A comparison of skating economy on-ice and on the skating treadmill.

The purpose of this study was to compare skating economy and oxygen uptake (VO2) on-ice and on the skating treadmill (TM). Male varsity hockey players (n = 15, age = 21.0 yr) performed skating tests on a TM and on-ice. The subjects skated for 4 min at each of 3 submaximal velocities (18, 20, and 22 km . h(-1)), separated by 5 min of passive recovery. A VO2max test followed the submaximal tests and commenced at 24 km . h(-1) with the velocity increasing by 1 km . h(-1) every minute until volitional fatigue. VO2 was 39.7, 42.9, 46.0, and 53.4 ml . kg(-1) . min(-1) at 18, 20, 22, and maximum speed (km . h(-1)) on the TM. VO2 was significantly lower (p < .05) 31.5, 36.9, and 42.7 ml . kg(-1) . min(-1) at 18, 20, and 22 km . h(-1) on-ice. The on-ice VO2max (54.7 ml . kg(-1) . min(-1)) was similar to TM. Stride rate, stride length and heart rate (HR) were significantly different on-ice compared to TM. These results show that at submaximal velocities, VO2, HR, and stride rate are higher on TM compared to on-ice. VO2max was similar while HRmax was higher on the skating treadmill compared to on-ice

Oxidative enzyme activities of the vastus lateralis muscle and the functional status in patients with COPD.

BACKGROUND: Enzymatic and histochemical abnormalities of the peripheral muscle may play a role in exercise intolerance in patients with chronic obstructive pulmonary disease (COPD). A study was undertaken to measure the mitochondrial enzyme activity of the vastus lateralis muscle in patients with COPD and to evaluate the relationship between enzyme activities and functional status. METHODS: Fifty seven patients with COPD of mean (SD) age 66 (7) years with forced expiratory volume in one second (FEV(1)) 39 (15)% predicted and peak oxygen uptake (VO(2)) of 14 (4) ml/min/kg and 15 normal subjects of similar age were included in the study. Each subject performed a stepwise exercise test up to maximal capacity during which five-breath averages of VO(2) were measured. Muscle specimens were obtained by percutaneous needle biopsy of the vastus lateralis muscle and the activity of two mitochondrial enzymes (citrate synthase (CS) and 3-hydroxyacyl CoA dehydrogenase (HADH)) was measured. The functional status of the patients was classified according to peak VO(2). RESULTS: CS and HADH activities were markedly reduced in patients with COPD compared with normal subjects (22.3 (2.7) versus 29.5 (7.3) micromol/min/g muscle (p<0.0001) and 5. 1 (2.0) versus 6.7 (1.9) micromol/min/g muscle (p<0.005), respectively). The activity of CS decreased progressively with the deterioration in the functional status while that of HADH was not related to functional status. Using a stepwise regression analysis, percentage predicted functional residual capacity (FRC), the activity of CS, oxygen desaturation during exercise, age, and inspiratory capacity (% pred) were found to be significant determinants of peak VO(2). The regression model explained 59% of the variance in peak VO(2) (p<0.0001). CONCLUSIONS: The oxidative capacity of the vastus lateralis muscle is reduced in patients with moderate to severe COPD compared with normal subjects of similar age. In these individuals the activity of CS correlated significantly with peak exercise capacity and independently of lung function impairment.

Feasibility and efficacy of home exercise training before lung volume reduction.

BACKGROUND: Exercise training is recommended before lung volume reduction surgery (LVRS) in patients with emphysema. Unfortunately, many of these patients are referred from remote areas where there is no available rehabilitation program. The authors evaluated the feasibility and efficacy of a minimally supervised home-based exercise training program. METHODS: Twenty-three emphysematous patients (age 61 +/- 6, forced expiratory volume in 1 second = 29 +/- 7% predicted [mean +/- SD]) were recruited from our LVRS program. Measurements of pulmonary function, maximal and submaximal exercise capacity, 6-minute walking distance (6-MWD), muscle strength, and quality of life with the Chronic Respiratory Questionnaire were obtained before and after training. Home-based exercise training program included muscle exercises and aerobic training, and started with detailed teaching while the follow-up was ensured through weekly phone calls and a diary filled by each patient. RESULTS: Significant increases in 6-MWD (P < 0.001), quality of life (P < 0.005), peak work rate (P < 0.05), peak oxygen consumption (P < 0.05), endurance time (P < 0.005), and muscle strength were observed in the home-based exercise training program. CONCLUSIONS: Home-based exercise training for patients in preparation for LVRS was feasible, and induced significant improvement in exercise tolerance and quality of life.

Aerobic and strength training in patients with chronic obstructive pulmonary disease.

The purpose of this study was to evaluate whether strength training is a useful addition to aerobic training in patients with chronic obstructive pulmonary disease (COPD). Forty-five patients with moderate to severe COPD were randomized to 12 wk of aerobic training alone (AERO) or combined with strength training (AERO + ST). The AERO regimen consisted of three weekly 30-min exercise sessions on a calibrated ergocycle, and the ST regimen included three series of eight to 10 repetitions of four weight lifting exercises. Measurements of peripheral muscle strength, thigh muscle cross-sectional area (MCSA) by computed tomographic scanning, maximal exercise capacity, 6-min walking distance (6MWD), and quality of life with the chronic respiratory questionnaire were obtained at baseline and after training. Thirty-six patients completed the program and constituted the study group. The strength of the quadriceps femoris increased significantly in both groups (p < 0.05), but the improvement was greater in the AERO + ST group (20 +/- 12% versus 8 +/- 10% [mean +/- SD] in the AERO group, p < 0.005). The thigh MCSA and strength of the pectoralis major muscle increased in the AERO + ST group by 8 +/- 13% and 15 +/- 9%, respectively (p < 0.001), but not in the AERO group (3 +/- 6% and 2 +/- 10%, respectively, p > 0.05). These changes were significantly different in the two study groups (p < 0.01). The increase in strength of the latissimus dorsi muscle after training was modest and of similar magnitude for both groups. The changes in peak exercise work rate, 6MWD, and quality of life were comparable in the two groups. In conclusion, the addition of strength training to aerobic training in patients with COPD is associated with significantly greater increases in muscle strength and mass, but does not provide additional improvement in exercise capacity or quality of life.

Histochemical and morphological characteristics of the vastus lateralis muscle in patients with chronic obstructive pulmonary disease.

PURPOSE AND METHODS: In this study, we examined the fiber-type proportions, cross-sectional areas (CSA), and capillarization from needle biopsies of the vastus lateralis muscle in 20 patients with chronic obstructive pulmonary disease (COPD) (FEV1 = 37 +/- 11% predicted, peak VO2 = 13 +/- 4 mL.min-1.kg-1) and nine age-matched normal subjects (peak VO2 = 33 +/- 7 mL.min-1.kg-1). The effects of endurance training on these parameters were also evaluated in 11 of the 20 patients with COPD. RESULTS: The proportion of Type I fiber was smaller in COPD than normals (34 +/- 14% vs 58 +/- 16 in normals, P < 0.0005) with a corresponding increase in Type IIb fiber (P = 0.015). The CSA of Type I, IIa, and IIab fibers was also smaller in COPD. The capillary to fiber ratio tended to be reduced in patients, but this difference did not reach statistical significance (P = 0.15). The number of capillary contact for Type I, IIa, and IIab fibers was significantly reduced in COPD compared with normal subjects (P < 0.05). When corrected for the CSA, this parameter was similar for both groups. After training, peak VO2 increased by 11% (P < 0.05), the fiber-type proportion remained unchanged, and the CSA of Type I and IIa fibers increased by 31 and 21%, respectively (P < 0.05). Although the number of capillary contact for each fiber types increased with training, the capillary to fiber ratio and the number of capillary contact for the different fiber types relative to their CSA remain unchanged. CONCLUSIONS: We conclude that in COPD, 1) the vastus lateralis muscle is characterized by a marked decrease in Type I fiber proportion, an increase in Type IIb fiber proportion, a decrease in Type I, IIa, and IIab fiber CSA and by a relatively preserved capillarization; and 2) a 12-wk training program induces a significant increase in Type I and IIa CSA.

Peripheral muscle weakness in patients with chronic obstructive pulmonary disease.

Peripheral muscle weakness is commonly found in patients with chronic obstructive pulmonary disease (COPD) and may play a role in reducing exercise capacity. The purposes of this study were to evaluate, in patients with COPD: (1) the relationship between muscle strength and cross-sectional area (CSA), (2) the distribution of peripheral muscle weakness, and (3) the relationship between muscle strength and the severity of lung disease. Thirty-four patients with COPD and 16 normal subjects of similar age and body mass index were evaluated. Compared with normal subjects, the strength of three muscle groups (p < 0.05) and the right thigh muscle CSA, evaluated by computed tomography (83.4 +/- 16.4 versus 109.6 +/- 15.6 cm2, p < 0.0001), were reduced in COPD. The quadriceps strength/thigh muscle CSA ratio was similar for the two groups. The reduction in quadriceps strength was proportionally greater than that of the shoulder girdle muscles (p < 0.05). Similar observations were made whether or not patients had been exposed to systemic corticosteroids in the 6-mo period preceding the study, although there was a tendency for the quadriceps strength/thigh muscle CSA ratio to be lower in patients who had received corticosteroids. In COPD, quadriceps strength and muscle CSA correlated positively with the FEV1 expressed in percentage of predicted value (r = 0.55 and r = 0. 66, respectively, p < 0.0005). In summary, the strength/muscle cross-sectional area ratio was not different between the two groups, suggesting that weakness in COPD is due to muscle atrophy. In COPD, the distribution of peripheral muscle weakness and the correlation between quadriceps strength and the degree of airflow obstruction suggests that chronic inactivity and muscle deconditioning are important factors in the loss in muscle mass and strength.

Metabolic and hemodynamic responses of lower limb during exercise in patients with COPD.

Premature lactic acidosis during exercise in patients with chronic obstructive pulmonary disease (COPD) may play a role in exercise intolerance. In this study, we evaluated whether the early exercise-induced lactic acidosis in these individuals can be explained by changes in peripheral O2 delivery (O2). Measurements of leg blood flow by thermodilution and of arterial and femoral venous blood gases, pH, and lactate were obtained during a standard incremental exercise test to capacity in eight patients with severe COPD and in eight age-matched controls. No significant difference was found between the two groups in leg blood flow at rest or during exercise at the same power outputs. Blood lactate concentrations and lactate release from the lower limb were greater in COPD patients at all submaximal exercise levels (all P < 0.05). Leg D02 at a given power output was not significantly different between the two groups, and no significant correlation was found between this parameter and blood lactate concentrations. COPD patients had lower arterial and venous pH at submaximal exercise, and there was a significant positive correlation between venous pH at 40 W and the peak O2 uptake (r = 0.91, P < 0.0001). The correlation between venous pH and peak O2 uptake suggests that early muscle acidosis may be involved in early exercise termination in COPD patients. The early lactate release from the lower limb during exercise could not be accounted for by changes in peripheral O2. The present results point to skeletal muscle dysfunction as being responsible for the early onset of lactic acidosis in COPD.