Objective-C-reactive protein (CRP), an obesity-related inflammatory marker, is a promising predictor for cardiovascular disease and may be a mediator for atherogenesis. It has been reported that diet-induced weight loss lowered CRP levels. However, the effect of exercise training, another therapy that can reduce weight, on CRP is still unclear. We examined effects of exercise training with weight loss on CRP levels and conventional cardiovascular risks. Methods and Results-A total of 227 apparently healthy women were recruited, and 199 subjects (average age 52 years) completed a 2-month weight reduction program consisting of supervised aerobic exercises. After the program, weight was reduced from 65.8 to 62.8 kg (PϽ0.0001), and all conventional variables were remarkably improved. Similarly, CRP levels were significantly decreased, from 0.63 (0.28 to 1.19) to 0.41 (0.18 to 0.80) mg/L (PϽ0.0001). However, in contrast to other variables, the changes in CRP levels were not proportionally associated with the extent of weight reduction. In the quartile analysis of % weight reduction, the largest weight reduction quartile did not show significant decreases in CRP levels, whereas moderate quartile showed remarkable CRP decreases. Conclusions-Exercise

These results suggest that impaired muscle metabolism associated with early metabolic limitation determines exercise capacity during maximal systemic exercise in patients with CHF. There was a significant correlation between muscle metabolic capacity during systemic and local exercise in patients with CHF.

The use of anaerobic threshold in assessment of aerobic capacity was evaluated in 34 normal subjects and 47 patients with various kinds of chronic heart disease. Anaerobic threshold was determined as the oxygen consumption (W02) at which a linear relationship between pulmonary ventilation (yE) and V02 was lost during progressive treadmill exercise. Anaerobic threshold determined in this manner was validated with that determined by blood lactate measurements in eight normal subjects and nine cardiac patients (r = .962, p < .001). Thereafter, anaerobic threshold was determined only by respiratory measurements. In symptom-limited, maximal exercise, anaerobic threshold was reached well before maximal effort and corresponded to 70% of maximal V02 both in normal subjects and cardiac patients. Anaerobic threshold decreased as age progressed in normal subjects (r = -.70, p < .001). Anaerobic threshold in cardiac patients was lower than that in the normal subjects and decreased progressively as New York Heart Association functional classification advanced (normal, 32

Objective-To estimate muscle metabolism and oxygen delivery to skeletal muscle in patients with chronic heart failure. Methods-13 patients with chronic heart failure and 15 controls performed calf plantar flexion for six minutes at a constant workload of 50% of one repetition maximum. During recovery from exercise, skeletal muscle content of oxygenated haemoglobin (oxy-Hb) and the level of phosphocreatine (PCr) were measured by near-infrared spectroscopy and 31 P-magnetic resonance spectroscopy, respectively. Results-The mean (SD) time constants of PCr and oxy-Hb during recovery from exercise were significantly greater in patients with chronic heart failure than in normal subjects ( PCr: 76.3 (30.2) s v 36.5 (5.8) s; oxy-Hb: 48.3 (7.3) s v 30.1 (7.7) s; p < 0.01). Both time constants were similar in normal subjects, while the PCr was significantly greater than the oxy-Hb in patients with chronic heart failure. Conclusions-The slower recovery of PCr compared with oxy-Hb in patients with chronic heart failure indicates that haemoglobin resaturation is not a major rate limiting factor of PCr resynthesis. It is suggested that muscle metabolic recovery may depend more on oxygen utilisation than on haemoglobin resaturation or oxygen delivery in patients with chronic heart failure. (Heart 2000;83:161-166) Keywords: near-infrared spectroscopy; 31 P-magnetic resonance spectroscopy; chronic heart failure; exercise tolerance Studies have shown that the degree of exercise intolerance in patients with chronic heart failure is not significantly correlated with the extent of the central haemodynamic disturbance.1 2 This means that exercise capacity is not limited only by haemodynamics but also by peripheral abnormality. Studies using phosphorus-31 nuclear magnetic resonance spectroscopy ( 31 P-MRS) have shown that peripheral muscle metabolic abnormalities during exercise are important contributors to exercise intolerance in patients with chronic heart failure.3-8 Recent studies using nearinfrared spectroscopy (NIRS) to evaluate skeletal muscle oxygen kinetics have shown that peripheral muscle oxygenation is impaired during systemic exercise in patients with chronic heart failure.9 10 Both muscle metabolism and muscle oxygen kinetics are important determinants of exercise capacity and these factors have been separately evaluated in patients with chronic heart failure. In normal subjects, only a few studies have assessed both muscle metabolism and oxygen kinetics. McCully et al simultaneously measured oxygenated haemoglobin (oxy-Hb) and phosphocreatine (PCr) recovery after submaximal exercise in normal subjects using NIRS and 31 P-MRS respectively, and found that the time constants of these indices were similar.11 They suggested that oxy-Hb recovery is rate limiting for ATP synthesis, evaluated as the rate of PCr recovery after submaximal exercise. In patients with chronic heart failure, both skeletal muscle metabolism and oxygen delivery are impaired and these abnormalities are potential contributors to exercise into...

Exercising an average of 2.6 times per week for 6 months produced a significant improvement in cardiovascular risk profile in subjects with multiple cardiovascular risk factors through cumulative results of modest yet pervasive changes in all conventional risk factors, without increased adverse effects.

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