Prior maximal exercise decreases pulmonary diffusing capacity during subsequent exercise.

Pulmonary diffusion (DLCO) increases during exercise due to greater pulmonary capillary volume (Vc) and membrane diffusing capacity (DM). However, after heavy exercise there is a reduction in resting DLCO. It is unclear whether this post-exercise effect will attenuate the normal increase in DLCO, Vc and DM during subsequent exercise and whether this affects SpO2 (pulse oximeter). DLCO, Vc, DM, cardiac output and SpO2 were measured at rest, moderate (~70% VO2peak) and heavy (~90 VO2peak) exercise in 9 subjects during 2 sessions separated by ~90 min. DLCO, Vc and DM increased during exercise (P<0.05). DLCO (P<0.05) and Vc (P<0.10), but not DM or SpO2 were lower in session 2 compared to the first. Reductions in DLCO and Vc appeared to be smallest during rest (1-4%) and greatest at high-intensity exercise (8-20%), but the interaction was not significant. SpO2 decreased by 4.9% and 5.1% from rest to high-intensity exercise during the first and second exercise bout, but these changes were not different. These data confirm that a bout of high-intensity exercise reduces DLCO and Vc, and may indicate that these changes are exacerbated during subsequent high-intensity exercise. Despite these changes, SpO2 was not affected by previous exercise.

The larger exercise stroke volume in endurance-trained men does not result from increased left ventricular early or late inflow or tissue velocities.

AIM: To determine whether the larger exercise stroke volume in senior endurance-trained athletes results from an attenuation of age-related alterations in left ventricular (LV) early diastolic filling or a more vigorous late filling. METHODS: Body composition (DEXA), VO(2)peak, stroke volume (CO(2) rebreathing) and Doppler measures of early and late mitral inflow and mitral annular velocities were collected at seated upright rest and heart rate-matched exercise (100 and 120 bpm) in trained and untrained younger (18-30 years) men and trained and untrained older (60-80 years) healthy men. RESULTS: Ageing had a greater effect than training status on seated rest mitral inflow and tissue Doppler imaging parameters, as shown by a lower peak early-to-late mitral inflow velocity ratio (E/A ratio) and slower peak early mitral annular velocity (Em) in older compared with younger men. Exercise stroke volume was unaffected by healthy ageing; however, Em, an index of early LV lengthening rate and relaxation, was slower (P < 0.001), while measures of atrial systole were increased (P < 0.001) during exercise in older men. Stroke volume during exercise was larger in the trained men (P < 0.001); however, early and late mitral inflow and tissue velocities were not different between trained and untrained men. CONCLUSION: The larger exercise stroke volume in trained older male athletes does not seem to be related to faster filling or lengthening velocities during early or late filling. Thus, a larger, more compliant left ventricle in combination with an increased blood volume may explain the larger LV filling volumes in trained seniors.

Effect of reduced total blood volume on left ventricular volumes and kinetics in type 2 diabetes.

AIM: Although impaired left ventricular (LV) diastolic function is commonly observed in patients with type 2 diabetes, it remains unclear whether the impairment is caused by altered LV relaxation or changes in LV preload. The purpose of this study was to examine the influence of LV function and LV loading conditions on stroke volume in men with type 2 diabetes. METHODS: Cardiac magnetic resonance imaging scans were performed in eight men with type 2 diabetes and 11 non-diabetic men matched for age, weight and physical activity level. Total blood volume was determined with the Evans blue dye dilution technique. RESULTS: End-diastolic volume (EDV), the ratio of peak early to late mitral inflow velocity (E/A) and stroke volume were lower in men with type 2 diabetes than in non-diabetic individuals. Peak filling rate and peak ejection rate were not different between diabetic and non-diabetic individuals; however, men with type 2 diabetes had proportionally longer systolic duration than non-diabetic individuals. Heart rate was higher and total blood volume was lower in men with type 2 diabetes. The lower total blood volume was correlated with a lower EDV in men with type 2 diabetes. CONCLUSIONS: Men with type 2 diabetes have an altered cardiac cycle and lower end-diastolic and stroke volume. A lower total blood volume and higher heart rate in men with type 2 diabetes suggest that changes in LV preload, independent of changes in LV relaxation or contractility, influence LV diastolic filling and stroke volume in this population.

Impaired stroke volume and aerobic capacity in female adolescents with type 1 and type 2 diabetes mellitus.

AIM/HYPOTHESIS: This study was designed to determine whether type 2 diabetic adolescents have reduced aerobic capacity and to investigate the role of cardiac output and arteriovenous oxygen difference (a-vO(2)) in their exercise response. METHODS: Female adolescents (age 12-18 years) with type 2 diabetes mellitus (n = 8) and type 1 diabetes mellitus (n = 12) and obese (n = 10) and non-obese (n = 10) non-diabetic controls were recruited for this study. Baseline data included maximal aerobic capacity (cycle ergometer) and body composition. Cardiac output and a-vO(2) were determined at rest and during submaximal exercise. RESULTS: Diabetic groups had lower aerobic capacity than non-diabetic groups (p < 0.05). Adolescents with type 2 diabetes had lower aerobic capacity than the type 1 diabetic group. Maximal heart rate was lower in the type 2 diabetic group (p < 0.05). Exercise stroke volume was 30-40% lower at 100 and 120 beats per min in the diabetic than in the non-diabetic groups (p < 0.05). The a-vO(2) value was not different in any condition. CONCLUSIONS AND INTERPRETATION: Type 2 diabetic adolescents have reduced aerobic capacity and reduced heart rate response to maximal exercise. Furthermore, type 2 and type 1 diabetic adolescent girls have a blunted exercise stroke volume response compared with non-diabetic controls. Central rather than peripheral mechanisms contribute to the reduced aerobic capacity in diabetic adolescents. Although of short duration, type 2 diabetes in adolescence is already affecting cardiovascular function in adolescents.

Resistance training improves glycaemic control in obese type 2 diabetic men.

The purpose of this investigation was to determine whether moderate intensity resistance training (RT) improves glycaemic control in obese, type 2 diabetic men. Eighteen subjects were randomly assigned to a 10-week RT program, or a non-training control group (C). Glycosylated haemoglobin (HbA 1c ), fasting glucose and insulin, glucose and insulin 120 minutes (2h) after a 75 g oral glucose load, body composition and muscular strength and endurance were measured before and after the 10-week experimental period. In the RT group fasting glucose and insulin decreased with training (p < 0.05) and decreases in HbA 1c approached significance (p = 0.057). 2-h glucose and insulin did not change in either group. Fat free mass (FFM) increased by 3.5 % after RT but was unchanged in the controls. Fat mass (FM) increased 6.9 % in C but was unchanged in RT. Percent body fat was unchanged in both groups. Muscular strength and endurance increased by 25 to 52 % in the RT group but was unchanged in controls. Changes in fasting glucose and HbA 1c were inversely related to changes in FFM. These results suggest that RT is an effective form of exercise training which modestly improves glycaemic control and lowers fasting insulin levels in obese type 2 diabetics.

Muscle atrophy is prevented in patients with acute spinal cord injury using functional electrical stimulation.

Severe muscle atrophy occurs rapidly following traumatic spinal cord injury (SCI). Previous research shows that neuromuscular or 'functional' electrical stimulation (FES), particularly FES-cycle ergometry (FES-CE) can cause muscle hypertrophy in individuals with chronic SCI (> 1 year post-injury). However, the modest degree of hypertrophy in these already atrophied muscles has lessened earlier hopes that FES therapy would reduce secondary impairments of SCI. It is not known whether FES treatments are effective when used to prevent, rather than reverse, muscle atrophy in individuals with acute SCI. This study explored whether unloaded isometric FES contractions (FES-IC) or FES-CE decreased subsequent muscle atrophy in individual with acute SCI (< 3 months post-injury). Twenty-six subjects, 14-15 weeks post-traumatic SCI, were assigned to control, FES-IC, or FES-CE against progessively increasing resistance. Subjects were involved in the study for 3 or 6 months. Total body lean body mass (TB-LBM), lower limb lean body mass (LL-LBM), and gluteal lean body mass (G-LBM) were determined before the study, and at 3 and 6 months using dual energy X-ray absorptiometry (DEXA). Controls lost an average of 6.1%, 10.1%, 12.4%, after 3 months and 9.5%, 21.4%, 26.8% after 6 months in TB-LBM, LL-LBM and G-LBM respectively. Subjects in the FES-IC group consistently lost less lean body mass than controls, however, only 6 month G-LBM loss was significantly attenuated in this group relative to the controls. In the FES-CE group, LL-LBM and G-LBM loss were prevented at both 3 and 6 months, and TB-LBM loss was prevented at 6 months. In addition, FES-CE significantly increased G-LBM and LL-LBM after 6 months of training relative to pre-training levels. Within the control group, there was no significant relationship between LL-LBM loss (3 and 6 months) and the number of days between injury and baseline measurement. In summary, this study shows that FES-CE, but not FES-IC, training prevents muscle atrophy in acute SCI after 3 months of training, and causes significant hypertrophy after 6 months. The magnitude of differences in regionalized LBM between controls and FES-CE subject raises hopes that such treatment may indeed be beneficial in preventing secondary impairments of SCI if employed before extensive post-injury atrophy occurs.

Intermediate filament proteins increase during chronic stimulation of skeletal muscle.

Chronic low-frequency electrical stimulation of rabbit fast-twitch skeletal muscle induces increased levels of two intermediate filament proteins, desmin and vimentin, during the first 3 weeks of stimulation. These increases occur over the same timecourse as reported shifts in alpha-actinin expression and increased Z-disc width, but precede the fast-to-slow shifts in contractile proteins, which have been described by others. Desmin and vimentin levels increase during the first 2 weeks of stimulation, at which time the increase in desmin appears to plateau while vimentin continues to increase significantly through 3 weeks of stimulation. Absolute amounts of vimentin are lower than desmin at all time points, however increases in desmin and vimentin levels are strongly correlated during the stimulation period, suggesting that the two proteins are coordinately increased during the initial phases of muscle transformation. We suggest that rapid increases in the expression of intermediate filament proteins, which coincide with alterations in Z-disc structure, may indicate a fortification of the force-bearing ultrastructure of the muscle fibre in response to the increased activity that is induced by stimulation. The presence of vimentin and elevated levels of desmin expression suggest that mature skeletal muscle reverts toward a developmental program of intermediate filament protein expression during fast-to-slow transformation.