Treatment with controlled exercise is a safe program that appears to improve PCS symptoms when compared with a no-treatment baseline. A randomized controlled study is warranted.

With the aim of computing a complete energy balance of front crawl, the energy cost per unit distance (C = Ev(-1), where E is the metabolic power and v is the speed) and the overall efficiency (eta(o) = W(tot)/C, where W(tot) is the mechanical work per unit distance) were calculated for subjects swimming with and without fins. In aquatic locomotion W(tot) is given by the sum of: (1) W(int), the internal work, which was calculated from video analysis, (2) W(d), the work to overcome hydrodynamic resistance, which was calculated from measures of active drag, and (3) W(k), calculated from measures of Froude efficiency (eta(F)). In turn, eta(F) = W(d)/(W(d) + W(k)) and was calculated by modelling the arm movement as that of a paddle wheel. When swimming at speeds from 1.0 to 1.4 m s(-1), eta(F) is about 0.5, power to overcome water resistance (active body drag x v) and power to give water kinetic energy increase from 50 to 100 W, and internal mechanical power from 10 to 30 W. In the same range of speeds E increases from 600 to 1,200 W and C from 600 to 800 J m(-1). The use of fins decreases total mechanical power and C by the same amount (10-15%) so that eta(o) (overall efficiency) is the same when swimming with or without fins [0.20 (0.03)]. The values of eta(o) are higher than previously reported for the front crawl, essentially because of the larger values of W(tot) calculated in this study. This is so because the contribution of W(int) to W(tot )was taken into account, and because eta(F) was computed by also taking into account the contribution of the legs to forward propulsion.

Body drag, D, and the overall mechanical efficiency of swimming, e, were measured from the relationship between extra oxygen consumption and extra drag loads in 42 male and 22 female competitive swimmers using the front crawl at speeds ranging from 0.4 to 1.2 m/s. D increased from 3.4 (1.9) kg at 0.5 m/s to 8.2 (7.0) kg at 1.2 m/s, with D of women (in brackets) being significantly less (P less than 0.05) than that of men. Mechanical efficiency increased from 2.9% at 0.5 m/s to 7.4% at 1.2 m/s for men, the values for women being somewhat greater than those for men. The ratio, D/e was shown to be identical to the directly measured energy cost of swimming one unit distance, V02/d, and was independent of the velocity up to 1.2 m/s. It averaged 52 and 37 l/km for men and women respectively (P less than 0.05). When corrected for body surface area the values were 27 and 22 l/km-m2 for men and women, respectively (P less than 0.05). The underwater torque, T, a measure of the tendency of the feet to sink, was 1.44 kg-m for men and 0.70 kg-m for women (P less than 0.05). VO2/d increased linearly with T for both men and women of similar competitive experience. However, the proportionality constant delta VO2/d-delta T was significantly less for competitive than noncompetitive swimmers. The analysis of the relationship VO2/d vs. T provides a valuable approach to the understanding of the energetics of swimming.

Water covers over 70% of the earth, has varying depths and temperatures and contains much of the earth's resources. Head-out water immersion (HOWI) or submersion at various depths (diving) in water of thermoneutral (TN) temperature elicits profound cardiorespiratory, endocrine, and renal responses. The translocation of blood into the thorax and elevation of plasma volume by autotransfusion of fluid from cells to the vascular compartment lead to increased cardiac stroke volume and output and there is a hyperperfusion of some tissues. Pulmonary artery and capillary hydrostatic pressures increase causing a decline in vital capacity with the potential for pulmonary edema. Atrial stretch and increased arterial pressure cause reflex autonomic responses which result in endocrine changes that return plasma volume and arterial pressure to preimmersion levels. Plasma volume is regulated via a reflex diuresis and natriuresis. Hydrostatic pressure also leads to elastic loading of the chest, increasing work of breathing, energy cost, and thus blood flow to respiratory muscles. Decreases in water temperature in HOWI do not affect the cardiac output compared to TN; however, they influence heart rate and the distribution of muscle and fat blood flow. The reduced muscle blood flow results in a reduced maximal oxygen consumption. The properties of water determine the mechanical load and the physiological responses during exercise in water (e.g. swimming and water based activities). Increased hydrostatic pressure caused by submersion does not affect stroke volume; however, progressive bradycardia decreases cardiac output. During submersion, compressed gas must be breathed which introduces the potential for oxygen toxicity, narcosis due to nitrogen, and tissue and vascular gas bubbles during decompression and after may cause pain in joints and the nervous system.

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Some PCS patients have exercise intolerance due to abnormal CBF regulation that may be the result of concussion-induced altered sensitivity to CO2. Return of normal CBF control and exercise tolerance may be physiological markers of recovery from concussion.

The relationship between half time of the O2 uptake on-response (t1/2 VO2on, seconds) and early blood lactate accumulation (delta Lab, mmol.1(-1) at the onset of submaximal arm and/or leg exercise was the object of a cross-sectional study of sedentary subjects (S,n = 3), and kayakers (K, n = 8), and of a longitudinal study on 11 untrained subjects of specific arm vs. leg training. In supine arm cranking (W = 125 watts) S had an average t1/2 VO2on of 82 s and a delta Aab of 9.2 mmol.1(-1) compared to 47 +/- 7 s and 4 +/- 1.4 mmol.1(-1), respectively, for K. In longitudinal trainees shorter t1/2 VO2on was accompanied by lower Lab for the trained limbs. Specific limb conditioning in swimmers and runners resulted in shorter t1/2 VO2on. A linear relationship was observed between delta Lab and t1/2 VO2on having an intercept on the time axis at congruent to 20 s and a slope proportional to muscle mass. Trained muscles were grouped closest to the intercept indicating local acceleration of the rate of O2 transfer approaching the t1/2 VO2on for isolated perfused muscle at the onset of work. Since t1/2 VO2on, we conclude that factors distal to the capillary are specifically involved in the local training response.

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