In this study, the intensities of activity and movement patterns during men's basketball were investigated by videoing the movements and monitoring the heart rate and blood lactate responses of eight elite players during competition. The results are expressed according to ‘live time’, which is actual playing time, and ‘total time’, which includes live time as well as all stoppages in play. The mean (± s.d.) frequency of all activities was 997 ± 183, with a change in movement category every 2.0 s. A mean total of 105 ± 52 high‐intensity runs (mean duration 1.7 s) was recorded for each game, resulting in one high‐intensity run every 21 s during live time. Sixty percent of live time was spent engaged in low‐intensity activity, while 15% was spent in high‐intensity activity. The mean heart rate (HR) during live time was 169 ± 9 beats min^‐l (89 ± 2% peak HR attained during laboratory testing); 75% of live time was spent with a HR response of greater than 85% peak HR. The mean blood lactate concentration was 6.8 ± 2.8 mM, indicating the involvement of glycolysis in the energy demands of basketball. It is concluded that the physiological requirements of men's basketball are high, placing considerable demands on the cardiovascular and metabolic capacities of players.

Membrane excitability is a critical regulatory step in skeletal muscle contraction and is modulated by local ionic concentrations, conductances, ion transporter activities, temperature, and humoral factors. Intense fatiguing contractions induce cellular K⁺ efflux and Na⁺ and Cl⁻ influx, causing pronounced perturbations in extracellular (interstitial) and intracellular K⁺ and Na⁺ concentrations. Muscle interstitial K⁺ concentration may increase 1- to 2-fold to 11–13 mM and intracellular K⁺ concentration fall by 1.3- to 1.7-fold; interstitial Na⁺ concentration may decline by 10 mM and intracellular Na⁺ concentration rise by 1.5- to 2.0-fold. Muscle Cl⁻ concentration changes reported with muscle contractions are less consistent, with reports of both unchanged and increased intracellular Cl⁻ concentrations, depending on contraction type and the muscles studied. When considered together, these ionic changes depolarize sarcolemmal and t-tubular membranes to depress tetanic force and are thus likely to contribute to fatigue. Interestingly, less severe local ionic changes can also augment subtetanic force, suggesting that they may potentiate muscle contractility early in exercise. Increased Na⁺-K⁺-ATPase activity during exercise stabilizes Na⁺ and K⁺ concentration gradients and membrane excitability and thus protects against fatigue. However, during intense contraction some Na⁺-K⁺ pumps are inactivated and together with further ionic disturbances, likely precipitate muscle fatigue.

The production of reactive oxygen species in skeletal muscle is linked with muscle fatigue. This study investigated the effects of the antioxidant compound N-acetylcysteine (NAC) on muscle cysteine, cystine, and glutathione and on time to fatigue during prolonged, submaximal exercise in endurance athletes. Eight men completed a double-blind, crossover study, receiving NAC or placebo before and during cycling for 45 min at 71% peak oxygen consumption (V̇o_2 peak) and then to fatigue at 92% V̇o_2 peak. NAC was intravenously infused at 125 mg·kg⁻¹·h⁻¹ for 15 min and then at 25 mg·kg⁻¹·h⁻¹ for 20 min before and throughout exercise. Arterialized venous blood was analyzed for NAC, glutathione status, and cysteine concentration. A vastus lateralis biopsy was taken preinfusion, at 45 min of exercise, and at fatigue and was analyzed for NAC, total glutathione (TGSH), reduced glutathione (GSH), cysteine, and cystine. Time to fatigue at 92% V̇o_2 peak was reproducible in preliminary trials (coefficient of variation 5.6 ± 0.6%) and with NAC was enhanced by 26.3 ± 9.1% (NAC 6.4 ± 0.6 min vs. Con 5.3 ± 0.7 min; P < 0.05). NAC increased muscle total and reduced NAC at both 45 min and fatigue ( P < 0.005). Muscle cysteine and cystine were unchanged during Con, but were elevated above preinfusion levels with NAC ( P < 0.001). Muscle TGSH ( P < 0.05) declined and muscle GSH tended to decline ( P = 0.06) during exercise. Both were greater with NAC ( P < 0.05). Neither exercise nor NAC affected whole blood TGSH. Whereas blood GSH was decreased and calculated oxidized glutathione increased with exercise ( P < 0.05), both were unaffected by NAC. In conclusion, NAC improved performance in well-trained individuals, with enhanced muscle cysteine and GSH availability a likely mechanism.