This review describes processes for the distribution of K+ ([K+]) and lactate concentrations ([Lac-]) that are released from contracting muscle at high rates during high-intensity exercise. This results in increased interstitial and venous [K+] and [Lac-] in contracting muscle. Large and rapid increases in plasma [K+] and [Lac-] result in the transport of these ions into red blood cells (RBCs). These ions are distributed to noncontracting tissues within both the plasma and RBC compartments of blood. The extraction of K+ and Lac- from the circulation by noncontracting tissue serves to markedly attenuate exercise-induced increases in plasma [K+] and [Lac-]. This apparent regulation of the plasma compartment by noncontracting tissues helps to maintain favorable concentration gradients for the net movement of [K+] and [Lac-] into the venous side of the microcirculation from interstitial fluids of contracting muscle. This provides conditions that 1) reduce the increase in interstitial [K+], thereby decreasing the magnitude and rate of sarcolemmal depolarization, and 2) favor the sarcolemmal transport of Lac- from within contracting muscle cells, thereby regulating intracellular osmolality and H+ concentration. On cessation of exercise, net K+ uptake by recovering muscle is rapid, with 90-95% recovery of intracellular [K+] within 3.5 min, indicating a very high rate of Na+-K+ pump activity. The K+ extracted by noncontracting tissues during exercise may be slowly released during recovery. During the initial minutes of recovery, recovering muscle continues to release Lac- into the circulation, and noncontracting tissues continue to extract Lac- for up to 30 min. The uptake of Lac- by noncontracting tissues results in elevated intracellular [Lac-]. There is no evidence that Lac- extracted by noncontracting tissues is subsequently released; it is probably metabolized within these cells. We conclude that the uptake of K+ and Lac- by RBCs and noncontracting tissues regulates ion homeostasis within plasma and the interstitial and intracellular compartments of contracting muscle. The regulatory processes help to maintain the function of active muscles by delaying the onset of fatigue during exercise and to restore homeostasis during recovery.

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In 9 patients with stable coronary artery disease, measurements were made during a progressive incremental maximum exercise test of O(2) intake (VO(2)), CO(2) output (VCO(2)), mixed venous PCO(2) by an exponential rebreathing method, and end-tidal PCO(2) (PETCO(2)) to estimate arterial PCO(2) (PaCO(2)). By applying the Fick principle to CO2, these measurements were used to derive cardiac output at several incremental work loads. Each subject underwent two incremental exercise studies to establish the reproducibility of the technique, and also a steady state exercise study to compare steady state responses with unsteady state incremental exercise. The results were also compared to those previously obtained in healthy subjects. PvCO(2) showed a curvilinear increase with increasing VCO(2) with only a small intersubject variation. Cardiac output-oxygen uptake relationships (Q/VO(2)) were similar in the two incremental studies (intercepts 6.27 and 6.641/min; slopes 4.82 and 4.58 1/min), and also similar to that obtained previously in healthy subjects (intercept 6.441/min; slope 4.71 1/min). Low calculated values for cardiac output were obtained at high exercise levels during the incremental test in those subjects in whom PETCO(2) fell at the highest work loads. This effect could be corrected for by using a PETCO(2) obtained 1 min prior to rebreathing, suggesting that the low values of Q were an artifact due to a transient decrease in PaCO(2) secondary to hyperventilation. At any given VO(2) or VCO2, PvCO(2) and Q were the same in both steady state and unsteady state incremental exercise. The exponential CO(2) rebreathing method may be reliably applied to incremental exercise testing to evaluate the cardiac output responses to exercise in patients with cardiac disease.

Exercise training for patients with chronic heart failure reduced mortality and cardiac events and improved quality of life QUESTION In patients with chronic heart failure, can long-term exercise training reduce all-cause mortality and cardiac events and improve quality of life? DESIGN A randomized, unblinded, controlled trial with a mean follow-up of 3.4 years. SETTING A cardiology institute and hospital in Italy. PATIENTS A total of 110 patients with stable chronic heart failure were screened, and 99 (mean age, 55 years; 88% men) were studied. Other inclusion criteria were left ventricular ejection fraction of Յ40 and sinus rhythm. Exclusion criteria were unstable angina, recent acute myocardial infarction, decompensated congestive heart failure, hemodynamically important valvular heart disease, severe chronic pulmonary illness, uncontrolled hypertension, renal insufficiency, or orthopedic or neurologic limitations. Followup was 95%.