Immune and inflammation responses to a 3-day period of intensified running versus cycling

Highlight

• This study showed that a 3-day period of intensified training resulted in substantially more muscle damage, soreness, and systemic inflammation in runners compared to cyclists.

Abstract

Functional overreaching has been linked to alterations in immunity and host pathogen defense, but little is known as to whether or not running and cycling evoke different responses. This study compared inflammation, muscle damage and soreness, and innate immune function responses to a 3-day period of intensified exercise in trained long distance runners (N = 13, age 34.4 ± 2.4 year) and cyclists (N = 22, age 36.6 ± 1.7 year, P = 0.452). Upper respiratory tract infection (URTI) symptomatology was monitored for 12 weeks using the Wisconsin Upper Respiratory Symptom Survey (WURSS), and subjects from both athletic groups came to the lab during week five and exercised 2.5 h/day for 3 days in a row at 70% VO_2max. Blood samples were collected before and after the 3-day period of exercise, with recovery samples collected 1-, 14-, and 38 h-post-exercise. Samples were analyzed for muscle damage [creatine kinase (CK), myoglobin (MYO)], inflammation (CRP, IL-6, IL-8, IL-10, MCP), and innate immunity [granulocyte and monocyte phagocytosis (GR-PHAG and MO-PHAG) and oxidative burst activity (GR-OBA and MO-OBA)]. Runners compared to cyclists experienced significantly more muscle damage (CK 133% and MYO 404% higher post-3 days exercise), inflammation (CRP 87%, IL-6 256%, IL 8 61%, IL-10 32%, MCP 29%), and delayed onset of muscle soreness (DOMS, 87%). The 3-day period of exercise caused significant downturns in GR-PHAG, MO-PHAG, GR-OBA, MO-OBA by 14- and 38 h-recovery, but the pattern of change did not differ between groups. No group differences were measured for 12-week URTI severity (18.3 ± 5.6 and 16.6 ± 4.0, P = 0.803) and symptom scores (33.4 ± 12.6 and 24.7 ± 5.8, P = 0.477). These data indicate that a 3-day period of functional overreaching results in substantially more muscle damage and soreness, and systemic inflammation in runners compared to cyclists, but without group differences for 12-week URTI symptomatology and post-exercise decrements in innate immune function.

Introduction

Most athletes incorporate periodized training in their schedules, with phases of functional overreaching or short-term intensified training to enhance future performance (Meeusen et al., 2013). Single bouts of heavy exertion cause widespread perturbations in physiologic and immune biomarkers, and include transient alterations in innate immune function and elevations in stress hormones, pro-and anti-inflammatory cytokines, and reactive oxygen species (Henson et al., 2008, Nieman, 2009, Nieman et al., 2001, Suzuki et al., 2006). These data imply that periods of intensified exercise training may cause a more serious downturn in immune function and increased incidence of upper respiratory tract infection (URTI), but few well-designed studies have been conducted to verify this hypothesis (Meeusen et al., 2013). Even less is known regarding physiologic and immune responses to functional overreaching in runners compared to cyclists.

Exercise modes incorporating significant eccentric (e.g., running) compared to concentric (e.g., cycling) muscle contractions cause greater muscle damage (Proske and Allen, 2005). The general assumption is that exercise-induced muscle damage is related to alterations in innate immune function and systemic inflammation, but evidence is limited and inconsistent (Paulsen et al., 2012). Bruunsgaard et al. (1997) showed a relationship between elevated creatine kinase (CK) and IL-6 after 30 min of eccentric compared to concentric cycling. However, this has not been a consistent finding, with comparisons across studies difficult to make due to the incorporation of a wide variety of exercise challenges and inter-individual variation (Paulsen et al., 2012, Peake et al., 2005a, Peake et al., 2005b, Sugama et al., 2012, Suzuki et al., 2006, Toft et al., 2002). At the 160-km Western States Endurance Run (WSER), a strong relationship was found between CK, delayed onset of muscle soreness (DOMS), and a spectrum of systemic inflammation markers including C-reactive protein (CRP), IL-6, granulocyte colony stimulating factor (GC-SF), IL-1 receptor antagonist (IL-1ra), monocyte chemoattractant-1 (MCP-1), IL-10, and IL-8 (Nieman, 2009, Nieman et al., 2003, Nieman et al., 2005, Nieman et al., 2006, Nieman et al., 2007). During the week following the WSER, DOMS also showed modest positive correlations with many of the cytokines changes experienced during the race (Nieman, 2009). Contrary to expectations, the oxidative stress experienced by the WSER athletes was modest, with no significant correlations to cytokine, CK, and CRP changes (Nieman, 2009, Quindry et al., 2008). Multiple triggers of cytokine release during extreme exercise include elevations in stress hormones and other internal and external stress signals, and metabolic demands such as glycogen deficiency (Muñoz-Cánoves et al., 2013, Pedersen, 2012, Welc and Clanton, 2013).

In a randomized, crossover study of 10 triathletes, single 2.5-h bouts of running and cycling (∼75% VO_2max) resulted in similar innate immune responses but higher plasma IL-6 concentrations following running (Henson et al., 1999, Nieman et al., 1998a, Nieman et al., 1998b). In the current study, these data were extended by comparing muscle damage, inflammation, and innate immune biomarkers in runners and cyclists during a 3-day period of intensified training (2.5 h/day), and URTI symptomatology during a 12-week period. We hypothesized that runners compared to cyclists would experience higher muscle damage and inflammation during the 3-day functional overreaching period, with decreased innate immune function and higher overall URTI rates during 12-weeks of monitoring symptoms.