González-Alonso, José, Ricardo Mora-Rodrı́guez, Paul R. Below, and Edward F. Coyle.Dehydration markedly impairs cardiovascular function in hyperthermic endurance athletes during exercise. J. Appl. Physiol. 82(4): 1229–1236, 1997.—We identified the cardiovascular stress encountered by superimposing dehydration on hyperthermia during exercise in the heat and the mechanisms contributing to the dehydration-mediated stroke volume (SV) reduction. Fifteen endurance-trained cyclists [maximal O₂consumption (V˙o_{2 max}) = 4.5 l/min] exercised in the heat for 100–120 min and either became dehydrated by 4% body weight or remained euhydrated by drinking fluids. Measurements were made after they continued exercise at 71%V˙o_{2 max}for 30 min while 1) euhydrated with an esophageal temperature (T_es) of 38.1–38.3°C (control); 2) euhydrated and hyperthermic (39.3°C); 3) dehydrated and hyperthermic with skin temperature (T_sk) of 34°C; 4) dehydrated with T_esof 38.1°C and T_skof 21°C; and 5) condition 4 followed by restored blood volume. Compared with control, hyperthermia (1°C T_esincrease) and dehydration (4% body weight loss) each separately lowered SV 7–8% (11 ± 3 ml/beat; P < 0.05) and increased heart rate sufficiently to prevent significant declines in cardiac output. However, when dehydration was superimposed on hyperthermia, the reductions in SV were significantly ( P< 0.05) greater (26 ± 3 ml/beat), and cardiac output declined 13% (2.8 ± 0.3 l/min). Furthermore, mean arterial pressure declined 5 ± 2%, and systemic vascular resistance increased 10 ± 3% (both P < 0.05). When hyperthermia was prevented, all of the decline in SV with dehydration was due to reduced blood volume (∼200 ml). These results demonstrate that the superimposition of dehydration on hyperthermia during exercise in the heat causes an inability to maintain cardiac output and blood pressure that makes the dehydrated athlete less able to cope with hyperthermia.

This investigation determined the manner in which the cardiovascular system copes with the dehydration-induced reductions in cardiac output (Q) during prolonged exercise in the heat. On two separate occasions, seven endurance-trained subjects (maximal O2 consumption 4.70 +/- 0.41 l/min) cycled in the heat (35 degrees C) for 2 h, beginning at 62 +/- 2% maximal O2 consumption. During exercise, they randomly received either 0.2 liter of fluid and became dehydrated by 4.9 +/- 0.2% of their body weight [i.e., dehydration trial (DE)] or 3.6 +/- 0.4 liter of fluid and replaced 95% of fluid losses [i.e., euhydration trial (EU)]. During the 10- to 120-min period of EU, Q, mean arterial pressure (MAP), systemic vascular resistance (SVR), cutaneous vascular resistance (CVR), and plasma catecholamines did not change while esophageal temperature stabilized at 38.0 +/- 0.1 degrees C. Conversely, after 120 min of DE, Q and MAP were reduced 18 +/- 3 and 5 +/- 2%, respectively, compared with EU (P < 0.05). This was associated with a significantly higher SVR (17 +/- 6%) and plasma norepinephrine concentration (50 +/- 19%, P < 0.05). In addition, CVR was also significantly higher (126 +/- 16 vs. 102 +/- 6% of 20-min value; P < 0.05) during DE despite a 1.2 +/- 0.1 degrees C greater esophageal temperature (P < 0.05). In conclusion, significant reductions in Q are accompanied by significant increases in SVR and plasma norepinephrine and a slight although significant decline in MAP. The cutaneous circulation participates in this systemic vasoconstriction as indicated by increases in CVR despite significant hyperthermia.

This study analysed the effect of imposing a pause between the eccentric and concentric phases on the biological within-subject variation of velocity- and power–load isoinertial assessments. Seventeen resistance-trained athletes undertook a progressive loading test in the bench press (BP) and squat (SQ) exercises. Two trials at each load up to the one-repetition maximum (1RM) were performed using 2 techniques executed in random order: with (stop) and without (standard) a 2-s pause between the eccentric and concentric phases of each repetition. The stop technique resulted in a significantly lower coefficient of variation for the whole load–velocity relationship compared to the standard one, in both BP (2.9% vs. 4.1%; P = 0.02) and SQ (2.9% vs. 3.9%; P = 0.01). Test–retest intraclass correlation coefficients (ICCs) were r = 0.61–0.98 for the standard and r = 0.76–0.98 for the stop technique. Bland–Altman analysis showed that the error associated with the standard technique was 37.9% (BP) and 57.5% higher (SQ) than that associated with the stop technique. The biological within-subject variation is significantly reduced when a pause is imposed between the eccentric and concentric phases. Other relevant variables associated to the load–velocity and load–power relationships such as the contribution of the propulsive phase and the load that maximises power output remained basically unchanged.

The purpose of this study was to determine, i) the reliability of blood lactate and ventilatory-based thresholds, ii) the lactate threshold that corresponds with each ventilatory threshold (VT₁ and VT₂) and with maximal lactate steady state test (MLSS) as a proxy of cycling performance. Fourteen aerobically-trained male cyclists ( 62.1±4.6 ml·kg^-1·min^-1) performed two graded exercise tests (50 W warm-up followed by 25 W·min^-1) to exhaustion. Blood lactate, and data were collected at every stage. Workloads at VT₁ (rise in ;) and VT₂ (rise in ) were compared with workloads at lactate thresholds. Several continuous tests were needed to detect the MLSS workload. Agreement and differences among tests were assessed with ANOVA, ICC and Bland-Altman. Reliability of each test was evaluated using ICC, CV and Bland-Altman plots. Workloads at lactate threshold (LT) and LT+2.0 mMol·L^-1 matched the ones for VT₁ and VT₂, respectively (p = 0.147 and 0.539; r = 0.72 and 0.80; Bias = -13.6 and 2.8, respectively). Furthermore, workload at LT+0.5 mMol·L^-1 coincided with MLSS workload (p = 0.449; r = 0.78; Bias = -4.5). Lactate threshold tests had high reliability (CV = 3.4–3.7%; r = 0.85–0.89; Bias = -2.1–3.0) except for D_MAX method (CV = 10.3%; r = 0.57; Bias = 15.4). Ventilatory thresholds show high reliability (CV = 1.6%–3.5%; r = 0.90–0.96; Bias = -1.8–2.9) except for RER = 1 and V-Slope (CV = 5.0–6.4%; r = 0.79; Bias = -5.6–12.4). Lactate threshold tests can be a valid and reliable alternative to ventilatory thresholds to identify the workloads at the transition from aerobic to anaerobic metabolism.

The purpose of this study was to determine the oral dose of caffeine needed to increase muscle force and power output during all-out single multijoint movements. Thirteen resistance-trained men underwent a battery of muscle strength and power tests in a randomized, double-blind, crossover design, under four different conditions: (a) placebo ingestion (PLAC) or with caffeine ingestion at doses of (b) 3 mg · kg(-1) body weight (CAFF 3mg), (c) 6 mg · kg(-1) (CAFF 6mg), and (d) 9 mg · kg(-1) (CAFF 9mg). The muscle strength and power tests consisted in the measurement of bar displacement velocity and muscle power output during free-weight full-squat (SQ) and bench press (BP) exercises against four incremental loads (25%, 50%, 75%, and 90% one-repetition maximum [1RM]). Cycling peak power output was measured using a 4-s inertial load test. Caffeine side effects were evaluated at the end of each trial and 24 h later. Mean propulsive velocity at light loads (25%-50% 1RM) increased significantly above PLAC for all caffeine doses (5.4%-8.5%, P = 0.039-0.003). At the medium load (75% 1RM), CAFF 3mg did not improve SQ or BP muscle power or BP velocity. CAFF 9mg was needed to enhance BP velocity and SQ power at the heaviest load (90% 1RM) and cycling peak power output (6.8%-11.7%, P = 0.03-0.05). The CAFF 9mg trial drastically increased the frequency of the adverse side effects (15%-62%). The ergogenic dose of caffeine required to enhance neuromuscular performance during a single all-out contraction depends on the magnitude of load used. A dose of 3 mg · kg(-1) is enough to improve high-velocity muscle actions against low loads, whereas a higher caffeine dose (9 mg · kg(-1)) is necessary against high loads, despite the appearance of adverse side effects.

Euhydrated and dehydrated subjects exercised in a hot and a cold environment with our aim to identify factors that relate to reductions in stroke volume (SV). We hypothesized that reductions in SV with heat stress are related to the interaction of several factors rather than the effect of elevated skin blood flow. Eight male endurance-trained cyclists [maximal O₂ consumption (V˙o _{2 max}) 4.5 ± 0.1 l/min; means ± SE] cycled for 30 min (72%V˙o _{2 max}) in the heat (H; 35°C) or the cold (C; 8°C) when euhydrated or dehydrated by 1.5, 3.0, or 4.2% of their body weight. When euhydrated, SV and esophageal temperature (T_es 38.2–38.3°C) were similar in H and C, whereas skin blood flow was much higher in H vs. C (365 ± 64% higher; P < 0.05). With each 1% body weight loss, SV declined 6.4 ± 1.3 ml (4.8%) in H and 3.4 ± 0.4 ml (2.5%) in C, whereas T_es increased 0.21 ± 0.02 and 0.10 ± 0.02°C in H and C, respectively ( P < 0.05). However, reductions in SV were not associated with increases in skin blood flow. The reduced SV was highly associated with increased heart rate and reduced blood volume in both H ( R = 0.96; P < 0.01) and C ( R = 0.85; P < 0.01). In conclusion, these results suggest that SV is maintained in trained subjects during exercise in euhydrated conditions despite large differences in skin blood flow. Furthermore, the lowering of SV with dehydration appears largely related to increases in heart rate and reductions in blood volume.