Evidence for impaired skeletal muscle contraction-induced rapid vasodilation in aging humans

We tested the hypothesis that aging is associated with an impaired contraction-induced rapid vasodilation in healthy adults. We reasoned that employing single contractions of a small muscle mass would allow us to isolate the local rapid vasodilatory responses independent of systemic hemodynamic and sympathetic neural influences on forearm hemodynamics. We measured forearm blood flow (Doppler ultrasound) and arterial blood pressure (Finapres) on a beat-by-beat basis and calculated the changes in forearm vascular conductance (DeltaFVC) in response to forearm contractions in 18 young (24 +/- 1 yr) and 13 older (62 +/- 2 yr) healthy subjects. Single, 1-s dynamic forearm contractions were performed with the experimental arm slightly above heart level at 5, 10, 20, and 40% of the subjects' maximal voluntary contraction (MVC) in random order. In general, muscle contractions evoked a rapid increase in FVC that reached a peak within approximately four to five cardiac cycles postcontraction in both age groups. At 5% MVC, there were no significant age-related differences in contraction-induced forearm vasodilation. However, the peak vasodilatory responses were impaired approximately 40-45% in older adults at 10, 20, and 40% MVC, as were the total vasodilatory responses (area under curve approximately 40-50%; all P < 0.05). Additionally, the immediate vasodilation (first cardiac cycle postcontraction) for the 20% and 40% MVC trials was also impaired approximately 50% with age (P < 0.05). There were no significant age-group differences in MVC or forearm fat-free mass, and these variables were not correlated with local vasodilation within a given exercise intensity. Under the experimental conditions employed, the blunted responses with age reflect impaired local contraction-induced rapid vasodilation.     

Influence of age on cardiac baroreflex function during dynamic exercise in humans

We investigated the influence of aging on cardiac baroreflex function during dynamic exercise in seven young (22 +/- 1 yr) and eight older middle-aged (59 +/- 2 yr) healthy subjects. Carotid-cardiac baroreflex function was assessed at rest and during moderate-intensity steady-state cycling performed at 50% heart rate reserve (HRR). Five-second pulses of neck pressure and neck suction from +40 to -80 Torr were applied to determine the operating point gain (G(OP)) and maximal gain (G(MAX)) of the full carotid-cardiac baroreflex function curve and examine baroreflex resetting during exercise. At rest, mean arterial pressure (MAP) and heart rate were similar between the younger and older subjects. In contrast, the resting G(OP) and G(MAX) were significantly lower in the older subjects. The increase in MAP from rest to exercise was greater in the older subjects (Delta +20 +/- 2 older vs. Delta +6 +/- 3 younger mmHg; P < 0.001). However, the G(OP) was similar in both groups during exercise because of a reduction in the younger subjects. In contrast, G(MAX) was unchanged from rest and therefore remained lower in older subjects (-0.19 +/- 0.05 older vs. -0.42 +/- 0.05 younger beats.min(-1).mmHg(-1); 50% HRR; P < 0.001). Furthermore, exercise resulted in an upward and rightward resetting of the cardiac baroreflex function curve in both groups. Collectively, these findings suggest that the cardiac baroreflex function curve appropriately resets during exercise in older subjects but operates at a reduced G(MAX) primarily because of age-related reductions in carotid-cardiac control manifest at rest.     

Effect of aging on renal blood flow velocity during static exercise

During exercise, activation of the sympathetic nervous system causes reflex renal vasoconstriction. The effects of aging on this reflex are poorly understood. This study evaluated the effects of age on renal vasoconstrictor responses to handgrip. Seven older (65 +/- 9 yr) and nine younger (25 +/- 2 yr) subjects were studied. Beat-by-beat analyses of changes in renal blood flow velocity (RBV; duplex ultrasound) were performed during two handgrip paradigms. Arterial blood pressure (BP) and heart rate were also measured, and an index of renal vascular resistance (RVR) was calculated (BP/RBV). In protocol 1, fatiguing handgrip [40% of maximal voluntary contraction (MVC)] caused a greater increase in RVR in the older subjects (old 90% +/- 15 increase, young 52% +/- 4 increase; P = 0.03). During posthandgrip circulatory arrest (isolates muscle metaboreflex), the increases in RVR were only approximately 1/2 of the increase seen at end grip. In protocol 2, 15-s bouts of handgrip at graded intensities led to increases in RVR in both subject groups. This effect was not seen until 50% MVC workload (P < 0.05). RVR responses occurred early and were greater in older than in younger subjects at 50% MVC (32 +/- 6% vs. 16 +/- 5%; P = 0.02) and 70% MVC (39 +/- 11% vs. 24 +/- 8%; P = 0.02). Static exercise-induced renal vasoconstriction is enhanced with aging. Because the characteristics of this response suggest a predominant role for mechanoreceptor engagement, we hypothesize that mechanoreceptor responses are augmented with aging.     

Forearm blood flow responses to fatiguing isometric contractions in women and men

Previous studies suggest that women experience less vascular occlusion than men when generating the same relative contractile force. This study examined forearm blood flow (FBF) in women and men during isometric handgrip exercise requiring the same relative force. Thirty-eight subjects [20 women and 18 men, 22.8 +/- 0.6 yrs old (means +/- SE)] performed low- and moderate-force handgrip exercise on two occasions. Subjects performed five maximum voluntary contractions (MVC) before exercise to determine 20% and 50% MVC target forces. Time to task failure (TTF) was determined when the subject could not maintain force within 5% of the target force. Mean blood velocity was measured in the brachial artery with the use of Doppler ultrasonography. Arterial diameter was measured at rest and used to calculate absolute FBF (FBFa; ml/min) and relative FBF (FBFr; ml.min(-1).100 ml(-1)). Women generated less (P < 0.05) absolute maximal force (208 +/- 10 N) than men (357 +/- 17 N). The TTF was longer (P < 0.05) at 20% MVC for women (349 +/- 32 s) than for men (230 +/- 23 s), but no difference between the sexes was observed at 50% MVC (women: 69 +/- 5 s; men: 71 +/- 8 s). FBFa and FBFr increased (P < 0.05) from rest to TTF in both women and men during 20% and 50% MVC trials. FBFr was greater in women than in men at > or =30% TTF during 50% MVC. At exercise durations > or =60% of TTF, FBFa was lower (P < 0.05) in women than in men during handgrip at 20% MVC. Despite the longer exercise duration for women at the lower contraction intensity, FBFr was similar between the sexes, suggesting that muscle perfusion is matched to the exercising muscle mass independent of sex.     

The effect of age and gender on the relative fatigability of the human adductor pollicis muscle

The purpose of this study was to examine the relative influence of such factors as age, gender, and absolute force on the fatiguability of the human adductor pollicis muscle. 12 young males (YM, 25.3 +/- 2.1 y), 12 young females (YF. 23.5 +/- 2.1 y), 12 older males (OM, 71.7 +/- 5.6 y) and 12 older females (OF, 69.5 +/- 4.6 y) participated. Three minutes of intermittent (5 s contraction, 2 s rest) maximal voluntary contractions (MVC) were used to fatigue the adductor pollicis muscle; the ulnar nerve was also stimulated in each 2 s rest period to evoke a maximal twitch. Males were stronger than females in both voluntary and evoked force (PT) in the young age group (MVC: YM, 10.0 +/- 2.7 kg vs. YF, 6.6 +/- 1.1 kg, P < 0.05) (PT: YM, 0.99 +/- 0.21 kg vs. YF, 0.71 +/- 0.12 kg, P < 0.05). In the older adults, however, males were stronger only in the evoked twitch (OM, 0.73 +/- 0.24 kg vs. OF, 0.48 +/- 0.07 kg, P < 0.05). There was no significant effect of gender or absolute muscle force on relative fatigability; the only variable found to significantly affect fatigability was age. Older adults were significantly less fatigable than young adults as indicated by the voluntary fatigue index (FI) (percentage of force reduction from baseline; FI-young, 40.2 +/- 12.6% vs. FI-old, 25.2 +/- 12.3%). This age effect, however, was more prominent in males than females (FI-YM, 44.7 +/- 10.5% vs. FI-OM, 24.2 +/- 10.7%, P < 0.01; FI-YF, 37.8 +/- 14.1% vs. FI-OF, 26.3 +/- 14.5%, P = 0.13). In conclusion, age was found to be the strongest single predictor of fatigability during short duration, intermittent exercise in human adductor pollicis muscle.     

Changes of muscular sound during sustained isometric contraction up to exhaustion

The sound (SMG) generated by the biceps muscle during isometric exercise at 20, 40, 60, and 80% of maximum voluntary contraction (MVC) up to exhaustion has been recorded by a contact transducer and integrated (iSMG), together with the surface electromyogram (EMG) in eight young untrained men. At the onset of exercise, iSMG and integrated surface EMG (iEMG) amplitude increased linearly with exercise. iSMG remained constant for 253 +/- 73 (SD), 45 +/- 16, 21 +/- 5, and 0 s at the four levels of contraction. Then iSMG increased linearly at 20% MVC, fluctuated at 40% MVC, and decreased exponentially at 60 and 80% MVC. iSMG exhaustion-to-onset ratio was 5.0 at 20%, 1.0 at 40%, and 0.2 at 60 and 80% MVC. On the contrary, independently of exercise intensity, iEMG increased with time, being 1.4 higher at exhaustion than at the onset. The nonunivocal iSMG changes with time and effort of exercise suggest that the sound may be a useful tool to acquire different information to EMG and output force during muscle contraction up to fatigue.     

O2 uptake kinetics, pyruvate dehydrogenase activity, and muscle deoxygenation in young and older adults during the transition to moderate-intensity exercise

The adaptation of pulmonary O(2) uptake (Vo(2)(p)) kinetics is slowed in older compared with young adults during the transition to moderate-intensity exercise. In this study, we examined the relationship between Vo(2)(p) kinetics and mitochondrial pyruvate dehydrogenase (PDH) activity in young (n = 7) and older (n = 6) adults. Subjects performed cycle exercise to a work rate corresponding to approximately 90% of estimated lactate threshold. Phase 2 Vo(2)(p) kinetics were slower (P < 0.05) in older (tau = 40 +/- 17 s) compared with young (tau = 21 +/- 6 s) adults. Relative phosphocreatine (PCr) breakdown was greater (P < 0.05) at 30 s in older compared with young adults. Absolute PCr breakdown at 6 min was greater (P < 0.05) in older compared with young adults. In young adults, PDH activity increased (P < 0.05) from baseline to 30 s, with no further change observed at 6 min. In older adults, PDH activity during baseline exercise was similar to that seen in young adults. During the exercise transition, PDH activity did not increase (P > 0.05) at 30 s of exercise but was elevated (P < 0.05) after 6 min. The change in deoxyhemoglobin (HHb) was greater for a given Vo(2)(p) in older adults, and there was a similar time course of HHb accompanying the slower Vo(2)(p) kinetics in the older adults, suggesting a slower adaptation of bulk O(2) delivery in older adults. In conclusion, the slower adaptation of Vo(2)(p) in older adults is likely a result of both an increased metabolic inertia and lower O(2) availability.     

Muscle endurance is greater for old men compared with strength-matched young men.

The purpose was to compare the time to task failure for a sustained isometric contraction performed at a submaximal intensity with the elbow flexor muscles by young and old men who were matched for strength. Eight young men (18-31 yr) and eight old men (67-76 yr) sustained an isometric contraction at 20% of maximal voluntary contraction (MVC) torque until the target torque could no longer be achieved for at least 5 s. The maximal torque exerted at the wrist was similar for the young and old men before the fatiguing task (65.9 +/- 8.0 vs. 65.4 +/- 8.7 N x m; P > 0.05), and they experienced similar reductions in MVC torque after the fatiguing contraction (31.4 +/- 10.6%; P < 0.05). The time to task failure was longer for the old men (22.6 +/- 7.4 min) compared with the strength-matched young men (13.0 +/- 5.2 min; P < 0.05), despite each group sustaining a similar torque during the fatiguing contraction (P > 0.05). The increases in torque fluctuations, electromyographic (EMG) bursting activity, and heart rate were greater for young men compared with the old men, and they were less at task failure for the old men (P < 0.05). Mean arterial pressure increased at a similar rate for both groups of men (P > 0.05), whereas the averaged EMG activity and rating of perceived exertion reached similar values at task failure for the young and old men (P > 0.05). These findings indicate that the longer time to task failure for the old men when performing the submaximal contraction was not due the absolute target torque exerted during the contraction.     

High-dose ascorbic acid infusion abolishes chronic vasoconstriction and restores resting leg blood flow in healthy older men.

Resting whole leg blood flow and vascular conductance decrease linearly with advancing age in healthy adult men. The potential role of age-related increases in oxidative stress in these changes is unknown. Resting leg blood flow during saline and ascorbic acid infusion was studied in 10 young (25 +/- 1 yr) and 11 older (63 +/- 2 yr) healthy normotensive men. Plasma oxidized LDL, a marker of oxidative stress, was greater in the older men (P < 0.05). Absolute resting femoral artery blood flow at baseline (iv saline control infusion) was 25% lower in the older men (238 +/- 25 vs. 316 +/- 38 ml/min; P < 0.05), and it was inversely related to plasma oxidized LDL (r = -0.56, P < 0.01) in all subjects. Infusion of supraphysiological concentrations of ascorbic acid increased femoral artery blood flow by 37% in the older men (to 327 +/- 52 ml/min; P < 0.05), but not in the young men (352 +/- 41 ml/min; P = 0.28), thus abolishing group differences (P = 0.72). Mean arterial blood pressure was greater in the older men at baseline (86 +/- 4 vs. 78 +/- 2 mmHg; P < 0.05), but it was unaffected by ascorbic acid infusion (P >/= 0.70). As a result, the lower baseline femoral artery blood flow in the older men was mediated solely by a 32% lower femoral artery vascular conductance (P < 0.05). Baseline femoral vascular conductance also was inversely related to plasma oxidized LDL (r = -0.65, P < 0.01). Ascorbic acid increased femoral vascular conductance by 36% in the older men (P < 0.05) but not in the young men (P = 0.31). In conclusion, ascorbic acid infused at concentrations known to scavenge reactive oxygen species restores resting femoral artery blood flow in healthy older adult men by increasing vascular conductance. These results support the hypothesis that oxidative stress plays a major role in the reduced resting whole leg blood flow and increased leg vasoconstriction observed with aging in men.     

Levels of serum creatine kinase and myoglobin in women after two isometric exercise conditions

The purpose of this study was to measure serum creatine kinase (CK) activity and serum myoglobin (MG) concentrations in women after two unilateral isometric knee extension exercises. Forty maximal voluntary contractions (MVC) were held for 10 s, with either a 5 s (10:5) or 20 s 10:20 exercise (349.4 +/- 66.1 mU . ml-1) and 6 h and MG values were measured pre, 0, 3, 6, and 18 h post exercise. For CK, the highest post exercise values were observed at 6 h following the 10:20 exercise (349.4 +/- 66.1 mU . ml-1) and 6 h following the 10:5 exercise (194.1 +/- 18.6 mU . ml-1). For MG, the highest values were found 3 h after the 10:20 exercise (148.9 +/- 61.7 ng . ml-1) and 6 h after the 10:5 exercise (67.3 +/- 10.9 ng . ml-1). Serum CK and MG levels were significantly greater (p less than 0.01) after the 10:20 exercise bout. The data demonstrate that CK and MG values for women increase significantly after isometric exercise. Since greater tension levels were maintained during the 10:20 exercise it is hypothesized that increased serum CK and MG values after isometric exercise may be related to the tension generated by the contracting muscle.     

Effects of exercise intensity on the sweating response to a sustained static exercise.

To investigate how the sweating response to a sustained handgrip exercise depends on changes in the exercise intensity, the sweating response to exercise was measured in eight healthy male subjects. Each subject lay in the supine position in a climatic chamber (35 degrees C and 50% relative humidity) for approximately 60 min. This exposure caused sudomotor activation by increasing skin temperature without a marked change in internal temperature. After this period, each subject performed isometric handgrip exercise [15, 30, 45, and 60% maximal voluntary contraction (MVC)] for 60 s. Although esophageal and mean skin temperatures did not change with a rise in exercise intensity and were similar at all exercise intensities, the sweating rate (SR) on the forearm increased significantly (P < 0.05) from baseline (0.094 +/- 0.021 mg. cm(-2). min(-1) at 30% MVC, 0.102 +/- 0.022 mg. cm(-2). min(-1) at 45% MVC, 0.059 +/- 0.009 mg. cm(-2). min(-1) at 60% MVC) in parallel with exercise intensity above exercise intensity at 30% MVC (0.121 +/- 0.023 mg. cm(-2). min(-1) at 30% MVC, 0.242 +/- 0.051 mg. cm(-2). min(-1) at 45% MVC, 0.290 +/- 0.056 mg. cm(-2). min(-1) at 60% MVC). Above 45% MVC, SR on the palm increased significantly from baseline (P < 0.05). Although SR on the forearm and palm tended to increase with a rise in exercise intensity, there was a difference in the time courses of SR between sites. SR on the palm showed a plateau after abrupt increase, whereas SR on the forearm increased progressively during exercise. These results suggest that the increase in SR with the increase in sustained handgrip exercise intensity is due to nonthermal factors and that the magnitude of these factors during the exercise may be responsible for the magnitude of SR.     

Age-related enhancement of fatigue resistance is evident in men during both isometric and dynamic tasks.

It has been suggested that the effects of old age on the ability to resist fatigue may be task dependent. To test one aspect of this hypothesis, we compared the neuromuscular responses of nine young (26 +/- 4 yr, mean +/- SD) and nine older (72 +/- 4 yr) healthy, relatively sedentary men to intermittent isometric (3 min, 5 s contract/5 s rest) and dynamic (90 at 90 degrees /s) maximum voluntary contractions (MVC) of the ankle dorsiflexor muscles. To assess the mechanisms of fatigue (defined as the ratio of postexercise MVC to preexercise MVC), we also measured isometric central activation ratios (CAR), tetanic torque, contractile properties, and compound muscle action potentials before and immediately after exercise. Because dynamic contractions are more neurally complex and metabolically demanding than isometric contractions, we expected an age-related fatigue resistance observed during isometric exercise to be absent during dynamic exercise. In contrast, older men (O) fatigued less than young (Y) during both isometric (O = 0.77 +/- 0.07, Y = 0.66 +/- 0.02, mean +/- SE; P < 0.01) and dynamic (O = 0.45 +/- 0.07, Y = 0.27 +/- 0.02; P = 0.04) contractions (ratio of postexercise to preexercise MVC), with no evidence of peripheral activation failure in either group. We observed no obvious limitations in central activation in either group, as assessed using isometric CAR methods, after both isometric and dynamic contractions. Preexercise half-time of tetanic torque relaxation, which was longer in O compared with Y, was linearly associated with fatigue resistance during both protocols (r = 0.62 and 0.66, P < or = 0.004, n = 18). These results suggest that relative fatigue resistance is enhanced in older adults during both isometric and isokinetic contractions and that age-related changes in fatigue may be due largely to differences within the muscle itself.     

The impact of aging and habitual physical activity on static respiratory work at rest and during exercise

We investigated the effects of aging on the elastic properties of lung tissue and the chest wall, simultaneously quantifying the contribution of each component to static inspiratory muscle work in resting and exercising adults. We further evaluated the interaction of aging and habitual physical activity on respiratory mechanics. Static lung volumes and elastic properties of the lung and chest wall (pressure-volume relaxation maneuvers) in 29 chronically sedentary and 29 habitually active subjects, grouped by age, were investigated: young (Y, 20-30 years), middle-aged (M, 40-50 years), and older (O, >60 years). Using static pressure-volume data, we computed the elastic work of breathing (joules per liter, J.l(-1)), including inspiratory muscle work, over resting and exercising tidal volume excursions. Elastic work of the lung (Y = 0.79 +/- 0.05; M = 0.47 +/- 0.05; O = 0.43 +/- 0.05 J.l(-1)) and chest wall (Y = -0.49 +/- 0.06; M = -0.12 +/- 0.07; O = 0.04 +/- 0.05 J.l(-1) ) changed significantly with age (P < 0.05). With aging, a parallel displacement of the chest wall pressure-volume curve resulted in a shift from energy being stored primarily during expiration to energy storage during inspiration, and driving expiration, both at rest and during exercise. Although deviating significantly from young adults, this did not significantly elevate static inspiratory muscle work but resulted in a redistribution of the tissues on which this work was performed and the phase of the respiratory cycle in which it occurred. Nevertheless, static inspiratory muscle work remained similar across age groups, at rest and during exercise, and habitual physical activity failed to influence these changes.     

Oxygen uptake kinetics for moderate exercise are speeded in older humans by prior heavy exercise.

This study examined the effect of heavy-intensity warm-up exercise on O(2) uptake (VO(2)) kinetics at the onset of moderate-intensity (80% ventilation threshold), constant-work rate exercise in eight older (65 +/- 2 yr) and seven younger adults (26 +/- 1 yr). Step increases in work rate from loadless cycling to moderate exercise (Mod(1)), heavy exercise, and moderate exercise (Mod(2)) were performed. Each exercise bout was 6 min in duration and separated by 6 min of loadless cycling. VO(2) kinetics were modeled from the onset of exercise by use of a two-component exponential model. Heart rate (HR) kinetics were modeled from the onset of exercise using a single exponential model. During Mod(1), the time constant (tau) for the predominant rise in VO(2) (tau VO(2)) was slower (P < 0.05) in the older adults (50 +/- 10 s) than in young adults (19 +/- 5 s). The older adults demonstrated a speeding (P < 0.05) of VO(2) kinetics when moderate-intensity exercise (Mod(2)) was preceded by high-intensity warm-up exercise (tau VO(2), 27 +/- 3 s), whereas young adults showed no speeding of VO(2) kinetics (tau VO(2), 17 +/- 3 s). In the older and younger adults, baseline HR preceding Mod(2) was elevated compared with Mod(1), but the tau for HR kinetics was slowed (P < 0.05) in Mod(2) only for the older adults. Prior heavy-intensity exercise in old, but not young, adults speeded VO(2) kinetics during Mod(2). Despite slowed HR kinetics in Mod(2) in the older adults, an elevated baseline HR before the onset of Mod(2) may have led to sufficient muscle perfusion and O(2) delivery. These results suggest that, when muscle blood flow and O(2) delivery are adequate, muscle O(2) consumption in both old and young adults is limited by intracellular processes within the exercising muscle.     

Effects of prior heavy-intensity exercise on pulmonary O2 uptake and muscle deoxygenation kinetics in young and older adult humans.

Pulmonary O2 uptake (VO2p) and muscle deoxygenation kinetics were examined during moderate-intensity cycling (80% lactate threshold) without warm-up and after heavy-intensity warm-up exercise in young (n = 6; 25 +/- 3 yr) and older (n = 5; 68 +/- 3 yr) adults. We hypothesized that heavy warm-up would speed VO2p kinetics in older adults consequent to an improved intramuscular oxygenation. Subjects performed step transitions (n = 4; 6 min) from 20 W to moderate-intensity exercise preceded by either no warm-up or heavy-intensity warm-up (6 min). VO2p was measured breath by breath. Oxy-, deoxy-(HHb), and total hemoglobin and myoglobin (Hb(tot)) of the vastus lateralis muscle were measured continuously by near-infrared spectroscopy (NIRS). VO2p (phase 2; tau) and HHb data were fit with a monoexponential model. After heavy-intensity warm-up, oxyhemoglobin (older subjects: 13 +/- 9 microM; young subjects: 9 +/- 8 microM) and Hb(tot) (older subjects: 12 +/- 8 microM; young subjects: 14 +/- 10 microM) were elevated (P < 0.05) relative to the no warm-up pretransition baseline. In older adults, tauVO2p adapted at a faster rate (P < 0.05) after heavy warm-up (30 +/- 7 s) than no warm-up (38 +/- 5 s), whereas in young subjects, tauVO2p was similar in no warm-up (26 +/- 7 s) and heavy warm-up (25 +/- 5 s). HHb adapted at a similar rate in older and young adults after no warm-up; however, in older adults after heavy warm-up, the adaptation of HHb was slower (P < 0.01) compared with young and no warm-up. These data suggest that, in older adults, VO2p kinetics may be limited by a slow adaptation of muscle blood flow and O2 delivery.     

Regulation of middle cerebral artery blood velocity during dynamic exercise in humans: influence of aging.

Although cerebral autoregulation (CA) appears well maintained during mild to moderate intensity dynamic exercise in young subjects, it is presently unclear how aging influences the regulation of cerebral blood flow during physical activity. Therefore, to address this question, middle cerebral artery blood velocity (MCAV), mean arterial pressure (MAP), and the partial pressure of arterial carbon dioxide (Pa(CO(2))) were assessed at rest and during steady-state cycling at 30% and 50% heart rate reserve (HRR) in 9 young (24 +/- 3 yr; mean +/- SD) and 10 older middle-aged (57 +/- 7 yr) subjects. Transfer function analysis between changes in MAP and mean MCAV (MCAV(mean)) in the low-frequency (LF) range were used to assess dynamic CA. No age-group differences were found in Pa(CO(2)) at rest or during cycling. Exercise-induced increases in MAP were greater in older subjects, while changes in MCAV(mean) were similar between groups. The cerebral vascular conductance index (MCAV(mean)/MAP) was not different at rest (young 0.66 +/- 0.04 cm x s(-1) x mmHg(-1) vs. older 0.67 +/- 0.03 cm x s(-1) x mmHg(-1); mean +/- SE) or during 30% HRR cycling between groups but was reduced in older subjects during 50% HRR cycling (young 0.67 +/- 0.03 cm x s(-1) x mmHg(-1) vs. older 0.56 +/- 0.02 cm x s(-1) x mmHg(-1); P < 0.05). LF transfer function gain and phase between MAP and MCAV(mean) was not different between groups at rest (LF gain: young 0.95 +/- 0.05 cm x s(-1) x mmHg(-1) vs. older 0.88 +/- 0.06 cm x s(-1) x mmHg(-1); P > 0.05) or during exercise (LF gain: young 0.80 +/- 0.05 cm x s(-1) x mmHg(-1) vs. older 0.72 +/- 0.07 cm x s(-1) x mmHg(-1) at 50% HRR; P > 0.05). We conclude that despite greater increases in MAP, the regulation of MCAV(mean) is well maintained during dynamic exercise in healthy older middle-aged subjects.     

Mechanical effects of muscle contraction do not blunt sympathetic vasoconstriction in humans

Sympathetic vasoconstrictor responses are blunted in the vascular beds of contracting muscle (functional sympatholysis), but the mechanism(s) have been difficult to elucidate. We tested the hypothesis that the mechanical effects of muscle contraction blunt sympathetic vasoconstriction in human muscle. We measured forearm blood flow (Doppler ultrasound) and calculated the reductions in forearm vascular conductance (FVC) in response to reflex increases in sympathetic activity evoked via lower body negative pressure (LBNP). In protocol 1, eight young adults were studied under control resting conditions and during simulated muscle contractions using rhythmic forearm cuff inflations (20 inflations/min) with cuff pressures of 50 and 100 mmHg with the arm below heart level (BH), as well as 100 mmHg with the arm at heart level (HL). Forearm vasoconstrictor responses (%DeltaFVC) during LBNP were -26 +/- 2% during control conditions and were not blunted by simulated contractions (range = -31 +/- 3% to -43 +/- 6%). In protocol 2, eight subjects were studied under control conditions and during rhythmic handgrip exercise (20 contractions/min) using workloads of 15% maximum voluntary contraction (MVC) at HL and BH (similar metabolic demand, greater mechanical muscle pump effect for the latter) and 5% MVC BH alone and in combination with superimposed forearm compressions of 100 mmHg (similar metabolic demand, greater mechanical component of contractions for the latter). The forearm vasoconstrictor responses during LBNP were blunted during 15% MVC exercise with the arm at HL (-1 +/- 3%) and BH (-2 +/- 3%) compared with control (-25 +/- 3%; both P < 0.005) but were intact during both 5% MVC alone (-24 +/- 4%) and with superimposed compressions (-23 +/- 4%). We conclude that mechanical effects of contraction per se do not cause functional sympatholysis in the human forearm and that this phenomenon appears to be coupled with the metabolic demand of contracting skeletal muscle.     

Role of skin blood flow and sweating rate in exercise thermoregulation after bed rest.

Two potential mechanisms, reduced skin blood flow (SBF) and sweating rate (SR), may be responsible for elevated intestinal temperature (T(in)) during exercise after bed rest and spaceflight. Seven men underwent 13 days of 6 degrees head-down bed rest. Pre- and post-bed rest, subjects completed supine submaximal cycle ergometry (20 min at 40% and 20 min at 65% of pre-bed rest supine peak exercise capacity) in a thermoneutral room. After bed rest, T(in) was elevated at rest (+0.31 +/- 0.12 degrees C) and at the end of exercise (+0.33 +/- 0.07 degrees C). Percent increase in SBF during exercise was less after bed rest (211 +/- 53 vs. 96 +/- 31%; P < or = 0.05), SBF/T(in) threshold was greater (37.09 +/- 0.16 vs. 37.33 +/- 0.13 degrees C; P < or = 0.05), and slope of SBF/T(in) tended to be reduced (536 +/- 184 vs. 201 +/- 46%/ degrees C; P = 0.08). SR/T(in) threshold was delayed (37.06 +/- 0.11 vs. 37.34 +/- 0.06 degrees C; P < or = 0.05), but the slope of SR/T(in) (3.45 +/- 1.22 vs. 2.58 +/- 0.71 mg x min-1 x cm-2 x degrees C-1) and total sweat loss (0.42 +/- 0.06 vs. 0.44 +/- 0.08 kg) were not changed. The higher resting and exercise T(in) and delayed onset of SBF and SR suggest a centrally mediated elevation in the thermoregulatory set point during bed rest exposure.     

Postexercise muscle glycogen resynthesis in obese insulin-resistant Zucker rats.

We determined the effect of an acute bout of swimming (8 x 30 min) followed by either carbohydrate administration (0.5 mg/g glucose ip and ad libitum access to chow; CHO) or fasting (Fast) on postexercise glycogen resynthesis in soleus muscle and liver from female lean (ZL) and obese insulin-resistant (ZO) Zucker rats. Resting soleus muscle glycogen concentration ([glycogen]) was similar between genotypes and was reduced by 73 (ZL) and 63% (ZO) after exercise (P < 0.05). Liver [glycogen] at rest was greater in ZO than ZL (334 +/- 31 vs. 247 +/- 16 micromol/g wet wt; P < 0.01) and fell by 44 and 94% after exercise (P < 0.05). The fractional activity of glycogen synthase (active/total) increased immediately after exercise (from 0.22 +/- 0.05 and 0.32 +/- 0.04 to 0.63 +/- 0.08 vs. 0.57 +/- 0.05; P < 0.01 for ZL and ZO rats, respectively) and remained elevated above resting values after 30 min of recovery. During this time, muscle [glycogen] in ZO increased 68% with CHO (P < 0.05) but did not change in Fast. Muscle [glycogen] was unchanged in ZL from postexercise values after both treatments. After 6 h recovery, GLUT-4 protein concentration was increased above resting levels by a similar extent for both genotypes in both fasted (approximately 45%) and CHO-supplemented (approximately 115%) rats. Accordingly, during this time CHO refeeding resulted in supercompensation in both genotypes (68% vs. 44% for ZL and ZO). With CHO, liver [glycogen] was restored to resting levels in ZL but remained at postexercise values for ZO after both treatments. We conclude that the increased glucose availability with carbohydrate refeeding after glycogen-depleting exercise resulted in glycogen supercompensation, even in the face of muscle insulin-resistance.     

Effect of exercise at three exercise intensities on salivary cortisol

Changes in cortisol concentration in response to exercise at 3 different intensities were quantified. Ten apparently healthy, recreationally active males participated. On 4 separate occasions, subjects were assigned a random order of 1-hour cycle ergometer bouts of exercise at 44.5 +/- 5.5%, 62.3 +/- 3.8%, and 76.0 +/- 6.0% (mean +/- SD) of VO2peak and a resting control session. Saliva samples were collected before exercise at 10, 20, 40, and 59 minutes of exercise and at 20 minutes of recovery. Differences in cortisol concentration were assessed via multivariate analysis of variance (alpha = 0.05) Tukey post hoc analysis when indicated. During the highest-intensity exercise session, cortisol was significantly higher at 59 minutes of exercise (p = 0.004) and at 20 minutes of recovery (p = 0.016) than at those same time points during the resting control session. No significant differences in cortisol concentration were noted among resting, low-, and moderate-intensity exercise. Exercise <40 minutes in duration elicited no significant differences at any intensity. These data indicate that only exercise of high intensity and long duration results in significant elevations of salivary cortisol.