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Featured Application: This training regimen can be used as a time-efficient protocol for people with lower levels of aerobic fitness to kickstart their fitness journey. The training loads applied can be used as initial mesocycle loads for untrained participants, noting that, through effective periodization, the HITT intensities will periodically increase to provide an ongoing adaptive stimulus. Further, for aerobically trained individuals (>40 mL/kg/min), we suggest that this program be modified by increasing the prescribed training intensities to induce a sufficient stimulus to increase their baseline strength and aerobic parameters. An alternative use of this intervention is as a short (off-/pre-season) training regimen within sports clubs to boost strength and endurance parameters through a brief, but intense, time-efficient training approach. Finally, the described intervention could be implemented in occupational settings (e.g., fly-in–fly-out work camp labour workers in mines), where the benefit from incorporating a systematic training regimen, especially when the time devoted to exercise is limited, can lead to general health benefits. There is conflicting evidence on whether concurrent aerobic endurance and resistance training (RT) leads to synergistic enhancements in aerobic capacity and muscular strength or causes interference, limiting performance gains. We developed a concurrent training (CT) intervention, including full-body dynamic RT combined with high-intensity interval training (HIIT), on a cycle ergometer to determine whether a brief CT intervention is beneficial to both muscular strength and aerobic capacity. In an exploratory pilot study, participants (n = 10; male = 4) undertook a four-week CT intervention consisting of RT, including six compound movements (bench press, squat, deadlift, Pendley row, squat jumps, and rack pulls), plus cycle HIIT. The pre-/post-intervention improvements were assessed via bench press and leg press 3RM testing, an isometric mid-thigh pull, a countermovement jump, and the change in the relative V ˙ O2max. We observed significant (p < 0.1) increases in the bench press (6.4%), leg press (6.7%), IMTP (11.1%), and relative V ˙ O2max (7%) results. Interestingly, the participants with the highest pre-intervention relative V ˙ O2max demonstrated no performance improvements. These pilot test results suggest that CT is an effective strategy that enables synergistic enhancements that can be observed with very low training volumes. This suggests that CT is an effective strategy for improving muscular strength and aerobic endurance in non-elite physically active individuals. [ABSTRACT FROM AUTHOR]

In contrast to their exercise-trained counterparts, the maximal oxidative rate of skeletal muscle in sedentary humans appears not to benefit from supplemental O2 availability but is impacted by severe hypoxia, suggesting a metabolic limitation either at or below ambient [O.sub.2] levels. However, the critical level of [O.sub.2] availability at which maximal metabolic rate is reduced in sedentary humans is unknown. Using [sup.31]P magnetic resonance spectroscopy and arterial oximetry, phosphocreatine (PCr) recovery kinetics and arterial oxygenation were assessed in six sedentary subjects performing 5-min bouts of plantar flexion exercise followed by 6 min of recovery. Each trial was repeated while breathing one of four different fractions of inspired [O.sub.2] ([MATHEMATICAL EXPRESSION NOT REPRODUCIBLE IN ASCII]) (0.10, 0.12, 0.15, and 0.21). The PCr recovery rate constant (a marker of oxidative capacity) was unaffected by reductions in [MATHEMATICAL EXPRESSION NOT REPRODUCIBLE IN ASCII],remaining at a value of 1.5 [+ or -] 0.2 [min.sup.-1] until arterial [O.sub.2] saturation ([MATHEMATICAL EXPRESSION NOT REPRODUCIBLE IN ASCII]) fell to less than ~92%, the average value reached breathing an [MATHEMATICAL EXPRESSION NOT REPRODUCIBLE IN ASCII] of 0.15. Below this [MATHEMATICAL EXPRESSION NOT REPRODUCIBLE IN ASCII], the PCr rate constant fell significantly by 13 and 31% to 1.3 [+ or -] 0.2 and 1.0 [+ or -] 0.2 [min.sup.-1] (p < 0.05) as [MATHEMATICAL EXPRESSION NOT REPRODUCIBLE IN ASCII] was reduced to 82 [+ or -] 3 and 77 [+ or -] 2%, respectively. In conclusion, this study has revealed that [O.sub.2] availability does not impact maximal oxidative rate in sedentary humans until the [O.sub.2] level falls well below that of ambient air, indicating a metabolic limitation in normoxia. oxidative capacity; [sup.31]P-magnetic resonance spectroscopy; exercise

Aim: Complete arthrocentesis of the effusive knee ameliorates patient pain, reduces intra‐articular and intraosseous pressure, removes inflammatory cytokines, and has been shown to substantially improve the therapeutic outcomes of intra‐articular injections. However, conventional arthrocentesis incompletely decompresses the knee, leaving considerable residual synovial fluid in the intra‐articular space. The present study determined whether external pneumatic circumferential compression of the effusive knee permitted more successful arthrocentesis and complete joint decompression. Methods: Using a paired sample design, 50 consecutive effusive knees underwent conventional arthrocentesis and then arthrocentesis with pneumatic compression. Pneumatic compression was applied to the superior knee using a conventional thigh blood pressure cuff inflated to 100 mm Hg which compressed the suprapatellar bursa and patellofemoral joint, forcing fluid from the superior knee to the anterolateral portal where the fluid could be accessed. Arthrocentesis success and fluid yield in mL before and after pneumatic compression were determined. Results: Successful diagnostic arthrocentesis (≥3 mL) of the effusive knee was 82% (41/50) with conventional arthrocentesis and increased to 100% (50/50) with pneumatic compression (P =.001). Synovial fluid yields increased by 144% (19.8 ± 17.1 mL) with pneumatic compression (conventional arthrocentesis; 13.7 ± 16.4 mL, pneumatic compression: 33.4 ± 26.5 mL; 95% CI: 10.9 < 19.7 < 28.9 mL, P <.0001). Conclusions: Conventional arthrocentesis routinely does not fully decompress the effusive knee. External circumferential pneumatic compression markedly improves arthrocentesis success and fluid yield, and permits complete decompression of the effusive knee. Pneumatic compression of the effusive knee with a thigh blood pressure cuff is an inexpensive and widely available technique to improve arthrocentesis outcomes. [ABSTRACT FROM AUTHOR]

Strenuous exercise elicits transient functional and biochemical cardiac imbalances. Yet, the extent to which these responses are altered owing to aging is unclear. Accordingly, echocardiograph-derived left ventricular (LV) and right ventricular (RV) global longitudinal strain (GLS) and high-sensitivity cardiac troponin I (hs-cTnI) were assessed before (pre) and after (post) a 60-min high-intensity cycling race intervention (CRIT60) in 11 young (18-30 yr) and 11 middle-aged (40-65 yr) highly trained male cyclists, matched for cardiorespiratory fitness. LV and RV GLS were measured at rest and during a semirecumbent exercise challenge performed at the same intensity (young: 93 ± 10; middle-aged: 85 ± 11W, P = 0.60) pre- and post-CRIT60. Augmentation (change from rest-to-exercise challenge) of LV GLS (pre: -2.97 ± 0.65; post: -0.82 ± 0.48%, P = 0.02) and RV GLS (pre: -2.08 ± 1.28; post: 3.08 ± 2.02%, P = 0.01) was attenuated and completely abolished, in the young following CRIT60, while augmentation of LV GLS (pre: -3.21 ± 0.41; post: -3.99 ± 0.55%, P = 0.22) and RV GLS (pre: -3.47 ± 1.44; post: -1.26 ± 1.00%, P = 0.27) was preserved in middle-aged following CRIT60. While serum hs-cTnI concentration increased followingCRIT60 in the young (pre: 7.3 ± 1.6; post: 17.7 ± 1.6 ng/L, P < 0.01) and middle-aged (pre: 4.5 ± 0.6; post: 10.7 ± 2.0 ng/L, P < 0.01), serum hs-cTnI concentration increased to a greater extent in the young than in the middle-aged following CRIT60 (P < 0.01). These findings suggest that functional and biochemical cardiac perturbations induced by high-intensity exercise are attenuated in middle-aged relative to young individuals. Further study is warranted to determine whether acute exercise-induced cardiac perturbations alter the adaptive myocardial remodeling response. NEW & NOTEWORTHY High-intensity endurance exercise elicits acute cardiac imbalances that may be an important stimulus for adaptive cardiac remodeling. This study highlights that following a bout of high-intensity exercise that is typical of routine day-today cycling training, exercise-induced autonomic, biochemical, and functional cardiac imbalances are attenuated in middle-aged relative to young well-trained cyclists. These findings suggest that aging may alter exercise-induced stress stimulus response that initiates cardiac remodeling in athlete's heart. [ABSTRACT FROM AUTHOR]

Introduction/objectives: We hypothesized that mechanical compression of the knee in rheumatoid arthritis (RA) would mobilize occult extractable fluid and improve arthrocentesis success. Methods: Sixty-seven consecutive knees with RA and 186 knees with OA and were included. Conventional arthrocentesis was performed and success and volume (milliliters) determined; the needle was left intraarticularly, and mechanical compression was applied with an elastomeric knee brace. Arthrocentesis was then resumed until fluid return ceased. Fluid was characterized as to volume and cell counts. Results: In the RA, knee mechanical compression decreased failed diagnostic arthrocentesis from 56.7% (38/67) to 26.9% (18/67) (− 47.4%, p = 0.003) and increased absolute arthrocentesis yield from 4.7 ± 10.3 ml to 9.8 ± 9.8 ml (108% increase, 95% CI − 8.5 < − 5.1 < − 1.7 p = 0.0038). Total extractable fluid yield was 96% greater in RA (9.8 ± 9.8 ml) than OA (5.0 ± 9.4 ml, p = 0.0008), and occult extractable fluid was 77% greater in RA than OA (RA 5.3 ± 8.7 ml, OA 3.0 ± 5.5 ml, p = 0.046). Large effusions versus small effusions in RA demonstrated increased neutrophils in synovial fluid (p = 0.04) but no difference in radiologic arthritis grade (p = 0.87). In contrast, large effusions versus small effusions in OA demonstrated no difference in neutrophils in synovial fluid (p = 0.87) but significant different radiologic arthritis grade (p = 0.04). Conclusion: Mechanical compression improves the success of diagnostic and therapeutic knee arthrocentesis in both RA and OA. Large effusions in RA are associated with increased neutrophil counts but not arthritis grade; in contrast, large effusions in OA are associated with more severe arthritis grades but not increased neutrophil counts. Key points • Mechanical compression of the painful knee improves arthrocentesis success and fluid yield in both rheumatoid arthritis and osteoarthritis. • The painful rheumatoid knee contains approximately 100% more fluid than the osteoarthritic knee. • Large effusions in the osteoarthritic knee are characterized by higher grades of mechanical destruction but not increased neutrophil counts. • In contrast, large effusions in the rheumatoid knee are characterized by higher synovial fluid neutrophil counts but not the grade of mechanical destruction, indicating different mechanisms of effusion formation in rheumatoid arthritis versus osteoarthritis. [ABSTRACT FROM AUTHOR]

Aims Strenuous endurance exercise acutely increases myocardial wall stress and evokes transient functional cardiac perturbations. However, it is unclear whether exercise-induced functional cardiac disturbances are ubiquitous throughout the myocardium or are segment specific. The aim of this study was to examine the influence of high-intensity endurance exercise on global and segmental left (LV) and right (RV) ventricular tissue deformation (strain). Methods and results Echocardiography was used to measure strain in 23 active men (age: 28 ± 2 years; VO2 peak: 4.5 ± 0.7 L -1) at rest and during a standardized low-intensity exercise challenge, before and after a 90-min high-intensity endurance cycling intervention. Following the cycling intervention, LV and RV global strain decreased at rest (LV: -18.4 ± 0.4% vs. -17.7 ± 0.4%, P < 0.05; RV: -27.6 ± 0.7% vs. -26.4 ± 0.6%, P < 0.05) and by a greater extent during the low-intensity exercise challenge (LV: -21.3 ± 0.4% vs. -19.2 ± 0.5%, P < 0.01; RV: -28.4 ± 0.8% vs. -23.5 ± 0.9%, P < 0.01). Reductions in LV strain were unique to regions of RV attachment (e.g. LV septum: -24.4 ± 0.5% vs. -21.4 ± 0.6%, P < 0.01) with lateral (-18.9 ± 0.4% vs. -18.4 ± 0.5%) and posterior segments (-19.5 ± 0.4% vs. -18.8 ± 0.7%) unaffected. Similarly, augmentation of strain from rest to exercise was abolished in the RV free wall (-1.1 ± 1.0% vs. 2.9 ± 1.2%, P < 0.01), reduced in the septum (-4.6 ± 0.4% vs. -2.4 ± 0.5%, P < 0.01), and unchanged in the lateral (-1.2 ± 0.6% vs. -0.9 ± 0.6%) and posterior walls (-1.7 ± 0.6% vs. -1.3 ± 0.7%). Conclusion Changes in ventricular strain following high-intensity exercise are more profound in the right ventricle than in the left ventricle. Reductions in LV strain were unique to the septal myocardium and may reflect ventricular interactions secondary to exercise-induced RV dysfunction. [ABSTRACT FROM AUTHOR]

It remains incompletely understood whether there is an association between the transcriptome profiles of skeletal muscle and blood leukocytes in response to exercise or other physiological stressors. We have previously analyzed the changes in the muscle and blood neutrophil transcriptome in eight trained men before and 3, 48, and 96 h after 2 h cycling and running. Because we collected muscle and blood in the same individuals and under the same conditions, we were able to directly compare gene expression between the muscle and blood neutrophils. Applying weighted gene coexpression network analysis (WGCNA) as an advanced network-driven method to these original data sets enabled us to compare the muscle and neutrophil transcriptomes in a rigorous and systematic manner. Two gene networks were identified that were preserved between skeletal muscle and blood neutrophils, functionally related to mitochondria and posttranslational processes. Strong preservation measures (Zsummary > 10) for both muscle-neutrophil gene networks were evident within the postexercise recovery period. Muscle and neutrophil gene coexpression was strongly correlated in the mitochondria-related network (r = 0.97; P = 3.17E-2). We also identified multiple correlations between muscular gene subnetworks and exercise-induced changes in blood leukocyte counts, inflammation, and muscle damage markers. These data reveal previously unidentified gene coexpression between skeletal muscle and blood neutrophils following exercise, showing the value of WGCNA to understand exercise physiology. Furthermore, these findings provide preliminary evidence in support of the notion that blood neutrophil gene networks may potentially help us to track physiological and pathophysiological changes in the muscle. [ABSTRACT FROM AUTHOR]

BACKGROUND: The purpose of the present study was to investigate the effects of regular treadmill walking on plasma factors that increase low-shear blood viscosity and red blood cell aggregation in older women with type 2 diabetes. METHODS: Eighteen women with type 2 diabetes (age: 69±3 yr; body mass index: 30.5±5.0 kg·m-2) performed 12-wk of 120 min·wk-1 of supervised treadmill walking at an intensity equivalent to the gas-exchange threshold. Peak exercise values, anthropometry and blood indices of diabetic status, markers of inflammation, and plasma fibrinogen were analysed during a 6-wk pre-training 'control' period, and then after 6 and 12-wk of regular walking. RESULTS: Regular walking significantly increased peak oxygen uptake (p = 0.01). Body mass, waist to hip ratio, and glycaemic control did not change. Systolic and diastolic blood pressures decreased by 8.5% (p < 0.01) and 7.2% (p < 0.01) respectively, cholesterol to high-density lipoprotein (HDL) ratio decreased by 9.6% (p = 0.01), and HDL concentration significantly increased (p = 0.01). While 12 wk of regular walking did not significantly alter plasma concentrations of interleukin-6 (IL-6), tumour necrosis factorα, or C-reactive protein, plasma fibrinogen concentration decreased by 6.9% (p < 0.01) and plasma interleukin-10 (IL-10) concentration increased from 1.15±0.32 to 1.62±0.22 mmol·L-1 (p < 0.04). CONCLUSIONS: Improved plasma inflammatory profile and decreased plasma fibrinogen concentration is induced by regular walking, independent of glycaemic control. These factors may mediate the improved haemorheology associated with exercise training in metabolic disorders. [ABSTRACT FROM AUTHOR]

Polygenic profiling has been proposed for elite endurance performance, using an additive model determining the proportion of optimal alleles in endurance athletes. To investigate this model’s utility for elite triathletes, we genotyped seven polymorphisms previously associated with an endurance polygenic profile (ACE Ins/Del, ACTN3 Arg577Ter, AMPD1 Gln12Ter, CKMM 1170bp/985+185bp, HFE His63Asp, GDF8 Lys153Arg and PPARGC1A Gly482Ser) in a cohort of 196 elite athletes who participated in the 2008 Kona Ironman championship triathlon. Mean performance time (PT) was not significantly different in individual marker analysis. Age, sex, and continent of origin had a significant influence on PT and were adjusted for. Only the AMPD1 endurance-optimal Gln allele was found to be significantly associated with an improvement in PT (model p = 5.79 x 10−17, AMPD1 genotype p = 0.01). Individual genotypes were combined into a total genotype score (TGS); TGS distribution ranged from 28.6 to 92.9, concordant with prior studies in endurance athletes (mean±SD: 60.75±12.95). TGS distribution was shifted toward higher TGS in the top 10% of athletes, though the mean TGS was not significantly different (p = 0.164) and not significantly associated with PT even when adjusted for age, sex, and origin. Receiver operating characteristic curve analysis determined that TGS alone could not significantly predict athlete finishing time with discriminating sensitivity and specificity for three outcomes (less than median PT, less than mean PT, or in the top 10%), though models with the age, sex, continent of origin, and either TGS or AMPD1 genotype could. These results suggest three things: that more sophisticated genetic models may be necessary to accurately predict athlete finishing time in endurance events; that non-genetic factors such as training are hugely influential and should be included in genetic analyses to prevent confounding; and that large collaborations may be necessary to obtain sufficient sample sizes for powerful and complex analyses of endurance performance. [ABSTRACT FROM AUTHOR]

Transient reductions in myocardial strain coupled with cardiac-specific biomarker release have been reported following prolonged exercise (<180min). However, it is unknown if: a) shorter duration exercise (60min) can perturb cardiac function; or b) if exercise-induced reductions in strain are masked by hemodynamic changes that are associated with passive recovery from exercise. Left (LV) and right ventricular (RV) global longitudinal strain (GLS), LV torsion (LVT), and high-sensitivity cardiac troponin (hs-cTnT) were measured in fifteen competitive cyclists (Age: 28±3 yr; VO2peak: 4.8±0.6 L•min-1) before and after a 60-min high-intensity cycling race intervention (CRIT60). At both time points (pre- and post-CRIT60) strain and torsion were assessed at rest and during a standardized low-intensity exercise challenge (power output: 96±8 W) in a semi-recumbent position using echocardiography. During rest, hemodynamic conditions were different from pre- to post-CRIT60 (MAP: 96±1 vs 86±2 mmHg, p>0.001) and there were no changes in strain or torsion. In contrast, during the standardized low-intensity exercise challenge hemodynamic conditions were unchanged from pre- to post-CRIT60 (MAP: 98±1 vs 97±1 mmHg, ns), but strain decreased (LVGLS: -20.3±0.5% vs -18.5±0.4%, p>0.01; RVGLS: -26.4±1.6% vs -22.4±1.5%, p>0.05), while LVT remained unchanged. Serum hs-cTnT increased by 345% after the CRIT 60 (6.0±0.6 vs 20.7±6.9 ngL-1, p>0.05). This study demonstrates that exercise-induced functional and biochemical cardiac perturbations are not confined to ultra-endurance sporting events, and transpire during exercise that is typical of day-to-day training undertaken by endurance athletes. The clinical significance of cumulative exposure to endurance exercise warrants further study. [ABSTRACT FROM AUTHOR]

Reprogramming of gene expression is fundamental for skeletal muscle adaptations in response to endurance exercise. This study investigated the time course-dependent changes in the muscular transcriptome after an endurance exercise trial consisting of 1 h of intense cycling immediately followed by 1 h of intense running. Skeletal muscle samples were taken at baseline, 3 h, 48 h, and 96 h postexercise from eight healthy, endurance-trained men. RNA was extracted from muscle. Differential gene expression was evaluated using Illumina microarrays and validated with qPCR. Gene set enrichment analysis identified enriched molecular signatures chosen from the Molecular Signatures Database. Three hours postexercise, 102 gene sets were upregulated [family wise error rate (FWER), P < 0.05], including groups of genes related with leukocyte migration, immune and chaperone activation, and cyclic AMP responsive element binding protein (CREB) 1 signaling. Forty-eight hours postexercise, among 19 enriched gene sets (FWER, P < 0.05), two gene sets related to actin cytoskeleton remodeling were upregulated. Ninety-six hours postexercise, 83 gene sets were enriched (FWER, P < 0.05), 80 of which were upregulated, including gene groups related to chemokine signaling, cell stress management, and extracellular matrix remodeling. These data provide comprehensive insights into the molecular pathways involved in acute stress, recovery, and adaptive muscular responses to endurance exercise. The novel 96 h postexercise transcriptome indicates substantial transcriptional activity potentially associated with the prolonged presence of leukocytes in the muscles. This suggests that muscular recovery, from a transcriptional perspective, is incomplete 96 h after endurance exercise involving muscle damage. [ABSTRACT FROM AUTHOR]

Although phosphorus magnetic resonance spectroscopy (31P-MRS)-based evidence suggests that in vivo peak mitochondrial respiration rate in young untrained adults is limited by the intrinsic mitochondrial capacity of ATP synthesis, it remains unknown whether a large, locally targeted increase in convective O2 delivery would alter this interpretation. Consequently, we examined the effect of superimposing reactive hyperemia (RH), induced by a period of brief ischemia during the last minute of exercise, on oxygen delivery and mitochondrial function in the calf muscle of nine young adults compared with free-flow conditions (FF). To this aim, we used an integrative experimental approach combining 31P-MRS, Doppler ultrasound imaging, and near-infrared spectroscopy. Limb blood flow [area under the curve (AUC), 1.4 ± 0.8 liters in FF and 2.5 ± 0.3 liters in RH, P < 0.01] and convective O2 delivery (AUC, 0.30 ± 0.16 liters in FF and 0.54 ± 0.05 liters in RH, P < 0.01), were significantly increased in RH compared with FF. RH was also associated with significantly higher capillary blood flow (P < 0.05) and faster tissue reoxygenation mean response times (70 ± 15 s in FF and 24 ± 15 s in RH, P < 0.05). This resulted in a 43% increase in estimated peak mitochondrial ATP synthesis rate (29 ± 13 mM/min in FF and 41 ± 14 mM/min in RH, P < 0.05) whereas the phosphocreatine (PCr) recovery time constant in RH was not significantly different (P = 0.22). This comprehensive assessment of local skeletal muscle O2 availability and utilization in untrained subjects reveals that mitochondrial function, assessed in vivo by 31P-MRS, is limited by convective O2 delivery rather than an intrinsic mitochondrial limitation. [ABSTRACT FROM AUTHOR]

Neutrophils serve as an intriguing model for the study of innate immune cellular activity induced by physiological stress. We measured changes in the transcriptome of circulating neutrophils following an experimental exercise trial (EXTRI) consisting of 1 h of intense cycling immediately followed by 1 h of intense running. Blood samples were taken at baseline, 3 h, 48 h, and 96 h post-EXTRI from eight healthy, endurance-trained, male subjects. RNA was extracted from isolated neutrophils. Differential gene expression was evaluated using Illumina microarrays and validated with quantitative PCR. Gene set enrichment analysis identified enriched molecular signatures chosen from the Molecular Signatures Database. Blood concentrations of muscle damage indexes, neutrophils, interleukin (IL)-6 and IL-10 were increased (P < 0.05) 3 h post-EXTRI. Upregulated groups of functionally related genes 3 h post-EXTRI included gene sets associated with the recognition of tissue damage, the IL-1 receptor, and Toll-like receptor (TLR) pathways (familywise error rate, P value < 0.05). The core enrichment for these pathways included TLRs, lowaffinity immunoglobulin receptors, S100 calcium binding protein A12, and negative regulators of innate immunity, e.g., IL-1 receptor antagonist, and IL-1 receptor associated kinase-3. Plasma myoglobin changes correlated with neutrophil TLR4 gene expression (r - 0.74; P < 0.05). Neutrophils had returned to their nonactivated state 48 h post-EXTRI, indicating that their initial proinflammatory response was transient and rapidly counterregulated. This study provides novel insight into the signaling mechanisms underlying the neutrophil responses to endurance exercise, suggesting that their transcriptional activity was particularly induced by damage-associated molecule patterns, hypothetically originating from the leakage of muscle components into the circulation. [ABSTRACT FROM AUTHOR]

Heart rate variability (HRV) and haemorheology adaptations to 12 wk of varied-dose treadmill walking were investigated in women aged 65-74 yr with type 2 diabetes. Subjects were randomly allocated into two groups where exercise frequency and session duration were manipulated (Group 1 : 2 × 60 min·wk-1 or Group 2 : 4 × 30 min·wk-1), but intensity and accumulated weekly duration of exercise were consistent between groups (100% gas-exchange threshold; 120 min·wk-1). Twelve weeks of exercise training significantly improved peak oxygen uptake, time to exhaustion, and gas-exchange threshold (p < 0.05), independent of exercise group. Exercise training did not significantly change glycaemic control or body mass. Red blood cell (RBC) aggregation and RBC deformability significantly decreased (p < 0.05) for both groups. No change in HRV was observed for Group 1, whereas several key indicators of HRV were significantly improved in Group 2 (p < 0.05). The present study was the first to report decreased RBC aggregation following an exercise-only intervention and that exercise training improved RBC aggregation without a concomitant improvement in glycaemic control. The accumulated weekly exercise duration may be the most important training component for the prescription of exercise in older women with type 2 diabetes. [ABSTRACT FROM AUTHOR]

Exercise triggers hormesis, conditioning hearts against damaging consequences of subsequent ischemia- reperfusion (I/R). We test whether "low-stress" voluntary activity modifies I/R tolerance and molecular determinants of cardiac survival. Male C57BL/6 mice were provided 7-day access to locked (7SED) or rotating (7EX) running-wheels before analysis of cardiac prosurvival (Akt, ERK 1/2) and prodeath (GSK3β) kinases, transcriptomic adaptations, and functional tolerance of isolated hearts to 25-min ischemia/ 45-min reperfusion. Over 7 days, 7EX mice increased running from 2.1 ± 0.2 to 5.3 ± 0.3 km/day (mean speed 38 ± 2 m/min), with activity improving myocardial I/R tolerance: 7SED hearts recovered 43 ± 3% of ventricular force with diastolic contracture of 33 ± 3 mmHg, whereas 7EX hearts recovered 63 ± 5% of force with diastolic dysfunction reduced to 23 ± 2 mmHg (P < 0.05). Cytosolic expression (total protein) of Akt and GSK3β was unaltered, while ERK 1/2 increased 30% in 7EX vs. 7SED hearts. Phosphorylation of Akt and ERK 1/2 was unaltered, whereas GSK3β phosphorylation increased ~90%. Microarray interrogation identified significant changes (≥1.3-fold expression change, ≤5% FDR) in 142 known genes, the majority (92%) repressed. Significantly modified paths/ networks related to inflammatory/immune function (particularly interferon- dependent), together with cell movement, growth, and death. Of only 14 induced transcripts, 3 encoded interrelated sarcomeric proteins titin, α-actinin, and myomesin-2, while transcripts for protective actin-stabilizing ND1-L and activator of mitochondrial biogenesis ALAS1 were also induced. There was no transcriptional evidence of oxidative heat-shock or other canonical "stress" responses. These data demonstrate that relatively brief voluntary activity substantially improves cardiac ischemic tolerance, an effect independent of shifts in Akt, but associated with increased total ERK 1/2 and phospho-inhibition of GSK3β. Transcriptomic data implicate inflammatory/immune and sarcomeric modulation in activity-dependent protection. [ABSTRACT FROM AUTHOR]

Impaired metabolism in peripheral skeletal muscles potentially contributes to exercise intolerance in chronic obstructive pulmonary disease (COPD). We used 31P-magnetic resonance spectroscopy (31P-MRS) to examine the energy cost and skeletal muscle energetics in six patients with COPD during dynamic plantar flexion exercise compared with six well-matched healthy control subjects. Patients with COPD displayed a higher energy cost of muscle contraction compared with the controls (control: 6.1 ± 3.1% of rest·min-1·W-1, COPD: 13.6 ± 8.3% of rest·min-1·W-1, P = 0.01). Although, the initial phosphocreatine resynthesis rate was also significantly attenuated in patients with COPD compared with controls (control: 74 ± 17% of rest/min, COPD: 52 ± 13% of rest/min, P = 0.04), when scaled to power output, oxidative ATP synthesis was similar between groups (6.5 ± 2.3% of rest·min-1·W-1 in control and 7.8 ± 3.9% of rest·min-1·W-1 in COPD, P = 0.52). Therefore, our results reveal, for the first time that in a small subset of patients with COPD a higher ATP cost of muscle contraction may substantially contribute to the lower mechanical efficiency previously reported in this population. In addition, it appears that some patients with COPD have preserved mitochondrial function and normal energy supply in lower limb skeletal muscle. [ABSTRACT FROM AUTHOR]

Impaired heart rate variability (HRV)and haemorheology are independently associated with cardiovascular disease and diabetic complications. The aim of the present study was to investigate the relationships between parameters of HRV,and red blood cell (RBC) aggregation and deformability, in older women with type 2 diabetes. Twenty women (age 69 ± 2 yr) with uncomplicated type 2 diabetes and twenty controls (age 69 ± 3 yr) participated in the study. Beat-to-beat cardiac (RR) intervals over 5 min were analysed for HRV parameters in the time and frequency domains. Blood was sampled for RBC deformability, as well as RBC aggregation in two suspending mediums: haematocrit adjusted plasma and 3% dextran 70. RBC aggregation was increased and HRV was impaired for those with type 2 diabetes when compared with control. RBC aggregation was negatively related to low frequency power of HRV, and was positively related to high frequency power of HRV, for subjects with type 2 diabetes. RBC deformability was positively related to HRV only for those with type 2 diabetes. Impaired haemorheology is associated with reduced HRV in older women with type 2 diabetes, suggesting changes in the microcirculation may result in impaired modulation of cardiac cycles. [ABSTRACT FROM AUTHOR]

The contribution of respiratory muscle O2 uptake to the development of the slow component of O2 uptake kinetics is unclear. The aim of the present study was to examine the impact of respiratory muscle unloading (via breathing, a He–O2 mixture) on the amplitude of during exercise performed below (B-RCT) and above the respiratory compensation threshold (A-RCT). We hypothesized that breathing He–O2 would reduce the amplitude of the by a greater amount during exercise performed A-RCT than B-RCT. Eight healthy male recreational cyclists performed constant-load cycling in four sets of conditions: (1) B-RCT breathing normal air; (2) B-RCT breathing He–O2; (3) A-RCT breathing normal air; and (4) A-RCT breathing He–O2. Breathing He–O2 did not significantly attenuate the during exercise performed B-RCT (–3 ± 14%, P > 0.05). However, breathing He–O2 significantly reduced the during exercise A-RCT (–45 ± 6%, P < 0.05). The attenuated while breathing He–O2 is likely to reflect a decreased . Minute ventilation was not different between normal air and He–O2 breathing trials either B-RCT or A-RCT. However, operating lung volume was significantly lower when breathing He–O2 during exercise performed A-RCT (–12 ± 3%, P < 0.05). These findings suggest that comprises a greater proportion of the when exercise is performed A-RCT compared with B-RCT. Therefore, the impact of breathing He–O2 was more pronounced during exercise A-RCT. Furthermore, changes in operating lung volume and the work of breathing appear to play an important role in the development of the . [ABSTRACT FROM AUTHOR]

Several letters to the editor are presented in response to the article "In Health and in a Normoxic Environment, Vo2 maxmax Is/Is Not Limited Primarily By Cardiac Output and Locomotor Muscle Blood Flow," which appeared in the "Point: Counterpoint," section of the "Journal of Applied Physiology," in the February 2006 issue.

Previously, it was demonstrated in exercise-trained humans that phosphocreatine (PCr) recovery is significantly altered by fraction of inspired O2 (FIO2), suggesting that in this population under normoxic conditions, O2 availability limits maximal oxidative rate. Haseler LJ, Hogan ML, and Richardson RS. J Appl Physiol 86: 2013-2018, 1999. To further elucidate these population-specific limitations to metabolic rate, we used 31P-magnetic resonance spectroscopy to study the exercising human gastrocnemius muscle under conditions of varied FIO2 in sedentary subjects. To test the hypothesis that PCr recovery from submaximal exercise in sedentary subjects is not limited by O2 availability, but rather by their mitochondrial capacity, six sedentary subjects performed three bouts of 6-min steady-state submaximal plantar flexion exercise followed by 5 min of recovery while breathing three different FIO2 (0.10, 0.21, and 1.00). PCr recovery time constants were significantly longer in hypoxia (47.0 ± 3.2 s), but there was no difference between hyperoxia (31.8 ± 1.9 s) and normoxia (30.0 ± 2.1 s) (mean ± SE). End-exemise pH was not significantly different across treatments. These results suggest that the maximal muscle oxidative rate of these sedentary subjects, unlike their exercise-trained counterparts, is limited by mitochondrial capacity and not O2 availability in normoxia. Additionally, the significant elongation of PCr recovery in these subjects in hypoxia illustrates the reliance on O2 supply at the other end of the O2 availability spectrum in both sedentary and active populations. [ABSTRACT FROM AUTHOR]

31P-magnetic resonance spectroscopy was used to study phosphocreatine (PCr) onset kinetics in exercising human gastrocnemius muscle under varied fractions of inspired 02 (FIO2). Five male subjects performed three identical work bouts (5 min duration; order randomised) at a submaximal workload while breathing 0.1, 0.21 or 1.0 FIO2. Either a single or double exponential model was fitted to the PCr kinetics. The phase I τ (0.1, 38.6 ± 7.5; 0.21, 34.5 ± 7.9; 1.0, 38.6 ± 9.2 s) and amplitude, A1 (0.1, 0.34 ± 0.03; 0.21, 0.28 ± 0.05; 1.0, 0.28 ± 0.03,% fall in PCr) were invariant (both P > 0.05) across FIO2 trials. The initial rate of change in PCr hydrolysis at exercise onset, calculated as A1/τ1 (%PCr reduction s-1), was the same across FIO2 trials. A PCr slow component (phase II) was present at an FIO2 of 0.1 and 0.21; however, breathing 1.0 FIO2 ablated the slow component. The onset of the slow component resulted in a greater (P ≤ 0.05) overall percentage fall in PCr (both phase I and II) as FIO2 decreased (0.43 ± 0.05, 0.34 ± 0.05, 0.28 ± 0.03) for 0.1, 0.21 and 1.0 FIO2, respectively. These data demonstrate that altering FIO2 does not affect the initial phase I PCr onset kinetics, which supports the notion that O2 driving pressure does not limit PCr kinetics at the onset of submaximal exercise. Thus, these data imply that the manner in which microvascular and intracellular PO2 regulates PCr hydrolysis in exercising muscle is not due to the initial kinetic fall in PCr at exercise onset. [ABSTRACT FROM AUTHOR]