Farr, Trevor M (2019) The effects of muscle mass, digoxin and high-intensity interval training on arterial and venous [K+], excitability and fatigue during and after intense exercise. PhD thesis, Victoria University.

Abstract

Potassium (K+) regulation during exercise is vital in preserving muscle membrane excitability, a failure of which has been linked to muscle fatigue. This thesis investigated the regulation of arterial and venous plasma K+ concentration ([K+]) during and following intense exercise and its importance for exercise performance, muscular force and excitability via three interventional studies, comparing two- versus one-legged cycling (Study 1), acute oral digoxin versus placebo intake (Study 2), and high-intensity intermittent training versus non-training control (Study 3). Study 1. The effects of different contracting muscle mass were investigated on arterial and venous plasma [K+], fatigability and muscle torque following exhaustive two- versus one- legged high-intensity intermittent cycling exercise. Eleven recreationally active adults performed two- (2L) and one-legged (1L) trials, which comprised cycling for six, 2 min repetitions at 80% V̇ O2peak, then at 90% V̇ O2peak continued to fatigue. Radial arterial (a) and antecubital venous (v) plasma [K+] ([K+]a, [K+]v, respectively) were measured prior to and during exercise bouts, and for 30 min recovery. The quadriceps maximal isometric voluntary contraction (MVC), as well as potentiated quadriceps twitch force (Qtw,pot), doublet and tetani (20 Hz) and vastus medialis (VM) and vastus lateralis (VL) M-wave (amplitude, duration and area) evoked via magnetic stimulation, were measured prior to exercise, 1 min after exercise bouts 1, 3 and 6, and up to 30 min in recovery. Plasma [K+]a increased throughout exercise (P < 0.05, time main effect), being greater in 2L than 1L (P < 0.05, treatment main effect) and with [K+]a being greater in 2L than 1L during 90% V̇ O2peak after 2 min and at fatigue, reaching 6.03 ± 0.58 vs 5.21 ± 0.52 mmol.1-1 at fatigue for 2L and 1L, respectively (P < 0.05). Plasma [K+]v increased at fatigue for 2L and 1L, reaching 5.98 ± 0.64 and 5.34 ± 0.43 mmol.1-1 respectively, but did not differ significantly between trials. The [K+]a-v difference across the inactive forearm was higher throughout exercise to fatigue (P < 0.05, time main effect) and was greater in 2L than 1L (treatment main effect, P < 0.05). Plasma [Lac-]a increased throughout exercise, reaching 7.40 ± 1.74 and 5.28 ± 1.12 mmol.1-1 at fatigue for 2L and 1L, respectively (P < 0.05), with 2L greater than 1L during recovery at 2-30 min (P < 0.05). The MVC was decreased after exercise and in recovery (P < 0.05, time main effect), falling at fatigue (P < 0.05) by 17% for 2L (rest 135 ± 59 vs. fatigue 112 ± 57 Nm) and by 26% for 1L (rest 144 ± 57 vs. fatigue 107 ± 63 Nm). Each of the evoked Qtw,pot, doublet and 20 Hz torque declined after fatigue and remained depressed at 30 min recovery (P < 0.05, time main effect), with Qtw,pot less in 1L than 2L at 30 min recovery (P < 0.05). The twitch M-wave amplitude declined throughout exercise and recovery, whilst duration was extended after fatiguing exercise, in both VM and VL (P < 0.05, time main effect), with area also reduced after fatigue only in VM (P < 0.05); there were no significant differences between 1L and 2L. In conclusion, exercise with a large contracting muscle mass augmented [K+]a, suggesting a greater K+ release from contracting muscles. The greater [K+]a-v across the forearm in 2L cycling suggests also greater K+ uptake by inactive muscle, probably via activation of muscle Na+,K+-ATPase. Nonetheless, plasma [K+] was tightly regulated during intense exercise, with only relatively small differences evident between trials, despite substantially differing contracting muscle mass. Despite elevated [K+]a, 2L was accompanied by lesser percentage declines in MVC compared to 1L exercise; whilst the M-wave characteristics give some evidence of excitability changes with fatigue, but with minimal differences between trials. Thus, the slightly greater [K+]a disturbances during cycling to fatigue with 2L than 1L exercise, were not accompanied by greater post-exercise reductions in muscle torque and changes in M-wave characteristics. Study 2. The effects of acute digoxin intake on K+ regulation, muscle performance, muscle excitability, and fatigability were investigated in ten recreationally active adults, in a randomised, crossover, double-blind, counterbalanced study design. Ten healthy adults received orally 0.50 mg digoxin or placebo 60 min prior to cycling exercise, which was 1 min at 60% V̇ O2peak and at 95% V̇ O2peak, then continued at 95% V̇ O2peak until fatigue. Radial arterial (a) [K+] ([K+]a) was measured pre-exercise, during exercise and for up to 60 min recovery. Quadriceps MVC, as well as muscle torque (Qtw,pot, doublet and 20 Hz tetani) and M-wave characteristics (amplitude, duration and area) evoked via magnetic stimulation were measured pre-exercise, 1 min following exercise and for 60 min recovery. Serum digoxin concentration at 60 min post-ingestion was 3.36 ± 0.8 nM (mean ± SD) in digoxin and less than the detectable level of 0.2 nM in placebo. Time to fatigue was 7.8% shorter during digoxin than placebo (P < 0.05). Plasma [K+]a increased during exercise and decreased early in recovery, being lower than baseline at 3-20 min recovery (P < 0.05, time main effect). During digoxin, plasma [K+]a was slightly greater than placebo (4.93 ± 0.2 vs. 4.88 ± 0.2, respectively) and the post-exercise [K+]a decline was less ( b o t h P < 0.05, treatment main effect). After exercise, the MVC torque, Qtw,pot, doublet and 20 Hz tetani (percentage pre- exercise) each decreased 1 min after fatigue and remained less than baseline at 60 min post- exercise (P < 0.05, time main effect) but did not differ between trials. Following exercise to fatigue the M-wave characteristics demonstrated variability between muscles and with time; amplitude was increased post-exercise in VL, duration increased at 60 min recovery in both VL and VM, whilst area increased at 60 min recovery in VM and 10 min post-exercise in VL (P < 0.05, treatment main effect). In VL, duration was greater with digoxin than placebo at fatigue (P < 0.05). Thus digoxin impaired cycling exercise performance to fatigue, with a slight increase in [K+]a but did not affect the fatigue-induced reductions in MVC, evoked torque or M-wave characteristics, other than a prolonged M-wave duration in VL. Hence, although plasma [K+] was increased and fatigability during cycling lessened with digoxin, it was not possible to conclude that acute digoxin treatment is linked to worsened muscle excitability. Study 3. The effects of High Intensity Interval Training (HIIT) were investigated on plasma [K+]a and [K+]v, muscle performance and muscle excitability Sixteen healthy adult participants were randomly allocated to training (HIIT, n = 8) or control (CON, n = 8). Exercise testing comprised a 2 min cycling bout at each of 60% V̇ O2peak and 80% V̇ O2peak, then followed by two 30s maximal sprints, separated by 120 s; these tests were repeated Pre and Post HIIT and CON. Radial arterial (a) and antecubital venous (v) blood samples were measured prior to and during exercise bouts, and in recovery for 60 min. Quadriceps MVC, and the potentiated quadriceps twitch force (Qtw,pot), doublet and tetani (20 Hz) and the vastus medialis (VM) and vastus lateralis (VL) M-wave (amplitude, duration area) evoked via magnetic stimulation, were measured prior to exercise, 1 min after 80% V̇ O2peak, after sprint exercise bouts, and for 60 min recovery. HIIT comprised repeated 30 s sprints during 3 sessions per week for 7 weeks. Plasma [K+]a was increased above rest during 60% and 80% V̇ O2peak exercise and returned to resting values at 2 min recovery, for both HIIT and CON (P < 0.05, time main effect). There was no trial main effect for [K+]a. For HIIT, there was a significant trial x time interaction, with lower [K+]a evident at Post compared to Pre during 80% V̇ O2peak and at 1 min recovery after the sprint bouts (P < 0.05). Plasma [K+]v increased during 60% V̇ O2peak, 80% V̇ O2peak exercise and the two sprint bouts (P < 0.05, time main effect) and was slightly above rest late in recovery (P < 0.05, time main effect); there was no trial main effect for [K+]v. There were significant trial x time interactions with higher [K+]v Post than Pre at fatigue for HIIT (P < 0.05) and 1 min recovery for CON (P < 0.05). The [K+]a-v difference across the forearm was increased with submaximal and sprint exercise for both HIIT and for CON (P < 0.05,time main effect ). Plasma [K+]a-v did not differ between trials. The peak power, total work and fatigue index were unchanged after HIIT. Sprint performance during the four 30 s sprints of the last training session after HIIT was unchanged compared to the first training session. There were decreases for all torque values with fatigue and also changes in M-wave characteristics (amplitude, duration and area). For MVC, there was no trial main effect, although MVC during HIIT was greater than CON after the first sprint bout (88 ± 9 vs. 65 ± 14% pre-exercise MVC, respectively, P < 0.05, trial x time interaction). For each of the quadriceps twitch, doublet and 20 Hz tetani torque or M-wave characteristics, there were no differences between trials. Thus, whilst HIIT improved K+ regulation with submaximal exercise and after two sprint bouts, this did not result in corresponding improvements in muscle voluntary and evoked contractile performance and muscle excitability. In conclusion, this thesis investigated the effects of differences in the active muscle mass, acute digoxin treatment and HIIT, on each of K+ regulation, muscle performance, muscle excitability and fatigue in humans. Plasma [K+]a increased during exercise then decreased early in recovery, with elevations in plasma [K+]a during 2L compared to 1L cycling, and in digoxin compared to placebo, lower [K+]a after HIIT during sub-maximal exercise and 1 min after sprint exercise. Interestingly, the MVC torque decline was less for 2L than 1L and for HIIT Post compared to Pre, whilst no difference was found between digoxin and placebo trials. The time to fatigue showed no significant difference between trials during the active muscle mass study but was 7.8% shorter for digoxin than placebo. Whilst considerable variability was evident in M- wave measures, there is evidence to suggest impaired muscle excitability after exercise. Thus, greater active muscle mass, acute digoxin and HIIT interventions that differentially affected K+ regulation during and after exercise did not show corresponding changes in muscle voluntary or evoked torque or excitability after exercise.

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