We compared the effects of two resistance training (RT) programs only differing in the repetition velocity loss allowed in each set: 20% (VL20) vs 40% (VL40) on muscle structural and functional adaptations. Twenty-two young males were randomly assigned to a VL20 (n = 12) or VL40 (n = 10) group. Subjects followed an 8-week velocity-based RT program using the squat exercise while monitoring repetition velocity. Pre- and post-training assessments included: magnetic resonance imaging, vastus lateralis biopsies for muscle cross-sectional area (CSA) and fiber type analyses, one-repetition maximum strength and full load-velocity squat profile, countermovement jump (CMJ), and 20-m sprint running. VL20 resulted in similar squat strength gains than VL40 and greater improvements in CMJ (9.5% vs 3.5%, P < 0.05), despite VL20 performing 40% fewer repetitions. Although both groups increased mean fiber CSA and whole quadriceps muscle volume, VL40 training elicited a greater hypertrophy of vastus lateralis and intermedius than VL20. Training resulted in a reduction of myosin heavy chain IIX percentage in VL40, whereas it was preserved in VL20. In conclusion, the progressive accumulation of muscle fatigue as indicated by a more pronounced repetition velocity loss appears as an important variable in the configuration of the resistance exercise stimulus as it influences functional and structural neuromuscular adaptations.

Background-A classic, unresolved physiological question is whether central cardiorespiratory and/or local skeletal muscle circulatory factors limit maximal aerobic capacity (V O 2 max) in humans. Severe heat stress drastically reduces V O 2 max, but the mechanisms have never been studied. Methods and Results-To determine the main contributing factor that limits V O 2 max with and without heat stress, we measured hemodynamics in 8 healthy males performing intense upright cycling exercise until exhaustion starting with either high or normal skin and core temperatures (ϩ10°C and ϩ1°C). Heat stress reduced V O 2 max, 2-legged V O 2 , and time to fatigue by 0.4Ϯ0.1 L/min (8%), 0.5Ϯ0.2 L/min (11%), and 2.2Ϯ0.4 minutes (28%), respectively (all PϽ0.05), despite heart rate and core temperature reaching similar peak values. However, before exhaustion in both heat stress and normal conditions, cardiac output, leg blood flow, mean arterial pressure, and systemic and leg O 2 delivery declined significantly (all 5% to 11%, PϽ0.05), yet arterial O 2 content and leg vascular conductance remained unchanged. Despite increasing leg O 2 extraction, leg V O 2 declined 5% to 6% before exhaustion in both heat stress and normal conditions, accompanied by enhanced muscle lactate accumulation and ATP and creatine phosphate hydrolysis. Conclusions-These results demonstrate that in trained humans, severe heat stress reduces V O 2 max by accelerating the declines in cardiac output and mean arterial pressure that lead to decrements in exercising muscle blood flow, O 2 delivery, and O 2 uptake. Furthermore, the impaired systemic and skeletal muscle aerobic capacity that precedes fatigue with or without heat stress is largely related to the failure of the heart to maintain cardiac output and O 2 delivery to locomotive muscle. Key Words: hemodynamics Ⅲ blood flow, regional Ⅲ cardiac output Ⅲ hemodynamics Ⅲ heat stress D uring heavy exercise, large volumes of oxygen are transported through the links of the cardiorespiratory transport system to mitochondrial cytochromes for synthesis of ATP in the electron transport chain. The fastest rate at which the body can utilize O 2 during heavy exercise is defined as the maximum rate of oxygen uptake (V O 2 max), which is an index of maximal cardiovascular function, provided pulmonary function and ambient O 2 concentration are normal. 1 The working skeletal muscle cells, which account for more than 90% of the energy spent during severe exercise, largely determine V O 2 max. 1-4 Long-standing yet unresolved debates center on whether central cardiorespiratory and/or local skeletal muscle circulatory and metabolic factors limit V O 2 max. [1][2][3][4][5][6][7] Severe heat stress has been shown to markedly suppress V O 2 max and work capacity without altering the initial rate of rise in whole-body V O 2 . 8 The mechanisms underlying the compensatory adjustments to heat stress early in exercise and the subsequent precipitated fatigue have never been investigated. During heavy exercise in normal environments, f...

During exercise, fatigue is defined as a reversible reduction in force- or power-generating capacity and can be elicited by "central" and/or "peripheral" mechanisms. During skeletal muscle contractions, both aspects of fatigue may develop independent of alterations in convective O(2) delivery; however, reductions in O(2) supply exacerbate and increases attenuate the rate of accumulation. In this regard, peripheral fatigue development is mediated via the O(2)-dependent rate of accumulation of metabolic by-products (e.g., inorganic phosphate) and their interference with excitation-contraction coupling within the myocyte. In contrast, the development of O(2)-dependent central fatigue is elicited 1) by interference with the development of central command and/or 2) via inhibitory feedback on central motor drive secondary to the peripheral effects of low convective O(2) transport. Changes in convective O(2) delivery in the healthy human can result from modifications in arterial O(2) content, blood flow, or a combination of both, and they can be induced via heavy exercise even at sea level; these changes are exacerbated during acute and chronic exposure to altitude. This review focuses on the effects of changes in convective O(2) delivery on the development of central and peripheral fatigue.

The present study examined whether the blood flow to exercising muscles becomes reduced when cardiac output and systemic vascular conductance decline with dehydration during prolonged exercise in the heat. A secondary aim was to determine whether the upward drift in oxygen consumption (V̇O2) during prolonged exercise is confined to the active muscles. Seven euhydrated, endurance‐trained cyclists performed two bicycle exercise trials in the heat (35 °C; 40–50% relative humidity; 61 ± 2% of maximal V̇O2), separated by 1 week. During the first trial (dehydration trial, DE), they bicycled until volitional exhaustion (135 ± 4 min, mean ± s.e.m.), while developing progressive dehydration and hyperthermia (3.9 ± 0.3% body weight loss; 39.7 ± 0.2 °C oesophageal temperature, Toes). In the second trial (control trial), they bicycled for the same period of time while maintaining euhydration by ingesting fluids and stabilizing Toes at 38.2 ± 0.1 °C after 30 min exercise. In both trials, cardiac output, leg blood flow (LBF), vascular conductance and V̇O2 were similar after 20 min exercise. During the 20 min‐exhaustion period of DE, cardiac output, LBF and systemic vascular conductance declined significantly (8–14%; P < 0.05) yet muscle vascular conductance was unaltered. In contrast, during the same period of control, all these cardiovascular variables tended to increase. After 135 ± 4 min of DE, the 2.0 ± 0.6 l min−1 lower blood flow to the exercising legs accounted for approximately two‐thirds of the reduction in cardiac output. Blood flow to the skin also declined markedly as forearm blood flow was 39 ± 8% (P < 0.05) lower in DE vs. control after 135 ± 4 min. In both trials, whole body V̇O2 and leg V̇O2 increased in parallel and were similar throughout exercise. The reduced leg blood flow in DE was accompanied by an even greater increase in femoral arterial‐venous O2 (a‐vO2) difference. It is concluded that blood flow to the exercising muscles declines significantly with dehydration, due to a lowering in perfusion pressure and systemic blood flow rather than increased vasoconstriction. Furthermore, the progressive increase in oxygen consumption during exercise is confined to the exercising skeletal muscles.

Acute hypoxia (AH) reduces maximal O2 consumption (VO2 max), but after acclimatization, and despite increases in both hemoglobin concentration and arterial O2 saturation that can normalize arterial O2 concentration ([O2]), VO2 max remains low. To determine why, seven lowlanders were studied at VO2 max (cycle ergometry) at sea level (SL), after 9-10 wk at 5,260 m [chronic hypoxia (CH)], and 6 mo later at SL in AH (FiO2 = 0.105) equivalent to 5,260 m. Pulmonary and leg indexes of O2 transport were measured in each condition. Both cardiac output and leg blood flow were reduced by approximately 15% in both AH and CH (P < 0.05). At maximal exercise, arterial [O2] in AH was 31% lower than at SL (P < 0.05), whereas in CH it was the same as at SL due to both polycythemia and hyperventilation. O2 extraction by the legs, however, remained at SL values in both AH and CH. Although at both SL and in AH, 76% of the cardiac output perfused the legs, in CH the legs received only 67%. Pulmonary VO2 max (4.1 +/- 0.3 l/min at SL) fell to 2.2 +/- 0.1 l/min in AH (P < 0.05) and was only 2.4 +/- 0.2 l/min in CH (P < 0.05). These data suggest that the failure to recover VO2 max after acclimatization despite normalization of arterial [O2] is explained by two circulatory effects of altitude: 1) failure of cardiac output to normalize and 2) preferential redistribution of cardiac output to nonexercising tissues. Oxygen transport from blood to muscle mitochondria, on the other hand, appears unaffected by CH.

To unravel the mechanisms by which maximal oxygen uptake (VO2 max) is reduced with severe acute hypoxia in humans, nine Danish lowlanders performed incremental cycle ergometer exercise to exhaustion, while breathing room air (normoxia) or 10.5% O2 in N2 (hypoxia, approximately 5,300 m above sea level). With hypoxia, exercise PaO2 dropped to 31-34 mmHg and arterial O2 content (CaO2) was reduced by 35% (P < 0.001). Forty-one percent of the reduction in CaO2 was explained by the lower inspired O2 pressure (PiO2) in hypoxia, whereas the rest was due to the impairment of the pulmonary gas exchange, as reflected by the higher alveolar-arterial O2 difference in hypoxia (P < 0.05). Hypoxia caused a 47% decrease in VO2 max (a greater fall than accountable by reduced CaO2). Peak cardiac output decreased by 17% (P < 0.01), due to equal reductions in both peak heart rate and stroke VOlume (P < 0.05). Peak leg blood flow was also lower (by 22%, P < 0.01). Consequently, systemic and leg O2 delivery were reduced by 43 and 47%, respectively, with hypoxia (P < 0.001) correlating closely with VO2 max (r = 0.98, P < 0.001). Therefore, three main mechanisms account for the reduction of VO2 max in severe acute hypoxia: 1) reduction of PiO2, 2) impairment of pulmonary gas exchange, and 3) reduction of maximal cardiac output and peak leg blood flow, each explaining about one-third of the loss in VO2 max.

The rate of gastric emptying and the plasma GLP-1 and PYY responses to feeding with cow milk protein solutions in humans are independent of the degree of protein fractionation and are not altered by small differences in the amino acid composition or protein solubility. In contrast, the GIP response is accentuated when milk proteins are delivered as peptide hydrolysates.

To determine whether conditions for O 2 utilization and O2 off-loading from the hemoglobin are different in exercising arms and legs, six cross-country skiers participated in this study. Femoral and subclavian vein blood flow and gases were determined during skiing on a treadmill at ϳ76% maximal O 2 uptake (V O2 max) and at V O2 max with different techniques: diagonal stride (combined arm and leg exercise), double poling (predominantly arm exercise), and leg skiing (predominantly leg exercise). The percentage of O 2 extraction was always higher for the legs than for the arms. At maximal exercise (diagonal stride), the corresponding mean values were 93 and 85% (n ϭ 3; P Ͻ 0.05). During exercise, mean arm O 2 extraction correlated with the PO2 value that causes hemoglobin to be 50% saturated (P 50: r ϭ 0.93, P Ͻ 0.05), but for a given value of P 50, O2 extraction was always higher in the legs than in the arms. Mean capillary muscle O 2 conductance of the arm during double poling was 14.5 (SD 2.6) ml ⅐ min Ϫ1 ⅐ mmHg Ϫ1 , and mean capillary PO 2 was 47.7 (SD 2.6) mmHg. Corresponding values for the legs during maximal exercise were 48.3 (SD 13.0) ml ⅐ min Ϫ1 ⅐ mmHg Ϫ1 and 33.8 (SD 2.6) mmHg, respectively. Because conditions for O 2 off-loading from the hemoglobin are similar in leg and arm muscles, the observed differences in maximal arm and leg O 2 extraction should be attributed to other factors, such as a higher heterogeneity in blood flow distribution, shorter mean transit time, smaller diffusing area, and larger diffusing distance, in arms than in legs. diffusing capacity; fatigue; oxygen extraction; performance; training MUSCULAR OXYGEN UPTAKE depends on extrinsic factors such as O 2 delivery and the intrinsic factors that regulate both the transfer of O 2 from the erythrocytes to the mitochondria and the subsequent utilization of O 2 in the mitochondria. However, the diffusive transfer of O 2 is not only determined by intrinsic factors, because it also depends on mean capillary O 2 tension. It is currently assumed that during exercise with a small muscle mass, intrinsic factors are the main determinants of peak local muscular V O 2 , because the O 2 delivery is extraordinary high (3,44,61). During exercise with a large muscle mass, the V O 2 peak of the lower extremities appears to be O 2 delivery dependent (6,7,16,33,35,57). O 2 extraction across the lower extremities may reach maximal values between 90 and 92% of the arterial O 2 content (Ca O 2 ), and the PO 2 in the femoral vein may be close to 10 mmHg in active subjects (6,7,16), leaving little room for further extraction. However, in sedentary subjects, the maximal O 2 extraction across the legs lies close to 70% of the Ca O 2 (59), implying that their peak muscular V O 2 also may be limited by intrinsic factors (20). In physically active but nonarm-trained subjects, a low O 2 extracting capacity has been reported for the arms (1,11,51,70). Moreover, arm training resulted in only a marginal improvement in the O 2 extraction of the arms (51). Therefore, ...