Reductions in Systemic and Skeletal Muscle Blood Flow and Oxygen Delivery Limit Maximal Aerobic Capacity in Humans

Abstract

Background-A classic, unresolved physiological question is whether central cardiorespiratory and/or local skeletal muscle circulatory factors limit maximal aerobic capacity (V O 2 max) in humans. Severe heat stress drastically reduces V O 2 max, but the mechanisms have never been studied. Methods and Results-To determine the main contributing factor that limits V O 2 max with and without heat stress, we measured hemodynamics in 8 healthy males performing intense upright cycling exercise until exhaustion starting with either high or normal skin and core temperatures (ϩ10°C and ϩ1°C). Heat stress reduced V O 2 max, 2-legged V O 2 , and time to fatigue by 0.4Ϯ0.1 L/min (8%), 0.5Ϯ0.2 L/min (11%), and 2.2Ϯ0.4 minutes (28%), respectively (all PϽ0.05), despite heart rate and core temperature reaching similar peak values. However, before exhaustion in both heat stress and normal conditions, cardiac output, leg blood flow, mean arterial pressure, and systemic and leg O 2 delivery declined significantly (all 5% to 11%, PϽ0.05), yet arterial O 2 content and leg vascular conductance remained unchanged. Despite increasing leg O 2 extraction, leg V O 2 declined 5% to 6% before exhaustion in both heat stress and normal conditions, accompanied by enhanced muscle lactate accumulation and ATP and creatine phosphate hydrolysis. Conclusions-These results demonstrate that in trained humans, severe heat stress reduces V O 2 max by accelerating the declines in cardiac output and mean arterial pressure that lead to decrements in exercising muscle blood flow, O 2 delivery, and O 2 uptake. Furthermore, the impaired systemic and skeletal muscle aerobic capacity that precedes fatigue with or without heat stress is largely related to the failure of the heart to maintain cardiac output and O 2 delivery to locomotive muscle. Key Words: hemodynamics Ⅲ blood flow, regional Ⅲ cardiac output Ⅲ hemodynamics Ⅲ heat stress D uring heavy exercise, large volumes of oxygen are transported through the links of the cardiorespiratory transport system to mitochondrial cytochromes for synthesis of ATP in the electron transport chain. The fastest rate at which the body can utilize O 2 during heavy exercise is defined as the maximum rate of oxygen uptake (V O 2 max), which is an index of maximal cardiovascular function, provided pulmonary function and ambient O 2 concentration are normal. 1 The working skeletal muscle cells, which account for more than 90% of the energy spent during severe exercise, largely determine V O 2 max. 1-4 Long-standing yet unresolved debates center on whether central cardiorespiratory and/or local skeletal muscle circulatory and metabolic factors limit V O 2 max. [1][2][3][4][5][6][7] Severe heat stress has been shown to markedly suppress V O 2 max and work capacity without altering the initial rate of rise in whole-body V O 2 . 8 The mechanisms underlying the compensatory adjustments to heat stress early in exercise and the subsequent precipitated fatigue have never been investigated. During heavy exercise in normal environments, f...

Induction and decay of short-term heat acclimation

“…Heatand-exercise induced hypohydration manifests itself as hyperosmotic hypovolaemia (Nadel et al 1980), which impairs cutaneous blood flow and sweat rate, and raises heart rate, core temperature, glycogenolysis, perceived exertion and permeability of tight-membranes (Mack and Nadel 1996;Gonzalez-Alonso et al 1998;Gonzalez-Alonso et al 1999;Blatteis 2000;Gonzalez-Alonso and Calbert 2003;Maughan 2003;Watson et al 2005). The consequence is impaired exercise tolerance and performance in temperate conditions which has previously been debated (Sawka and Noakes 2007).…”

Self-paced exercise in hot and cool conditions is associated with the maintenance of %V̇o2peak within a narrow range

“…Indeed, a narrowing core-to-skin temperature gradient during exercise-heat stress increases the skin blood flow requirement for heat dissipation (5,35,36). The combination of an increase in cutaneous blood volume and a temperature-mediated rise in intrinsic heart rate decreases cardiac filling, which leads to reductions in stroke volume and maximal cardiac output when heart rate approaches maximum (6,13,15,36). During prolonged constant-load exercise to exhaustion, for example, this forces the cardiovascular system toward a functional limit at submaximal workloads (e.g., power output), ultimately reducing maximal oxygen uptake (V O 2max ) (2,24,29).…”

Point:Counterpoint: Maximal oxygen uptake is/is not limited by a central nervous system governor

“…For maximum exercise in health terminates before the onset of myocardial ischemia (22) and according to a majority of [but not all (8,16)] studies before the Q "plateaus" (7,12,30). The most effective method to prevent myocardial ischemia is to "limit" peripheral blood flow (9) (chapter 84, Figs.…”