A comparison of the immediate effects of resistance, aerobic, and concurrent exercise on postexercise hypotension

A comparison of the immediate effects of resistance, aerobic, and concurrent exercise on postexercise hypotension. The influence of resistance exercise (RE), aerobic exercise (AE), and concurrent exercise (CE) on postexercise hypotension (PEH) is not known. We investigated the immediate blood pressure (BP) lowering effects of exercise after RE, AE, and CE sessions among healthy subjects. Twenty-one men (20.7 ± 0.7 years) performed 4 experimental sessions each in a within-subject design: control (CTL-seated rest for 60 minutes), RE (3 sets at 80% 1RM for 8 exercises, including upper and lower limbs), AE (7-minutes warm-up followed by 50 minutes of cycle ergometer exercise at 65% VO?peak and 3-minute cooldown), and CE (2 sets at 80% 1RM for 6 exercises among those which composed the RE session, plus 20 minutes of cycle ergometer exercise at 65% VO?peak, 7-minute warm-up and 3-minute cooldown, exactly in this order). The total duration of each exercise session was approximately 60 minutes. Systolic blood pressure (SBP) and diastolic blood pressure (DBP) were assessed by ambulatory monitoring at rest (20 minutes) and every 10 minutes after the exercise during 120 minutes while in the laboratory. The duration of the decrease in SBP was longer after AE and CE (120 minutes) compared to RE (80 minutes); and for DBP after AE (50 minutes) compared to CE (40 minutes) and RE (20 minutes) (p < 0.05). The magnitude of the decrease in SBP and DBP was similar after all exercise sessions and significantly different from CTL (p < 0.05) (SBP: RE = 4.1 ± 2.0 mm Hg, AE = 6.3 ± 1.3 mm Hg, CE = 5.1 ± 2.2 mm Hg; DBP: RE = 1.8 ± 1.1 mm Hg, AE = 1.8 ± 1.0 mm Hg, CE = 1.6 ± 0.6 mm Hg). It was concluded that exercise sessions combining aerobic and resistance activities are as effective as AE sessions and more effective than RE sessions to promote PEH.     

Effects of resistance training intensity, volume, and session format on the postexercise hypotensive response

The effect of resistance exercise (RE) on the postexercise systolic and diastolic blood pressure (SBP and DBP) response in young men was investigated. Group 1 (G1) and group 2 (G2) performed three 6 repetition maximum (6RM) sets in a set repetition format for 5 and 6 exercises, respectively. G1 and G2 also performed a circuit and set repetition format session, respectively, using 50% of the 6RM for 3 sets of 12 repetitions (12-repetition protocol). SBP and DBP were determined before and up to 60 minutes postexercise. G1's postexercise SBP demonstrated a significant decrease from its preexercise SBP, lasting 50 minutes after both RE sessions. G2's postexercise SBP demonstrated a significant difference from its preexercise SBP after the 6RM and 12-repetition protocol, lasting 60 and 40 minutes, respectively. The only significant difference in the DBP from rest was at 10 minutes postexercise for G2 after the 12-repetition-per-set protocol. In summary, results indicate that RE intensity affects the duration, but not the magnitude, of the postexercise hypotensive response.     

Concurrent resistance and aerobic exercise stimulates both myofibrillar and mitochondrial protein synthesis in sedentary middle-aged men

We determined myofibrillar and mitochondrial protein fractional synthesis rates (FSR), intramuscular signaling protein phosphorylation, and mRNA expression responses after isolated bouts of resistance exercise (RE), aerobic exercise (AE), or in combination [termed concurrent exercise (CE)] in sedentary middle-aged men. Eight subjects (age = 53.3 ± 1.8 yr; body mass index = 29.4 ± 1.4 kg·m(2)) randomly completed 8 × 8 leg extension repetitions at 70% of one repetition-maximum, 40 min of cycling at 55% peak aerobic power output (AE), or (consecutively) 50% of the RE and AE trials (CE). Biopsies were obtained (during a primed, constant infusion of l-[ring-(13)C(6)]phenylalanine) while fasted, and at 1 and 4 h following postexercise ingestion of 20 g of protein. All trials increased mitochondrial FSR above fasted rates (RE = 1.3-fold; AE = 1.5; CE = 1.4; P < 0.05), although only CE (2.2) and RE (1.8) increased myofibrillar FSR (P < 0.05). At 1 h postexercise, phosphorylation of Akt on Ser(473) (CE = 7.7; RE = 4.6) and Thr(308) (CE = 4.4; RE = 2.9), and PRAS40 on Thr(246) (CE = 3.8; AE = 2.5) increased (P < 0.05), with CE greater than AE for Akt Ser(473)-Thr(308) and greater than RE for PRAS40 (P < 0.05). Despite increased phosphorylation of Akt-PRAS40, phosphorylation of mammalian target of rapamycin (Ser(2448)) remained unchanged (P > 0.05), while rpS6 (Ser(235/236)) increased only in RE (10.4) (P < 0.05). CE and AE both resulted in increased peroxisome proliferator receptor-γ coactivator 1-α (PGC1α) expression at 1 h (CE = 2.9; AE = 2.8; P < 0.05) and 4 h (CE = 2.6; AE = 2.4) and PGC1β expression at 4 h (CE = 2.1; AE = 2.6; P < 0.05). These data suggest that CE-induced acute stimulation of myofibrillar and mitochondrial FSR, protein signaling, and mRNA expression are equivalent to either isolate mode (RE or AE). These results occurred without an interference effect on muscle protein subfractional synthesis rates, protein signaling, or mRNA expression.     

Concurrent aerobic exercise interferes with the satellite cell response to acute resistance exercise

The addition of aerobic exercise (AE) to a resistance exercise (RE) program (concurrent exercise, CE) can interfere with maximum muscle fiber growth achieved with RE. Further, CE appears to markedly affect the growth of myosin heavy chain (MHC) I, but not MHC IIa fibers. The mechanism responsible for this "interference" is unclear. Satellite cell (SC) responsiveness to exercise appears to influence muscle adaptation but has not yet been examined following acute concurrent exercise. Thus, we assessed the fiber-type-specific SC response to RE, AE, and CE exercise. Eight college-aged males completed the following two exercise trials: the RE trial, which consisted of unilateral leg extensions and presses (4 sets ≥ 10 repetitions: 75% 1 repetition maximum, RM); and the AE/CE trial, which included an identical RE protocol with the opposite leg, immediately followed by subjects cycling for 90 min (60% W(max)). Muscle biopsies were obtained from the vastus lateralis before and 4 days after each session. Samples were cross-sectioned, stained with antibodies against NCAM, Ki-67, and MHC I, counterstained with DAPI, and analyzed for SC density (SC per fiber), SC activation, and fiber type. SC density increased to a greater extent following RE (38 ± 10%), compared with CE (-6 ± 8%). Similarly, MHC I muscle fiber SC density displayed a greater increase following RE (46 ± 14%), compared with AE (-7 ± 17%) and CE (-8 ± 8%). Our data indicate that the SC response to RE is blunted when immediately followed by AE, at least in MHC I muscle fibers, and possibly MHC II fibers. This suggests that the physiological environment evoked by AE might attenuate the eventual addition of myonuclei important for maximum muscle fiber growth and consequent force-producing capacity.     

Plasma and salivary steroid hormone responses of men to high-intensity cycling and resistance exercise

Hormonal responses to exercise could be used as a marker of overreaching. A short exercise protocol that induces robust hormonal elevations in a normal trained state should be able to highlight hormonal changes during overreaching. This study compared plasma and salivary cortisol and testosterone responses to 4 exercise trials; these were (a) continuous cycle to fatigue at 75% peak power output (Wmax) (FAT); (b) 30-minute cycle alternating 1-minute 60% and 1 minute 90% Wmax (60/90); (c) 30-minute cycle alternating 1-minute 55% and 4-minute 80% Wmax (55/80); and (d) Squatting 8 sets of 10 repetitions at 10 repetition maximum (RESIST). Blood and saliva samples were collected pre-exercise and at 0, 10, 20, 30, 40, 50, and 60 minute postexercise. Pre- to postexercise plasma cortisol increased in all exercise trials, except 60/90. Increases in 55/80 remained above pre-exercise levels for the entire postexercise period. Salivary cortisol increased from pre- to postexercise in FAT and 55/80 trials only. Once elevated after 55/80, it remained so for the postexercise period. Plasma testosterone increased from pre- to postexercise in all trials except 55/80. Saliva testosterone increased from pre- to postexercise in all trials with the longest elevation occurring after 55/80. Area under the curve analysis indicated that the exercise response of salivary hormones was greater in all cycle trials (cortisol) and in the 60/90 and 55/80 trials (testosterone) compared with the other trials. This study indicates that the 55/80 cycle protocol induces a prolonged salivary and plasma cortisol and salivary testosterone response compared with the other trials and so may be a useful diagnostic tool of overreaching.     

Acute exercise reduces the response to colon distension in T(5) spinal rats

Individuals with spinal cord injuries above thoracic level 6 (T(6)) experience life-threatening bouts of hypertension, termed autonomic dysreflexia (AD). AD is mediated by peripheral alpha-adrenergic receptor supersensitivity as well as a reorganization of spinal pathways controlling sympathetic preganglionic neurons. A single bout of dynamic exercise may be a safe therapeutic approach to reduce the severity of AD because mild-to-moderate dynamic exercise reduces postexercise alpha-adrenergic receptor responsiveness, lowers postexercise sympathetic nerve activity, and reduces the postexercise response to stress. Therefore, this study was designed to test the hypothesis that mild-to-moderate dynamic exercise attenuates the postexercise response to colon distension (mechanism to elicit AD). To test this hypothesis, six male Wistar rats (406 +/- 23 g), 5 wk post-T(5) spinal cord transection, were instrumented with an arterial catheter. After recovery, the response to graded colon distension (10, 30, 50, and 80 mmHg, in random order) was determined before and after a single bout of mild-to-moderate dynamic exercise (9-12 m/min, 0% grade for 40 min). After exercise, the pressor response to graded colon distension was significantly attenuated (preexercise change: 2 +/- 1, 9 +/- 1, 14 +/- 1, and 24 +/- 2 vs. postexercise change: 2 +/- 1, 2 +/- 1, 9 +/- 1, and 12 +/- 3 mmHg). Thus acute exercise is a safe, therapeutic approach to reduce the severity of AD in paraplegic subjects.     

Evidence for sympatholysis at the onset of forearm exercise.

The effect of augmented sympathetic outflow on forearm vascular conductance after single handgrip contractions of graded intensity was examined to determine whether sympatholysis occurs early in exercise (n = 7). While supine, subjects performed contractions that were 1 s in duration and 15, 30, and 60% of maximal voluntary contraction (MVC) in intensity. The contractions were repeated during control and lower body negative pressure (LBNP) (-40 mmHg) sessions. Forearm blood flow (FBF; Doppler ultrasound) and mean arterial pressure were measured continuously for 30 s before and 60 s after the single contractions. Vascular conductance (VC) was calculated. Total postcontraction blood flow increased in an exercise intensity-dependent manner. Compared with control, LBNP caused a reduction in baseline and postexercise FBF (P < 0.05), VC (P < 0.01), as well as total excess flow (P < 0.01). Specifically, during LBNP, baseline FBF and VC were reduced by 29 and 34% of control, respectively (P < 0.05). After the 15% MVC contraction, peak VC during LBNP was reduced by a magnitude similar to that during baseline (i.e., ~30%), but it was only reduced by 15% during both the 30 and 60% MVC trials (P < 0.01). It was concluded that the stimuli for exercise hyperemia during moderate and heavy, but not mild, handgrip exercise intensities, diminish the vasoconstrictor effects of LBNP. Furthermore, these data demonstrate that this sympatholysis occurs early in exercise.     

Effect of acute high-intensity interval exercise on postexercise biventricular function in mild heart failure

We studied the acute effect of high-intensity interval exercise on biventricular function using cardiac magnetic resonance imaging in nine patients [age: 49 ± 16 yr; left ventricular (LV) ejection fraction (EF): 35.8 ± 7.2%] with nonischemic mild heart failure (HF). We hypothesized that a significant impairment in the immediate postexercise end-systolic volume (ESV) and end-diastolic volume (EDV) would contribute to a reduction in EF. We found that immediately following acute high-intensity interval exercise, LV ESV decreased by 6% and LV systolic annular velocity increased by 21% (both P < 0.05). Thirty minutes following exercise (+30 min), there was an absolute increase in LV EF of 2.4% (P < 0.05). Measures of preload, left atrial volume and LV EDV, were reduced immediately following exercise. Similar responses were observed for right ventricular volumes. Early filling velocity, filling rate, and diastolic annular velocity remained unchanged, while LV untwisting rate increased 24% immediately following exercise (P < 0.05) and remained 18% above baseline at +30 min (P < 0.05). The major novel findings of this investigation are 1) that acute high-intensity interval exercise decreases the immediate postexercise LV ESV and increases LV EF at +30 min in patients with mild HF, and this is associated with a reduction in LV afterload and maintenance of contractility, and 2) that despite a reduction in left atrial volume and LV EDV immediately postexercise, diastolic function is preserved and may be modulated by enhanced LV peak untwisting rate. Acute high-intensity interval exercise does not impair postexercise biventricular function in patients with nonischemic mild HF.     

Human soleus single muscle fiber function with exercise or nutrition countermeasures during 60 days of bed rest

The soleus muscle has been consistently shown to atrophy more than other leg muscles during unloading and is difficult to protect using various exercise countermeasure paradigms. However, the efficacy of aerobic exercise, a known stimulus for oxidative adaptations, has not been tested in combination with resistance exercise (RE), a known hypertrophic stimulus. We hypothesized that a concurrent exercise program (AE + RE) would preserve soleus fiber myosin heavy chain (MHC) I size and function during 60 days of bed rest. A secondary objective was to test the hypothesis that a leucine-enriched high protein diet would partially protect soleus single fiber characteristics. Soleus muscle biopsies were obtained before and after bed rest from a control (BR; n = 7), nutrition (BRN; n = 8), and exercise (BRE; n = 6) group. Single muscle fiber diameter (Dia), peak force (Po), contractile velocity, and power were studied. BR decreased (P < 0.05) MHC I Dia (-14%), Po (-38%), and power (-39%) with no change in contractile velocity. Changes in MHC I size (-13%) and contractile function (approximately 30%) from BRN were similar to BR. BRE decreased (P < 0.05) MHC I Dia (-13%) and Po (-23%), while contractile velocity increased (P < 0.05) 26% and maintained power. These soleus muscle data show 1) the AE + RE exercise program maintained MHC I power but not size and strength, and 2) the nutrition countermeasure did not benefit single fiber size and contractile function. The divergent response in size and functional MHC I soleus properties with the concurrent exercise program was a unique finding further highlighting the challenges of protecting the unloaded soleus.     

Effects of exercise and food restriction on rat skeletal muscles.

Studies were undertaken to compare the effects of exercise and food restriction on body weight (BW), muscle weight (MW), muscle fiber size, and proportion of muscle fiber types. 20 male Fischer 344 rats were randomly assigned to four equal groups: ad libitum-fed control (AC), ad libitum-fed exercise (AE), food restricted control (RC) and food restricted exercise (RE). From 6 weeks of age, RC and RE rats received 60% of the daily food intake of AC and AE rats, respectively. At 7 months of age, AE and RE rats began 40-50 min of daily treadmill exercise. Running speed increased from 1.2 to 1.6 miles/hour and the grade increased to 15% during the first 2 weeks of training. After 10 weeks of training, rats were weighed, sacrificed, and the soleus (SOL), plantaris (PLN) and extensor digitorum longus (EDL) muscles were removed at in situ rest length, weighed, and quick-frozen. Standard histochemical assays were performed, and muscle fiber cross-sectional area was determined planimetrically. Training had little effect on MW or BW, but food restriction greatly reduced BW. This resulted in greater MW/BW ratio in RC and RE than AC and AE rats, respectively. Exercise also increased SOL muscle fiber area in ad libitum-fed but not food restricted rats resulting in smaller fibers in SOL of RE than AE. No changes in percentage of SOL fiber types occurred with food restriction or exercise. In PLN, the percentage of fast-twitch oxidative fibers of AE and RE was greater than in AC and RC, but there was no effect of food restriction or exercise on fiber area.(ABSTRACT TRUNCATED AT 250 WORDS)     

Effect of resistance exercise on postprandial lipemia.

The purpose of this study was to examine the effect of resistance exercise on postprandial lipemia. Fourteen young men and women participated in each of three treatments: 1) control (Con), 2) resistance exercise (RE), and 3) aerobic exercise (AE) estimated to have an energy expenditure (EE) equal that for RE. Each trial consisted of performing a treatment on day 1 and ingesting a fat-tolerance test meal 16 h later (day 2). Resting metabolic rate and fat oxidation were measured at baseline and at 3 and 6 h postprandial on day 2. Blood was collected at baseline and at 0.5, 1, 2, 3, 4, 5, and 6 h after meal ingestion. RE and AE were similar in EE [1.7 +/- 0.1 vs. 1.6 +/- 0.1 (SE) MJ, respectively], as measured by using the Cosmed K4b(2). Baseline triglycerides (TG) were significantly lower after RE than after Con (19%) and AE (21%). Furthermore, the area under the postprandial response curve for TG, adjusted for baseline differences, was significantly lower after RE than after Con (14%) and AE (18%). Resting fat oxidation was significantly greater after RE than after Con (21%) and AE (28%). These results indicate that resistance exercise lowers baseline and postprandial TG, and increases resting fat oxidation, 16 h after exercise.     

H2-receptor-mediated vasodilation contributes to postexercise hypotension.

The early (approximately 30 min) postexercise hypotension response after a session of aerobic exercise is due in part to H1-receptor-mediated vasodilation. The purpose of this study was to determine the potential contribution of H2-receptor-mediated vasodilation to postexercise hypotension. We studied 10 healthy normotensive men and women (ages 23.7 +/- 3.4 yr) before and through 90 min after a 60-min bout of cycling at 60% peak O2 uptake on randomized control and H2-receptor antagonist days (300 mg oral ranitidine). Arterial pressure (automated auscultation), cardiac output (acetylene washin) and femoral blood flow (Doppler ultrasound) were measured. Vascular conductance was calculated as flow/mean arterial pressure. Sixty minutes postexercise on the control day, femoral (delta62.3 +/- 15.6%, where Delta is change; P < 0.01) and systemic (delta13.8 +/- 5.3%; P = 0.01) vascular conductances were increased, whereas mean arterial pressure was reduced (Delta-6.7 +/- 1.1 mmHg; P < 0.01). Conversely, 60 min postexercise with ranitidine, femoral (delta9.4 +/- 9.2%; P = 0.34) and systemic (delta-2.8 +/- 4.8%; P = 0.35) vascular conductances were not elevated and mean arterial pressure was not reduced (delta-2.2 +/- 1.3 mmHg; P = 0.12). Furthermore, postexercise femoral and systemic vascular conductances were lower (P < 0.05) and mean arterial pressure was higher (P = 0.01) on the ranitidine day compared with control. Ingestion of ranitidine markedly reduces vasodilation after exercise and blunts postexercise hypotension, suggesting H2-receptor-mediated vasodilation contributes to postexercise hypotension.     

Exercise increases serum Hsp72 in humans

Recent evidence suggests that heat shock proteins (Hsps) may have an important systemic role as a signal to activate the immune system. Since acute exercise is known to induce Hsp72 (the inducible form of the 70-kDa family of Hsp) in a variety of tissues including contracting skeletal muscle, we hypothesized that such exercise would result in the release of Hsp72 from stressed cells into the blood. Six humans (5 males, 1 female) ran on a treadmill for 60 minutes at a workload corresponding to 70% of their peak oxygen consumption. Blood was sampled from a forearm vein at rest (R), 30 minutes during exercise, immediately postexercise (60 minutes), and 2, 8, and 24 hours after exercise. These samples were analyzed for serum Hsp72 protein. In addition, plasma creatine kinase (CK) was measured at these time points as a crude marker of muscle damage. With the exception of the sample collected at 30 minutes, muscle biopsies (n = 5 males) were also obtained from the vastus lateralis at the time of blood sampling and analyzed for Hsp72 gene and protein expression. Serum Hsp72 protein increased from rest, both during and after exercise (0.13 0.10 vs 0.87+/-0.24 and 1.02+/-0.41 ng/mL at rest, 30 and 60 minutes, respectively, P < 0.05, mean SE). In addition, plasma CK was elevated (P < 0.05) 8 hours postexercise. Skeletal muscle Hsp72 mRNA expression increased 6.5-fold (P < 0.05) from rest 2 hours postexercise, and although there was a tendency for Hsp72 protein expression to be elevated 2 and 8 hours following exercise compared with rest, results were not statistically significant. The increase in serum Hsp72 preceded any increase in Hsp72 gene or protein expression in contracting muscle, suggesting that Hsp72 was released from other tissues or organs. This study is the first to demonstrate that acute exercise can increase Hsp72 in the peripheral circulation, suggesting that during stress these proteins may indeed have a systemic role.     

Arterial distensibility: acute changes following dynamic exercise in normal subjects

The time course of acute changes in large artery distensibility immediately and for 60 min following maximum treadmill exercise in normal subjects was characterized by simultaneously measuring upper and lower limb pulse wave velocity (PWV). A new oscillometric technique was used, which has proven to be sensitive to changes in distensibility induced by acute changes in vascular tone independently of blood pressure. The observed changes in PWV are attributable to changes in vascular tone corresponding to recovery from a systemic net constrictor response and a local net dilator response to exercise with persisting postexercise vasodilatation. They are inadequately explained by associated changes in blood pressure and cannot be attributed to changes in heart rate or viscosity. Modeled as a system of n coupled linear differential equations, the minimum (and adequate) order required to reproduce these patterns was n = 1 for the upper and n = 2 for the exercising lower limb. The economy of the solution suggests entrainment among the multiple interactive mechanisms governing vasomotor control.     

Salivary testosterone and cortisol responses in professional rugby players after four resistance exercise protocols

The acute response of free salivary testosterone (T) and cortisol (C) concentrations to four resistance exercise (RE) protocols in 23 elite men rugby players was investigated. We hypothesized that hormonal responses would differ among individuals after four distinct RE protocols: four sets of 10 repetitions (reps) at 70% of 1 repetition maximum (1RM) with 2 minutes' rest between sets (4 x 10-70%); three sets of five reps at 85% 1RM with 3 minutes' rest (3 x 5-85%); five sets of 15 reps at 55% 1RM with 1 minute's rest (5 x 15-55%); and three sets of five reps at 40% 1RM with 3 minutes' rest (3 x 5-40%). Each athlete completed each of the four RE protocols in a random order on separate days. T and C concentrations were measured before exercise (PRE), immediately after exercise (POST), and 30 minutes post exercise (30 POST). Each protocol consisted of four exercises: bench press, leg press, seated row, and squats. Pooled T data did not change as a result of RE, whereas C declined significantly. Individual athletes differed in their T response to each of the protocols, a difference that was masked when examining the pooled group data. When individual data were retrospectively tabulated according to the protocol in which each athlete showed the highest T response, a significant protocol-dependent T increase for all individuals was revealed. Therefore, RE induced significant individual, protocol-dependent hormonal changes lasting up to 30 minutes after exercise. These individual responses may have important ramifications for modulating adaptation to RE and could explain the variability often observed in studies of hormonal response to RE.     

Effect of systemic nitric oxide synthase inhibition on postexercise hypotension in humans.

An acute bout of aerobic exercise results in a reduced blood pressure that lasts several hours. Animal studies suggest this response is mediated by increased production of nitric oxide. We tested the extent to which systemic nitric oxide synthase inhibition [N(G)-monomethyl-L-arginine (L-NMMA)] can reverse the drop in blood pressure that occurs after exercise in humans. Eight healthy subjects underwent parallel experiments on 2 separate days. The order of the experiments was randomized between sham (60 min of seated upright rest) and exercise (60 min of upright cycling at 60% peak aerobic capacity). After both sham and exercise, subjects received, in sequence, systemic alpha-adrenergic blockade (phentolamine) and L-NMMA. Phentolamine was given first to isolate the contribution of nitric oxide to postexercise hypotension by preventing reflex changes in sympathetic tone that result from systemic nitric oxide synthase inhibition and to control for alterations in resting sympathetic activity after exercise. During each condition, systemic and regional hemodynamics were measured. Throughout the study, arterial pressure and vascular resistances remained lower postexercise vs. postsham despite nitric oxide synthase inhibition (e.g., mean arterial pressure after L-NMMA was 108.0+/-2.4 mmHg postsham vs. 102.1+/-3.3 mmHg postexercise; P<0.05). Thus it does not appear that postexercise hypotension is dependent on increased production of nitric oxide in humans.     

Active intervals between sets of resistance exercises potentiate the magnitude of postexercise hypotension in elderly hypertensive women

Active and passive intervals (AI, PI) between exercise series promote different hemodynamic responses; however, the impact of these intervals on the blood pressure response has not yet been investigated. The objective of this study was to compare the impact of AIs and PIs during resistance exercises with the magnitude of postexercise hypotension (PEH). Elderly hypertensive women (n = 21, 61.2 ± 2 years of age) completed 4 sessions for upper or lower limbs with AI or PI (3 sets, 15 repetitions, 60% load of 15 repetition maximum (RM), and an interval of 90 seconds between sets). Blood pressure was measured 10 minutes before and at 10, 20, 30, 40, and 50 minutes after the exercise sessions. The heart rate at the end of each AI was always significantly higher than that after the PI, but the perceived exertion as measured by the Perceived Exertion Scale (OMNI-RPE) was similar to that of PI exercise protocols. In the lower limb exercises, AI resulted in significantly and consistently higher PEH than in exercises with PI for both systolic (from 20 minutes postexercise) and diastolic (from 10 minutes postexercise) pressures. The upper limb exercises promoted much more discrete PEH in relation to the lower limb exercises, given that the AI promoted significantly higher PEH relative to the PI protocols, but only for systolic PEH and only from 30 minutes postexercise. This is the first time that AIs between sets in a session of resistance exercises have been shown to be a highly effective methodological strategy to increase PEH in elderly hypertensive women.     

Catecholamines, growth hormone, cortisol, insulin, and sex hormones in anaerobic and aerobic exercise

Seventeen male physical education students performed three types of treadmill exercise: (1) progressive exercise to exhaustion, (2) prolonged exercise of 50 min duration at the anaerobic threshold of 4 mmol . l-1 blood lactate (AE), (3) a single bout of short-term high-intensity exercise at 156% of maximal exercise capacity in the progressive test, leading to exhaustion within 1.5 min (ANE). Immediately before and after ANE and before, during, and after AE adrenaline, noradrenaline, growth hormone, cortisol, insulin, testosterone, and oestradiol were determined in venous blood, and glucose and lactate were determined in arterialized blood from the earlobe. Adrenaline and noradrenaline increased 15 fold during ANE and 3--4 fold and 6--9 fold respectively during AE. The adrenaline/noradrenaline ratio was 1 : 3 during ANE and 1 : 10 during AE. Cortisol increased by 35% in ANE (12% of which appeared in the postexercise period) and 54% in AE. Insulin increased during ANE but decreased during AE. Testosterone and oestradiol increased by 14% and 16% during ANE and by 22% and 28% during AE. The results point to a markedly higher emotional stress and higher sympatho-adrenal activity in anaerobic exercise. Growth hormone and cortisol appear to be the more affected by intense prolonged exercise. Taking plasma volume changes and changes of metabolic clearance rates into consideration, neither of the exercise tests appeared to affect secretion of testosterone and oestradiol.     

Antioxidant status and oxidative stress at rest and in response to acute exercise in judokas and sedentary men

It is well recognized that acute strenuous exercise is accompanied by an increase in free-radical production and subsequent oxidative stress, in addition to changes in blood antioxidant status. Chronic exercise provides protection against exercise-induced oxidative stress by upregulating endogenous antioxidant defense systems. Little is known regarding the protective effect afforded by judo exercise. Therefore, we determined antioxidant and oxidative stress biomarkers at rest and in response to acute exercise in 10 competitive judokas and 10 sedentary subjects after mixed exercise (anaerobic followed by aerobic). The subjects performed a Wingate test, followed by 30 minutes of aerobic exercise performed at 60% of maximal aerobic power. Blood samples were taken, by an intravenous catheter, at rest (R), immediately after the physical exercise (P0), and at 5 (P5), 10 (P10), and 20 (P20) minutes postexercise. The measured parameters included the activity of the antioxidant enzymes superoxide dismutase, glutathione peroxidase, and glutathione reductase, in addition to α-tocopherol, and total antioxidant status. Malondialdehyde was measured as a representation of lipid peroxidation. At rest, the judokas had higher values for all antioxidant and oxidative stress markers as compared to the sedentary subjects (p < 0.05). Plasma concentrations of all parameters except for α-tocopherol increased significantly above resting values for both the judokas and sedentary subjects (p < 0.05) and remained elevated at 20 minutes postexercise. A significant postexercise decrease was observed for α-tocopherol (p < 0.05) at P20 for judokas and at P5 for sedentary subjects. These data indicate that competitive judo athletes have higher endogenous antioxidant protection compared to sedentary subjects. However, both groups of subjects experience an increase in exercise-induced oxidative stress that is not different.     

Effects of resistance training on selected indexes of immune function in elderly women.

Women aged 67-84 yr were randomly assigned to either resistance exercise (RE, n = 15) or control group (C, n = 14). RE group completed 10 wk of resistance training, whereas C group maintained normal activity. Blood samples were obtained from the RE group (at the same time points as for resting C) at rest, immediately after resistance exercise, and 2 h after exercise before (week 0) and after (week 10) training. Mononuclear cell (CD3+, CD3+CD4+, CD3+CD8+, CD19+, and CD3-CD16+CD56+) number, lymphocyte proliferative (LP) response to mitogen, natural cell-mediated cytotoxicity (NCMC), and serum cortisol levels were determined. Strength increased significantly in RE subjects (%change 8-repetition maximum = 148%). No significant group, exercise time, or training effects were found for CD3+, CD3+CD4+, or CD3+CD8+ cells, but there was a significant exercise time effect for CD3-CD16+CD56+ cells. LP response was not different between groups, across exercise time, or after training. NCMC was increased immediately after exercise for RE subjects at week 0 and for RE and C groups at week 10. The week 0 and week 10 NCMC values were above baseline for both RE and C groups 2 h after exercise. In conclusion, acute resistance exercise did not result in postexercise suppression of NCMC or LP, and 10 wk of resistance training did not influence resting immune measures in women aged 67-84 yr.