.52 ± 0.1% at 1 min to 11.13 ± 2.36 ml/100 g tissue at 30 min and was significantly greater than that of sucrose. Co-perfusion of a PgP/MDR1 (e.g. verapamil) or MRP1/2 inhibitor (e.g. probenecid) significantly increased the brain distribution of CTS by 35.1-163.6%. The brain levels of CTS were only about 21% of those in plasma, and were significantly increased when coadministered with verapamil or probenecid in rats. The brain levels of CTS in rats subjected to middle cerebral artery occlusion and rats treated with quinolinic acid (a neurotoxin) were about 2- to 2.5-fold higher than the control rats. Moreover, the brain levels in mdr1a(-/-) and mrp1(-/-) mice were 10.9- and 1.5-fold higher than those in the wild-type mice, respectively. Taken collectively, these findings indicate that PgP and Mrp1 limit the brain penetration of CTS in rodents, suggesting a possible role of PgP and MRP1 in limiting the brain penetration of CTS in patients and causing drug resistance to Danshen therapy and interactions with conventional drugs that are substrates of PgP and MRP1. Further studies are needed to explore the role of other drug transporters in restricting the brain penetration of CTS and the clinical relevance.

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This study investigated the effect of reduced acetylcarnitine availability on oxidative metabolism during the transition from rest to steady-state exercise. Eight male subjects completed two randomised exercise trials at 68 % of the peak rate of O2 uptake (V̇O2,peak). On one occasion subjects ingested 1 g (kg body mass)−1 glucose 75 min prior to exercise (CHO), whereas the other trial acted as a control (CON). Muscle samples were obtained pre- and 75 min post-ingestion, and following 1 and 10 min of exercise. Plasma glucose and insulin were elevated (P < 0.05), and plasma free fatty acids (FFA) were lower at the onset of exercise in CHO. Acetylcarnitine (CON, 4.8 ± 1.8; CHO, 1.5 ± 0.9 mmol (kg dry mass (d.m.))−1, P < 0.05) and acetyl CoA (CON, 13.2 ± 2.3; CHO, 6.3 ± 0.6 μmol (kg d.m.)−1, P < 0.05) were lower at rest, whereas pyruvate dehydrogenase activation (PDHa) was greater in CHO compared with CON (CON, 0.78 ± 0.07; CHO, 1.44 ± 0.19 mmol min−1 (kg wet mass (w.m.))−1). Respiratory exchange ratio (RER) was significantly elevated during exercise in CHO. The acetyl groups increased at similar rates at the onset of exercise (1 min) and there was no difference in substrate phosphorylation as determined from lactate accumulation and phosphocreatine degradation between trials. Subsequently, oxidative metabolism during the transition from rest to steady-state exercise was not affected by prior carbohydrate ingestion. Although exercise resulted in the rapid activation of PDH in both trials, PDHa was greater at 1 min in CHO (CON, 2.36 ± 0.22; CHO, 2.91 ± 0.18 mmol min−1 (kg w.m.)−1). No differences in muscle metabolite levels and PDHa were observed after 10 min of moderate exercise between trials. In summary, at rest, carbohydrate ingestion induced multiple metabolic changes which included decreased acetylcarnitine availability and small increases in PDHa. The prior changes in PDHa and acetylcarnitine availability had no effect on substrate phosphorylation and oxidative metabolism at the onset of exercise. These data suggest that acetylcarnitine availability is unlikely to be the site of metabolic inertia during the transition from rest to steady-state moderate intensity exercise.

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µ-calpain and calpain-3 are Ca2+-dependent proteases found in skeletal muscle. Autolysis of calpains is observed using Western blot analysis as the cleaving of the full-length proteins to shorter products. Biochemical assays suggest that µ-calpain becomes proteolytically active in the presence of 2–200 µM Ca2+. Although calpain-3 is poorly understood, autolysis is thought to result in its activation, which is widely thought to occur at lower intracellular Ca2+ concentration levels ([Ca2+]i; ~1 µM) than the levels at which µ-calpain activation occurs. We have demonstrated the Ca2+-dependent autolysis of the calpains in human muscle samples and rat extensor digitorum longus (EDL) muscles homogenized in solutions mimicking the intracellular environment at various [Ca2+] levels (0, 2.5, 10, and 25 µM). Autolysis of calpain-3 was found to occur across a [Ca2+] range similar to that for µ-calpain, and both calpains displayed a seemingly higher Ca2+ sensitivity in human than in rat muscle homogenates, with ~15% autolysis observed after 1-min exposure to 2.5 µM Ca2+ in human muscle and almost none after 1- to 2-min exposure to the same [Ca2+]i level in rat muscle. During muscle activity, [Ca2+]i may transiently peak in the range found to autolyze µ-calpain and calpain-3, so we examined the effect of two types of exhaustive cycling exercise (30-s "all-out" cycling, n = 8; and 70% VO2 peak until fatigue, n = 3) on the amount of autolyzed µ-calpain or calpain-3 in human muscle. No significant autolysis of µ-calpain or calpain-3 occurred as a result of the exercise. These findings have shown that the time- and concentration-dependent changes in [Ca2+]i that occurred during concentric exercise fall near but below the level necessary to cause autolysis of calpains in vivo.

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The time sustained during a graded cycle exercise is ~10% longer in an upright compared with a supine posture. However, during constant-load cycling this effect is unknown. Therefore, we tested the postural effect on the performance of high-intensity constant-load cycling. Twenty-two active subjects (11 men, 11 women) performed two graded tests (one upright, one supine), and of those 22, 10 subjects (5 men, 5 women) performed three high-intensity constant-load tests (one upright, two supine). To test the postural effect on performance at the same absolute intensity, during the upright and one of the supine constant-load tests subjects cycled at 80% of the peak power output achieved during the upright graded test. To test the postural effect on performance at the same relative intensities, during the second supine test subjects cycled at 80% of the peak power output achieved during the supine graded test. Exercise time on the graded and absolute intensity constant-load tests for all subjects was greater (P<0.05) in the upright compared with supine posture (17.9±3.5 vs. 16.1±3.1 min for graded; 13.2±8.7 vs. 5.2±1.9 min for constant-load). This postural effect at the same absolute intensity was larger in men (19.4±8.5 upright vs. 6.6±1.6 supine, P<0.001) than women (7.1±2 upright vs. 3.9±1.4 supine, P>0.05) and it was correlated (P<0.05) with both the difference in VO2 between positions during the first minute of exercise (r=0.67) and the height of the subjects (r=0.72). In conclusion, there is a very large postural effect on performance during constant-load cycling exercise and this effect is significantly larger in men than women.

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Aims/hypothesis: The 5′-AMP-activated protein kinase (AMPK) pathway is intact in type 2 diabetic patients and is seen as a target for diabetes treatment. In this study, we aimed to assess the impact of the AMPK activator 5-aminoimidazole-4-carboxamide riboside (AICAR) on both glucose and fatty acid metabolism in vivo in type 2 diabetic patients.

Methods: Stable isotope methodology and blood and muscle biopsy sampling were applied to assess blood glucose and fatty acid kinetics following continuous i.v. infusion of AICAR (0.75 mg kg−1 min−1) and/or NaCl (0.9%) in ten male type 2 diabetic patients (age 64 ± 2 years; BMI 28 ± 1 kg/m2).
Results Plasma glucose rate of appearance (R a) was reduced following AICAR administration, while plasma glucose rate of disappearance (R d) was similar in the AICAR and control test. Consequently, blood glucose disposal (R d expressed as a percentage of R a) was increased following AICAR infusion (p < 0.001). Accordingly, a greater decline in plasma glucose concentration was observed following AICAR infusion (p < 0.001). Plasma NEFA R a and R d were both significantly reduced in response to AICAR infusion, and were accompanied by a significant decline in plasma NEFA concentration. Although AMPK phosphorylation in skeletal muscle was not increased, we observed a significant increase in acetyl-CoA carboxylase phosphorylation (p < 0.001).

Conclusions/interpretation
: The i.v. administration of AICAR reduces hepatic glucose output, thereby lowering blood glucose concentrations in vivo in type 2 diabetic patients. Furthermore, AICAR administration stimulates hepatic fatty acid oxidation and/or inhibits whole body lipolysis, thereby reducing plasma NEFA concentration.

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We have previously demonstrated that well-trained subjects who completed a 3 week training programme in which selected high-intensity interval training (HIT) sessions were commenced with low muscle glycogen content increased the maximal activities of several oxidative enzymes that promote endurance adaptations to a greater extent than subjects who began all training sessions with normal glycogen levels. The aim of the present study was to investigate acute skeletal muscle signalling responses to a single bout of HIT commenced with low or normal muscle glycogen stores in an attempt to elucidate potential mechanism(s) that might underlie our previous observations. Six endurance-trained cyclists/triathletes performed a 100 min ride at ∼70% peak O2 uptake (AT) on day 1 and HIT (8 × 5 min work bouts at maximal self-selected effort with 1 min rest) 24 h later (HIGH). Another six subjects, matched for fitness and training history, performed AT on day 1 then 1–2 h later, HIT (LOW). Muscle biopsies were taken before and after HIT. Muscle glycogen concentration was higher in HIGH versus LOW before the HIT (390 ± 28 versus 256 ± 67 μmol (g dry wt)−1). After HIT, glycogen levels were reduced in both groups (P < 0.05) but HIGH was elevated compared with LOW (229 ± 29 versus 124 ± 41 μmol (g dry wt)−1; P < 0.05). Phosphorylation of 5'AMP-activated protein kinase (AMPK) increased after HIT, but the magnitude of increase was greater in LOW (P < 0.05). Despite the augmented AMPK response in LOW after HIT, selected downstream AMPK substrates were similar between groups. Phosphorylation of p38 mitogen-activated protein kinase (p38 MAPK) was unchanged for both groups before and after the HIT training sessions. We conclude that despite a greater activation AMPK phosphorylation when HIT was commenced with low compared with normal muscle glycogen availability, the localization and phosphorylation state of selected downstream targets of AMPK were similar in response to the two interventions.

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Little research documents the contribution of upper limb and total body movement to energy expenditure (EE) during active video gaming. To address this, EE, heart rate (HR), and, upper limb and total body movement were assessed in 11- to 17-year-old adolescents whilst playing three active (Nintendo Wii) and one sedentary (XBOX 360) video games. Non-dominant upper limb activity, EE and HR were significantly greater during Wii Sports boxing [mean 267.2 (SD 115.8) J kg−1 min−1; 136.7 (24.5) beats min−1] than tennis or bowling (P ≤ 0.044). For all active games hip activity best predicted EE (R 2 ≥ 0.53), with two-measure models of HR and single-site activity data, and multi-site activity data, similarly explaining the variance in EE (R 2 ≥ 0.64). The physiological cost of upper-body orientated active video games increased when movement of both upper limbs was encouraged. Improvements in EE explanatory power provide support for multi-site activity monitoring during unique, non-ambulatory activities.