Efficacy of a web-based cognitive rehabilitation intervention for adult cancer survivors: A pilot study.

The purpose of this study was to evaluate the efficacy of a web-based cognitive rehabilitation intervention in survivors of adult-onset cancer and a sample of non-cancer community dwelling adults. Fifty-one participants were recruited and allocated to a cancer intervention group, a non-cancer intervention group, or a non-cancer waitlist group. Intervention groups completed a 4-week online program and all participants were assessed at baseline, post-intervention and 3-month follow-up. The primary outcome measure was subjective cognitive functioning. Secondary outcome measures included objective cognitive functioning, distress, quality of life (QoL), illness perception and program satisfaction. Results from the study found significant improvements on self-report measures of cognitive functioning in both treatment groups, as well as improvements on objective measures assessing attention and executive functioning. No intervention effects were observed for distress, QoL or illness perception. High participant satisfaction was observed with 75% of participants in the cancer group reporting being either "satisfied" or "very satisfied" with the program compared to 87% in the non-cancer treatment group. Initial evaluation of the program suggests that the web-based cognitive rehabilitation intervention shows potential for improving subjective and objective cognitive functioning in cancer survivors and community dwelling adults.

Health behaviour models and patient preferences regarding nutrition and physical activity after breast or prostate cancer diagnosis.

This study aimed to improve understanding of prostate and breast cancer survivors' physical activity and nutrition and the association of these behaviours with two models. The first model, the Commonsense Self-Regulation Model (CSM), addresses cognitive and emotional perceptions of illness whereas the Transtheoretical Model (TTM) focuses on stage of readiness to engage in a behaviour. Participants who had been diagnosed with either breast (n = 145) or prostate cancer (n = 92) completed measures of demographic and health information, illness representations, stage of change, self-efficacy and preferences regarding health behaviour interventions. Health behaviours in the past seven days were measured via the International Physical Activity Questionnaire and concordance with national dietary guidelines. As hypothesised, TTM variables (stage of change and self-efficacy) demonstrated independent associations with physical activity and nutrition in regression analyses. CSM variables were not independently associated with absolute levels of health behaviours but both TTM and CSM variables were independently associated with self-reported changes in physical activity and nutrition following prostate or breast cancer diagnosis. Many participants reported high interest in receiving lifestyle interventions, particularly soon after diagnosis. Results supported application of the TTM and CSM models for strengthening behaviour change intentions and actions in breast and prostate cancer survivors.

Muscle fatigue and excitation-contraction coupling responses following a session of prolonged cycling.

AIM: The mechanisms underlying the fatigue that occurs in human muscle following sustained activity are thought to reside in one or more of the excitation-contraction coupling (E-C coupling) processes. This study investigated the association between the changes in select E-C coupling properties and the impairment in force generation that occurs with prolonged cycling. METHODS: Ten volunteers with a peak aerobic power (VO(2peak)) of 2.95 ± 0.27 L min(-1) (mean ± SE), exercised for 2 h at 62 ± 1.3%. Quadriceps function was assessed and tissue properties (vastus lateralis) were measured prior to (E1-pre) and following (E1-post) exercise and on three consecutive days of recovery (R1, R2 and R3). RESULTS: While exercise failed to depress the maximal activity (V(max) ) of the Na(+) ,K(+) -ATPase (P = 0.10), reductions (P < 0.05) were found at E1-post in V(max) of sarcoplasmic reticulum Ca(2+) -ATPase (-22%), Ca(2+) -uptake (-26%) and phase 1(-33%) and 2 (-38%) Ca(2+) -release. Both V(max) and Ca(2+) -release (phase 2) recovered by R1, whereas Ca(2+) -uptake and Ca(2+) -release (phase 1) remained depressed (P < 0.05) at R1 and at R1 and R2 and possibly R3 (P < 0.06) respectively. Compared with E1-pre, fatigue was observed (P < 0.05) at 10 Hz electrical stimulation at E1-post (-56%), which persisted throughout recovery. The exercise increased (P < 0.05) overall content of the Na(+), K(+)-ATPase (R1, R2 and R3) and the isoforms ß2 (R1, R2 and R3) and ß3 (R3), but not ß1 or the α-isoforms (α1, α2 and α3). CONCLUSION: These results suggest a possible direct role for Ca(2+)-release in fatigue and demonstrate a single exercise session can induce overlapping perturbations and adaptations (particularly to the Na(+), K(+)-ATPase).

Muscle metabolic, enzymatic and transporter responses to a session of prolonged cycling.

A single session of prolonged work was employed to investigate changes in selected metabolic, transporter and enzymatic properties in muscle. Ten active but untrained volunteers (weight = 73.9 ± 4.2 kg) with a peak aerobic power [Formula: see text] of 2.95 ± 0.27 l min(-1), cycled for 2 h at 62 ± 1.3% [Formula: see text] Tissue extraction from the vastus lateralis occurred prior to (E1-Pre) and following (E1-Post) exercise and on 3 consecutive days of recovery (R1, R2, R3). The exercise resulted in decreases (P < 0.05) in ATP (-9.3%) and creatine phosphate (-49%) and increases in lactate (+100%), calculated free ADP (+253%) and free AMP (+1,207%), all of which recovered to E1-Pre by R1. Glycogen concentration, which was depressed (P < 0.05) by 75% at E1-Post, did not recover until R3. Compared to E1-Pre, the cycling also resulted in decreases (P < 0.05) in the activities of cytochrome c oxidase, phosphorylase, and hexokinase but not in citrate synthase (CS) or 3-hydroxy-CoA dehydrogenase at E1-Post. With the exception of CS, which was elevated (P < 0.05) at R3, all enzyme activities were not different from E1-Pre during recovery. For the glucose (GLUT1, GLUT4) and monocarboxylate (MCT1, MCT4) transporters, changes in expression levels (P < 0.05) were only observed for GLUT1 at R1 (+42%) and R3 (+33%). It is concluded that the metabolic stress produced by prolonged exercise is reversed by 1 day of recovery. One day of exercise also resulted in a potential upregulation in the citric acid cycle and glucose transport capabilities, adaptations which are expressed at variable recovery durations.

Coping in men with prostate cancer and their partners: a quantitative and qualitative study.

This study investigated coping and quality of life in men with prostate cancer (n= 105, 48-86 years of age) and their partners (n= 85, 48-84 years). Participants completed the Abbreviated Dyadic Adjustment Scale, Brief COPE, European Organisation for Research and Treatment of Cancer Core Quality of Life Questionnaire (QLQ-C30) and open-ended questions on appraisal and coping. Multivariate analyses showed that better quality of life was associated with higher education levels (role functioning and fatigue), lower avoidant coping (emotional, social, and physical functioning and fatigue), and higher relationship satisfaction (emotional functioning). Use of medication or combined treatments was associated with worse physical and role functioning. Partners reported similar quality of life for patients as the patient ratings, except that partners reported patients' emotional functioning as significantly worse and social functioning as significantly better than the patients' own ratings. Patients and partners reported both positive and negative aspects to prostate cancer, and mentioned a range of coping strategies. Similarities between patients and partners in their responses to prostate cancer were identified using both quantitative and qualitative methods. Some differences within dyads were also noted and previous suggestions to incorporate partners and significant others in education and treatment were supported.

Metabolic adaptations of oxidative muscle during spawning migration in the Atlantic salmon Salmo salar L.

The adaptability/plasticity of the highly oxidative red muscle in Atlantic salmon was demonstrated during spawning migration. Substrate concentrations and the enzymatic pathways of ATP production were examined in red muscle obtained from Atlantic salmon at different sites along their migratory route in the Exploits River, Newfoundland, Canada. Individuals were chronologically sampled from a seawater site, two sites upstream, and at spawning. The 20% decrease in salmon body weight during the later stages of migration was accompanied by large decreases (mg dry weight(-1)) in both glycogen (P < 0.01) and total muscle lipid (P < 0.01). In contrast, water content and protein concentration (mg dry weight(-1)) of the red muscle increased by 25 and 34%, respectively, at spawning. Enzymes of the glycolytic pathways demonstrated a significant (P < 0.001) decrease in maximal activity as migration proceeded whereas enzymes of the oxidative phosphorylation pathways, specifically the citric acid cycle enzymes, exhibited an increase (P < 0.001) in maximal activity at spawning. The antioxidant enzyme superoxide dismutase also demonstrated an increase (P < 0.001) in maximal activity during the latter stages of migration. These adaptations imply that the red epaxial muscle of Atlantic salmon has a more efficient means of oxidizing lipids, while minimizing free radical damage, during the later stages of migration and spawning, thereby potentially increasing post spawning survival.

Time-dependent effects of short-term training on muscle metabolism during the early phase of exercise.

In this study, we investigated the hypothesis that the metabolic adaptations observed during steady-state exercise soon after the onset of training would be displayed during the nonsteady period of moderate exercise and would occur in the absence of increases in peak aerobic power (Vo2peak) and in muscle oxidative potential. Nine untrained males [age = 20.8 +/- 0.70 (SE) yr] performed a cycle task at 62% Vo2peak before (Pre-T) and after (Post-T) training for 2 h/day for 5 days at task intensity. Tissue samples extracted from the vastus lateralis at 0 min (before exercise) and at 10, 60, and 180 s of exercise, indicated that at Pre-T, reductions (P < 0.05) in phosphocreatine and increases (P < 0.05) in creatine, inorganic phosphate, calculated free ADP, and free AMP occurred at 60 and 180 s but not at 10 s. At Post-T, the concentrations of all metabolites were blunted (P < 0.05) at 60 s. Training also reduced (P < 0.05) the increase in lactate and the lactate-to-pyruvate ratio observed during exercise at Pre-T. These adaptations occurred in the absence of change in Vo2peak (47.8 +/- 1.7 vs. 49.2 +/- 1.7 mlxkg(-1)xmin(-1)) and in the activities (molxkg protein(-1)xh(-1)) of succinic dehydrogenase (3.48 +/- 0.21 vs. 3.77 +/- 0.35) and citrate synthase (7.48 +/- 0.61 vs. 8.52 +/- 0.65) but not cytochrome oxidase (70.8 +/- 5.1 vs. 79.6 +/- 6.6 U/g protein; P < 0.05). It is concluded that the tighter metabolic control observed following short-term training is initially expressed during the nonsteady state, probably as a result of increases in oxidative phosphorylation that is not dependent on changes in Vo2peak while the role of oxidative potential remains uncertain.

Failure of hypoxia to exaggerate the metabolic stress in working muscle following short-term training.

This study investigated the effects of hypoxia (experiment 1) and the effects of hypoxia following short-term training (experiment 2) on metabolism in working muscle. In experiment 1, eight males with a peak aerobic power (VO2peak) of 45 +/- 1.7 ml x kg(-1) x min(-1) (x +/- SE) cycled for 15 min at 66.1 +/- 2.1% VO2peak while breathing room air [normoxia (N)] or 14% O(2) [hypoxia (H)]. In experiment 2, nine males with a VO2peak of 43.3 +/- 1.6 ml x kg(-1) x min(-1) performed a similar protocol at 60.7 +/- 1.4% VO2peak during N and during H following 5 days of submaximal exercise training (H + T). Tissue samples extracted from the vastus lateralis before exercise and at 1, 3, and 15 min of exercise indicated that compared with N, H resulted in lower (P < 0.05) concentrations (mmol/kg dry wt) of creatine phosphate and higher (P < 0.05) concentrations of creatine, inorganic phosphate, and lactate, regardless of exercise time. When the exercise was performed at H + T and compared with N, no differences were observed in creatine phosphate, creatine, inorganic phosphate, and lactate, regardless of duration. Given the well-documented effects of the short-term training model on elevating VO2 kinetics and attenuating the alterations in high-energy phosphate metabolism and lactate accumulation, it would appear that the mechanism underlying the reversal of these adaptations during H is linked to a more rapid increase in oxidative phosphorylation, mediated by increased oxygen delivery and/or mitochondrial activation.

Altered metabolic and transporter characteristics of vastus lateralis in chronic obstructive pulmonary disease.

To investigate energy metabolic and transporter characteristics in resting muscle of patients with moderate to severe chronic obstructive pulmonary disease [COPD; forced expiratory volume in 1 s (FEV(1)) = 42 +/- 6.0% (mean +/- SE)], tissue was extracted from resting vastus lateralis (VL) of 9 COPD patients and compared with that of 12 healthy control subjects (FEV(1) = 114 +/- 3.4%). Compared with controls, lower (P < 0.05) concentrations (mmol/kg dry wt) of ATP (19.6 +/- 0.65 vs. 17.8 +/- 0.69) and phosphocreatine (81.3 +/- 2.3 vs. 69.1 +/- 4.2) were observed in COPD, which occurred in the absence of differences in the total adenine nucleotide and total creatine pools. Higher concentrations were observed in COPD for several glycolytic metabolites (glucose-1-phosphate, glucose-6-phosphate, fructose-6-phosphate, pyruvate) but not lactate. Glycogen storage was not affected by the disease (289 +/- 20 vs. 269 +/- 20 mmol glucosyl units/kg dry wt). Although no difference between groups was observed for the glucose transporter GLUT1, GLUT4 was reduced by 28% in COPD. For the monocarboxylate transporters, MCT4 was 35% lower in COPD, with no differences observed for MCT1. These results indicate that in resting VL, moderate to severe COPD results in a reduction in phosphorylation potential, an apparent elevation of glycolytic flux rate, and a potential defect in glucose and lactate transport as a result of reduced levels of the principal isoforms.

Abnormal sarcoplasmic reticulum Ca2+-sequestering properties in skeletal muscle in chronic obstructive pulmonary disease.

The objective of this study was to investigate the hypothesis that alterations in sarcoplasmic reticulum (SR) Ca(2+)-cycling properties would occur in skeletal muscle in patients with moderate to severe chronic obstructive pulmonary disease (COPD). To investigate this hypothesis, tissue samples were obtained from the vastus lateralis of 8 patients with COPD [age 65.6 +/- 3.2 yr; forced expiratory volume in 1 s (FEV(1))/forced vital capacity (FVC) = 44 +/- 2%; mean +/- SE] and 10 healthy age-matched controls (CON, age 67.5 +/- 2.5 yr; FEV(1)/FVC = 77 +/- 2%), and homogenates were analyzed for a wide range of SR properties. Compared with CON, COPD displayed (in mumol.g protein(-1).min(-1)) a 16% lower maximal Ca(2+)-ATPase activity [maximal velocity (V(max)), 158 +/- 10 vs. 133 +/- 7, P < 0.05] and a 17% lower Ca(2+) uptake (4.65 +/- 0.039 vs. 3.85 +/- 0.26, P < 0.05) that occurred in the absence of differences in Ca(2+) release. The lower V(max) in COPD was also accompanied by an 11% lower (P < 0.05) Ca(2+) sensitivity, as measured by the Hill coefficient (defined as the relationship between Ca(2+)-ATPase activity and free cytosolic Ca(2+) concentration for 10-90% V(max)). For the sarco(endo)plasmic reticulum Ca(2+)-ATPase (SERCA) isoforms, SERCA1a was 16% higher (P < 0.05) and SERCA2a was 14% lower (P < 0.05) in COPD. It is concluded that moderate to severe COPD results in abnormalities in SR Ca(2+)-ATPase properties that cannot be explained by changes in the SERCA isoform phenotypes. The reduced catalytic properties of SERCA in COPD suggest a disturbance in Ca(2+) cycling, possibly resulting in impairment in Ca(2+)-mediated mechanical function and/or second messenger regulated processes.

Acute responses in muscle mitochondrial and cytosolic enzyme activities during heavy intermittent exercise.

To examine the effects of repetitive bouts of heavy exercise on the maximal activities of enzymes representative of the major metabolic pathways and segments, 13 untrained volunteers [peak aerobic power (Vo(2 peak)) = 44.3 +/- 2.3 ml.kg(-1).min(-1)] cycled at approximately 91% Vo(2 peak) for 6 min once per hour for 16 h. Maximal enzyme activities (V(max), mol.kg(-1).protein.h(-1)) were measured in homogenates from tissue extracted from the vastus lateralis before and after exercise at repetitions 1 (R1), 2 (R2), 9 (R9), and 16 (R16). For the mitochondrial enzymes, exercise resulted in reductions (P < 0.05) in cytochrome-c oxidase (COX, 14.6%), near significant reductions in malate dehydrogenase (4.06%; P = 0.06) and succinic dehydrogenase (4.82%; P = 0.09), near significant increases in beta-hydroxyacyl-CoA dehydrogenase (4.94%; P = 0.08), and no change in citrate synthase (CS, 2.88%; P = 0.37). For the cytosolic enzymes, exercise reduced (P < 0.05) V(max) in hexokinase (Hex, 4.4%), creatine phosphokinase (9.0%), total phosphorylase (13.5%), phosphofructokinase (16.6%), pyruvate kinase (PK, 14.1%) and lactate dehydrogenase (10.7%). Repetition-dependent reductions (P < 0.05) in V(max) were observed for CS (R1, R2 > R16), COX (R1, R2 > R16), Hex (1R, 2R > R16), and PK (R9 > R16). It is concluded that heavy exercise results in transient reductions in a wide range of enzymes involved in different metabolic functions and that in the case of selected enzymes, multiple repetitions of the exercise reduce average V(max).

Dissociation between changes in muscle Na+-K+-ATPase isoform abundance and activity with consecutive days of exercise and recovery.

The early plasticity of vastus lateralis Na(+)-K(+)-ATPase to the abrupt onset of prolonged submaximal cycling was studied in 12 untrained participants (Vo(2 peak) 44.8 +/- 2.0 ml x kg(-1) x min(-1), mean +/- SE) using a 6-day protocol (3 days of exercise plus 3 days of recovery). Tissue samples were extracted prior to (Pre) and following exercise (Post) on day 1 (E1) and day 3 (E3) and on each day of recovery (R1, R2, R3) and analyzed for changes in maximal protein (beta(max)) (vanadate-facilitated [(3)H]ouabain binding), alpha- and beta-isoform concentration (quantitative immunoblotting) and maximal Na(+)-K(+)-ATPase activity (V(max)) (3-O-methylfluorescein K(+)-stimulated phosphatase assay). For beta(max) (pmol/g wet wt), an increase (P < 0.05) of 11.8% was observed at R1 compared with E1-Pre (340 +/- 14 vs 304 +/- 17). For the alpha-isoforms alpha(1), alpha(2), and alpha(3), increases (P < 0.05) of 46, 42, and 31% were observed at R1, respectively. For the beta-isoform, beta(1) and beta(2) increased (P < 0.05) by 19 and 28% at R1, whereas beta(3) increased (P < 0.05) by 18% at R2. With the exception of alpha(2) and alpha(3), the increases in the isoforms persisted at R3. Exercise resulted in an average decrease (P < 0.05) in V(max) by 14.3%. No differences were observed in V(max) at E1 - Pre and E3 - Pre or between R1, R2, and R3. It is concluded that 3 days of prolonged exercise is a powerful stimulus for the rapid upregulation of the Na(+)-K(+)-ATPase subunit isoforms. Contrary to our hypothesis, the increase in subunit expression is not accompanied by increases in the maximal catalytic activity.

Rapid upregulation of GLUT-4 and MCT-4 expression during 16 h of heavy intermittent cycle exercise.

In this study, we have investigated the hypothesis that an exercise protocol designed to repeatedly induce a large dependence on carbohydrate and large increases in glycolytic flux rate would result in rapid increases in the principal glucose and lactate transporters in working muscle, glucose transporter (GLUT)-4 and monocarboxylate transporter (MCT)4, respectively, and in activity of hexokinase (Hex), the enzyme used to phosphorylate glucose. Transporter abundance and Hex activity were assessed in homogenates by Western blotting and quantitative chemiluminescence and fluorometric techniques, respectively, in samples of tissue obtained from the vastus lateralis in 12 untrained volunteers [peak aerobic power (.VO(2peak)) = 44.3 +/- 2.3 ml.kg(-1).min(-1)] before cycle exercise at repetitions 1 (R1), 2 (R2), 9 (R9), and 16 (R16). The 16 repetitions of the exercise were performed for 6 min at approximately 90% .VO(2peak), once per hour. Compared with R1, GLUT-4 increased (P < 0.05) by 28% at R2 and remained elevated (P < 0.05) at R9 and R16. For MCT-4, increases (P < 0.05) of 24% were first observed at R9 and persisted at R16. No changes were observed in GLUT-1 and MCT-1 or in Hex activity. The approximately 17- to 24-fold increase (P < 0.05) in muscle lactate observed at R1 and R2 was reduced (P < 0.05) to an 11-fold increase at R9 and R16. It is concluded that an exercise protocol designed to strain muscle carbohydrate reserves and to result in large increases in lactic acid results in a rapid upregulation of both GLUT-4 and MCT-4.

Muscle metabolic, SR Ca(2+) -cycling responses to prolonged cycling, with and without glucose supplementation.

This study investigated the effects of prolonged exercise, with and without glucose supplementation, on metabolism and sarcoplasmic reticulum (SR) Ca(2+)-handling properties in working vastus lateralis muscle. Fifteen untrained volunteers [peak O(2) consumption (Vo(2peak)) = 3.45 +/- 0.17 l/min; mean +/- SE] cycled at approximately 60% Vo(2peak) on two occasions, during which they were provided with either an artificially sweetened placebo beverage (NG) or a 6% glucose (G) beverage (~1.00 g carbohydrate/kg body mass). Beverage supplementation started at 30 min of exercise and continued every 15 min thereafter. SR Ca(2+) handling, metabolic, and substrate responses were assessed in tissue extracted from the vastus lateralis at rest, after 30 min and 90 min of exercise, and at fatigue in both conditions. Plasma glucose during G was 15-23% higher (P < 0.05) than those observed during NG following 60 min of exercise until fatigue. Cycle time to fatigue was increased (P < 0.05) by approximately 19% during G (137 +/- 7 min) compared with NG (115 +/- 6 min). Prolonged exercise reduced (P < 0.05) maximal Ca(2+)-ATPase activity (-18.4%), SR Ca(2+) uptake (-27%), and both Phase 1 (-22.2%) and Phase 2 (-34.2%) Ca(2+)-release rates during NG. The exercise-induced reductions in SR Ca(2+)-cycling properties were not altered during G. The metabolic responses to exercise were all unaltered by glucose supplementation, since no differences in respiratory exchange ratios, carbohydrate and lipid oxidation rates, and muscle metabolite and glycogen contents were observed between NG and G. These results indicate that the maintenance of blood glucose homeostasis by glucose supplementation is without effect in modifying the muscle metabolic, endogenous glycogen, or SR Ca(2+)-handling responses.

Muscle metabolic responses during 16 hours of intermittent heavy exercise.

The alterations in muscle metabolism were investigated in response to repeated sessions of heavy intermittent exercise performed over 16 h. Tissue samples were extracted from the vastus lateralis muscle before (B) and after (A) 6 min of cycling at approximately 91% peak aerobic power at repetitions one (R1), two (R2), nine (R9), and sixteen (R16) in 13 untrained volunteers (peak aerobic power = 44.3 +/- 0.66 mL.kg-1.min-1, mean +/- SE). Metabolite content (mmol.(kg dry mass)-1) in homogenates at R1 indicated decreases (p < 0.05) in ATP (21.9 +/- 0.62 vs. 17.7 +/- 0.68) and phosphocreatine (80.3 +/- 2.0 vs. 8.56 +/- 1.5) and increases (p < 0.05) in inosine monophosphate (IMP, 0.077 +/- 0.12 vs. 3.63 +/- 0.85) and lactate (3.80 +/- 0.57 vs. 84.6 +/- 10.3). The content (micromol.(kg dry mass)-1) of calculated free ADP ([ADPf], 86.4 +/- 5.5 vs. 1014 +/- 237) and free AMP ([AMPf], 0.32 +/- 0.03 vs. 78.4 +/- 31) also increased (p < 0.05). No differences were observed between R1 and R2. By R9 and continuing to R16, pronounced reductions (p < 0.05) at A were observed in IMP (72.2%), [ADPf] (58.7%), [AMPf] (85.5%), and lactate (41.3%). The 16-hour protocol resulted in an 89.7% depletion (p < 0.05) of muscle glycogen. Repetition-dependent increases were also observed in oxygen consumption during exercise. It is concluded that repetitive heavy exercise results in less of a disturbance in phosphorylation potential, possibly as a result of increased mitochondrial respiration during the rest-to-work non-steady-state transition.

Muscle sarcoplasmic reticulum calcium regulation in humans during consecutive days of exercise and recovery.

The study investigated the hypothesis that three consecutive days of prolonged cycle exercise would result in a sustained reduction in the Ca(2+)-cycling properties of the vastus lateralis in the absence of changes in the sarcoplasmic (endoplasmic) reticulum Ca(2+)-ATPase (SERCA) protein. Tissue samples were obtained at preexercise (Pre) and postexercise (Post) on day 1 (E1) and day 3 (E3) and during recovery day 1 (R1), day 2 (R2), and day 3 (R3) in 12 active but untrained volunteers (age 19.2 +/- 0.27 yr; mean +/- SE) and analyzed for changes (nmol.mg protein(-1).min(-1)) in maximal Ca(2+)-ATPase activity (V(max)), Ca(2+) uptake and Ca(2+) release (phase 1 and phase 2), and SERCA isoform expression (SERCA1a and SERCA2a). At E1, reductions (P < 0.05) from Pre to Post in V(max) (150 +/- 7 vs. 121 +/- 7), Ca(2+) uptake (7.79 +/- 0.28 vs. 5.71 +/- 0.33), and both phases of Ca(2+) release (phase 1, 20.3 +/- 1.3 vs. 15.2 +/- 1.1; phase 2, 7.70 +/- 0.60 vs. 4.99 +/- 0.48) were found. In contrast to V(max), which recovered at Pre E3 and then remained stable at Post E3 and throughout recovery, Ca(2+) uptake remained depressed (P < 0.05) at E3 Pre and Post and at R1 as did phase 2 of Ca(2+) release. Exercise resulted in an increase (P < 0.05) in SERCA1a (14% at R2) but not SERCA2a. It is concluded that rapidly adapting mechanisms protect V(max) following the onset of regular exercise but not Ca(2+) uptake and Ca(2+) release.

Muscle Na+-K+-ATPase response during 16 h of heavy intermittent cycle exercise.

This study investigated the effects of a 16-h protocol of heavy intermittent exercise on the intrinsic activity and protein and isoform content of skeletal muscle Na(+)-K(+)-ATPase. The protocol consisted of 6 min of exercise performed once per hour at approximately 91% peak aerobic power (Vo(2 peak)) with tissue sampling from vastus lateralis before (B) and immediately after repetitions 1 (R1), 2 (R2), 9 (R9), and 16 (R16). Eleven untrained volunteers with a Vo(2 peak) of 44.3 +/- 2.3 ml x kg(-1) x min(-1) participated in the study. Maximal Na(+)-K(+)-ATPase activity (V(max), in nmol x mg protein(-1) x h(-1)) as measured by the 3-O-methylfluorescein K(+)-stimulated phosphatase assay was reduced (P < 0.05) by approximately 15% with exercise regardless of the number of repetitions performed. In addition, V(max) at R9 and R16 was lower (P < 0.05) than at R1 and R2. Vanadate-facilitated [(3)H]ouabain determination of Na(+)-K(+)-ATPase content (maximum binding capacity, pmol/g wet wt), although unaltered by exercise, increased (P < 0.05) 8.3% by R9 with no further increase observed at R16. Assessment of relative changes in isoform abundance measured at B as determined by quantitative immunoblotting showed a 26% increase (P < 0.05) in the alpha(2)-isoform by R2 and a 29% increase in alpha(3) by R9. At R16, beta(3) was lower (P < 0.05) than at R2 and R9. No changes were observed in alpha(1), beta(1), or beta(2). It is concluded that repeated sessions of heavy exercise, although resulting in increases in the alpha(2)- and alpha(3)-isoforms and decreases in beta(3)-isoform, also result in depression in maximal catalytic activity.

Protection of muscle membrane excitability during prolonged cycle exercise with glucose supplementation.

To determine if exercise-induced depressions in neuromuscular function are altered with oral glucose supplementation, 15 untrained participants (Vo2 peak = 45 +/- 2 ml x kg(-1) x min(-1), mean +/- SE) performed prolonged cycle exercise at approximately 60% Vo2 peak on two occasions: without glucose supplementation (NG) and with oral glucose supplementation (G). The oral G began at 30 min of exercise and was administered every 15 min (total ingested = 1.23 +/- 0.11 g carbohydrate/kg body mass). Quadriceps isometric properties and membrane excitability were assessed prior to exercise, after 90 min of exercise, and at fatigue. Cycle time to fatigue was greater (P < 0.05) in G compared with NG (137 +/- 7 vs. 115 +/- 6 min). Progressive reductions (P < 0.05) in maximal voluntary contraction (MVC, N) were observed for NG at 90 min (441 +/- 29) and at fatigue (344 +/- 33) compared with pre-exercise (666 +/- 30). At fatigue in G, the reduction in MVC was not as pronounced (P < 0.05) as in NG. Motor unit activation assessed with the interpolated twitch technique during an MVC following exercise was not different between conditions. During cycling, the G condition also resulted in a higher (P < 0.05) muscle compound potential (M-wave) amplitude (mV) at both 90 min (+50%) and at fatigue (+87%) compared with NG. Similar effects were also found M-wave area (mV/ms). These results suggest that the ergogenic effect of glucose supplementation occurs not as a result of decreased neural activation but to improved muscle function, possibly as a consequence of protection of muscle membrane excitability.

Glucose supplements increase human muscle in vitro Na+-K+-ATPase activity during prolonged exercise.

Regulation of maximal Na(+)-K(+)-ATPase activity in vastus lateralis muscle was investigated in response to prolonged exercise with (G) and without (NG) oral glucose supplements. Fifteen untrained volunteers (14 males and 1 female) with a peak aerobic power (Vo(2)(peak)) of 44.8 +/- 1.9 ml.kg(-1).min(-1); mean +/- SE cycled at approximately 57% Vo(2)(peak) to fatigue during both NG (artificial sweeteners) and G (6.13 +/- 0.09% glucose) in randomized order. Consumption of beverage began at 30 min and continued every 15 min until fatigue. Time to fatigue was increased (P < 0.05) in G compared with NG (137 +/- 7 vs. 115 +/- 6 min). Maximal Na(+)-K(+)-ATPase activity (V(max)) as measured by the 3-O-methylfluorescein phosphatase assay (nmol.mg(-1).h(-1)) was not different between conditions prior to exercise (85.2 +/- 3.3 or 86.0 +/- 3.9), at 30 min (91.4 +/- 4.7 vs. 91.9 +/- 4.1) and at fatigue (92.8 +/- 4.3 vs. 100 +/- 5.0) but was higher (P < 0.05) in G at 90 min (86.7 +/- 4.2 vs. 109 +/- 4.1). Na(+)-K(+)-ATPase content (beta(max)) measured by the vanadate facilitated [(3)H]ouabain-binding technique (pmol/g wet wt) although elevated (P < 0.05) by exercise (0<30, 90, and fatigue) was not different between NG and G. At 60 and 90 min of exercise, blood glucose was higher (P < 0.05) in G compared with NG. The G condition also resulted in higher (P < 0.05) serum insulin at similar time points to glucose and lower (P < 0.05) plasma epinephrine and norepinephrine at 90 min of exercise and at fatigue. These results suggest that G results in an increase in V(max) by mechanisms that are unclear.

Effects of prior exercise and a low-carbohydrate diet on muscle sarcoplasmic reticulum function during cycling in women.

The effects of exercise and diet on sarcoplasmic reticulum Ca(2+)-cycling properties in female vastus lateralis muscle were investigated in two groups of women following four different conditions. The conditions were 4 days of a low-carbohydrate (Lo CHO) and glycogen-depleting exercise plus a Lo CHO diet (Ex + Lo CHO) (experiment 2) and 4 days of normal CHO (Norm CHO) and glycogen-depleting exercise plus Norm CHO (Ex + Norm CHO) (experiment 1). Peak aerobic power (Vo2peak)) was 38.1 +/- 1.4 (SE); n = 9 and 35.6 +/- 1.4 ml.kg(-1).min(-1); n = 9, respectively. Sarcoplasmic reticulum properties measured in vitro in homogenates (micromol.g protein(-1).min(-1)) indicated exercise-induced reductions (P < 0.05) in maximal Ca(2+)-ATPase activity (0 > 30, 60 min > fatigue), Ca(2+) uptake (0 > 30 > 60 min, fatigue), and Ca(2+) release, both phase 1 (0, 30 > 60 min, fatigue) and phase 2 (0 > 30, 60 min, fatigue; 30 min > fatigue) in Norm CHO. Exercise was without effect in altering the Hill slope (n(H)), defined as the slope of relationship between Ca(2+)-ATPase activity and Ca(2+) concentration. No differences were observed between Norm CHO and Ex+Norm CHO. Compared with Norm CHO, Lo CHO resulted in a lower (P < 0.05) Ca(2+) uptake, phase 1 Ca(2+) release (30 min), and n(H). Ex + Lo CHO resulted in a greater (P < 0.05) Ca(2+) uptake and n(H) compared with Lo CHO. The results demonstrate that Lo CHO alone can disrupt SR Ca(2+) cycling and that, with the exception of Ca(2+) release, a glycogen-depleting session of exercise before Lo CHO can reverse the effects.