A prospective evaluation of non-interval- and interval-based exercise training progressions in rodents

2013

Self Cite

Key points• Sympathetic nervous system activity causes tonic vasoconstriction in resting and contracting skeletal muscle. Vasoactive molecules released from the active skeletal muscle and/or endothelium have been shown to inhibit sympathetic vasoconstriction, a phenomenon defined as functional sympatholysis.• A definitive mechanism responsible for functional sympatholysis has yet to be identified; however, nitric oxide (NO) appears to be involved.• It is unknown whether exercise training alters the inhibition of sympathetic vasoconstriction and NO-mediated sympatholysis in resting and contracting skeletal muscle.• The present findings demonstrate that short-term exercise training augments functional sympatholysis in a training-intensity-dependent manner through a NO-dependent mechanism. These novel findings advance our understanding of the effects of exercise training on the regulation of sympathetic vasoconstriction in resting and contracting skeletal muscle.Abstract We tested the hypothesis that short-term mild-(M) and heavy-intensity (H) exercise training would enhance sympatholysis through a nitric oxide (NO)-dependent mechanism. Sprague-Dawley rats (n = 36) were randomly assigned to sedentary (S) or to M (20 m min −1 5% gradient) or H exercise training groups (40 m min −1 5% gradient). Rats assigned to M and H groups trained on 5 days week −1 for 4 weeks, with the volume of training being matched between groups. Rats were anaesthetized and instrumented for stimulation of the lumbar sympathetic chain and the measurement of arterial blood pressure and femoral artery blood flow. The triceps surae muscle group was stimulated to contract rhythmically at 30 and 60% of maximal contractile force (MCF). The percentage change of femoral vascular conductance (%FVC) in response to sympathetic stimulation delivered at 2 and 5 Hz was determined at rest and during contraction at 30 and 60% MCF. The vascular response to sympathetic stimulation was reduced as a function of MCF in all rats (P < 0.05). At 30% MCF, the magnitude of sympatholysis (%FVC restcontraction; %FVC) was greater in H compared with M and S groups ( %FVC at 2 Hz, S, 9 ± 5; M, 11 ± 8; and H, 18 ± 7; and %FVC at 5 Hz, S, 6 ± 6; M, 12 ± 9; and H, 18 ± 7; P < 0.05) and was greater in H and M compared with S at 60% MCF ( %FVC at 2 Hz, S, 15 ± 5; M, 25 ± 3; and H, 36 ± 6; and %FVC at 5 Hz, S, 22 ± 6; M, 33 ± 9; and H, 39 ± 9; P < 0.05). Blockade of NO synthase did not alter the magnitude of sympatholysis in S during contraction at 30 or 60% MCF. In contrast, NO synthase inhibition diminished sympatholysis in H at 30% MCF and in M and H at 60% MCF (P < 0.05). The present findings indicate that short-term

Section: Methodssupporting

confidence: 77%

Short‐term exercise training enhances functional sympatholysis through a nitric oxide‐dependent mechanism

Jendzjowsky¹,

2013

Self Cite

“…This training progression allowed all rats in the exercise‐trained group to run continuously for 600 m at the prescribed speed and grade within 11 ± 2 days. This training paradigm is regularly used in our laboratory and has been shown to increase heart mass, heart mass: body mass ratio, soleus citrate synthase activity and endothelium‐dependent vasodilation (Jendzjowsky & DeLorey, , , ).…”

Section: Methodsmentioning

confidence: 99%

Exercise training augments neuronal nitric oxide synthase‐mediated inhibition of sympathetic vasoconstriction in contracting skeletal muscle of rats

Jendzjowsky

Just

2014

Self Cite

Key pointsr Sympathetic nervous system activity causes tonic vasoconstriction in resting and contracting skeletal muscle. Nitric oxide (NO) has been shown to inhibit sympathetic vasoconstriction.r NO derived from both the neuronal and endothelial isoforms of NO synthase (NOS) has been shown to contribute to the inhibition of sympathetic vasoconstriction.r Our laboratory recently demonstrated that exercise training augmented NO-dependent inhibition of sympathetic vasoconstriction. However, the NOS isoform responsible for the increase in NO-mediated inhibition of sympathetic vasoconstriction following exercise training has not been established.r The present findings demonstrate that exercise training improves neuronal NOS-mediated inhibition of sympathetic vasoconstriction in contracting skeletal muscle.Abstract We tested the hypothesis that exercise training would increase neuronal nitric oxide synthase (nNOS)-mediated inhibition of sympathetic vasoconstriction in resting and contracting skeletal muscle. Sprague-Dawley rats (n = 18) were randomized to sedentary or exercise-trained (40 m min −1 , 5°grade; 5 days week −1 for 4 weeks) groups. Following completion of sedentary behaviour or exercise training, rats were anaesthetized and instrumented with a brachial artery catheter, femoral artery flow probe and stimulating electrodes on the lumbar sympathetic chain. The percentage change of femoral vascular conductance (%FVC) in response to sympathetic chain stimulations delivered at 2 and 5 Hz was determined at rest and during triceps surae muscle contraction before (control) and after selective nNOS blockade with S-methyl-L-thiocitrulline (SMTC, 0.6 mg kg −1 , I.V.) and subsequent non-selective NOS blockade with L-NAME (5 mg kg −1 , I.V.; SMTC + L-NAME). At rest, sympathetic vasoconstrictor responsiveness was greater (P < 0.05) in exercise-trained compared to sedentary rats in control, SMTC and SMTC + L-NAME conditions. During contraction, the constrictor response was not different (P > 0.05) between exercise trained (2 Hz: −11 ± 4%FVC; 5 Hz: −21 ± 5%FVC) and sedentary rats (2 Hz: −7 ± 6%FVC; 5 Hz: −18 ± 10%FVC) in control conditions. SMTC augmented (P < 0.05) sympathetic vasoconstriction in sedentary and exercise-trained rats; however, sympathetic vasoconstrictor responsiveness was greater (P < 0.05) in exercise-trained (2 Hz: −27 ± 5%FVC; 5 Hz: −39 ± 5%FVC) compared to sedentary (2 Hz: −17 ± 6%FVC; 5 Hz: −27 ± 8%FVC) rats during selective nNOS inhibition. SMTC + L-NAME further augmented (P < 0.05) sympathetic vasoconstrictor responsiveness by a similar magnitude (P > 0.05) in exercise-trained and sedentary rats. These data demonstrate that exercise training augmented nNOS-mediated inhibition of sympathetic vasoconstriction in contracting muscle.C 2014 The Authors.

“…The total volume of ET was matched between M and H groups by having all rats run the same distance during each exercise bout. This training paradigm is routinely used in our laboratory and has been shown to increase heart mass, heart mass/body mass ratio, soleus citrate synthase activity and endothelium‐dependent vasodilation (Jendzjowsky & DeLorey, 2011, 2012, 2013).…”

Section: Methodsmentioning

confidence: 99%

Short‐term exercise training augments α₂‐adrenoreceptor‐mediated sympathetic vasoconstriction in resting and contracting skeletal muscle

Jendzjowsky¹,

2013

Self Cite

Key points• Postsynaptic α 1 -and α 2 -adrenoreceptors produce tonic vasoconstriction in resting and contracting skeletal muscle.• Muscular contraction attenuates sympathetic vasoconstriction (functional sympatholysis). The blunting of sympathetic vasoconstriction during contraction has been mechanistically linked to a reduction in postsynaptic α 1 -and α 2 -adrenoreceptor responsiveness and nitric oxide.• We recently demonstrated that exercise training augmented sympathetic vasoconstrictor responsiveness and functional sympatholysis. Whether these vascular adaptations were mediated by changes to postsynaptic adrenoreceptors was not investigated.• The present findings demonstrate that exercise training augmented α 2 -adrenoreceptormediated vasoconstriction in resting and contracting skeletal muscle.• These data indicate that exercise training alters the relative contributions of α-adrenoreceptors to sympathetic vasoconstriction in resting and contracting skeletal muscle and that the regulation of sympathetic vasoconstriction becomes more complex following exercise training.Abstract We hypothesized that exercise training (ET) would alter α 2 -adrenoreceptor-mediated sympathetic vasoconstriction. Sprague-Dawley rats (n = 30) were randomized to sedentary (S), mild-(M) or heavy-intensity (H) treadmill ET groups (5 days per week for 4 weeks). Following the ET component of the study, rats were anaesthetized, and instrumented for lumbar sympathetic chain stimulation, triceps surae muscle contraction and measurement of femoral vascular conductance (FVC). The percentage change of FVC in response to sympathetic stimulation was determined at rest and during contraction in control, α 2 blockade (yohimbine) and combined α 2 + nitric oxide (NO) synthase (NOS) blockade (N ω -nitro-L-arginine methyl ester hydrochloride, L-NAME) conditions. ET augmented (P < 0.05) sympathetic vasoconstrictor responses at rest and during contraction. Yohimbine reduced (P < 0.05) the vasoconstrictor response in ET rats at rest (M: 2 Hz: 8 ± 2%, 5 Hz: 9 ± 4%; H: 2 Hz: 14 ± 5%, 5 Hz: 11 ± 6%) and during contraction (M: 2 Hz: 9 ± 2%, 5 Hz: 9 ± 5%; H: 2 Hz: 8 ± 3%, 5 Hz: 6 ± 6%) but did not change the response in S rats. The addition of L-NAME caused a larger increase (P < 0.05) in the vasoconstrictor response in ET than in S rats at rest (2 Hz: S: 8 ± 2%, M: 15 ± 3%, H: 23 ± 7%; 5 Hz: S: 8 ± 5%, M: 15 ± 3%, H: 17 ± 5%) and during contraction (2 Hz: S: 9 ± 3%, M: 18 ± 3%, H: 22 ± 6%; 5 Hz: S: 9 ± 5%, M: 22 ± 4%, H:26 ± 9%). Sympatholysis was greater (P < 0.05) in ET than in S rats. Blockade of α 2 -adrenoreceptors and NOS reduced (P < 0.05) sympatholysis in