The aging process causes many changes in muscle strength, and analysis of explosive force from handgrip strength seems to be useful and promising in studying the aging musculoskeletal system. Therefore, the purpose of this study was to investigate if explosive force parameters [rate of force development (RFD) and contractile impulse (CI) over the time interval of 0-200 ms from the onset of contraction] during handgrip efforts decline differently than maximum handgrip strength with increasing age. Twenty healthy young women (20-27 years) and 65 healthy elderly women, assigned into three age groups (50-64, 65-74, and 75-86 years), participated in this study. All participants performed two maximal grip attempts. Handgrip data were recorded as force-time curves, peak force, and explosive force parameters. Our results revealed that peak force decreased significantly (p < 0.05) for those who are 65 years old, while explosive force parameters decreased significantly (p < 0.05) for those aged 50 years. These data indicate that the decline in explosive grip force-generating capacity may begin earlier (i.e., for those aged 50 years old) than peak force during the aging process. Our findings suggest that the aging process reduces the explosive grip force-generating capacity before affecting peak force.

We have previously demonstrated that acute third ventricle injections of both Pb 2+ and Cd 2+ impair the dipsogenic response elicited by three different situations: dehydration and central cholinergic or angiotensinergic stimulation. ß-Adrenergic activation is part of the multifactorial integrated systems operating in drinking behavior control in the central nervous system. In the present study acute third ventricle injections of Pb 2+ (3, 30 and 300 pmol/rat) or Cd 2+ (0.3, 3 and 30 pmol/ rat) blocked the dipsogenic response induced by third ventricle injections of isoproterenol (ISO; 160 nmol/rat) in a dose-dependent manner. Normohydrated animals receiving ISO + NaAc (sodium acetate) or saline (controls) displayed a high water intake after 120 min (ISO + saline = 5.78 ± 0.54 ml/100 g; ISO + NaAc = 6.00 ± 0.6 ml/100 g). After the same period, animals receiving ISO but pretreated with PbAc at the highest dose employed (300 pmol/rat) drank 0.78 ± 0.23 ml/100 g while those receiving ISO and pretreated with the highest dose of CdCl 2 (30 pmol/rat) presented a water intake of 0.7 ± 0.30 ml/100 g. Third ventricle injections of CdCl 2 (3 nmol/rat) or PbAc (3 nmol/rat) did not modify food intake in rats deprived of food for 24 h. Thus, general central nervous system depression explaining the antidipsogenic action of the metals can be safely excluded. It is concluded that both Pb 2+ and Cd 2+ inhibit water intake induced by central ß-adrenergic stimulation. Received April 11, 1996 Accepted December 17, 1996 Key wordsHuman exposure to heavy metals such as cadmium (Cd 2+ ) and lead (Pb 2+ ) may bring about several adverse reactions. Neurotoxicity induced by heavy metals is well-documented in humans and experimental animals (1). Both Cd 2+ and Pb 2+ reach the central nervous system either by crossing the bloodbrain barrier or via retrograde axonal transport (2,3).The presence of heavy metals in the central nervous system disrupts the functional integrity of several neurotransmitter pathways. Many independent reports confirm alterations in brain monoaminergic receptors and uptake after Pb 2+ (4) and Cd 2+ (5,6) intoxication.We have recently used a new approach to study the acute actions of heavy metals on

We investigated differences in sex responses in serum CK activity and renal function measured by glomerular filtration rate (GFR) after an exercise session. Twenty-two healthy and trained volunteers (11 males and 11 females) performed 17 resistance exercises with 3 × 12 repetitions in a circuit training fashion. Subjects provided blood samples prior to exercise session, and at 24, 48, and 72 h following exercise sessions for creatine kinase and creatinine. Twenty-four-hour urine samples were collected before and 72 h after the exercise. Estimate (e) GFR was obtained by using the Chronic Kidney Disease Epidemiology Collaboration equation adjusted for males and females. After the exercise session, males showed greater serum CK activity than females (p < 0.02), serum creatinine increased 31.3 % for males and 29.8 % for females, and urinary creatinine decreased on average 5.4 % for males and 0.6 % for females, with no significant differences (p > 0.05) between sex for serum and urinary creatinine. eGFR decreased significantly for males (~10 %) and females (~8 %), but also without a difference between the sexes (p > 0.05). The correlation between CK and eGFR was significant for males (r = -0.794; p = 0.003), and females (r = -0.8875; p < 0.001). A significant negative correlation between CK activity and the eGFR indice of renal function in both males and females was observed. Additionally, the renal function compromise was similar for both sexes, despite males presenting greater exercise-induced skeletal muscle damage when compared to females.

We have demonstrated that central administration of zinc in minute amounts induces a significant antidipsogenic action in dehydrated rats as well as in rats under central cholinergic and angiotensinergic stimulation. Here we show that acute third ventricle injections of zinc also block water intake induced by central ß-adrenergic stimulation in Wistar rats (190-250 g). Central inhibition of opioid pathways by naloxone reverses the zinc-induced antidipsogenic effect in dehydrated rats. After 120 min, rats receiving third ventricle injections of isoproterenol (160 nmol/rat) exhibited a significant increase in water intake (5.78 ± 0.54 ml/100 g body weight) compared to saline-treated controls (0.15 ± 0.07 ml/100 g body weight). Pretreatment with zinc (3.0, 30.0 and 300.0 pmol/rat, 45 min before isoproterenol injection) blocked water intake in a dose-dependent way. At the highest dose employed a complete blockade was demonstrable (0.54 ± 0.2 ml/100 g body weight). After 120 min, control (NaAc-treated) dehydrated rats, as expected, exhibited a high water intake (7.36 ± 0.39 ml/100 g body weight). Central administration of zinc blocked this response (2.5 ± 0.77 ml/100 g body weight). Naloxone pretreatment (82.5 nmol/ rat, 30 min before zinc administration) reverted the water intake to the high levels observed in zinc-free dehydrated animals (7.04 ± 0.56 ml/ 100 g body weight). These data indicate that zinc is able to block water intake induced by central ß-adrenergic stimulation and that zincinduced blockade of water intake in dehydrated rats may be, at least in part, due to stimulation of central opioid peptides. Correspondence